Furthermore, the pres- ence of structural CAD could be expected to affect the pres- sure-flow relationships in the coronary arteries, with a lower tolerance of diastolic pressures. There is evidence from clini- cal trials to both support and refute the existence of a J curve. The first retrospective study in 1979 reported a 5-fold increase in MI among treated patients with DBP (Korotkoff phase IV) values <90 mmHg,133 roughly equivalent to <80 to 85 mmHg using the more universal Korotkoff phase V. This observation was confirmed by a subsequent meta-analysis in and a reanalysis of the 1985 MRC trial of mild hyper- tension, which reported an increased MI prevalence in those with achieved DBP <80 mmHg.135 However, other investiga- tors using the same data have drawn opposite conclusions about whether a J curve really exists.136,137 A secondary analysis of data from INVEST138,139 of patients with known CAD and hypertension showed a J-shaped relationship between BP and the primary outcome (all-cause death, nonfatal stroke, and nonfatal MI), all-cause death, and total MI, with a nadir at 119/84 mmHg. This was not the case for stroke. These post hoc results were also cited in an analysis by Thune et al140 and an accompanying editorial141 as support for the existence of a J curve and a warning against exces- sive lowering of BP. However, what was not mentioned was that patients in that trial who had a BP <120/70 mmHg (the level below which the risk of adverse outcomes seemed to rise) were older and had a history of more MI, coronary artery bypass grafting or percutaneous coronary intervention, stroke or transient ischemic attack, diabetes mellitus, HF, and cancer, all confounding factors. 