Grace SL, Russell KL, Reid RD, Oh P, Anand S, Rush J, Williamson K, Gupta M, Alter DA, Stewart DE; Cardiac Rehabilitation Care Continuity Through Automatic Referral Evaluation (CRCARE) Investigators. Effect of cardiac rehabilitation referral strategies on utilization rates: a prospective, controlled study. Arch Intern Med. 2011;171:235 241. doi: 10.1001/archinternmed.2010.501. 338. Eder B, Hofmann P, von Duvillard SP, Brandt D, Schmid JP, Pokan R, Wonisch M. Early 4-week cardiac rehabilitation exercise train- ing in elderly patients after heart surgery. J Cardiopulm Rehabil Prev. 2010;30:85 92. doi: 10.1097/HCR.0b013e3181be7e32. 339. Harkness K, Smith KM, Taraba L, Mackenzie CL, Gunn E, Arthur HM. Effect of a postoperative telephone intervention on attendance at intake for cardiac rehabilitation after coronary artery bypass graft surgery. Heart Lung. 2005;34:179 186. 340. Pack QR, Mansour M, Barboza JS, Hibner BA, Mahan MG, Ehrman JK, Vanzant MA, Schairer JR, Keteyian SJ. An early appointment to out- patient cardiac rehabilitation at hospital discharge improves attendance at orientation: a randomized, single-blind, controlled trial. Circulation. 2013;127:349 355. doi: 10.1161/CIRCULATIONAHA.112.121996. 341. Grace SL, Gravely-Witte S, Brual J, Suskin N, Higginson L, Alter D, Stewart DE. Contribution of patient and physician factors to cardiac rehabilitation referral: a prospective multilevel study. Nat Clin Pract Cardiovasc Med. 2008;5:653 662. doi: 10.1038/ncpcardio1272. 342. Hibbard JH, Stockard J, Mahoney ER, Tusler M. Development of the Patient Activation Measure (PAM): conceptualizing and measuring acti- vation in patients and consumers. Health Serv Res. 2004;39(pt 1):1005 1026. doi: 10.1111/j.1475-6773.2004.00269.x. 343. Hibbard JH, Mahoney ER, Stock R, Tusler M. Do increases in patient activation result in improved self-management behaviors? Health Serv Res. 2007;42:1443 1463. doi: 10.1111/j.1475-6773.2006.00669.x. 344. Mosen DM, Schmittdiel J, Hibbard J, Sobel D, Remmers C, Bellows J. Is patient activation associated with outcomes of care for adults with chronic conditions? J Ambul Care Manage. 2007;30:21 29. 345.


Is patient activation associated with outcomes of care for adults with chronic conditions? J Ambul Care Manage. 2007;30:21 29. 345. Remmers C, Hibbard J, Mosen DM, Wagenfield M, Hoye RE, Jones C. Is patient activation associated with future health outcomes and health- care utilization among patients with diabetes? J Ambul Care Manage. 2009;32:320 327. doi: 10.1097/JAC.0b013e3181ba6e77. 346. Hibbard JH, Greene J, Tusler M. Improving the outcomes of disease management by tailoring care to the patient s level of activation. Am J Manag Care. 2009;15:353 360. 347. Beckie TM. A behavior change intervention for women in cardiac reha- bilitation. J Cardiovasc Nurs. 2006;21:146 153. 348. Fix GM, Bokhour BG. Understanding the context of patient expe- riences in order to explore adherence to secondary prevention guidelines after heart surgery. Chronic Illn. 2012;8:265 277. doi: 10.1177/1742395312441037. 349. Blanchard CM, Reid RD, Morrin LI, McDonnell L, McGannon K, Rhodes RE, Spence JC, Edwards N. Demographic and clinical determi- nants of moderate to vigorous physical activity during home-based car- diac rehabilitation: the Home-Based Determinants of Exercise (HOME) study. J Cardiopulm Rehabil Prev. 2010;30:240 245. doi: 10.1097/ HCR.0b013e3181d0c4ae. 350. Griffo R, Ambrosetti M, Tramarin R, Fattirolli F, Temporelli PL, Vestri AR, De Feo S, Tavazzi L; ICAROS Investigators. Effective secondary prevention through cardiac rehabilitation after coronary revascularization and predictors of poor adherence to lifestyle modifi- cation and medication: results of the ICAROS Survey. Int J Cardiol. 2013;167:1390 1395. doi: 10.1016/j.ijcard.2012.04.069. 351. Moore SM, Kramer FM. Women s and men s preferences for car- diac rehabilitation program features. J Cardiopulm Rehabil. 1996;16:163 168. 352. Todaro JF, Shen BJ, Niaura R, Tilkemeier PL. Prevalence of depres- sive disorders in men and women enrolled in cardiac rehabilitation. J Cardiopulm Rehabil. 2005;25:71 75; quiz 76. 353. Moore SM, Dolansky MA, Ruland CM, Pashkow FJ, Blackburn GG.


Moore SM, Dolansky MA, Ruland CM, Pashkow FJ, Blackburn GG. Predictors of women s exercise maintenance after cardiac rehabilitation. J Cardiopulm Rehabil. 2003;23:40 49. 354. Schuster PM, Wright C, Tomich P. Gender differences in the outcomes of participants in home programs compared to those in structured car- diac rehabilitation programs. Rehabil Nurs. 1995;20:93 101. 355. Eshah NF. Jordanian acute coronary syndrome patients learn- ing needs: implications for cardiac rehabilitation and second- ary prevention programs. Nurs Health Sci. 2011;13:238 245. doi: 10.1111/j.1442-2018.2011.00608.x. 356. Squires RW, Montero-Gomez A, Allison TG, Thomas RJ. Long-term disease management of patients with coronary disease by cardiac reha- bilitation program staff. J Cardiopulm Rehabil Prev. 2008;28:180 186; quiz 187 188. doi: 10.1097/01.HCR.0000320068.35728.12. 357. Moore SM, Charvat JM. Using the CHANGE intervention to enhance long-term exercise. Nurs Clin North Am. 2002;37:273 283, vi vii. 358. Parry MJ, Watt-Watson J, Hodnett E, Tranmer J, Dennis CL, Brooks D. Cardiac Home Education and Support Trial (CHEST): a pilot study. Can J Cardiol. 2009;25:e393 e398. 359. Leemrijse CJ, van Dijk L, J rstad HT, Peters RJ, Veenhof C. The effects of Hartcoach, a life style intervention provided by telephone on the reduction of coronary risk factors: a randomised trial. BMC Cardiovasc Disord. 2012;12:47. doi: 10.1186/1471-2261-12-47. 360. Scholz U, Knoll N, Sniehotta FF, Schwarzer R. Physical activity and depressive symptoms in cardiac rehabilitation: long-term effects of a self-management intervention. Soc Sci Med. 2006;62:3109 3120. doi: 10.1016/j.socscimed.2005.11.035. 361. Gallagher R, McKinley S. Anxiety, depression and perceived con- trol in patients having coronary artery bypass grafts. J Adv Nurs. 2009;65:2386 2396. doi: 10.1111/j.1365-2648.2009.05101.x. 362. Martin F. Recognizing depression after a coronary artery bypass graft. Br J Nurs. 2006;15:703 706. 363. Goyal TM, Idler EL, Krause TJ, Contrada RJ. Quality of life follow- ing cardiac surgery: impact of the severity and course of depressive symptoms.


Quality of life follow- ing cardiac surgery: impact of the severity and course of depressive symptoms. Psychosom Med. 2005;67:759 765. doi: 10.1097/01. psy.0000174046.40566.80. 364. Blumenthal JA, Lett HS, Babyak MA, White W, Smith PK, Mark DB, Jones R, Mathew JP, Newman MF; NORG Investigators. Depression as a risk factor for mortality after coronary artery bypass surgery. Lancet. 2003;362:604 609. doi: 10.1016/S0140-6736(03)14190-6. 365. Connerney I, Shapiro PA, McLaughlin JS, Bagiella E, Sloan RP. Relation between depression after coronary artery bypass surgery and 12-month outcome: a prospective study. Lancet. 2001;358:1766 1771. doi: 10.1016/S0140-6736(01)06803-9. 366. Freedland KE, Skala JA, Carney RM, Rubin EH, Lustman PJ, D vila- Rom nVG, Steinmeyer BC, Hogue CW Jr. Treatment of depression after coronary artery bypass surgery: a randomized controlled trial. Arch Gen Psychiatry. 2009;66:387 396. doi: 10.1001/archgenpsychiatry.2009.7. 367. Rollman BL, Belnap BH, LeMenager MS, Mazumdar S, Houck PR, Counihan PJ, Kapoor WN, Schulberg HC, Reynolds CF 3rd. Telephone- delivered collaborative care for treating post-CABG depression: a ran- domized controlled trial. JAMA. 2009;302:2095 2103. doi: 10.1001/ jama.2009.1670. 368. Beckie TM, Beckstead JW, Schocken DD, Evans ME, Fletcher GF. The effects of a tailored cardiac rehabilitation program on depressive symp- toms in women: a randomized clinical trial. Int J Nurs Stud. 2011;48:3 12. doi: 10.1016/j.ijnurstu.2010.06.005. 369. Dao TK, Youssef NA, Armsworth M, Wear E, Papathopoulos KN, Gopaldas R. Randomized controlled trial of brief cognitive behav- ioral intervention for depression and anxiety symptoms preopera- tively in patients undergoing coronary artery bypass graft surgery. J Thorac Cardiovasc Surg. 2011;142:e109 e115. doi: 10.1016/j. jtcvs.2011.02.046. 370. Chocron S, Vandel P, Durst C, Laluc F, Kaili D, Chocron M, Etievent JP. Antidepressant therapy in patients undergoing coronary artery bypass grafting: the MOTIV-CABG trial. Ann Thorac Surg. 2013;95:1609 1618. doi: 10.1016/j.athoracsur.2013.02.035. 371. Jensen B , Rasmussen LS, Steinbr chel DA.


2013;95:1609 1618. doi: 10.1016/j.athoracsur.2013.02.035. 371. Jensen B , Rasmussen LS, Steinbr chel DA. Cognitive outcomes in elderly high-risk patients 1 year after off-pump versus on-pump coro- nary artery bypass grafting: a randomized trial. Eur J Cardiothorac Surg. 2008;34:1016 1021. doi: 10.1016/j.ejcts.2008.07.053. 372. Andrew MJ, Baker RA, Bennetts J, Kneebone AC, Knight JL. A com- parison of neuropsychologic deficits after extracardiac and intracardiac surgery. J Cardiothorac Vasc Anesth. 2001;15:9 14. 373. Fearn SJ, Pole R, Wesnes K, Faragher EB, Hooper TL, McCollum CN. Cerebral injury during cardiopulmonary bypass: emboli impair mem- ory. J Thorac Cardiovasc Surg. 2001;121:1150 1160. doi: 10.1067/ mtc.2001.114099. 374. Raymond PD, Hinton-Bayre AD, Radel M, Ray MJ, Marsh NA. Assessment of statistical change criteria used to define significant change in neuropsychological test performance following cardiac surgery. Eur J Cardiothorac Surg. 2006;29:82 88. doi: 10.1016/j.ejcts.2005.10.016. 375. Selnes OA, Goldsborough MA, Borowicz LM Jr, Enger C, Quaskey SA, McKhann GM. Determinants of cognitive change after coronary artery bypass surgery: a multifactorial problem. Ann Thorac Surg. 1999;67:1669 1676. 376. Selnes OA, Pham L, Zeger S, McKhann GM. Defining cognitive change after CABG: decline versus normal variability. Ann Thorac Surg. 2006;82:388 390. doi: 10.1016/j.athoracsur.2006.02.060. 377. Rosengart TK, Sweet JJ, Finnin E, Wolfe P, Cashy J, Hahn E, Marymont J, Sanborn T. Stable cognition after coronary artery bypass grafting: comparisons with percutaneous intervention and normal controls. Ann Thorac Surg. 2006;82:597 607. doi: 10.1016/j.athoracsur.2006.03.026. 378. Sweet JJ, Finnin E, Wolfe PL, Beaumont JL, Hahn E, Marymont J, Sanborn T, Rosengart TK. Absence of cognitive decline one year after coronary bypass surgery: comparison to nonsurgical and healthy controls. Ann Thorac Surg. 2008;85:1571 1578. doi: 10.1016/j. athoracsur.2008.01.090. 379. Selnes OA, Grega MA, Borowicz LM Jr, Royall RM, McKhann GM, Baumgartner WA.


