Heart rate as a risk factor in cardiovascular disease

Heart rate as a risk factor in cardiovascular disease

Heart rate as a risk factor in cardiovascular disease: Lower heart rates have been associated with better survival, as in athletes. Average adult heart rate is between 60 to 100 beats per minute. Heart rate gradually decreases with age. Heart rate also adapts to body’s metabolic demand. Measurement of heart rate has to be checked for a minimum of 60 seconds after a five minute rest period. Maximum predicted heart rate is given by the formula: 220-age (William Haskell and Samuel Fox, 1970). But there can be significant inter-individual variation as well as variation with training.

Intrinsic heart rate can be measured after total sympathetic and parasympathetic blockade. Target heart rate for aerobic training ranges from 50-85% of the maximum predicted heart rate. Heart rate reserve is the difference between the maximum predicted heart rate and the resting heart rate. Heart rate reserve increases with exercise training as the resting heart rate drops. To achieve fat burning with exercise, 50-65% of the maximum predicted heart rate has to be achieved (fat burning zone).

Recovery heart rate is also important. Impaired heart rate recovery also predicts all cause and cardiovascular mortality just like chronotropic incompetence. Allowance has to be given for those on beta blockers while assessing chronotropic incompetence.
Tachycardiomyopathy is a reversible form of tachycardia induced cardiomyopathy. But the reversibility is lost in long standing cases. Time course of recovery may be as long as 12 months. Bradycardia induced cardiomyopathy may occur in some infants with complete heart heart block, which may persist even after pacemaker implantation.

Resting heart rate is being increasingly recognized as a risk factor for increased cardiovascular morbidity and mortality. The incidence of sudden cardiac death has also been found to increase with heart rate.

Heart rate predicts both sudden and non sudden death from acute myocardial infarction. Increase in heart rate in this setting predisposes to life threatening ventricular arrhythmias. The beneficial effect of beta blockers may be mediated by a decrease in heart rate.