Aortic Pulse-Wave Velocity and Its Relationship to Mortality in Diabetes and Glucose Intolerance: An Integrated Index of Vascular Function? Association of sleep apnea and type II diabetes: a population-based study. Assessment of endothelial function using peripheral waveform analysis: a clinical application. Elevated C-Reactive Protein in Patients With Obstructive Sleep Apnea Increased arterial wave reflections predict severe cardiovascular events in patients undergoing percutaneous coronary interventions. Impairment of Endothelium-Dependent Vasodilation of Resistance Vessels in Patients With Obstructive Sleep Apnea Effects of long-term treatment for obstructive sleep apnea on pulse wave velocity Ethnic differences in arterial stiffness and wave reflections after cigarette smoking Elevated Levels of C-Reactive Protein and Interleukin-6 in Patients With Obstructive Sleep Apnea Syndrome Are Decreased by Nasal Continuous Positive Airway Pressure Circadian variation in the frequency of onset of acute myocardial infarction. Prognostic Value of Aortic Pulse Wave Velocity as Index of Arterial Stiffness in the General Population Effects of continuous positive airway pressure on early signs of atherosclerosis in obstructive sleep apnea. Effect of different antihypertensive drug classes on central aortic pressure. CPAP and measures of cardiovascular risk in males with OSAS Arterial stiffness increases during obstructive sleep apneas. Effect of continuous positive airway pressure therapy on aortic stiffness in patients with obstructive sleep apnea syndrome. Effects of continuous positive airway pressure treatment and withdrawal in patients with obstructive sleep apnea on arterial stiffness and central BP.
Background —Arterial distensibility measures , generally from pulse-wave velocity ( PWV ) , are widely used with little knowledge of relationships to patient outcome . We tested whether aortic PWV predicts cardiovascular and all-cause mortality in type 2 diabetes and glucose-tolerance – tested ( GTT ) multiethnic population sample s. Methods and Results — Participants were r and omly sample d from ( 1 ) a type 2 diabetes outpatient clinic and ( 2 ) primary care population registers , from which nondiabetic control subjects were given a GTT .  Brachial blood pressures  and Doppler-derived aortic PWV  were measured . Mortality data over 10 years ’ follow-up were obtained . At any level of systolic blood pressure ( SBP ) , aortic PWV was greater in subjects with diabetes than in controls . Mortality risk doubled in subjects with diabetes ( hazard ratio 2.34 , 95 % CI 1.5 to 3.74 ) and in those with glucose intolerance ( 2.12 , 95 % CI 1.11 to 4.0 ) compared with controls . For all groups combined , age , sex , and SBP predicted mortality ; the addition of PWV independently predicted all-cause and cardiovascular mortality ( hazard ratio 1.08 , 95 % CI 1.03 to 1.14 for each 1 m/s increase ) but displaced SBP . Glucose tolerance status and smoking were other independent contributors , with African-Caribbeans experiencing reduced mortality risk ( hazard ratio 0.41 , 95 % CI 0.25 to 0.69 ) . Conclusions —Aortic PWV is a powerful independent predictor of mortality in both diabetes and GTT population sample s. In displacing SBP as a prognostic factor , aortic PWV is probably further along the causal pathway for arterial disease and may represent a useful integrated index of vascular status and hence cardiovascular risk RATIONALE Cross-sectional association has been reported between sleep-disordered breathing ( SDB ) and insulin resistance , but no prospect i ve studies have been performed to determine whether SDB is causal in the development of diabetes . OBJECTIVES The purpose of our study was to investigate the prevalence and incidence of type II diabetes  in subjects with SDB and whether an independent relationship exists between them . METHODS A cross-sectional and longitudinal analysis was performed in 1,387 participants of the Wisconsin Sleep Cohort .  