Selnes OA, Grega MA, Borowicz LM Jr, Royall RM, McKhann GM, Baumgartner WA. Cognitive changes with coronary artery disease: a prospective study of coronary artery bypass graft patients and nonsurgi- cal controls. Ann Thorac Surg. 2003;75:1377 1384. 380. Newman MF, Kirchner JL, Phillips-Bute B, Gaver V, Grocott H, Jones RH, Mark DB, Reves JG, Blumenthal JA; Neurological Outcome Research Group and the Cardiothoracic Anesthesiology Research Endeavors Investigators. Longitudinal assessment of neurocogni- tive function after coronary-artery bypass surgery. N Engl J Med. 2001;344:395 402. doi: 10.1056/NEJM200102083440601. 381. Stygall J, Newman SP, Fitzgerald G, Steed L, Mulligan K, Arrowsmith JE, Pugsley W, Humphries S, Harrison MJ. Cognitive change 5 years after coronary artery bypass surgery. Health Psychol. 2003;22:579 586. doi: 10.1037/0278-6133.22.6.579. 382. Selnes OA, Grega MA, Bailey MM, Pham LD, Zeger SL, Baumgartner WA, McKhann GM. Cognition 6 years after surgical or medical ther- apy for coronary artery disease. Ann Neurol. 2008;63:581 590. doi: 10.1002/ana.21382. 383. Johnson T, Monk T, Rasmussen LS, Abildstrom H, Houx P, Korttila K, Kuipers HM, Hanning CD, Siersma VD, Kristensen D, Canet J, Iba az MT, Moller JT; ISPOCD2 Investigators. Postoperative cognitive dys- function in middle-aged patients. Anesthesiology. 2002;96:1351 1357. 384. Rasmussen LS, Moller JT. Central nervous system dysfunction after anesthesia in the geriatric patient. Anesthesiol Clin North America. 2000;18:59 70, vi. 385. Monk TG, Weldon BC, Garvan CW, Dede DE, van der Aa MT, Heilman KM, Gravenstein JS. Predictors of cognitive dysfunction after major noncardiac surgery. Anesthesiology. 2008;108:18 30. doi: 10.1097/01. anes.0000296071.19434.1e. 386. Ho PM, Arciniegas DB, Grigsby J, McCarthy M Jr, McDonald GO, Moritz TE, Shroyer AL, Sethi GK, Henderson WG, London MJ, VillaNueva CB, Grover FL, Hammermeister KE. Predictors of cogni- tive decline following coronary artery bypass graft surgery. Ann Thorac Surg. 2004;77:597 603. doi: 10.1016/S0003-4975(03)01358-4. 387.


Predictors of cogni- tive decline following coronary artery bypass graft surgery. Ann Thorac Surg. 2004;77:597 603. doi: 10.1016/S0003-4975(03)01358-4. 387. Goto T, Baba T, Honma K, Shibata Y, Arai Y, Uozumi H, Okuda T. Magnetic resonance imaging findings and postoperative neurologic dys- function in elderly patients undergoing coronary artery bypass grafting. Ann Thorac Surg. 2001;72:137 142. 388. Van Dijk D, Jansen EW, Hijman R, Nierich AP, Diephuis JC, Moons KG, Lahpor JR, Borst C, Keizer AM, Nathoe HM, Grobbee DE, De Jaegere PP, Kalkman CJ; Octopus Study Group. Cognitive outcome after off-pump and on-pump coronary artery bypass graft surgery: a ran- domized trial. JAMA. 2002;287:1405 1412. 389. Marasco SF, Sharwood LN, Abramson MJ. No improvement in neuro- cognitive outcomes after off-pump versus on-pump coronary revascu- larisation: a meta-analysis. Eur J Cardiothorac Surg. 2008;33:961 970. doi: 10.1016/j.ejcts.2008.03.022. 390. van Dijk D, Spoor M, Hijman R, Nathoe HM, Borst C, Jansen EW, Grobbee DE, de Jaegere PP, Kalkman CJ; Octopus Study Group. Cognitive and cardiac outcomes 5 years after off-pump vs on-pump coronary artery bypass graft surgery. JAMA. 2007;297:701 708. doi: 10.1001/jama.297.7.701. 391. Lamy A, Devereaux PJ, Prabhakaran D, Taggart DP, Hu S, Paolasso E, Straka Z, Piegas LS, Akar AR, Jain AR, Noiseux N, Padmanabhan C, Bahamondes JC, Novick RJ, Vaijyanath P, Reddy SK, Tao L, Olavegogeascoechea PA, Airan B, Sulling TA, Whitlock RP, Ou Y, Pogue J, Chrolavicius S,Yusuf S; CORONARY Investigators. Effects of off-pump and on-pump coronary-artery bypass grafting at 1 year. N Engl J Med. 2013;368:1179 1188. doi: 10.1056/NEJMoa1301228. 392. Eckel RH, Krauss RM. American Heart Association call to action: obe- sity as a major risk factor for coronary heart disease: AHA Nutrition Committee. Circulation. 1998;97:2099 2100. 393.


American Heart Association call to action: obe- sity as a major risk factor for coronary heart disease: AHA Nutrition Committee. Circulation. 1998;97:2099 2100. 393. Okorodudu DO, Jumean MF, Montori VM, Romero-Corral A, Somers VK, Erwin PJ, Lopez-Jimenez F. Diagnostic performance of body mass index to identify obesity as defined by body adiposity: a systematic review and meta-analysis. Int J Obes (Lond). 2010;34:791 799. doi: 10.1038/ijo.2010.5. 394. Romero-Corral A, Somers VK, Sierra-Johnson J, Jensen MD, Thomas RJ, Squires RW, Allison TG, Korinek J, Lopez-Jimenez F. Diagnostic performance of body mass index to detect obesity in patients with coro- nary artery disease. Eur Heart J. 2007;28:2087 2093. doi: 10.1093/ eurheartj/ehm243. 395. Coutinho T, Goel K, Corr a de S D, Carter RE, Hodge DO, Kragelund C, Kanaya AM, Zeller M, Park JS, Kober L, Torp-Pedersen C, Cottin Y, Lorgis L, Lee SH, Kim YJ, Thomas R, Roger VL, Somers VK, Kulik et al Secondary Prevention After CABG 963 Lopez-Jimenez F. Combining body mass index with measures of cen- tral obesity in the assessment of mortality in subjects with coronary disease: role of normal weight central obesity. J Am Coll Cardiol. 2013;61:553 560. doi: 10.1016/j.jacc.2012.10.035. 396. Coutinho T, Goel K, Corr a de S D, Kragelund C, Kanaya AM, Zeller M, Park JS, Kober L, Torp-Pedersen C, Cottin Y, Lorgis L, Lee SH, Kim YJ, Thomas R, Roger VL, Somers VK, Lopez-Jimenez F. Central obesity and survival in subjects with coronary artery disease: a system- atic review of the literature and collaborative analysis with individual subject data. J Am Coll Cardiol. 2011;57:1877 1886. doi: 10.1016/j. jacc.2010.11.058. 397.


J Am Coll Cardiol. 2011;57:1877 1886. doi: 10.1016/j. jacc.2010.11.058. 397. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC Jr; International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; International Association for the Study of Obesity. Harmonizing the metabolic syn- drome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640 1645. doi: 10.1161/ CIRCULATIONAHA.109.192644. 398. Angeloni E, Melina G, Benedetto U, Refice S, Capuano F, Roscitano A, Comito C, Sinatra R. Metabolic syndrome affects midterm outcome after coronary artery bypass grafting. Ann Thorac Surg. 2012;93:537 544. doi: 10.1016/j.athoracsur.2011.10.066. 399. Echahidi N, Pibarot P, Despr s JP, Daigle JM, Mohty D, Voisine P, Baillot R, Mathieu P. Metabolic syndrome increases operative mortality in patients undergoing coronary artery bypass grafting surgery. J Am Coll Cardiol. 2007;50:843 851. doi: 10.1016/j.jacc.2007.04.075. 400. Echahidi N, Mohty D, Pibarot P, Despr s JP, O Hara G, Champagne J, Philippon F, Daleau P, Voisine P, Mathieu P. Obesity and metabolic syn- drome are independent risk factors for atrial fibrillation after coronary artery bypass graft surgery. Circulation. 2007;116(suppl):I213 I219. doi: 10.1161/CIRCULATIONAHA.106.681304. 401. Girerd N, Pibarot P, Fournier D, Daleau P, Voisine P, O Hara G, Despr s JP, Mathieu P. Middle-aged men with increased waist circumference and elevated C-reactive protein level are at higher risk for postoperative atrial fibrillation following coronary artery bypass grafting surgery. Eur Heart J. 2009;30:1270 1278. doi: 10.1093/eurheartj/ehp091. 402.


Girerd N, Pibarot P, Fournier D, Daleau P, Voisine P, O Hara G, Despr s JP, Mathieu P. Middle-aged men with increased waist circumference and elevated C-reactive protein level are at higher risk for postoperative atrial fibrillation following coronary artery bypass grafting surgery. Eur Heart J. 2009;30:1270 1278. doi: 10.1093/eurheartj/ehp091. 402. Yilmaz MB, Guray U, Guray Y, Biyikoglu SF, Tandogan I, Sasmaz H, Korkmaz S. Metabolic syndrome negatively impacts early patency of saphenous vein grafts. Coron Artery Dis. 2006;17:41 44. 403. Kocz R, Hassan MA, Perala PR, Negargar S, Javadzadegan H, Nader ND. The effect of weight loss on the outcome after coronary artery bypass grafting in obese patients. Ann Card Anaesth. 2012;15:190 198. doi: 10.4103/0971-9784.97975. 404. Sierra-Johnson J, Wright SR, Lopez-Jimenez F, Allison TG. Relation of body mass index to fatal and nonfatal cardiovascular events after cardiac rehabilitation. Am J Cardiol. 2005;96:211 214. doi: 10.1016/j. amjcard.2005.03.046. 405. Batsis JA, Romero-Corral A, Collazo-Clavell ML, Sarr MG, Somers VK, Brekke L, Lopez-Jimenez F. Effect of weight loss on predicted car- diovascular risk: change in cardiac risk after bariatric surgery. Obesity (Silver Spring). 2007;15:772 784. doi: 10.1038/oby.2007.589. 406. Poirier P, Cornier MA, Mazzone T, Stiles S, Cummings S, Klein S, McCullough PA, Ren Fielding C, Franklin BA; on behalf of the American Heart Association Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Bariatric surgery and cardiovascular risk factors: a scientific statement from the American Heart Association. Circulation. 2011;123:1683 1701. doi: 10.1161/ CIR.0b013e3182149099. 407. Lopez-Jimenez F, Bhatia S, Collazo-Clavell ML, Sarr MG, Somers VK. Safety and efficacy of bariatric surgery in patients with coronary artery disease. Mayo Clin Proc. 2005;80:1157 1162. doi: 10.4065/80.9.1157. 408.


