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Cited by 1,318Lipoproteins and Cardiovascular HealthCardiovascular Health and Risk FactorsDiabetes, Cardiovascular Risks, and Lipoproteins

Is Relationship Between Serum Cholesterol and Risk of Premature Death From Coronary Heart Disease Continuous and Graded?: Findings in 356 222 Primary Screenees of the Multiple Risk Factor Intervention Trial (MRFIT)

Stamler, Jeremiah·1986·JAMA
DOI 10.1001/jama.1986.03380200061022
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Abstract

The 356 222 men aged 35 to 57 years, who were free of a history of hospitalization for myocardial infarction, screened by the Multiple Risk Factor Intervention Trial (MRFIT) in its recruitment effort, constitute the largest cohort with standardized serum cholesterol measurements and long-term mortality follow-up. For each five-year age group, the relationship between serum cholesterol and coronary heart disease (CHD) death rate was continuous, gradecf, and strong. For the entire group aged 35 to 57 years at entry, the age-adjusted risks of CHD death in cholesterol quintiles 2 through 5 (182 to 202, 203 to 220, 221 to 244, and ≥245 mg/dL [4.71 to 5.22, 5.25 to 5.69, 5.72 to 6.31, and ≥6.34 mmol/L]) relative to the lowest quintile were 1.29, 1.73, 2.21, and 3.42. Of all CHD deaths, 46% were estimated to be excess deaths attributable to serum cholesterol levels 180 mg/dL or greater (≥4.65 mmol/L), with almost half the excess deaths in serum cholesterol quintiles 2 through 4. The pattern of a continuous, graded, strong relationship between serum cholesterol and six-year age-adjusted CHD death rate prevailed for nonhypertensive nonsmokers, nonhypertensive smokers, hypertensive nonsmokers, and hypertensive smokers. These data of high precision show that the relationship between serum cholesterol and CHD is not a threshold one, with increased risk confined to the two highest quintiles, but rather is a continuously graded one that powerfully affects risk for the great majority of middle-aged American men. (JAMA1986;256:2823-2828)

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  • The reactivity hypothesis states exaggerated responses to stress cause pathophysiologic events leading to sustained blood pressure increases.

    “Specifically, the reactivity hypothesis states that exaggerated responses to stress cause a cascade of pathophysiologic events that can eventually lead to sustained increases in blood pressure (1,3,10-12).”

    From A high fat meal increases cardiovascular reactivity to psychological stress in healthy young adults (2007) · cites this paper as [1]

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Authors
Stamler, J.
Corresponding author
Stamler, Jeremiah
Venue
JAMA
Publisher
American Medical Association (AMA)
Published
1986-11-28
Volume
256
Issue
20
Pages
2823
ISSN
  • 0002-9955 (ISSN-L)
  • 0098-7484
DOI
10.1001/jama.1986.03380200061022
OpenAlex
W4296883165
Cited by
1,318
References
0
Citations by year
2026: 9 · 2025: 13 · 2024: 8 · 2023: 20 · 2022: 25 · 2021: 19 · 2020: 25 · 2019: 22 · 2018: 22 · 2017: 38 · 2016: 33 · 2015: 32 · 2014: 36 · 2013: 40 · 2012: 41
FWCI
43.46
Type
journal article
Language
en
Open access
closed
Locations
JAMA (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Risk Factors
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
serum cholesterol, coronary heart disease mortality, premature mortality, dose-response relationship, threshold hypothesis, middle-aged men, hypertension, smoking, Multiple Risk Factor Intervention Trial, excess mortality

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