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The Front Page of Medicine

Cardiology · 1961

Factors of Risk in the Development of Coronary Heart Disease (Framingham Heart Study)

Framingham Heart Study: Factors of Risk in the Development of Coronary Heart Disease, Six-Year Follow-up Experience

Image related to the Framingham Heart Study
NIH History Office from Bethesda / Public domain (Wikimedia Commons)

In the late 1940s, coronary heart disease was killing American men at epidemic rates, yet cardiology had almost no predictive tools. The prevailing assumption held that atherosclerosis was an inevitable accompaniment of aging, something that happened to patients rather than something patients could influence. The Framingham Heart Study was launched in 1948 precisely to challenge that assumption, enrolling 5,127 adult residents of Framingham, Massachusetts, and following them prospectively for cardiovascular events.

William Kannel, who led the analytic work on the first major outcome report, and Thomas Dawber, the epidemiologist who had directed the study since its founding, published their six-year findings in Annals of Internal Medicine in 1961. The paper quantified what had previously been clinical intuition: hypertension, elevated serum cholesterol, and cigarette smoking each predicted coronary events independently of one another, and their effects were roughly additive. The authors introduced the phrase 'risk factor' to describe these measurable antecedents, giving clinicians a vocabulary that did not yet exist.

The reception was not uniformly enthusiastic. Many cardiologists in 1961 remained skeptical that observational associations justified treating asymptomatic patients, and the therapeutic tools for lowering blood pressure were still limited and poorly tolerated. The causal role of dietary fat and serum cholesterol was actively debated, with physiologist Ancel Keys and his critics trading contested data across academic journals throughout the decade.

What the Framingham report provided was a durable empirical foundation. It reframed coronary disease as a condition with identifiable precursors that could, in principle, be measured during a routine office visit and modified before the first infarction. That shift in framing drove the design of subsequent intervention trials targeting lipids and blood pressure.

The cohort itself expanded over time, eventually enrolling the children of the original participants in 1971 and a grandchildren cohort in 2002. William Castelli, who directed the study for much of the 1970s and 1980s, extended the lipid findings to include HDL cholesterol as a protective factor. The treatment targets for LDL, blood pressure, and glucose now embedded in cardiovascular guidelines were calibrated in part against risk thresholds the Framingham data identified.

Key People

Read the original — PubMed

Ann Intern Med. 1961;55:33-50.

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