Safety and efficacy of bariatric surgery in patients with coronary artery disease. Mayo Clin Proc. 2005;80:1157 1162. doi: 10.4065/80.9.1157. 408. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A clinical trial of the effects of dietary patterns on blood pressure: DASH Collaborative Research Group. N Engl J Med. 1997;336:1117 1124. doi: 10.1056/NEJM199704173361601. 409. Batsis JA, Romero-Corral A, Collazo-Clavell ML, Sarr MG, Somers VK, Lopez-Jimenez F. Effect of bariatric surgery on the metabolic syn- drome: a population-based, long-term controlled study. Mayo Clin Proc. 2008;83:897 907. doi: 10.4065/83.8.897. 410. Chermesh I, Hajos J, Mashiach T, Bozhko M, Shani L, Nir RR, Bolotin G. Malnutrition in cardiac surgery: food for thought. Eur J Prev Cardiol. 2014;21:475 483. doi: 10.1177/2047487312452969. 411. Engelman DT, Adams DH, Byrne JG, Aranki SF, Collins JJ Jr, Couper GS, Allred EN, Cohn LH, Rizzo RJ. Impact of body mass index and albumin on morbidity and mortality after cardiac surgery. J Thorac Cardiovasc Surg. 1999;118:866 873. 412. Rapp-Kesek D, St hle E, Karlsson TT. Body mass index and albumin in the preoperative evaluation of cardiac surgery patients. Clin Nutr. 2004;23:1398 1404. doi: 10.1016/j.clnu.2004.06.006. 413. DiMaria-Ghalili RA. Changes in nutritional status and postoperative outcomes in elderly CABG patients. Biol Res Nurs. 2002;4:73 84. 414. DiMaria-Ghalili RA. Changes in body mass index and late postopera- tive outcomes in elderly coronary bypass grafting patients: a follow-up study. Biol Res Nurs. 2004;6:24 36. doi: 10.1177/1099800404264538. 415. van Venrooij LM, van Leeuwen PA, de Vos R, Borgmeijer-Hoelen MM, de Mol BA. Preoperative protein and energy intake and postoperative complications in well-nourished, non-hospitalized elderly cardiac surgery patients. Clin Nutr. 2009;28:117 121. doi: 10.1016/j.clnu.2009.01.016. 416.


Preoperative protein and energy intake and postoperative complications in well-nourished, non-hospitalized elderly cardiac surgery patients. Clin Nutr. 2009;28:117 121. doi: 10.1016/j.clnu.2009.01.016. 416. Racca V, Castiglioni P, Ripamonti V, Bertoli S, Calvo MG, Ferratini M. Nutrition markers in patients after heart surgery. JPEN J Parenter Enteral Nutr. 2010;34:143 150. doi: 10.1177/0148607109357627. 417. Osganian SK, Stampfer MJ, Rimm E, Spiegelman D, Hu FB, Manson JE, Willett WC. Vitamin C and risk of coronary heart disease in women. J Am Coll Cardiol. 2003;42:246 252. 418. Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC. Vitamin E consumption and the risk of coronary dis- ease in women. N Engl J Med. 1993;328:1444 1449. doi: 10.1056/ NEJM199305203282003. 419. Sesso HD, Buring JE, Christen WG, Kurth T, Belanger C, MacFadyen J, Bubes V, Manson JE, Glynn RJ, Gaziano JM. Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians Health Study II randomized controlled trial. JAMA. 2008;300:2123 2133. doi: 10.1001/jama.2008.600. 420. Sesso HD, Christen WG, Bubes V, Smith JP, MacFadyen J, Schvartz M, Manson JE, Glynn RJ, Buring JE, Gaziano JM. Multivitamins in the prevention of cardiovascular disease in men: the Physicians Health Study II randomized controlled trial. JAMA. 2012;308:1751 1760. doi: 10.1001/jama.2012.14805. 421. Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) Collaborative Group; Armitage JM, Bowman L, Clarke RJ, Wallendszus K, Bulbulia R, Rahimi K, Haynes R, Parish S, SleightP,PetoR,CollinsR.Effectsofhomocysteine-loweringwithfolicacid plus vitamin B12 vs placebo on mortality and major morbidity in myocar- dial infarction survivors: a randomized trial. JAMA. 2010;303:2486 2494. 422. Clarke R, Halsey J, Lewington S, Lonn E, Armitage J, Manson JE, B naa KH, Spence JD, Nyg rd O, Jamison R, Gaziano JM, Guarino P, Bennett D, Mir F, Peto R, Collins R; B-Vitamin Treatment Trialists Collaboration.


Clarke R, Halsey J, Lewington S, Lonn E, Armitage J, Manson JE, B naa KH, Spence JD, Nyg rd O, Jamison R, Gaziano JM, Guarino P, Bennett D, Mir F, Peto R, Collins R; B-Vitamin Treatment Trialists Collaboration. Effects of lowering homocysteine levels with B vitamins on cardiovascular disease, cancer, and cause-specific mortality: meta- analysis of 8 randomized trials involving 37 485 individuals. Arch Intern Med. 2010;170:1622 1631. doi: 10.1001/archinternmed.2010.348. 423. Myung SK, Ju W, Cho B, Oh SW, Park SM, Koo BK, Park BJ; Korean Meta-Analysis Study Group. Efficacy of vitamin and antioxidant sup- plements in prevention of cardiovascular disease: systematic review and meta-analysis of randomised controlled trials. BMJ. 2013;346:f10. 424. Mickle DA, Weisel RD, Burton GW, Ingold KU. Effect of orally admin- istered alpha-tocopheryl acetate on human myocardial alpha-tocopherol levels. Cardiovasc Drugs Ther. 1991;5(suppl 2):309 312. 425. Yau TM, Weisel RD, Mickle DA, Burton GW, Ingold KU, Ivanov J, Mohabeer MK, Tumiati L, Carson S. Vitamin E for coronary bypass operations: a prospective, double-blind, randomized trial. J Thorac Cardiovasc Surg. 1994;108:302 310. 426. Pyles LA, Fortney JE, Kudlak JJ, Gustafson RA, Einzig S. Plasma anti- oxidant depletion after cardiopulmonary bypass in operations for con- genital heart disease. J Thorac Cardiovasc Surg. 1995;110:165 171. 427. Louw JA, Werbeck A, Louw ME, Kotze TJ, Cooper R, Labadarios D. Blood vitamin concentrations during the acute-phase response. Crit Care Med. 1992;20:934 941. 428. Schindler R, Berndt S, Schroeder P, Oster O, Rave G, Sievers HH. Plasma vitamin E and A changes during cardiopulmonary bypass and in the postoperative course. Langenbecks Arch Surg. 2003;387:372 378. doi: 10.1007/s00423-002-0336-4. 429. Storti S, CerilloAG, RizzaA, Giannelli I, Fontani G, Glauber M, Clerico A. Coronary artery bypass grafting surgery is associated with a marked reduction in serum homocysteine and folate levels in the early postoper- ative period.


Storti S, CerilloAG, RizzaA, Giannelli I, Fontani G, Glauber M, Clerico A. Coronary artery bypass grafting surgery is associated with a marked reduction in serum homocysteine and folate levels in the early postoper- ative period. Eur J Cardiothorac Surg. 2004;26:682 686. doi: 10.1016/j. ejcts.2004.06.001. 430. Donnino MW, Cocchi MN, Smithline H, Carney E, Chou PP, Salciccioli J, Salciccoli J. Coronary artery bypass graft surgery depletes plasma thiamine levels. Nutrition. 2010;26:133 136. doi: 10.1016/j. nut.2009.06.004. 431. Zittermann A, Kuhn J, Dreier J, Knabbe C, Gummert JF, B rgermann J. Vitamin D status and the risk of major adverse cardiac and cerebrovas- cular events in cardiac surgery. Eur Heart J. 2013;34:1358 1364. doi: 10.1093/eurheartj/ehs468. 432. Armaganijan L, Lopes RD, Healey JS, Piccini JP, Nair GM, Morillo CA. Do omega-3 fatty acids prevent atrial fibrillation after open heart surgery? A meta-analysis of randomized controlled trials. Clinics (Sao Paulo). 2011;66:1923 1928. 433. He Z, Yang L, Tian J, Yang K, Wu J, Yao Y. Efficacy and safety of omega-3 fatty acids for the prevention of atrial fibrillation: a meta-analysis. Can J Cardiol. 2013;29:196 203. doi: 10.1016/j. cjca.2012.03.019. 434. Rasoli S, Kourliouros A, Harling L, Athanasiou T. Does prophylactic therapy with antioxidant vitamins have an effect on atrial fibrillation fol- lowing cardiac surgery? Interact Cardiovasc Thorac Surg. 2011;13:82 85. doi: 10.1510/icvts.2011.268326. 435. Udell JA, Zawi R, Bhatt DL, Keshtkar-Jahromi M, Gaughran F, Phrommintikul A, Ciszewski A, Vakili H, Hoffman EB, Farkouh ME, Cannon CP. Association between influenza vaccination and car- diovascular outcomes in high-risk patients: a meta-analysis. JAMA. 2013;310:1711 1720. doi: 10.1001/jama.2013.279206. 436. Bainton D, Jones GR, Hole D. Influenza and ischaemic heart disease: a possible trigger for acute myocardial infarction? Int J Epidemiol. 1978;7:231 239. 437.


Bainton D, Jones GR, Hole D. Influenza and ischaemic heart disease: a possible trigger for acute myocardial infarction? Int J Epidemiol. 1978;7:231 239. 437. Nichol KL, Margolis KL, Wuorenma J, Von Sternberg T. The efficacy and cost effectiveness of vaccination against influenza among elderly persons living in the community. N Engl J Med. 1994;331:778 784. doi: 10.1056/NEJM199409223311206. 438. Smeeth L, Thomas SL, Hall AJ, Hubbard R, Farrington P, Vallance P. Risk of myocardial infarction and stroke after acute infection or vaccina- tion. N Engl J Med. 2004;351:2611 2618. doi: 10.1056/NEJMoa041747. 439. Warren-Gash C, Smeeth L, Hayward AC. Influenza as a trigger for acute myocardial infarction or death from cardiovascular disease: a systematic review. Lancet Infect Dis. 2009;9:601 610. doi: 10.1016/ S1473-3099(09)70233-6. 440. Naghavi M, Barlas Z, Siadaty S, Naguib S, Madjid M, Casscells W. Association of influenza vaccination and reduced risk of recurrent myo- cardial infarction. Circulation. 2000;102:3039 3045. 441. Nichol KL, Nordin J, Mullooly J, Lask R, Fillbrandt K, Iwane M. Influenza vaccination and reduction in hospitalizations for cardiac dis- ease and stroke among the elderly. N Engl J Med. 2003;348:1322 1332. doi: 10.1056/NEJMoa025028. 442. Macintyre CR, Heywood AE, Kovoor P, Ridda I, Seale H, Tan T, Gao Z, Katelaris AL, Siu HW, Lo V, Lindley R, Dwyer DE. Ischaemic heart disease, influenza and influenza vaccination: a prospec- tive case control study. Heart. 2013;99:1843 1848. doi: 10.1136/ heartjnl-2013-304320. 443. Gurfinkel EP, de la Fuente RL, Mendiz O, Mautner B. Influenza vaccine pilot study in acute coronary syndromes and planned percutaneous cor- onary interventions: the FLU Vaccination Acute Coronary Syndromes (FLUVACS) Study. Circulation. 2002;105:2143 2147. 444. Gurfinkel EP, Leon de la Fuente R, Mendiz O, Mautner B. Flu vaccina- tion in acute coronary syndromes and planned percutaneous coronary interventions (FLUVACS) study. Eur Heart J. 2004;25:25 31. 445.


