An association between hypertension and coronary heart disease is well established. However, many misconceptions have arisen concerning the nature of this relationship. This report has explored prospectively in some detail the relation of antecedent blood pressure status to the risk of subsequent clinical manifestations of CHD over 14 years in a cohort of 5,127 men and women in Framingham, Massachusetts.
Risk of every manifestation of CHD including angina, coronary insufficiency, myocardial infarction and sudden death was distinctly and impressively related to the antecedent level of both systolic and diastolic blood pressure. Risk was related not solely to "hypertension" but was proportional to the level of the blood pressure—even at non-hypertensive pressures—from the lowest to the highest recorded. Also, risk appeared to be related to casual as well as to more basal pressures.
Gradients of rick of each manifestation of CHD were similar whether subjects were classified according to their systolic or diastolic pressure. More detailed analysis is required to determine the net contribution to risk of systolic versus diastolic pressure at specified ages in each sex. The clinical dictum that the cardiovascular consequences of "hypertension" derive principally from the diastolic pressure and that isolated systolic elevation is innocuous requires re-evaluation.
As regards CHD, women were found to tolerate hypertension no better than did men. While absolute incidence was greater in men, the same increment of relative risk was observed comparing normotensives with hypertensives in each sex.
There was no evidence to suggest a lack of a potent effect of elevated blood pressure on risk of CHD beyond age 50. Even elevated systolic pressures beyond age 50 carried a substantial increase in risk of CHD.
Casual blood pressure determinations are useful in determining risk of CHD. Labile blood pressure elevations may contribute to risk as well as fixed hypertension. The contribution of lability to risk at specified levels of blood pressure deserves further study.
Blood pressure appears to contribute to risk of CHD even in the absence of other conditions presumed to be associated with both hypertension and increased propensity to CHD. The seriousness of a "hypertensive" blood pressure, however, is markedly influenced by the coexisting blood lipid content and ECG abnormalities.
Hypertension is a common and a major contributor to CHD morbidity and mortality which is readily controlled by hygienic and pharmacologic measures. There is good rationale for advocating early, vigorous and sustained control of elevated pressure, labile or fixed, whether systolic or diastolic, at any age, in both sexes. There is good reason to expect that this should result in a substantial reduction in CHD morbidity and mortality.