Hypertension has traditionally been defined by the arbitrary criteria of systolic pressure > 140 mm Hg or diastolic pressure > 90 mm Hg.
Hypertension has traditionally been defined by the arbitrary criteria of systolic pressure > 140 mm Hg or diastolic pressure > 90 mm Hg. However, the need for a more flexible definition and a more flexible threshold for treatment, depending on the presence or absence of other cardiovascular risk factors, is increasingly accepted.
Recently, the term "prehypertension" has gained traction. Defined as a blood pressure of 120-139/81-90 mm Hg, it defines a group whose blood pressure is above optimal yet below the criteria for hypertension. Prehypertension is associated with an increased risk of developing hypertension and therefore merits lifestyle modification, although, at present, pharmacotherapy is not recommended unless dictated by other risk factors.
In determining whether or not to treat borderline hypertension, increasing attention is being paid to the presence or absence of intermediate markers of target-organ damage, such as left ventricular hypertrophy or microalbuminuria. Another important and very physiologically appropriate marker would be evidence of microvascular disease, the end result of the constellation of cardiovascular risk factors such as hypertension, hyperlipidemia, smoking, diabetes, and others. In his study, Erdogan identifies coronary microvascular disease by quantitating coronary flow reserve (CFR), a reflection of minimal coronary microvascular resistance. Study results demonstrated reduced CFR in 35% of hypertensive subjects and 18% of subjects with prehypertension, compared with none among normotensive subjects. Interestingly the left ventricular mass index of prehypertensive subjects did not differ from that of normotensive subjects, suggesting that the CFR could be a more sensitive test of target-organ effect.
This study offers an intriguing new approach to identifying patients at risk. It also suggests that prehypertension is associated with microvascular effects. The findings encourage consideration of treating prehypertension, perhaps specifically in those who have a reduced CFR. Obviously, such speculations are extremely premature.
In digesting these findings, several concerns merit consideration. First, of course, is intra-individual reproducibility of the test, which was not assessed. Second is the limitation of an arbitrary cutoff value, which inevitably misindentifies many individuals. Third, as the author suggests, it is unclear whether the low CFR represents microvascular disease or is instead a consequence of reduced diastolic relaxation. Fourth, although the term prehypertension lumps together systolic pressures in the broad range of 121 to 139 mm Hg, I would suspect that most of the prehypertensive subjects with a reduced CFR had a systolic pressure close to 140 mm Hg, although these data were not reported.
A final issue is the method for diagnosing prehypertension used in this study. Ambulatory blood pressure monitoring, the gold standard in research today, was not performed. Also, blood pressure was assessed after a 15-minute rest period, rather than the 5-minute rest period that is usually employed.1 In many individuals, readings can fall from the hypertensive to the prehypertensive range in 15 minutes, resulting in the mislabeling of hypertensive individuals as prehypertensive. Thus, many of the prehypertensive subjects who had a reduced CFR might have actually been hypertensive. This opens to question the finding of abnormal CFR in prehypertensive individuals.
Measurement of CFR offers an attractive physiological measure with the potential to refine assessment of hypertension and borderline hypertension. Ideally, treatment decisions would rely on pathophysiologic manifestations rather than a rigid blood pressure criterion. This study has important limitations, but the authors provide an intriguing proof of concept.