Flu vaccina- tion in acute coronary syndromes and planned percutaneous coronary interventions (FLUVACS) study. Eur Heart J. 2004;25:25 31. 445. Ciszewski A, Bilinska ZT, Brydak LB, Kepka C, Kruk M, Romanowska M, Ksiezycka E, Przyluski J, Piotrowski W, Maczynska R, Ruzyllo W. Influenza vaccination in secondary prevention from coronary isch- aemic events in coronary artery disease: FLUCAD study. Eur Heart J. 2008;29:1350 1358. doi: 10.1093/eurheartj/ehm581. 446. Phrommintikul A, Kuanprasert S, Wongcharoen W, Kanjanavanit R, Chaiwarith R, Sukonthasarn A. Influenza vaccination reduces cardio- vascular events in patients with acute coronary syndrome. Eur Heart J. 2011;32:1730 1735. doi: 10.1093/eurheartj/ehr004. 447. Davis MM, Taubert K, Benin AL, Brown DW, Mensah GA, Baddour LM, Dunbar S, Krumholz HM; American Heart Association; American College of Cardiology. Influenza vaccination as secondary preven- tion for cardiovascular disease: a science advisory from the American Heart Association/American College of Cardiology. Circulation. 2006;114:1549 1553. doi: 10.1161/CIRCULATIONAHA.106.178242. 448. Kuehn BM. CDC advisory committee recommends nearly univer- sal influenza vaccination. JAMA. 2010;303:1136. doi: 10.1001/ jama.2010.294. 449. Markewitz A, Faist E, Lang S, H ltner L, Weinhold C, Reichart B. An imbalance in T-helper cell subsets alters immune response after cardiac surgery. Eur J Cardiothorac Surg. 1996;10:61 67. 450. Franke A, Lante W, Kurig E, Z ller LG, Weinhold C, Markewitz A. Hyporesponsiveness of T cell subsets after cardiac surgery: a product of altered cell function or merely a result of absolute cell count changes in peripheral blood? Eur J Cardiothorac Surg. 2006;30:64 71. doi: 10.1016/j.ejcts.2006.03.029. Key Words: AHA Scientific Statements coronary artery bypass grafting prevention and control risk-reduction behavior


2016 by the American College of Cardiology Foundation, the American Heart Association, Inc., and the Heart Rhythm Society. Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIR.0000000000000311 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society WRITING COMMITTEE MEMBERS* Richard L. Page, MD, FACC, FAHA, FHRS, Chair; Jos A. Joglar, MD, FACC, FAHA, FHRS, Vice Chair; Mary A. Caldwell, RN, MBA, PhD, FAHA; Hugh Calkins, MD, FACC, FAHA, FHRS* ; Jamie B. Conti, MD, FACC* ; Barbara J. Deal, MD ; N.A.


Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIR.0000000000000311 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society WRITING COMMITTEE MEMBERS* Richard L. Page, MD, FACC, FAHA, FHRS, Chair; Jos A. Joglar, MD, FACC, FAHA, FHRS, Vice Chair; Mary A. Caldwell, RN, MBA, PhD, FAHA; Hugh Calkins, MD, FACC, FAHA, FHRS* ; Jamie B. Conti, MD, FACC* ; Barbara J. Deal, MD ; N.A. Mark Estes III, MD, FACC, FAHA, FHRS* ; Michael E. Field, MD, FACC, FHRS ; Zachary D. Goldberger, MD, MS, FACC, FAHA, FHRS ; Stephen C. Hammill, MD, FACC, FHRS ; Julia H. Indik, MD, PhD, FACC, FAHA, FHRS ; Bruce D. Lindsay, MD, FACC, FHRS* ; Brian Olshansky, MD, FACC, FAHA, FHRS* ; Andrea M. Russo, MD, FACC, FHRS* ; Win-Kuang Shen, MD, FACC, FAHA, FHRS ; Cynthia M. Tracy, MD, FACC ; Sana M. Al-Khatib, MD, MHS, FACC, FAHA, FHRS, Evidence Review Committee Chair ACC/AHA TASK FORCE MEMBERS Jonathan L. Halperin, MD, FACC, FAHA, Chair; Glenn N. Levine, MD, FACC, FAHA, Chair-Elect; Jeffrey L. Anderson, MD, FACC, FAHA, Immediate Past Chair ; Nancy M. Albert, PhD, RN, FAHA ; Sana M. Al-Khatib, MD, MHS, FACC, FAHA; Kim K. Birtcher, PharmD, AACC; Biykem Bozkurt, MD, PhD, FACC, FAHA; Ralph G. Brindis, MD, MPH, MACC; Joaquin E. Cigarroa, MD, FACC; Lesley H. Curtis, PhD, FAHA; Lee A. Fleisher, MD, FACC, FAHA; Federico Gentile, MD, FACC; Samuel Gidding, MD, FAHA; Mark A. Hlatky, MD, FACC; John Ikonomidis, MD, PhD, FAHA; Jose Joglar, MD, FACC, FAHA; Richard J. Kovacs, MD, FACC, FAHA ; E. Magnus Ohman, MD, FACC ; Susan J. Pressler, PhD, RN, FAHA; Frank W. Sellke, MD, FACC, FAHA ; Win-Kuang Shen, MD, FACC, FAHA ; Duminda N. Wijeysundera, MD, PhD *Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry and other entities may apply; see Appendix 1 for recusal information.


Mark Estes III, MD, FACC, FAHA, FHRS* ; Michael E. Field, MD, FACC, FHRS ; Zachary D. Goldberger, MD, MS, FACC, FAHA, FHRS ; Stephen C. Hammill, MD, FACC, FHRS ; Julia H. Indik, MD, PhD, FACC, FAHA, FHRS ; Bruce D. Lindsay, MD, FACC, FHRS* ; Brian Olshansky, MD, FACC, FAHA, FHRS* ; Andrea M. Russo, MD, FACC, FHRS* ; Win-Kuang Shen, MD, FACC, FAHA, FHRS ; Cynthia M. Tracy, MD, FACC ; Sana M. Al-Khatib, MD, MHS, FACC, FAHA, FHRS, Evidence Review Committee Chair ACC/AHA TASK FORCE MEMBERS Jonathan L. Halperin, MD, FACC, FAHA, Chair; Glenn N. Levine, MD, FACC, FAHA, Chair-Elect; Jeffrey L. Anderson, MD, FACC, FAHA, Immediate Past Chair ; Nancy M. Albert, PhD, RN, FAHA ; Sana M. Al-Khatib, MD, MHS, FACC, FAHA; Kim K. Birtcher, PharmD, AACC; Biykem Bozkurt, MD, PhD, FACC, FAHA; Ralph G. Brindis, MD, MPH, MACC; Joaquin E. Cigarroa, MD, FACC; Lesley H. Curtis, PhD, FAHA; Lee A. Fleisher, MD, FACC, FAHA; Federico Gentile, MD, FACC; Samuel Gidding, MD, FAHA; Mark A. Hlatky, MD, FACC; John Ikonomidis, MD, PhD, FAHA; Jose Joglar, MD, FACC, FAHA; Richard J. Kovacs, MD, FACC, FAHA ; E. Magnus Ohman, MD, FACC ; Susan J. Pressler, PhD, RN, FAHA; Frank W. Sellke, MD, FACC, FAHA ; Win-Kuang Shen, MD, FACC, FAHA ; Duminda N. Wijeysundera, MD, PhD *Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry and other entities may apply; see Appendix 1 for recusal information. HRS Representative. ACC/AHA Representative. ACC/AHA Task Force on Performance Measures Liaison. ACC/AHA Task Force on Clinical Practice Guidelines Liaison. Former Task Force member; current member during this writing effort.


Former Task Force member; current member during this writing effort. This document was approved by the American College of Cardiology Board of Trustees and Executive Committee, the American Heart Association Science Advisory and Coordinating Committee, and the Heart Rhythm Society Board of Trustees in August 2015 and the American Heart Association Executive Committee in September 2015. The Author Comprehensive Relationships Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/ CIR.0000000000000311/-/DC1. The Data Supplement files are available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIR.0000000000000311/-/DC2. The American Heart Association requests that this document be cited as follows: Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NAM 3rd, Field ME, Goldberger ZD, Hammill SC, Indik JH, Lindsay BD, Olshansky B, Russo AM, Shen W-K, Tracy CM, Al-Khatib SM. 2015 ACC/AHA/ HRS guideline for the management of adult patients with supraventricular tachycardia: a report of theAmerican College of Cardiology/American HeartAssociation Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2016;133;e506-e574. doi: 10.1161/CIR.0000000000000311. This article has been copublished in the Journal of the American College of Cardiology and HeartRhythm Journal. Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), the American Heart Association (professional.heart.org), and the Heart Rhythm Society (www.hrsonline.org). A copy of the document is available at http://professional.heart. org/statements by using either Search for Guidelines & Statements or the Browse By Topic area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com. Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://professional.heart.org/statements. Select the Guidelines & Statements drop-down menu, then click Publication Development.


Select the Guidelines & Statements drop-down menu, then click Publication Development. Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/Copyright- Permission-Guidelines_UCM_300404_Article.jsp. A link to the Copyright Permissions Request Form appears on the right side of the page. ACC/AHA/HRS Guideline Page et al 2015 ACC/AHA/HRS SVT Guideline e507 Table of Contents Preamble e507 1. Introduction e508 1.1. Methodology and Evidence Review e508 1.2. Organization of the GWC e510 1.3. Document Review and Approval e510 1.4. Scope of the Guideline e510 2. General Principles e510 2.1. Mechanisms and Definitions e510 2.2. Epidemiology, Demographics, and Public Health Impact e510 Evaluation of the Patient With Suspected or Documented SVT e511 Clinical Presentation and Differential Diagnosis on the Basis of Symptoms e511 2.3.2. Evaluation of the ECG e514 2.4. Principles of Medical Therapy e515 2.4.1. Acute Treatment: Recommendations e515 Ongoing Management: Recommendations e517 Basic Principles of Electrophysiological Study, Mapping, and Ablation e518 Mapping With Multiple and Roving Electrodes e518 Tools to Facilitate Ablation, Including 3-Dimensional Electroanatomic Mapping e518 Mapping and Ablation With No or Minimal Radiation e519 2.5.4. Ablation Energy Sources e519 3. Sinus Tachyarrhythmias e520 3.1. Physiological Sinus Tachycardia e521 3.2. Inappropriate Sinus Tachycardia e521 3.2.1. Acute Treatment e521 3.2.2. Ongoing Management: Recommendations e521 4. Nonsinus Focal Atrial Tachycardia and MAT e523 4.1. Focal Atrial Tachycardia e523 4.1.1. Acute Treatment: Recommendations e526 4.1.2. Ongoing Management: Recommendations e527 4.2. Multifocal Atrial Tachycardia e527 4.2.1. Acute Treatment: Recommendation e531 4.2.2. Ongoing Management: Recommendations e531 5. Atrioventricular Nodal Reentrant Tachycardia e531 5.1. Acute Treatment: Recommendations e532 5.2. Ongoing Management: Recommendations e533 6. Manifest and Concealed Accessory Pathways e534 Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways e535 6.1.1. Acute Treatment: Recommendations e535 6.1.2.


Manifest and Concealed Accessory Pathways e534 Management of Patients With Symptomatic Manifest or Concealed Accessory Pathways e535 6.1.1. Acute Treatment: Recommendations e535 6.1.2. Ongoing Management: Recommendations e536 6.2. Management of Asymptomatic Pre-Excitation . e537 6.2.1. PICOTS Critical Questions e537 Asymptomatic Patients With Pre-Excitation: Recommendations e538 Risk Stratification of Symptomatic Patients With Manifest Accessory Pathways: Recommendations e539 7. Atrial Flutter e539 7.1. Cavotricuspid Isthmus Dependent Atrial Flutter . e539 7.2. Non Isthmus-Dependent Atrial Flutters e540 7.3. Acute Treatment: Recommendations e541 7.4. Ongoing Management: Recommendations e542 8. Junctional Tachycardia e544 8.1. Acute Treatment: Recommendations e544 8.2. Ongoing Management: Recommendations e545 9. Special Populations e545 9.1. Pediatrics e545 9.2. Patients With Adult Congenital Heart Disease e549 9.2.1. Clinical Features e549 9.2.2. Acute Treatment: Recommendations e550 9.2.3. OngoingManagement:Recommendations e551 9.3. Pregnancy e553 9.3.1. Acute Treatment: Recommendations e553 9.3.2. Ongoing Management: Recommendations e554 9.4. SVT in Older Populations e555 Acute Treatment and Ongoing Management: Recommendation e555 10. Quality-of-Life Considerations e555 11. Cost-Effectiveness e555 12. Shared Decision Making e556 13. Evidence Gaps and Future Research Needs e556 References e557 Appendix 1. Author Relationships With Industry and Other Entities (Relevant) e570 Appendix 2. Reviewer Relationships With Industry and Other Entities (Relevant) e571 Appendix 3. Abbreviations e574 Preamble Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, based on systematic methods to evaluate and classify evidence, provide a cornerstone of quality cardio- vascular care.


