Relation of Heart Rate Parameters During Exercise Test to Sudden Death and All-Cause Mortality in Asymptomatic Men

Selcuk Adabag, Gregory A Grandits, Ronald J. Prineas, Richard S. Crow, Hanna E Bloomfield, Jim Neaton

Research output: Contribution to journalArticlepeer-review

68 Scopus citations

Abstract

Heart rate (HR) profile during exercise predicts all-cause mortality. However, less is known about its relation to sudden (vs nonsudden) death in asymptomatic people. The relation of exercise HR parameters (HR at rest, target HR achievement, HR increase, and HR recovery) with sudden death, coronary heart disease (CHD) death, myocardial infarction, and all-cause mortality was assessed in 12,555 men who participated in MRFIT. Subjects were 35 to 57 years old without clinical CHD, but with higher than average Framingham risk. Trial follow-up was 7 years, and extended follow-up after the trial for all-cause mortality was 25 years. After adjusting for cardiac risk factors, having to stop exercise before achieving 85% of age-specific maximal HR was associated with increased risk of sudden death (hazard ratio 1.8, 95% confidence interval [CI] 1.3 to 2.5, p = 0.001), CHD death (hazard ratio 1.4, 95% CI 1.2 to 1.5, p <0.001), and all-cause mortality (hazard ratio 1.3, 95% CI 1.2 to 1.4, p <0.001). Increased HR at rest (p = 0.001), attenuated HR increase (p = 0.02), delayed HR recovery (p = 0.04), and exercise duration (p <0.0001) were independent predictors of all-cause death in the overall study population and also in the subgroup that achieved target HR. In conclusion, middle-aged men without clinical CHD who stopped exercise before reaching 85% of maximal HR had a higher risk of sudden death. Other exercise HR parameters and exercise duration predicted all-cause mortality.

Original languageEnglish (US)
Pages (from-to)1437-1443
Number of pages7
JournalAmerican Journal of Cardiology
Volume101
Issue number10
DOIs
StatePublished - May 15 2008

Bibliographical note

Funding Information:
This work was supported by Grants No. R01-HL-43232, R01-HL-68140 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Dr. Adabag was supported by Grant No. 04S-CRCOE 001 from the Veterans Administration Clinical Science Research and Development Service, Washington, DC. Preventive cardiology

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