Full polysomnography was used to characterize SDB . Diabetes was defined in two ways : ( 1 ) physician-diagnosis alone or ( 2 ) for those with glucose measurements , either fasting glucose > or = 126 mg/dl or physician diagnosis . MEASUREMENTS AND MAIN RESULTS There was a greater prevalence of diabetes in subjects with increasing levels of SDB . A total of 14.7 % of subjects with an apnea-hypopnea index ( AHI ) of 15 or more had a diagnosis of diabetes compared with 2.8 % of subjects with an AHI of less than 5 . The odds ratio for having a physician diagnoses of diabetes mellitus with an AHI of 15 or greater versus an AHI of less than 5 was 2.30 ( 95 % confidence interval , 1.28 - 4.11 ; p = 0.005 ) after adjustment for age , sex , and body habitus . The odds ratio for developing diabetes mellitus within 4 yr with an AHI of 15 or more compared with an AHI of less than 5 was 1.62 ( 95 % confidence interval , 0.67 - 3.65 ; p = 0.24 ) when adjusting for age , sex , and body habitus . CONCLUSIONS Diabetes is more prevalent in SDB and this relationship is independent of other risk factors . However , it is not clear that SDB is causal in the development of diabetes OBJECTIVES The study was done to determine whether radial artery applanation tonometry can be used as a noninvasive method of assessing global endothelial function . BACKGROUND ; It is known that beta(2)-receptor stimulation results in endothelial release of nitric oxide . Furthermore , for over a century glyceryl trinitrate ( GTN ) has been known to markedly affect the arterial pressure waveform , even in the absence of significant blood pressure ( BP ) changes . Therefore , it was hypothesized that the change in the peripheral pressure waveform , as measured using tonometry and quantified using the augmentation index ( AIx ) and in response to Salbutamol ( Salb ) , would allow assessment of global endothelial function . METHODS The study contained three parts . In the first study , Salb ( 400 microg ) was administered to 11 healthy subjects via inhalation after either intravenous N-omega-nitro-monomethyl-L-arginine ( L-NMMA ) ( 3 mg/kg over 5 min ) or control solution ( normal saline ) in the supine , rested , fasted condition . The BP , heart rate and waveform responses were recorded each 5 min following Salb for 20 min . Next , GTN was given and responses recorded 5 min later . In the second study , both the reproducibility of Salb and the GTN responses were assessed in 9 subjects studied twice on separate days . In the third study , the Salb and GTN responses of 12 subjects with angiographic coronary artery disease ( CAD ) were compared with 10 age-matched control subjects with no atherosclerotic risk factors . RESULTS After control infusion , AIx decreased following Salb , from 50.8 + /- 4.3 % to 44.8 + /- 4.2 % , a change of -11.8 + /- 3.7 % , p < 0.01 . After L-NMMA , AIx did not significantly change following Salb ( 54.2 + /- 5.1 % vs. 52.9 + /- 5.3 % , -2.0 + /- 3.1 % ) . The GTN-induced decreases in AIx were similar after either infusion ( 35.1 + /- 3.3 % vs. 36.5 + /- 3.3 % ) . Reproducibility of Salb-induced changes in AIx between studies performed on separate days was good ( r = 0.80 , p < 0.01 ) . Salb-induced changes in AIx in CAD patients were significantly less compared to control subjects ( -2.4 + /- 1.9 % vs. -13.2 + /- 2.4 % , respectively , p < 0.002 ) . The GTN-induced changes were not significantly different ( -27.6 + /- 4.2 vs. -38.9 + /- 4.4 % , p = 0.07 ) . CONCLUSIONS The peripheral arterial pressure waveform is sensitive to beta(2)-stimulation . Changes are related to nitric oxide release , are reproducible and can distinguish between clinical subject groups . Arterial waveform changes following Salb may thus provide a noninvasive method of measuring " global " arterial endothelial function Background —Obstructive sleep apnea ( OSA ) has been increasingly linked to cardiovascular and cerebrovascular disease . Inflammatory processes associated with OSA may contribute to cardiovascular morbidity in these patients . We tested the hypothesis that OSA patients have increased plasma C-reactive protein ( CRP ) . Methods and Results —We studied 22 patients ( 18 males and 4 females ) with newly diagnosed OSA , who were free of other diseases , had never been treated for OSA , and were taking no medications . We compared CRP measurements in these patients to measurements obtained in 20 control subjects ( 15 males and 5 females ) who were matched for age and body mass index , and in whom occult OSA was excluded .  