These guidelines, based on systematic methods to evaluate and classify evidence, provide a cornerstone of quality cardio- vascular care. In response to reports from the Institute of Medicine1,2 and a mandate to evaluate new knowledge and maintain relevance at the point of care, the ACC/AHA Task Force on Clinical Practice Guidelines (Task Force) modified its methodology.3 5 The relationships between guidelines, data standards, appro- priate use criteria, and performance measures are addressed Intended Use Practice guidelines provide recommendations applicable to patients with or at risk of developing cardiovascular dis- ease. The focus is on medical practice in the United States, but guidelines developed in collaboration with other organi- zations may have a broader target. Although guidelines may inform regulatory or payer decisions, they are intended to improve quality of care in the interest of patients. Evidence Review Guideline Writing Committee (GWC) members review the lit- erature; weigh the quality of evidence for or against particular tests, treatments, or procedures; and estimate expected health outcomes. In developing recommendations, the GWC uses evidence-based methodologies that are based on all available Literature searches focus on randomized controlled trials (RCTs) but also include registries, nonrandomized comparative and descriptive studies, case series, cohort stud- ies, systematic reviews, and expert opinion. Only selected ref- erences are cited. The Task Force recognizes the need for objective, indepen- dent Evidence Review Committees (ERCs) that include meth- odologists, epidemiologists, clinicians, and biostatisticians who systematically survey, abstract, and assess the evidence to address key clinical questions posed in the PICOTS format (P=population, I=intervention, C=comparator, O=outcome, Practical considerations, including time and resource constraints, limit the ERCs to evidence that is relevant to key clinical questions and lends itself to sys- tematic review and analysis that could affect the strength of corresponding recommendations.


The Task Force recognizes the need for objective, indepen- dent Evidence Review Committees (ERCs) that include meth- odologists, epidemiologists, clinicians, and biostatisticians who systematically survey, abstract, and assess the evidence to address key clinical questions posed in the PICOTS format (P=population, I=intervention, C=comparator, O=outcome, Practical considerations, including time and resource constraints, limit the ERCs to evidence that is relevant to key clinical questions and lends itself to sys- tematic review and analysis that could affect the strength of corresponding recommendations. Recommendations devel- oped by the GWC on the basis of the systematic review are marked SR . Guideline-Directed Medical Therapy The term guideline-directed medical therapy refers to care defined mainly by ACC/AHA Class I recommendations. For these and all recommended drug treatment regimens, the reader should confirm dosage with product insert mate- rial and carefully evaluate for contraindications and interac- tions. Recommendations are limited to treatments, drugs, and devices approved for clinical use in the United States. Class of Recommendation and Level of Evidence The Class of Recommendation (COR; ie, the strength of the rec- ommendation) encompasses the anticipated magnitude and cer- taintyofbenefitinproportiontorisk.TheLevelofEvidence(LOE) rates evidence supporting the effect of the intervention on the basis of the type, quality, quantity, and consistency of data from clinical trials and other reports (Table 1).5,7 Unless otherwise stated, recom- mendations are sequenced by COR and then by LOE.Where com- parative data exist, preferred strategies take precedence. When >1 drug, strategy, or therapy exists within the same COR and LOE and no comparative data are available, options are listed alphabetically. Each recommendation is followed by supplemental text linked to supporting references and evidence tables. Relationships With Industry and Other Entities The ACC and AHA sponsor the guidelines without com- mercial support, and members volunteer their time.


Relationships With Industry and Other Entities The ACC and AHA sponsor the guidelines without com- mercial support, and members volunteer their time. The Task Force zealously avoids actual, potential, or perceived con- flicts of interest that might arise through relationships with industry or other entities (RWI). All GWC members and reviewers are required to disclose current industry relation- ships or personal interests from 12 months before initiation of the writing effort. Management of RWI involves selecting a balanced GWC and assuring that the chair and a majority of committee members have no relevant RWI (Appendix 1). Members are restricted with regard to writing or voting on sec- tions to which their RWI apply. For transparency, members comprehensive disclosure information is available online. Comprehensive disclosure information for the Task Force is also available online. The Task Force strives to avoid bias by selecting experts from a broad array of backgrounds represent- ing different geographic regions, sexes, ethnicities, intellectual perspectives/biases, and scopes of clinical practice, and by inviting organizations and professional societies with related interests and expertise to participate as partners or collaborators. Individualizing Care in Patients With Associated Conditions and Comorbidities Managing patients with multiple conditions can be complex, especially when recommendations applicable to coexisting ill- nesses are discordant or interacting.8 The guidelines are intended to define practices meeting the needs of patients in most, but not all, circumstances. The recommendations should not replace clinical judgment. Clinical Implementation Management in accordance with guideline recommendations is effective only when followed. Adherence to recommendations can be enhanced by shared decision making between clinicians and patients, with patient engagement in selecting interventions based on individual values, preferences, and associated con- ditions and comorbidities. Consequently, circumstances may arise in which deviations from these guidelines are appropriate.


Consequently, circumstances may arise in which deviations from these guidelines are appropriate. Policy The recommendations in this guideline represent the official policy of the ACC and AHA until superseded by published addenda, statements of clarification, focused updates, or revised full-text guidelines. To ensure that guidelines remain current, new data are reviewed biannually to determine whether recommendations should be modified. In general, full revisions are posted in 5-year cycles.3,5 Jonathan L. Halperin, MD, FACC, FAHA Chair, ACC/AHA Task Force on Clinical Practice Guidelines 1.1. Methodology and Evidence Review The recommendations listed in this guideline are, whenever possible, evidence based. An extensive evidence review was conducted in April 2014 that included literature published through September 2014. Other selected references published through May 2015 were incorporated by the GWC. Literature included was derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. The relevant data are included in evidence tables in the Online Data Supplement. Key search words included but were not limited to the following: abla- tion therapy (catheter and radiofrequency; fast and slow pathway), accessory pathway (manifest and concealed), antiarrhythmic drugs, atrial fibrillation, atrial tachycardia, atrioventricular nodal reentrant (reentry, reciprocating) tachycardia, atrioventricular reentrant (reentry, reciprocat- ing) tachycardia, beta blockers, calcium channel blockers, cardiac imaging, cardioversion, cost effectiveness, cryother- apy, echocardiography, elderly (aged and older), focal atrial tachycardia, Holter monitor, inappropriate sinus tachycardia, Page et al 2015 ACC/AHA/HRS SVT Guideline e509 junctional tachycardia, multifocal atrial tachycardia, parox- ysmal supraventricular tachycardia, permanent form of junc- tional reciprocating tachycardia, pre-excitation, pregnancy, quality of life, sinoatrial node, sinus node reentry, sinus tachycardia, supraventricular tachycardia, supraventricular arrhythmia, tachycardia, tachyarrhythmia, vagal maneuvers (Valsalva maneuver), and Wolff-Parkinson-White syndrome.


Key search words included but were not limited to the following: abla- tion therapy (catheter and radiofrequency; fast and slow pathway), accessory pathway (manifest and concealed), antiarrhythmic drugs, atrial fibrillation, atrial tachycardia, atrioventricular nodal reentrant (reentry, reciprocating) tachycardia, atrioventricular reentrant (reentry, reciprocat- ing) tachycardia, beta blockers, calcium channel blockers, cardiac imaging, cardioversion, cost effectiveness, cryother- apy, echocardiography, elderly (aged and older), focal atrial tachycardia, Holter monitor, inappropriate sinus tachycardia, Page et al 2015 ACC/AHA/HRS SVT Guideline e509 junctional tachycardia, multifocal atrial tachycardia, parox- ysmal supraventricular tachycardia, permanent form of junc- tional reciprocating tachycardia, pre-excitation, pregnancy, quality of life, sinoatrial node, sinus node reentry, sinus tachycardia, supraventricular tachycardia, supraventricular arrhythmia, tachycardia, tachyarrhythmia, vagal maneuvers (Valsalva maneuver), and Wolff-Parkinson-White syndrome. Additionally, the GWC reviewed documents related to supra- ventricular tachycardia (SVT) previously published by the ACC, AHA, and Heart Rhythm Society (HRS). References selected and published in this document are representative and not all-inclusive. An independent ERC was commissioned to perform a systematic review of key clinical questions, the results of which were considered by the GWC for incorporation into this guideline. The systematic review report on the management of asymptomatic patients with Wolff-Parkinson-White (WPW) syndrome is published in conjunction with this guideline.9 Table 1. Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care* 1.2. Organization of the GWC The GWC consisted of clinicians, cardiologists, electrophysi- ologists (including those specialized in pediatrics), and a nurse (in the role of patient representative) and included representa- tives from the ACC, AHA, and HRS. 1.3. Document Review and Approval This document was reviewed by 8 official reviewers nomi- nated by the ACC, AHA, and HRS, and 25 individual content reviewers.


Document Review and Approval This document was reviewed by 8 official reviewers nomi- nated by the ACC, AHA, and HRS, and 25 individual content reviewers. Reviewers RWI information was distributed to the GWC and is published in this document (Appendix 2). This document was approved for publication by the gov- erning bodies of the ACC, the AHA, and the HRS. 1.4. Scope of the Guideline The purpose of this joint ACC/AHA/HRS document is to provide a contemporary guideline for the management of adults with all types of SVT other than atrial fibrillation (AF). Although AF is, strictly speaking, an SVT, the term SVT generally does not refer to AF. AF is addressed in the 2014 ACC/AHA/HRS Guideline for the Management of Atrial Fibrillation (2014 AF guideline).10 The present guide- line addresses other SVTs, including regular narrow QRS complex tachycardias, as well as other, irregular SVTs (eg, atrial flutter with irregular ventricular response and multi- focal atrial tachycardia [MAT]). This guideline supersedes the 2003 ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias. 11 It incor- porates new and existing knowledge derived from published clinical trials, basic science, and comprehensive review arti- cles, along with evolving treatment strategies and new drugs. Some recommendations from the earlier guideline have been updated as warranted by new evidence or a better under- standing of existing evidence, whereas other inaccurate, irrelevant, or overlapping recommendations were deleted or modified. Whenever possible, we reference data from the acute clinical care environment; however, in some cases, the reference studies from the invasive electrophysiology labo- ratory inform our understanding of arrhythmia diagnosis and management.


Whenever possible, we reference data from the acute clinical care environment; however, in some cases, the reference studies from the invasive electrophysiology labo- ratory inform our understanding of arrhythmia diagnosis and management. Although this document is aimed at the adult population ( 18 years of age) and offers no specific recom- mendations for pediatric patients, as per the reference list, we examined literature that included pediatric patients. In some cases, the data from noninfant pediatric patients helped inform this guideline. In the current healthcare environment, cost consider- ation cannot be isolated from shared decision making and patient-centered care. The AHA and ACC have acknowl- edged the importance of value in health care, calling for eventual development of a Level of Value for practice rec- ommendations in the 2014 ACC/AHA Statement on Cost/ Value Methodology in Clinical Practice Guidelines and Although quality-of-life and cost- effectiveness data were not sufficient to allow for devel- opment of specific recommendations, the GWC agreed the data warranted brief discussion (Sections 10 and 11). Throughout this document, and associated with all rec- ommendations and algorithms, the importance of shared decision making should be acknowledged. Each approach, ranging from observation to drug treatment to ablation, must be considered in the setting of a clear discussion with the patient regarding risk, benefit and personal preference. See Section 12 for additional information. In developing this guideline, the GWC reviewed prior pub- lished guidelines and related statements. Table 2 contains a list of guidelines and statements deemed pertinent to this writing effort and is intended for use as a resource, thus obviating the need to repeat existing guideline recommendations. 2. General Principles 2.1. Mechanisms and Definitions For the purposes of this guideline, SVT is defined as per Table 3, which provides definitions and the mechanism(s) of each type of SVT.


