For the remainder of life, DBP decreases and pulse pressure widens, whereas car- diovascular risk increases exponentially. Age is by far the most important risk factor for CAD; the prevalence of fatal ischemic cardiac events increases by 64-fold as age doubles from 40 to 80 years. However, a high SBP, a low DBP, and a wide pulse pressure are each independent risk factors for CAD, but SBP was a better predictor of outcomes than pulse Thus, the effects of a low DBP or wide pulse pressure cannot be separated easily from those of aging in predicting the risk of a fatal MI. This important confounder may explain much of the confusion over the existence of a J curve in observational studies. These results suggest that wide pulse pressure is a signifi- cant determinant of whether the DBP is a major risk predictor. Therefore, in those studies that reported a J curve, possible explanations include diminished myocardial perfusion during diastole, an age-related increase in pulse pressure reflecting stiffer large arteries, or an epiphenomenon related to a known or undetected underlying illness (eg, cancer, HF), so-called reverse causality in which the pre-existing illness explains both the low BP and the high risk of death. There is also direct evidence against the concept of the J curve. For example, in the CAMELOT trial,150 had angiographically documented CAD, and the mean entry BP was 129/77 mmHg. Treatment with either an ACE inhibi- tor or a CCB lowered BP by an additional 5/2 mmHg, with no evidence of a J-curve in either treated group. 3.2.3. Clinical Trials to Specifically Evaluate Lower BP Goals Data from controlled trials designed primarily to evaluate lower BP goals in hypertensive subjects have not shown a J curve. 