Plasma CRP levels were significantly higher in patients with OSA than in controls ( median [ range ] 0.33 [ 0.09 to 2.73 ] versus 0.09 [ 0.02 to 0.9 ] mg/dL , P < 0.0003 ) . In multivariate analysis , CRP levels were independently associated with OSA severity ( F=6.8 , P = 0.032 ) . Conclusions —OSA is associated with elevated levels of CRP , a marker of inflammation and of cardiovascular risk . The severity of OSA is proportional to the CRP level AIMS Increased arterial wave reflections are associated with the presence and extent of coronary atherosclerosis and with cardiovascular mortality in selected population s. We prospect ively evaluated their prognostic value in the short- and long-term following percutaneous coronary interventions ( PCIs ) . METHODS AND RESULTS We non-invasively quantified wave reflections [ expressed as augmentation index corrected for heart rate of 75 b.p.m . ( AIx@75 ) ] using applanation tonometry of the radial artery and a vali date d transfer function to obtain the corresponding aortic values in 262 patients undergoing PCI .  During 2-year follow-up , 61 patients reached the primary endpoint [ death , myocardial infa rct ion ( MI ) , and restenosis ] . Increasing tertiles of Alx@75 were related to the rate of patients reaching the primary endpoint [ 15.2 , 20 and 35.3 % , respectively ( P = 0.001 ) ] , as well as the secondary endpoints total mortality , myocardial infa rct ion and death plus myocardial infa rct ion ( RR for the third vs. the first tertile 4.33 , 3.25 and 3.46 , respectively , P < 0.05 ) . In a multivariable Cox-regression model , AIx@75 added prognostic value above and beyond clinical risk factors , angiographic variables , and medications ( RR 1.8 , 95%CI 1.18 - 2.76 per increasing AIx@75-tertile , P < 0.01 ) . CONCLUSION Increased arterial wave reflections are independently associated with an increased risk for severe short- and long-term cardiovascular events in patients undergoing PCI Background — Patients with obstructive sleep apnea ( OSA ) experience repetitive episodic hypoxemia with consequent sympathetic activation and marked blood pressure surges , each of which may impair endothelial function . We tested the hypothesis that patients with OSA have impaired endothelium-dependent vasodilation , even in the absence of overt cardiovascular disease . Methods and Results —We studied 8 patients with OSA ( age 44±4 years ) and 9 obese control subjects ( age 48±3 years ) . Patients with OSA were newly diagnosed , never treated for OSA , on no medications , and free of any other known diseases . All obese control subjects underwent complete overnight polysomnographic studies to exclude occult OSA . Resistance-vessel function was tested by use of forearm blood flow responses to intra-arterial infusions of acetylcholine ( a vasodilator that stimulates endothelial release of nitric oxide ) , sodium nitroprusside ( an exogenous nitric oxide donor ) , and verapamil ( a calcium channel blocker ) . Conduit-vessel function was also evaluated by ultrasonography . Brachial artery diameter was measured under baseline conditions , during reactive hyperemia ( with flow increase causing endothelium-dependent dilatation ) , and after sublingual administration of nitroglycerin ( an endothelium-independent vasodilator ) . Patients with OSA had a blunted vasodilation in response to acetylcholine ( P < 0.007 ) , but responses to sodium nitroprusside and verapamil were not significantly different from those of control subjects . No significant difference in conduit-vessel dilation was evident between OSA patients and obese control subjects . Conclusions — Patients with OSA have an impairment of resistance-vessel endothelium-dependent vasodilation . This may be implicated in the pathogenesis of hypertension and heart failure in this condition Continuous positive airway pressure ( CPAP ) treatment improves endothelial function and sympathetic activity in patients with obstructive sleep apnea ( OSA ) . However , the long-term effects of CPAP on pulse wave velocity ( PWV ) , which reflects arterial stiffness that is associated with cardiovascular events , have not been evaluated in OSA patients with or without hypertension ( HT ) . In this study , 212 male OSA patients who had been receiving CPAP treatment for 2 years and were divided into two groups , those with HT ( n=114 ) and those without ( n=98 ) , were studied . In both HT and normotensive ( NT ) patients , PWV decreased significantly over the first 6 months of treatment ( P=0.005 and 0.010 , respectively ) , before increasing gradually from 6 to 24 months . Body mass index ( BMI ) , body weight , heart rate ( HR ) , systolic blood pressure ( SBP ) and diastolic blood pressure ( DBP ) levels decreased significantly in the HT group over the 2 years of CPAP treatment ( P<0.001 for all ) . In contrast , only HR decreased significantly in the NT group over the 2 years of treatment ( P<0.001 ) . Multivariate