Mechanisms and Definitions For the purposes of this guideline, SVT is defined as per Table 3, which provides definitions and the mechanism(s) of each type of SVT. The term SVT does not generally include AF, and this document does not discuss the manage- ment of AF. 2.2. Epidemiology, Demographics, and Public Health Impact The epidemiology of SVT, including its frequency, pat- terns, causes, and effects, is imprecisely defined because of incomplete data and failure to discriminate among AF, atrial flutter, and other supraventricular arrhythmias. The best available evidence indicates that the prevalence of SVT in the general population is 2.29 per 1000 persons.32 When adjusted by age and sex in the US population, the incidence of paroxysmal supraventricular tachycardia (PSVT) is esti- mated to be 36 per 100 000 persons per year.32 There are approximately 89 000 new cases per year and 570 000 per- sons with PSVT.32 Compared with patients with cardiovas- cular disease, those with PSVT without any cardiovascular disease are younger (37 versus 69 years; P=0.0002) and have faster PSVT (186 bpm versus 155 bpm; P=0.0006). Women have twice the risk of men of developing PSVT.32 Individuals >65 years of age have >5 times the risk of younger persons of developing PSVT.32 Patients with PSVT who are referred to specialized cen- ters for management with ablation are younger, have an equal sex distribution, and have a low frequency of cardio- The frequency of atrioventricular nodal reentrant tachycardia (AVNRT) is greater in women than in men. This may be due to an actual higher incidence in women, or it may reflect referral bias.


This may be due to an actual higher incidence in women, or it may reflect referral bias. In persons who are middle-aged or older, AVNRT is more common, whereas in adolescents, the prevalence may be more balanced between atrioventricular reentrant tachycardia (AVRT) and AVNRT, or AVRT may be more prevalent.32 The relative frequency of tachycardia mediated by an accessory pathway decreases with age. The incidence of manifest pre-excitation or WPW pattern on ECG tracings in the general population is 0.1% to 0.3%. However, not all patients with manifest ventricu- lar pre-excitation develop PSVT.47 49 The limited data on the public health impact of SVT indicate that the arrhythmia is commonly a reason for emergency department and primary care physician visits but is infrequently the primary reason for hospital admission.11,50,51 Page et al 2015 ACC/AHA/HRS SVT Guideline e511 2.3. Evaluation of the Patient With Suspected or Documented SVT 2.3.1. Clinical Presentation and Differential Diagnosis on the Basis of Symptoms Patients seen in consultation for palpitations often describe symptoms with characteristic features suggestive of SVT that may guide physicians to appropriate testing and a definitive diagnosis. The diagnosis of SVT is often made in the emergency department, but it is common to elicit symptoms suggestive of SVT before initial electrocardiogram/electrocardiographic (ECG) documentation.


The diagnosis of SVT is often made in the emergency department, but it is common to elicit symptoms suggestive of SVT before initial electrocardiogram/electrocardiographic (ECG) documentation. SVT symptom onset often begins in adulthood; in 1 study in adults, the mean age of symptom onset was 32 18 years of age for AVNRT, versus 23 14 years of age In contrast, in a study conducted in pediatric popu- lations, the mean ages of symptom onset of AVRT and AVNRT In comparison with AVRT, patients with AVNRT are more likely to be female, with an age AVNRT onset has been reported after the age of 50 years in 16% and before the age of 20 years in Among women with SVT and no other cardiovascular disease, the onset of symptoms occurred during childbearing years (eg, 15 to 50 years) in 58%.32 The first onset of SVT occurred in only 3.9% of women during pregnancy, but among women with an established history of SVT, 22% reported that pregnancy exacerbated their symptoms.58 SVT has an impact on quality of life, which varies according to the frequency of episodes, the duration of SVT, and whether symptoms occur not only with exercise but also at rest.53,59 retrospective study in which the records of patients <21 years of age with WPW pattern on the ECG were reviewed, 64% of patients had symptoms at presentation, and an additional 20% developed symptoms during follow-up.60 Modes of presentation included documented SVT in 38%, palpitations in 22%, chest pain in 5%, syncope in 4%, AF in 0.4%, and sudden cardiac death (SCD) in 0.2%.60 Although this was a pediatric population, it provided symptom data that are likely applicable to adults.


SVT symptom onset often begins in adulthood; in 1 study in adults, the mean age of symptom onset was 32 18 years of age for AVNRT, versus 23 14 years of age In contrast, in a study conducted in pediatric popu- lations, the mean ages of symptom onset of AVRT and AVNRT In comparison with AVRT, patients with AVNRT are more likely to be female, with an age AVNRT onset has been reported after the age of 50 years in 16% and before the age of 20 years in Among women with SVT and no other cardiovascular disease, the onset of symptoms occurred during childbearing years (eg, 15 to 50 years) in 58%.32 The first onset of SVT occurred in only 3.9% of women during pregnancy, but among women with an established history of SVT, 22% reported that pregnancy exacerbated their symptoms.58 SVT has an impact on quality of life, which varies according to the frequency of episodes, the duration of SVT, and whether symptoms occur not only with exercise but also at rest.53,59 retrospective study in which the records of patients <21 years of age with WPW pattern on the ECG were reviewed, 64% of patients had symptoms at presentation, and an additional 20% developed symptoms during follow-up.60 Modes of presentation included documented SVT in 38%, palpitations in 22%, chest pain in 5%, syncope in 4%, AF in 0.4%, and sudden cardiac death (SCD) in 0.2%.60 Although this was a pediatric population, it provided symptom data that are likely applicable to adults. A confounding factor in diagnosing SVT is the need to differen- tiate symptoms of SVT from symptoms of panic and anxiety disorders or any condition of heightened awareness of sinus tachycardia (such as postural orthostatic tachycardia syndrome).


A confounding factor in diagnosing SVT is the need to differen- tiate symptoms of SVT from symptoms of panic and anxiety disorders or any condition of heightened awareness of sinus tachycardia (such as postural orthostatic tachycardia syndrome). In 1 study, the criteria for panic disorder were fulfilled in 67% of patients with SVT that remained unrecognized after their ini- tial evaluation. Physicians attributed symptoms of SVT to panic, anxiety, or stress in 54% of patients, with women more likely to be mislabeled with panic disorder than men.61 When AVNRT and AVRT are compared, symptoms appear to differ substantially. Patients with AVNRT more frequently describe symptoms of shirt flapping or neck pounding 54,62 that may be related to pulsatile reversed flow when the right atrium contracts against a closed tricuspid valve (cannon a-waves). During 1 invasive study of patients with AVNRT and AVRT, both arrhythmias decreased arterial pressure and increased left atrial pressure, but simulation of SVT mecha- nism by timing the pacing of the atria and ventricles showed significantly higher left atrial pressure in simulated AVNRT than in simulatedAVRT.62 Polyuria is particularly common with AVNRT and is related to higher right atrial pressures and ele- vated levels of atrial natriuretic protein in patients with AVNRT compared with patients who have AVRT or atrial flutter.63 Table 2.


During 1 invasive study of patients with AVNRT and AVRT, both arrhythmias decreased arterial pressure and increased left atrial pressure, but simulation of SVT mecha- nism by timing the pacing of the atria and ventricles showed significantly higher left atrial pressure in simulated AVNRT than in simulatedAVRT.62 Polyuria is particularly common with AVNRT and is related to higher right atrial pressures and ele- vated levels of atrial natriuretic protein in patients with AVNRT compared with patients who have AVRT or atrial flutter.63 Table 2. Associated Guidelines and Statements Title Organization Publication Year (Reference) Guidelines Atrial fibrillation AHA/ACC/HRS 201410 Stable ischemic heart disease ACC/AHA/ACP/ AATS/ PCNA/ SCAI/STS Valvular heart disease AHA/ACC 201414 Assessment of cardiovascular risk Heart failure ACC/AHA 201316 Antithrombotic therapy for valvular heart disease Atrial fibrillation ESC 201218 Device-based therapy ACC/AHA/HRS 201220 Atrial fibrillation CCS 201421 Hypertrophic cardiomyopathy ACC/AHA 201123 Secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease Adult congenital heart disease * Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) Statements Catheter ablation in children and patients with congenital heart disease Postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope Arrhythmias in adult congenital heart disease Catheter and surgical ablation of atrial fibrillation CPR and emergency cardiovascular care * *A revision to the current document is being prepared, with publication expected in late 2015.


Associated Guidelines and Statements Title Organization Publication Year (Reference) Guidelines Atrial fibrillation AHA/ACC/HRS 201410 Stable ischemic heart disease ACC/AHA/ACP/ AATS/ PCNA/ SCAI/STS Valvular heart disease AHA/ACC 201414 Assessment of cardiovascular risk Heart failure ACC/AHA 201316 Antithrombotic therapy for valvular heart disease Atrial fibrillation ESC 201218 Device-based therapy ACC/AHA/HRS 201220 Atrial fibrillation CCS 201421 Hypertrophic cardiomyopathy ACC/AHA 201123 Secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease Adult congenital heart disease * Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) Statements Catheter ablation in children and patients with congenital heart disease Postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope Arrhythmias in adult congenital heart disease Catheter and surgical ablation of atrial fibrillation CPR and emergency cardiovascular care * *A revision to the current document is being prepared, with publication expected in late 2015. AATS indicates American Association for Thoracic Surgery; ACC, American College of Cardiology; ACCP, American College of Chest Physicians; ACP, American College of Physicians; AHA, American Heart Association; CCS, Canadian Cardiovascular Society; CPR, cardiopulmonary resuscitation; ECAS, European Cardiac Arrhythmia Society; EHRA, European Heart Rhythm Association; ESC, European Society of Cardiology; HRS, Heart Rhythm Society; JNC, Joint National Committee; NHLBI, National Heart, Lung, and Blood Institute; PACES, Pediatric and Congenital Electrophysiology Society; PCNA, Preventive Cardiovascular Nurses Association; SCAI, Society for Cardiovascular Angiography and Interventions; and STS, Society of Thoracic Surgeons. Table 3. Relevant Terms and Definitions Arrhythmia/Term Definition Supraventricular tachycardia (SVT) An umbrella term used to describe tachycardias (atrial and/or ventricular rates in excess of 100 bpm at rest), the mechanism of which involves tissue from the His bundle or above.


Relevant Terms and Definitions Arrhythmia/Term Definition Supraventricular tachycardia (SVT) An umbrella term used to describe tachycardias (atrial and/or ventricular rates in excess of 100 bpm at rest), the mechanism of which involves tissue from the His bundle or above. These SVTs include inappropriate sinus tachycardia, AT (including focal and multifocal AT), macroreentrant AT (including typical atrial flutter), junctional tachycardia, AVNRT, and various forms of accessory pathway-mediated reentrant tachycardias. In this guideline, the term does not include AF. Paroxysmal supraventricular tachycardia (PSVT) A clinical syndrome characterized by the presence of a regular and rapid tachycardia of abrupt onset and termination. These features are characteristic of AVNRT or AVRT, and, less frequently, AT. PSVT represents a subset of SVT. Atrial fibrillation (AF) A supraventricular arrhythmia with uncoordinated atrial activation and, consequently, ineffective atrial contraction. ECG characteristics include: 1) irregular atrial activity, 2) absence of distinct P waves, and 3) irregular R-R intervals (when atrioventricular conduction is present). AF is not addressed in this document. Sinus tachycardia Rhythm arising from the sinus node in which the rate of impulses exceeds 100 bpm. Physiologic sinus tachycardia Appropriate increased sinus rate in response to exercise and other situations that increase sympathetic tone. Inappropriate sinus tachycardia Sinus heart rate >100 bpm at rest, with a mean 24-h heart rate >90 bpm not due to appropriate physiological responses or primary causes such as hyperthyroidism or anemia. Atrial tachycardia (AT) Focal AT An SVT arising from a localized atrial site, characterized by regular, organized atrial activity with discrete P waves and typically an isoelectric segment between P waves. At times, irregularity is seen, especially at onset ( warm-up ) and termination ( warm-down ). Atrial mapping reveals a focal point of origin.


