Does Lowering Your Heart Rate Help You Live Longer?

Only in specific heart disease, and not consistently. A pooled analysis of 11 trials found beta-blockers lowered all-cause mortality in heart failure patients in sinus rhythm (hazard ratio 0.73), whatever their starting heart rate. In the same 11 trials, patients with AFib got the same 12-beat drop and no mortality benefit (hazard ratio 0.96). Ivabradine cut heart failure hospitalization and heart failure deaths in one trial and changed nothing in another. None of this evidence tests lowering resting heart rate in people without heart disease.

Do beta-blockers lower mortality by lowering heart rate?

In heart failure with sinus rhythm, beta-blockers lowered mortality. The reason is less clear than the result. A pooled analysis of individual patient data from 11 double-blind trials covered 14,166 patients in sinus rhythm and 3,034 with AFib.

Beta-blockers cut ventricular rate by 12 beats per minute in both groups. In sinus rhythm, mortality was lower on beta-blockers than on placebo (hazard ratio 0.73, 95% CI 0.67 to 0.79). That held whatever the starting heart rate. In AFib, the same rate cut came with no mortality effect (hazard ratio 0.96, 0.81 to 1.12).

So a slower heart alone did not deliver the benefit in AFib. A lower achieved heart rate went with better prognosis only in sinus rhythm.

What did a pure heart-rate-lowering drug show?

Ivabradine lowers heart rate without other cardiac effects. Two large trials tested it with different results.

SHIFT enrolled 6,558 patients with heart failure, an ejection fraction of 35% or lower and a heart rate of 70 or higher. The primary composite of cardiovascular death or heart failure admission fell from 29% on placebo to 24% on ivabradine (hazard ratio 0.82, 95% CI 0.75 to 0.90). Hospital admissions for worsening heart failure and deaths from heart failure each had a hazard ratio of 0.74. Symptomatic bradycardia occurred in 5% against 1%.

A companion SHIFT analysis found risk of the primary outcome was more than doubled in the highest heart rate group on placebo (hazard ratio 2.34). It also found that adjusting for heart rate change at 28 days neutralized the drug's effect. That points to heart rate reduction as the mechanism in this population.

BEAUTIFUL tested ivabradine in 10,917 patients with coronary artery disease and an ejection fraction below 40%. Heart rate fell 6 beats per minute. The primary composite did not change (hazard ratio 1.00, 95% CI 0.91 to 1.1). In the subgroup at 70 or above, it also did not change (0.91, 0.81 to 1.04). Secondary endpoints of myocardial infarction admission and revascularization did fall in that subgroup.

Does one clinic reading predict risk in patients with devices?

Not for death at one year. The German DEVICE registry analyzed 1,589 recipients of implanted defibrillators or resynchronization devices. Resting heart rate came from a 12-lead ECG at enrollment. Of these patients, 46.1% were above 70 beats per minute.

One-year all-cause mortality was 5.4% in both groups. Major cardio- and cerebrovascular events were 5.9% against 6.1%. All-cause hospital admission was higher above 70, at 29.0% against 23.1%, driven by non-cardiovascular admissions.

Does heart rate tracked over months predict better than one reading?

Three later analyses track heart rate over time. One of them found it predicts better than a baseline reading. A pooled analysis covered 5,428 heart failure patients in sinus rhythm. It defined cumulative load as the area under the heart rate curve at or above 70 beats per minute. Higher load went with more major cardiac events (hazard ratio 1.31, 95% CI 1.24 to 1.38). It beat baseline heart rate, mean heart rate and time in target range at prediction.

In 3,921 AFib patients from the AFFIRM study, average heart rate of 80 or above went with higher mortality (adjusted hazard ratio 2.01, 95% CI 1.59 to 2.55).

In 7,517 older hypertensive patients from the STEP trial, the pattern was U-shaped. Both the lowest and highest cumulative heart rate quartiles carried more cardiovascular events than the middle. The highest quartile had a hazard ratio of 2.21 and the lowest 1.71. There was no such trend for all-cause mortality. That complicates a rule of lower always being better.

All three are observational or post hoc. They describe who did worse, not what lowering the number does. Shorter-horizon uses of the same number are covered in resting heart rate trend as a recovery indicator.

What does this not settle?

The drug trials enrolled patients with heart failure or coronary disease with reduced ejection fraction. In BEAUTIFUL, 87% were already on beta-blockers. No study here tests a drug that lowers resting heart rate in adults without heart disease.

The population-level link between higher resting heart rate and mortality is covered in resting heart rate and longevity. Whether that link is causal, so that lowering the number would lower risk, is what a 2023 review calls undefined for the normal population.

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