regression analysis revealed that age ( P=0.008 ) , decreases in DBP ( P<0.001 ) and HR ( P<0.001 ) and higher initial levels of serum high-density lipoprotein – cholesterol ( P=0.040 ) were independent factors related to changes in PWV over the 2 years of CPAP treatment in all patients . In conclusion , we found a significant decrease in PWV in both NT and HT patients after 6 months of CPAP treatment . In HT patients , long-term CPAP treatment significantly decreases blood pressure , which may contribute to explain the PWV improvement Background Smoking increases plasma nicotine . Nicotine releases catecholamines and alters arterial distensibility . The nicotine intake per cigarette is greater and serum cotinine levels , the proximate metabolite of nicotine , are higher in Blacks than in Whites . We tested the hypothesis that cigarette smoking increases the pulse wave velocity ( PWV ) , a marker of arterial stiffness , and the augmentation index ( AI ) , a measure of wave reflection , more in Blacks than in Whites . Methods We matched Black ( n = 30 ) and White ( n = 30 ) smokers for age , gender , body mass index and height . We determined  carotid-femoral PWV ( PWVCF )  and carotid-radial PWV ( PWVCR ) ( Complior ) , the AI derived from the aortic pressure waveform ( applanation tonometry , Sphygmocor ) ,  blood pressure , heart rate ( HR ) and cotinine levels  before and after cigarette smoking . We also performed measurements in 16 participants after sham smoking . Results Smoking increased the AI , PWVCF and PWVCR in the whole population ( all P < 0.05 , n = 60 ) . Increases in the AI and PWV were positively related to serum cotinine levels ( all P < 0.05 ) . Smoking increased serum cotinine ( P = 0.01 ) and mean blood pressure ( P = 0.03 ) more , but raised the HR to a lesser extent , in Blacks [ + 8 ± 4 versus + 13 ± 6 beats/min in Whites ( mean ± SD ) , P = 0.01 ] . Blacks disclosed larger increases in AI adjusted for HR ( Blacks , + 7.2 ± 8 versus Whites , + 4.4 ± 8 % ; P = 0.03 ) , PWVCF ( Blacks , + 1.1 ± 0.2 versus Whites , + 0.6 ± 0.3 m/s ; P < 0.01 ) and PWVCR ( Blacks , + 1.4 ± 0.1 versus Whites , + 0.7 ± 0.4 m/s ; P < 0.01 ) normalized for the mean blood pressure . No changes were observed with sham smoking . Conclusions Smoking acutely increases the PWV and AI in Blacks more than in Whites . Differences in nicotine metabolism and β-adrenergic sensitivity could explain these findings Background —C-reactive protein ( CRP ) and interleukin (IL)-6 are important risk factors for atherosclerosis and coronary heart disease . In the present study , we examined serum levels of CRP and IL-6 , IL-6 production by monocytes , and the effect of nasal continuous positive airway pressure ( nCPAP ) in patients with obstructive sleep apnea syndrome ( OSAS ) . Methods and Results —After polysomnography , venous blood was collected at 5 am from 30 patients with OSAS and 14 obese control subjects .  Serum levels of CRP and IL-6 and spontaneous production of IL-6 by monocytes were investigated . In addition , the effects of 1 month of nCPAP were studied in patients with moderate to severe OSAS .  Levels of CRP and IL-6 were significantly higher in patients with OSAS than in obese control subjects ( CRP P < 0.001 , IL-6 P < 0.05 ) . IL-6 production by monocytes was also higher in patients with OSAS than in obese control subjects ( P < 0.01 ) . In patients with OSAS , the primary factors influencing levels of CRP were severity of OSAS and body mass index and those influencing levels of IL-6 were body mass index and nocturnal hypoxia . nCPAP significantly decreased levels of both CRP ( P < 0.0001 ) and IL-6 ( P < 0.001 ) and spontaneous IL-6 production by monocytes ( P < 0.01 ) . Conclusions —Levels of CRP and IL-6 and spontaneous production of IL-6 by monocytes are elevated in patients with OSAS but are decreased by nCPAP . Therefore , OSAS is associated with increased risks for cardiovascular morbidity and mortality , and nCPAP may be useful for decreasing these risks To determine whether the onset of myocardial infa rct ion occurs r and omly throughout the day , we analyzed the time of onset of pain in 2999 patients admitted with myocardial infa rct ion . A marked circadian rhythm in the frequency of onset was detected , with a peak from 6 a.m. to noon ( P less than 0.01 ) . In 703 of the patients , the time of the first elevation in the plasma creatine kinase MB ( CK-MB ) level could be used to time the onset of myocardial infa rct