At times, irregularity is seen, especially at onset ( warm-up ) and termination ( warm-down ). Atrial mapping reveals a focal point of origin. Sinus node reentry tachycardia A specific type of focal AT that is due to microreentry arising from the sinus node complex, characterized by abrupt onset and termination, resulting in a P-wave morphology that is indistinguishable from sinus rhythm. Multifocal atrial tachycardia (MAT) An irregular SVT characterized by 3 distinct P-wave morphologies and/or patterns of atrial activation at different rates. The rhythm is always irregular. Atrial flutter Cavotricuspid isthmus dependent atrial flutter: typical Macroreentrant AT propagating around the tricuspid annulus, proceeding superiorly along the atrial septum, inferiorly along the right atrial wall, and through the cavotricuspid isthmus between the tricuspid valve annulus and the Eustachian valve and ridge. This activation sequence produces predominantly negative sawtooth flutter waves on the ECG in leads 2, 3, and aVF and a late positive deflection in V1. The atrial rate can be slower than the typical 300 bpm (cycle length 200 ms) in the presence of antiarrhythmic drugs or scarring. It is also known as typical atrial flutter or cavotricuspid isthmus dependent atrial flutter or counterclockwise atrial flutter. Cavotricuspid isthmus dependent atrial flutter: reverse typical Macroreentrant AT that propagates around in the direction reverse that of typical atrial flutter. Flutter waves typically appear positive in the inferior leads and negative in V1. This type of atrial flutter is also referred to as reverse typical atrial flutter or clockwise typical atrial flutter. Atypical or non cavotricuspid isthmus dependent atrial flutter Macroreentrant ATs that do not involve the cavotricuspid isthmus. A variety of reentrant circuits may include reentry around the mitral valve annulus or scar tissue within the left or right atrium.


A variety of reentrant circuits may include reentry around the mitral valve annulus or scar tissue within the left or right atrium. A variety of terms have been applied to these arrhythmias according to the re-entry circuit location, including particular forms, such as LA flutter and LA macroreentrant tachycardia or incisional atrial re-entrant tachycardia due to re-entry around surgical scars. Junctional tachycardia A nonreentrant SVT that arises from the AV junction (including the His bundle). Atrioventricular nodal reentrant tachycardia (AVNRT) A reentrant tachycardia involving 2 functionally distinct pathways, generally referred to as fast and slow pathways. Most commonly, the fast pathway is located near the apex of Koch s triangle, and the slow pathway inferoposterior to the compact AV node tissue. Variant pathways have been described, allowing for slow-slow AVNRT. Typical AVNRT AVNRT in which a slow pathway serves as the anterograde limb of the circuit and the fast pathway serves as the retrograde limb (also called slow-fast AVNRT ). Atypical AVNRT AVNRT in which the fast pathway serves as the anterograde limb of the circuit and a slow pathway serves as the retrograde limb (also called fast-slow AV node reentry ) or a slow pathway serves as the anterograde limb and a second slow pathway serves as the retrograde limb (also called slow-slow AVNRT ). Accessory pathway For the purpose of this guideline, an accessory pathway is defined as an extranodal AV pathway that connects the myocardium of the atrium to the ventricle across the AV groove. Accessory pathways can be classified by their location, type of conduction (decremental or nondecremental), and whether they are capable of conducting anterogradely, retrogradely, or in both directions.


Accessory pathways can be classified by their location, type of conduction (decremental or nondecremental), and whether they are capable of conducting anterogradely, retrogradely, or in both directions. Of note, accessory pathways of other types (such as atriofascicular, nodo-fascicular, nodo-ventricular, and fasciculoventricular pathways) are uncommon and are discussed only briefly in this document (Section 7). Manifest accessory pathways A pathway that conducts anterogradely to cause ventricular pre-excitation pattern on the ECG. (Continued) Page et al 2015 ACC/AHA/HRS SVT Guideline e513 True syncope is infrequent with SVT, but complaints of light-headedness are common. In patients with WPW syn- drome, syncope should be taken seriously but is not neces- sarily associated with increased risk of SCD.64 The rate of AVRT is faster when AVRT is induced during exercise,65 yet the rate alone does not explain symptoms of near- syncope. Elderly patients with AVNRT are more prone to syncope or near-syncope than are younger patients, but the tachycardia rate is generally slower in the elderly.66,67 The drop in blood pressure (BP) during SVT is greatest in the first 10 to 30 seconds and somewhat normalizes within 30 to 60 seconds, despite minimal changes in rate.68,69 Shorter ventriculoatrial intervals are associated with a greater mean decrease in BP.69 Studies have demonstrated a relationship between hemodynamic changes and the relative timing of atrial and ventricular activation. In a study of patients with AVNRT with short versus long ventriculoatrial intervals, there was no significant difference in tachycardia cycle ; however, the induction of typical AVNRT caused a marked initial fall in systemic BP, followed by only partial recovery that resulted in stable hypotension and a reduction in cardiac output due to a decrease in stroke volume.


In a study of patients with AVNRT with short versus long ventriculoatrial intervals, there was no significant difference in tachycardia cycle ; however, the induction of typical AVNRT caused a marked initial fall in systemic BP, followed by only partial recovery that resulted in stable hypotension and a reduction in cardiac output due to a decrease in stroke volume. In comparison, atypical AVNRT, having a longer ventriculoatrial interval, exhibited a lesser degree of initial hypotension, a complete recovery of BP, and no significant change in cardiac output.70 The contrasting hemodynamic responses without sig- nificant differences in heart rate during SVT confirm that rate alone does not account for these hemodynamic changes. Atrial contraction on a closed valve might impair pulmonary drain- age and lead to neural factors that account for these observa- tions. These findings were confirmed in a study performed in the electrophysiological (EP) laboratory: When pacing was used to replicate the timing of ventricular and atrial activation during SVT, the decrease in BP was greatest with simultane- ous ventriculoatrial timing, smaller with a short vertriculoatrial interval, and smallest with a long ventriculoatrial interval.71 An increase in central venous pressure followed the same trend. Sympathetic nerve activity increased with all 3 pacing modali- ties but was most pronounced with simultaneous atrial and ventricular pacing or a short ventriculoatrial interval. In a study of the relationship of SVT with driving, 57% of patients with SVT experienced an episode while driving, and 24% of these considered it to be an obstacle to driving.72 This sentiment was most common in patients who had experienced syncope or near-syncope. Among patients who experienced SVT while driving, 77% felt fatigue, 50% had symptoms of near-syncope, and 14% experienced syncope. Women had more symptoms in each category.


Among patients who experienced SVT while driving, 77% felt fatigue, 50% had symptoms of near-syncope, and 14% experienced syncope. Women had more symptoms in each category. See Online Data Supplement 1 for additional data on clinical presentation and differential diagnosis on the basis of symptoms. Concealed accessory pathway A pathway that conducts only retrogradely and does not affect the ECG pattern during sinus rhythm. Pre-excitation pattern An ECG pattern reflecting the presence of a manifest accessory pathway connecting the atrium to the ventricle. Pre-excited ventricular activation over the accessory pathway competes with the anterograde conduction over the AV node and spreads from the accessory pathway insertion point in the ventricular myocardium. Depending on the relative contribution from ventricular activation by the normal AV nodal/His Purkinje system versus the manifest accessory pathway, a variable degree of pre-excitation, with its characteristic pattern of a short P-R interval with slurring of the initial upstroke of the QRS complex (delta wave), is observed. Pre-excitation can be intermittent or not easily appreciated for some pathways capable of anterograde conduction; this is usually associated with a low-risk pathway, but exceptions occur. Asymptomatic pre-excitation (isolated pre-excitation) The abnormal pre-excitation ECG pattern in the absence of documented SVT or symptoms consistent with SVT. Wolff-Parkinson-White syndrome Syndrome characterized by documented SVT or symptoms consistent with SVT in a patient with ventricular pre-excitation during sinus rhythm. Atrioventricular reentrant tachycardia (AVRT) A reentrant tachycardia, the electrical pathway of which requires an accessory pathway, the atrium, atrioventricular node (or second accessory pathway), and ventricle. Orthodromic AVRT An AVRT in which the reentrant impulse uses the accessory pathway in the retrograde direction from the ventricle to the atrium, and the AV node in the anterograde direction.


Orthodromic AVRT An AVRT in which the reentrant impulse uses the accessory pathway in the retrograde direction from the ventricle to the atrium, and the AV node in the anterograde direction. The QRS complex is generally narrow or may be wide because of pre-existing bundle-branch block or aberrant conduction. Antidromic AVRT An AVRT in which the reentrant impulse uses the accessory pathway in the anterograde direction from the atrium to the ventricle, and the AV node for the retrograde direction. Occasionally, instead of the AV node, another accessory pathway can be used in the retrograde direction, which is referred to as pre-excited AVRT. The QRS complex is wide (maximally pre-excited). Permanent form of junctional reciprocating tachycardia (PJRT) A rare form of nearly incessant orthodromic AVRT involving a slowly conducting, concealed, usually posteroseptal accessory pathway. Pre-excited AF AF with ventricular pre-excitation caused by conduction over 1 accessory pathway(s). AF indicates atrial fibrillation; AT, atrial tachycardia; AV, atrioventricular; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia; bpm, beats per minute; ECG, electrocardiogram/electrocardiographic; LA, left atrial; MAT, multifocal atrial tachycardia; PJRT, permanent form of junctional reciprocating tachycardia; PSVT, paroxysmal supraventricular tachycardia; SVT, supraventricular tachycardia; and WPW, Wolff-Parkinson-White. Table 3. Continued Arrhythmia/Term Definition 2.3.2. Evaluation of the ECG Figures 1 to 6 provide representative ECGs, with Figure 1 showing ventricular tachycardia (VT) and Figures 2 to 5 showing some of the most common types of these SVTs. A 12-lead ECG obtained during tachycardia and during sinus rhythm may reveal the etiology of tachycardia. For the patient who describes prior, but not current, symptoms of palpitations, the resting ECG can identify pre-excitation that should prompt a referral to a cardiac electrophysiologist. A wide-complex tachycardia (QRS duration >120 ms) may represent either VT or a supraventricular rhythm with abnormal conduction.


A wide-complex tachycardia (QRS duration >120 ms) may represent either VT or a supraventricular rhythm with abnormal conduction. Conduction abnormalities may be due to rate-related aberrant conduction, pre-existing bundle- branch block seen in sinus rhythm, or an accessory pathway that results in pre-excitation (Table 4). The presence of atrio- ventricular (AV) dissociation (with ventricular rate faster than atrial rate) or fusion complexes representing dissociation of supraventricular impulses from a ventricular rhythm provides the diagnosis of VT (Figure 1). Other criteria are useful but not diagnostic. Concordance of the precordial QRS com- plexes such that all are positive or negative suggests VT or pre-excitation, whereas QRS complexes in tachycardia that are identical to those seen in sinus rhythm are consistent with SVT. Other, more complicated ECG algorithms have been developed to distinguish VT from SVT, such as the Brugada criteria, which rely on an examination of the QRS morphol- ogy in the precordial leads,73 and the Vereckei algorithm, which is based on an examination of the QRS complex in lead (Table 5). The failure to correctly identify VT can be potentially life threatening, particularly if misdiagnosis results in VT being treated with verapamil or diltiazem. Adenosine is suggested in the 2010 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 8: Adult Advanced Cardiovascular Life Support (2010 Adult if a wide-complex tachycardia is mono- morphic, regular, and hemodynamically tolerated, because adenosine may help convert the rhythm to sinus and may help in the diagnosis. When doubt exists, it is safest to assume any wide-complex tachycardia is VT, particularly in patients with known cardiovascular disease, such as prior myocardial infarction. For a patient presenting in SVT, the 12-lead ECG can potentially identify the arrhythmia mechanism (Figure 7).


