Increased heart rate is associated with a prothrombotic state: The Framingham Heart Study

Although a higher heart rate is associated with an increased risk of cardiovascular disease, the mechanism is not well understood. As thrombosis has an important role in plaque development and acute coronary syndromes, the increase related to heart rate may result from a prothrombotic imbalance.

We investigated the relation between heart rate and thrombotic potential in 3451 participants from the Offspring Cohort of the Framingham Heart Study (mean age 54 years, 55% women). Participants were divided into quintiles based on heart rate derived from a resting electrocardiogram.

Higher heart rates were associated with significant age-adjusted increases in fibrinogen, viscosity, factor VII antigen, and impaired fibrinolytic potential (plasminogen activator inhibitor and tissue plasminogen activator antigen) among men and women, and von Willebrand factor antigen among men. Fibrinogen levels were 9% higher among men with a heart rate of 80.9 ± 8.1 beats/min (quintile 5) vs. 50.0 ± 3.9 beats/min (quintile 1) (314 vs. 287 mg/dl, p < 0.001 for linear trend) and 13% higher among women (83.5 ± 7.7 beats/min vs. 53.7 ± 3.5 beats/min (330 vs. 291 mg/dl, p < 0.001). The significant relations persisted after multivariate adjustment, other than among men, in whom factor VII was not significant and fibrinogen was borderline significant (p = 0.065).

Higher heart rates are associated with a prothrombotic state. Because these factors are also associated with endothelial dysfunction and inflammation, these findings are consistent with an injurious effect of higher heart rates on the endothelium. Measures to reduce thrombotic potential may be of particular value in people with higher heart rates.