Should the Treatment of Hypertension be based on Blood Pressure Level Only or on Total Cardiovascular Risk?

Hypertension is an important determinant in the spectrum of cardiovascular disease (CVD), and treating hypertension is a central tenet of modern cardiac care. However, the decision of whether to initiate therapy based on cardiovascular risk factors or absolute blood pressure (BP) measurements is less defined. The Framingham study began the cardiology community’s focus on epidemiological risk in the pursuit of the etiology of cardiac disease.[1] Historically, antihypertensive therapy was determined by signs of the development of overt end-organ damage in patients but became modified with accumulation of epidemiological data. Hypertension was established as a causal risk factor, with a significant reduction in BP being correlated with a reduction in hypertensive heart failure in those with CVD. The Framingham study established cardiovascular prospective population epidemiological research and preventative cardiology. The “risk factor” concept evolved, indicating that multiple interrelated factors promote increased risk of the development of coronary heart disease (CHD).[2] To date, no single essential factor has been identified. Epidemiologists began to conceptualize vascular disease as an outcome of multiple forces, and hypertension is primed among these. This research determined the influence of hypertension on the full clinical spectrum of CVD including sudden death, silent and overt myocardial infarction, heart failure, and clinical and silent strokes. The study determined population CVD incidence attributable to hypertension at a time when only mortality statistics was available, and most recently, the lifetime risk of developing it and its vascular consequences. The study also provided some valuable insights into mechanisms of hypertension-induced CVD. In the past, initiation of antihypertensive treatment was often delayed until there was evidence of target organ involvement. Framingham study data indicated that this practice was imprudent as 40–50% of hypertensive persons developed overt cardiovascular events before evidence of target organ damage such as proteinuria, cardiomegaly, or electrocardiogram abnormalities. However, patients with CVD appear to also benefit, with reductions in hypertensive heart failure. Within the original Framingham study subgroup of patients who have Abstract