For a patient presenting in SVT, the 12-lead ECG can potentially identify the arrhythmia mechanism (Figure 7). The tachycardia should first be classified according to whether there is a regular or irregular ventricular rate.An irregular ven- tricular rate suggests AF, MAT, or atrial flutter with variable AV conduction. When AF is associated with a rapid ventricu- lar response, the irregularity of the ventricular response is less easily detected and can be misdiagnosed as a regular SVT.76 If the atrial rate exceeds the ventricular rate, then atrial flutter or AT (focal or multifocal) is usually present (rare cases of AVNRT with 2:1 conduction have been described77 ). If the SVT is regular, this may represent AT with 1:1 con- duction or an SVT that involves theAV node. Junctional tachy- cardias, which originate in the AV junction (including the His bundle), can be regular or irregular, with variable conduction to the atria. SVTs that involve the AV node as a required com- ponent of the tachycardia reentrant circuit include AVNRT and 6). In these reentrant tachycardias, the retrogradely con- ducted P wave may be difficult to discern, especially if bundle- branch block is present. In typical AVNRT, atrial activation is nearly simultaneous with the QRS, so the terminal portion of the P wave is usually located at the end of the QRS complex, appearing as a narrow and negative deflection in the inferior leads (a pseudo S wave) and a slightly positive deflection at the end of the QRS complex in lead V1 (pseudo R ). In ortho- dromic AVRT (with anterograde conduction down the AV node), the P wave can usually be seen in the early part of the ST-T segment.


In ortho- dromic AVRT (with anterograde conduction down the AV node), the P wave can usually be seen in the early part of the ST-T segment. In typical forms of AVNRT and AVRT, because the P wave is located closer to the prior QRS complex than the subsequent QRS complex, the tachycardias are referred to as having a short RP. They also have a 1:1 relationship between the P wave and QRS complex, except in rare cases of AVNRT in which 2:1 AV block or various degrees of AV block can occur. In unusual cases of AVNRT (such as fast-slow ), the P wave is closer to the subsequent QRS complex, providing a long RP. The RP is also long during an uncommon form of AVRT, referred to as the permanent form of junctional recip- rocating tachycardia (PJRT), in which an unusual accessory bypass tract with decremental (slowly conducting) retro- grade conduction during orthodromicAVRT produces delayed atrial activation and a long RP interval. A long RP interval is typical of AT because the rhythm is driven by the atrium and conducts normally to the ventricles. In AT, the ECG will typically show a P wave with a morphol- ogy that differs from sinus that is usually seen near the end of or shortly after the T wave (Figure 5). In sinus node reentry Figure 1. ECG showing AV dissociation during VT in a patient with a wide QRS complex tachycardia. *P waves are marked with arrows. AV indicates atrioventricular; ECG, electrocardio- gram; and VT, ventricular tachycardia. Reproduced with permis- sion from Blomstr m-Lundqvist et al.11 Page et al 2015 ACC/AHA/HRS SVT Guideline e515 tachycardia, a form of focal AT, the P-wave morphology is identical to the P wave in sinus rhythm. 2.4.


Reproduced with permis- sion from Blomstr m-Lundqvist et al.11 Page et al 2015 ACC/AHA/HRS SVT Guideline e515 tachycardia, a form of focal AT, the P-wave morphology is identical to the P wave in sinus rhythm. 2.4. Principles of Medical Therapy See Figure 8 for the algorithm for acute treatment of tachy- cardia of unknown mechanism; Figure 9 for the algorithm for ongoing management of tachycardia of unknown mechanism; Table 6 for acute drug therapy for SVT (intravenous adminis- tration); and Table 7 for ongoing drug therapy for SVT (oral administration). 2.4.1. Acute Treatment: Recommendations Because patients with SVT account for approximately emer- gency physicians may be the first to evaluate patients whose tachycardia mechanism is unknown and to have the opportunity to diagnose the mechanism of arrhythmia. It is important to record a 12-lead ECG to differentiate tachy- cardia mechanisms according to whether the AV node is an obligate component (Section 2.3.2), because treatment that targets the AV node will not reliably terminate tachycardias Figure 2. Typical AVNRT and normal sinus rhythm after conversion. Upper panel: The arrow points to the P waves, which are inscribed at the end of the QRS complex, seen best in the inferior leads and as a slightly positive R (pseudo r prime) in lead V1. The reentrant circuit involves anterograde conduction over a slow atrioventricular node pathway, followed by retrograde conduction in a fast atrioventricular node pathway. Typical AVNRT is a type of short RP tachycardia. Middle panel: When the patient is in sinus rhythm, the arrow indicates where the R is absent in V1. Bottom panels: Magnified portions of lead V1 in AVNRT (left) and sinus rhythm (right) are shown. AVNRT indicates atrioventricular nodal reentrant tachycardia. that are not AV node dependent.


AVNRT indicates atrioventricular nodal reentrant tachycardia. that are not AV node dependent. Also, if the QRS duration is >120 ms, it is crucial to distinguish VT from SVT with aberrant conduction, pre-existing bundle-branch block, or pre-excitation (Table 4). In particular, the administration of verapamil or diltiazem for treatment of either VT or a pre-excited AF may lead to hemodynamic compromise or may accelerate the ventricular rate and lead to ventricular fibrillation. Recommendations for Acute Treatment of SVT of Unknown Mechanism COR LOE Recommendations I B-R 1. Vagal maneuvers are recommended for acute treatment in patients with regular SVT.82 84 See Online Data and 3. For acute conversion of SVT, vagal maneuvers, including Valsalva and carotid sinus massage, can be performed quickly and should be the first-line intervention to terminate SVT. These maneuvers should be performed with the patient in the supine position. Vagal maneuvers typically will not be effective if the rhythm does not involve the AV node as a requisite component of a reentrant circuit.


Vagal maneuvers typically will not be effective if the rhythm does not involve the AV node as a requisite component of a reentrant circuit. There is no gold standard for proper Valsalva maneuver technique but, in general, the patient raises intrathoracic pressure by bearing down against a closed glottis for 10 to 30 seconds, equivalent to at least 30 mm Hg to 40 mm Hg.82,84 Carotid massage is performed after absence of bruit has been confirmed by auscultation, by applying steady pressure over the right or left carotid sinus Another vagal maneuver based on the classic diving reflex consists of applying an ice-cold, wet towel to the ; in a laboratory setting, facial immersion in water at 10 C (50 F) has proved effective in terminating tachycardia, as well.86 One study involving 148 patients with SVT demonstrated that Valsalva was more successful than carotid sinus massage, and switching from 1 technique to the other resulted in an overall success rate of 27.7%.82 The practice of applying pressure to the eyeball is potentially dangerous and has been abandoned. I B-R 2. Adenosine is recommended for acute treatment in patients with regular SVT.42,51,83,87 92 See Online Data and 3. Adenosine has been shown in nonrandomized trials in the emergency department or prehospital setting to effectively terminate SVT that is due to either AVNRT or AVRT, with success rates ranging from 78% to 96%. Although patients may experience side effects, such as chest discomfort, shortness of breath, and flushing, serious adverse effects are rare because of the drug s very short half-life.93 Adenosine may also be useful diagnostically, to unmask atrial flutter or AT, but it is uncommon for adenosine to terminate these atrial arrhythmias.91 It should be administered via proximal IV as a rapid bolus infusion followed by a saline flush.


Although patients may experience side effects, such as chest discomfort, shortness of breath, and flushing, serious adverse effects are rare because of the drug s very short half-life.93 Adenosine may also be useful diagnostically, to unmask atrial flutter or AT, but it is uncommon for adenosine to terminate these atrial arrhythmias.91 It should be administered via proximal IV as a rapid bolus infusion followed by a saline flush. Continuous ECG recording during adenosine administration may help diagnostically and can also distinguish drug failure due to failure to terminate the arrhythmias versus successful termination with immediate arrhythmia reinitiation. I B-NR Synchronized cardioversion is recommended for acute treatment in patients with hemodynamically unstable SVT when vagal maneuvers or adenosine are ineffective or not feasible.94 See Online Data Supplement 3. Sinus rhythm must be promptly restored in patients with SVT who are hemodynamically unstable. The safety and effectiveness of cardioversion in the prehospital setting was analyzed in a cohort of patients with hemodynamically unstable SVT who had failed to convert with vagal maneuvers and intravenous pharmacological therapy, and cardioversion successfully restored sinus rhythm in all patients.94 The 2010 adult ACLS guideline75 advises synchronized cardioversion for any persistent SVT resulting in hypotension, acutely altered mental status, signs of shock, chest pain, or acute heart failure symptoms but recommends that adenosine be considered first if the tachycardia is regular and has a narrow QRS complex. Figure 3. Atypical AVNRT. Arrows point to the P wave. The reentrant circuit involves anterograde conduction over a fast atrioventricular node pathway, followed by retrograde conduction in a slow atrioventricular node pathway, resulting in a retrograde P wave (negative polarity in inferior leads) with long RP interval. This ECG does not exclude PJRT or a low septal atrial tachycardia, which can appear very similar to this ECG.


This ECG does not exclude PJRT or a low septal atrial tachycardia, which can appear very similar to this ECG. AVNRT indicates atrioventricular nodal reentrant tachycardia; ECG, electrocardiogram; and PJRT, permanent form of junctional reciprocating tachycardia. Page et al 2015 ACC/AHA/HRS SVT Guideline e517 2.4.2. Ongoing Management: Recommendations The recommendations and algorithm (Figure 9) for ongoing management, along with other recommendations and algo- rithms for specific SVTs that follow, are meant to include consideration of patient preferences and clinical judgment; this may include consideration of consultation with a car- diologist or clinical cardiac electrophyisiologist, as well as patient comfort with possible invasive diagnostic and therapeutic intervention. Recommendations for treatment options (including drug therapy, ablation, or observation) must be considered in the context of frequency and dura- tion of the SVT, along with clinical manifestations, such as symptoms or adverse consequences (eg, development of cardiomyopathy). Recommendations for Ongoing Management of SVT of Unknown Mechanism COR LOE Recommendations I B-R Oral beta blockers, diltiazem, or verapamil is useful for ongoing management in patients with symptomatic SVT who do not have ventricular pre-excitation during sinus rhythm.46,98,99 See Online Data Supplement 2. Although many patients prefer to undergo potentially curative therapy with ablation, given its high success rate, and although ablation may be mandatory therapy for patients in certain occupations (eg, pilots, bus drivers), patients may prefer not to undergo ablation or may not have access to a cardiac electrophysiologist. In these latter cases, pharmacological therapy with AV nodal blockers is an appropriate option for long-term prophylactic therapy. Pharmacological therapy with verapamil (dosage up to 480 mg/day) has been studied in RCTs, with reductions documented in SVT episode frequency and duration as recorded by Holter monitoring or subjective episode frequency recording in diaries.98 Evidence for beta blockers is limited.


Pharmacological therapy with verapamil (dosage up to 480 mg/day) has been studied in RCTs, with reductions documented in SVT episode frequency and duration as recorded by Holter monitoring or subjective episode frequency recording in diaries.98 Evidence for beta blockers is limited. One small study randomized patients with SVT to digoxin (0.375 mg/day), propranolol (240 mg/day), or verapamil (480 mg/day), with 1 week of placebo washout between drug regimens.99 Reduction in the number of episodes and duration of SVT (ascertained by diary and weekly 24-h Holter) was similar among the treatment groups, and all 3 medications were well tolerated.99 I B-NR 2. EP study with the option of ablation is useful for the diagnosis and potential treatment of SVT.36,100 106 See Online Data Supplement 2. EP testing with the option of ablation is useful as first-line therapy for treatment of symptomatic SVT, as it provides the potential for definitive cure without the need for chronic pharmacological therapy. Large registry studies report high success rates for ablation of both AVNRT and AVRT, with low frequency of potentially serious complications (Table 8). I C-LD 3. Patients with SVT should be educated on how to perform vagal maneuvers for ongoing management of SVT.82 See Online Data Supplement 2. When properly performed, vagal maneuvers can terminate SVT, so patient education on this maneuver may help to avoid a more prolonged tachycardia episode and reduce the need to seek medical attention. Vagal maneuvers should be performed with the patient in the supine position.