ion objective ly . CK-MB-estimated timing confirmed the existence of a circadian rhythm , with a three-fold increase in the frequency of onset of myocardial infa rct ion at peak ( 9 a.m. ) as compared with trough ( 11 p.m. ) periods . The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents  before myocardial infa rct ion but was present in those not receiving such therapy . If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted , the circadian timing of myocardial infa rct ion may result from a variation in the tendency to thrombosis . If the rhythmic processes that drive the circadian rhythm of myocardial-infa rct ion onset can be identified , their modification may delay or prevent the occurrence of infa rct ion Background — Few population studies addressed the prognostic significance of aortic pulse wave velocity ( APWV ) above and beyond other cardiovascular risk factors . Methods and Results — We studied a sex- and age-stratified r and om sample of 1678 Danes aged 40 to 70 years . We used Cox regression to investigate the prognostic value of  APWV , office pulse pressure ( PP ) , and 24-hour ambulatory PP  while adjusting for mean arterial pressure ( MAP ) and other covariates . Over a median follow-up of 9.4 years , the incidence of fatal and nonfatal cardiovascular end points , cardiovascular mortality , and fatal and nonfatal coronary heart disease amounted to 154 , 62 , and 101 cases , respectively . We adjusted for sex , age , body mass index , MAP measured in the office ( conventional PP and APWV ) or by ambulatory monitoring ( 24-hour PP ) , smoking , and alcohol intake . With these adjustments , APWV maintained its prognostic significance in relation to each end point ( P<0.05 ) , whereas office and 24-hour PP lost their predictive value ( P>0.19 ) , except for office PP in relation to coronary heart disease ( P=0.02 ) . For each 1-SD increment in  APWV  ( 3.4 m/s ) , the risk of an event increased by 16 % to 20 % . In sensitivity analyses , APWV still predicted all cardiovascular events after st and ardization to a heart rate of 60 beats per minute , after adjustment for 24-hour MAP instead of office MAP , and /or after additional adjustment for the ratio of total to HDL serum cholesterol and diabetes mellitus at baseline . Conclusions — In a general Danish population , APWV predicted a composite of cardiovascular outcomes above and beyond traditional cardiovascular risk factors , including 24-hour MAP RATIONALE  Obstructive sleep apnea ( OSA ) is associated with adverse cardiovascular outcomes , including myocardial infa rct ion and stroke . Atherosclerosis is a key mechanism for these cardiovascular events . Recent cross-sectional studies showed the presence of early signs of atherosclerosis in patients with OSA who were free of comorbidities . OBJECTIVES To determine the impact of treatment with continuous positive airway pressure ( CPAP ) on atherosclerosis . METHODS We r and omly assigned 24 patients with severe OSA ( age , 46 + /- 6 yr ) who were free of comorbidities to receive no treatment ( control , n = 12 ) or CPAP ( n = 12 ) for 4 months . Carotid intima-media thickness , arterial stiffness ( evaluated by pulse-wave velocity ) , carotid diameter , 24-hour blood pressure monitoring , C-reactive protein , and catecholamines were determined at baseline and after 4 months . MEASUREMENTS AND MAIN RESULTS At baseline , all measurements were similar in both groups and did not change in the control group after 4 months . In contrast , a significant decrease occurred in carotid intima-media thickness ( 707 + /- 105 vs. 645 + /- 95 microm , P = 0.04 ) , pulse-wave velocity ( 10.4 + /- 1.0 vs. 9.3 + /- 0.9 m/s , P < 0.001 ) , C-reactive protein ( 3.7 + /- 1.8 vs. 2.0 + /- 1.2 mg/L , P = 0.001 ) , and catecholamines ( 365 + /- 125 vs. 205 + /- 51 ng/ml , P < 0.001 ) after 4 months of CPAP . Carotid diameter did not change significantly . Regarding the whole group , changes in carotid intima-media thickness were correlated with changes in catecholamines ( r = 0.41 , P < 0.05 ) . Changes in pulse-wave velocity were correlated with changes in C-reactive protein ( r = 0.58 , P < 0.01 ) and catecholamines ( r = 0.54 , P < 0.01 ) . CONCLUSIONS The treatment of OSA significantly improves early signs of atherosclerosis , supporting the concept that OSA is an independent risk factor for atherosclerosis . Clinical trial registered with www . clinical trials.gov ( NCT 00400543 ) Central aortic systolic blood pressure ( BP ) is an important determinant of cardiac workload and cardiac hypertrophy . The relationship of central aortic systolic BP and brachial BP varies depending on the stiffness of blood vessels . It is not certain whether the different drug classes affect the brachial and aortic systolic BP in a similar manner . In a double-blind crossover study , we measured the effects of the four major drug classes compared with placebo on central aortic pressure . Central aortic pressure and various indices were determined using the Sphygmo Cor apparatus . The study was undertaken in patients aged 65 to 85 years with systolic BP > 150 mm Hg at study entry . Results are reported for 32 patients who had satisfactory applanation tonometry in all five periods .  Calcium channel blockers and diuretics caused a greater fall in brachial artery systolic BP than angiotensin-converting enzyme ( ACE ) inhibitors or beta-blocking drugs . On placebo , central aorta augmentation pressure and index were 23 mm Hg and 33.3 % ; on ACE inhibitors the values were 18 mm Hg and 30 % ; on beta-blockers , 26 mm Hg and 38.5 % ; on calcium channel blockers , 16 mm Hg and 28 % ; and on diuretics , 17 mm Hg and 28.8 % . The augmentation pressure on beta-blocking drugs was greater than on the other three drug classes ( P < .05 ) , and augmentation pressures on ACE inhibitors , calcium channel blockers , and diuretics were less than on placebo ( P < .05 ) . The lowest central aortic pressures were achieved with calcium blocking drugs and diuretics . Therapy based on brachial artery recordings may thus overestimate the effect of beta-blocking drugs on central aortic systolic BP and underestimate the effectiveness of ACE inhibitors and calcium blocking drugs . The clinical importance of this discrepancy needs to be evaluated Obstructive sleep apnoea syndrome ( OSAS ) has been associated with hypertension , stroke and myocardial ischaemia in epidemiological and observational studies . Continuous positive airway pressure ( CPAP ) is the treatment of choice for OSAS , but the impact of this intervention on established risk factors for cardiovascular disease remains incompletely understood . A total of 102 males with moderate-to-severe OSAS were r and omised to therapeutic ( n = 51 ) or subtherapeutic ( n = 51 ) CPAP treatment for 4 weeks to investigate the effects of active treatment on 24-h urinary catecholamine excretion , baroreflex sensitivity ( BRS ) , arterial stiffness ( augmentation index ) and 24-h ambulatory blood pressure ( ABP ) . After 4 weeks of therapeutic CPAP , significant reductions were seen in urine normetanephrine excretion ( from mean±sd 179.7±80.1 to 132.7±46.5 µmol·mol−1 creatinine ) and augmentation index ( from 14.5±11.3 to 9.1±13.8 % ) compared with the subtherapeutic control group . Furthermore , therapeutic CPAP significantly improved BRS ( from 7.1±3.3 to 8.8±4.2 ms·mmHg−1 ) and reduced mean arterial ABP by 2.6±5.4 mmHg . In conclusion , treatment of obstructive sleep apnoea with continuous positive airway pressure may lower cardiovascular risk by reducing sympathetic nerve activity , ambulatory blood pressure and arterial stiffness and by increasing sensitivity of the arterial baroreflex STUDY OBJECTIVES  Obstructive sleep apnea ( OSA ) appears to be an independent risk factor for diurnal systemic hypertension , but the specific biologic markers for this association have not been well established . Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans . However , arterial stiffness has not been measured in association with obstructive apneas in patients with OSA , nor related to systemic blood pressure ( BP ) activity in this setting . Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA , by demonstrating that ( 1 ) arterial stiffness increases acutely in association with obstructive apnea and hypopnea , and that ( 2 ) such increased stiffness may occur in the absence of acute BP increase . DESIGN Prospect i ve , cross-sectional . SETTING A tertiary-care university-based sleep and ventilatory disorders center . PATIENTS Forty-four normo- and hypertensive adult patients ( 11 women , 33 men ) with polysomnographically diagnosed moderate to severe OSA . INTERVENTIONS N/A. MEASUREMENTS AND RESULTS Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography .  Arterial augmentation index ( AAI ) , a measure of arterial stiffness , was calculated as the ratio of augmented systolic BP ( SBP ) to pulse pressure and expressed as a percentage for the following conditions : awake , the first 10 ( " early apnea " ) and last 10 ( " late apnea " ) cardiac cycles of obstructive events , and the first 15 cardiac cycles following apnea termination ( " post apnea " ) . Mean AAI ( + /-SD ) for the group was significantly increased during NREM sleep from early apnea to late apnea ( 12.02 + /- 2.70 % vs 13.35 + /- 3.54 % , p<0.05 , ANOVA ) . During REM ( analyzed in 20 patients ) , MI again significantly increased from early apnea to late apnea ( 11.75 + /- 2.81 % vs 13.43 + /- 4.97 % ) . Conversely , neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM ( SBP 130 + /- 14 mmHg vs 129 + /- 14 mmHg ) or REM ( SBP 128 + /- 22 mmHg vs 127 + /- 21 mmHg ) . CONCLUSIONS Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep , in the absence of measurable BP change . These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implication s concerning cardiovascular sequelae in patients with OSA OBJECTIVE The most significant complications seen in patients with obstructive sleep apnea syndrome ( OSAS ) are associated with the cardiovascular system . The present study assessed aortic stiffness in patients with OSAS and evaluated the effect of continuous positive airway pressure ( CPAP ) therapy on aortic stiffness . METHOD Twenty-four patients with newly diagnosed , previously untreated , moderate or severe OSAS ( apnea-hypopnea index > 15 ) and a control group of 17 healthy patients were included in the study .  M-mode recordings of the ascending aorta were taken from the parasternal long axis by echocardiograhy , and systolic and diastolic diameters of the aorta were measured . Aortic elastic parameters , aortic strain , and distensibility were calculated . Measurements were repeated after 6 months of CPAP therapy in patients with OSAS and were compared with baseline values . RESULTS In patients with OSAS , compared with the control group , aortic strain ( 6.7%+/- 2.1 % vs. 12.4%+/- 3.1 % ; P < 0.001 ) and aortic distensibility ( 2.8 + /- 0.9 x 10(-6 ) cm(2 ) dyn(-1 ) vs. 5.5 + /- 1.7 x 10(-6 ) cm(2 ) dyn(-1 ) ; P < 0.001 ) were evidently lower , and there was a significant correlation between aortic elastic parameters and AHI . After a 6-month course of CPAP therapy , significant increases were observed in aortic strain ( 6.1%+/- 1.5 % vs. 7.3%+/- 1.7 % ; P < 0.001 ) and aortic distensibility ( 2.5 + /- 0.7 x 10(-6 ) cm(2 ) dyn(-1 ) vs. 3.1 + /- 0.9 x 10(-6 ) cm(2 ) dyn(-1 ) ; P < 0.001 ) in patients with OSAS . CONCLUSION Aortic strain and distensibility were lower in patients with OSAS than in control patients , and CPAP treatment provided improvement in aortic elastic parameters BACKGROUND Obstructive sleep apnea ( OSA ) is associated with increased BP and other cardiometabolic risk factors . The aim of the present study was to determine whether arterial stiffness and central BP ( two important cardiovascular risk factors ) would change , independent of peripheral BP following either the initiation of or withdrawal from nasal continuous positive airway pressure ( CPAP ) treatment in subjects with OSA . METHODS AND RESULTS Arterial stiffness and peripheral and central BP were measured at baseline , and then either at 2 months after starting CPAP therapy ( intervention group , n=20 ) or 7 nights after withdrawal from CPAP therapy ( withdrawal group , n=20 ) using pulse wave analysis . In the intervention group , there were reductions in arterial stiffness ( ie , the aortic augmentation index fell by 2.5 % ) and central systolic BP ( fell by 4.2 mm Hg ) without a concomitant reduction in peripheral BP . The change in arterial stiffness was associated with CPAP compliance ( r=-0.47 ) . In contrast , in the withdrawal group there were no overall changes in arterial stiffness or BP . However , there was an early morning increase in diastolic BP and heart rate relative to late evening . CONCLUSION These results suggest that clinical ly important changes in arterial stiffness and central BP may occur following effective CPAP treatment of OSA without parallel changes in peripheral BP
Obstructive sleep apnea is a prevalent disease that is associated with significant morbidity and mortality , particularly due to cardiovascular disease .
An emerging cardiovascular risk factor , arterial stiffness , may also be involved in the cardiovascular complications of obstructive sleep apnea .
The purpose of this review was to summarize the current literature regarding the effect of obstructive sleep apnea on arterial stiffness .