Heart rate recovery is the decrease in heart rate that occurs immediately after exercise. In a serious of elegant experiments performed some years ago, Imai et al 1 demonstrated that an initial steep fall of heart rate immediately after exercise could be blunted by administration of atropine. Furthermore, patients with congestive heart failure, who are known to have markedly deranged autonomic balance, did not have the initial steep fall in heart rate observed in athletes and normal subjects. Imai et al 1 concluded that heart rate recovery is a manifestation of reactivated vagal tone that occurs normally after exercise.
Because heart rate recovery is related to autonomic balance, it has been hypothesized that it predicts in its own right an adverse outcome in patients with and those without cardiovascular disease. 2 Indeed, an extensive literature has developed over the past 10 to 15 years showing that disturbances in autonomic balance have a strong and robust association with morbidity and mortality. 3 One part of this fascinating and important picture is that vagal tone appears to play a critical role in protecting the heart against potentially lethal arrhythmias. 3 A number of studies have been published showing that heart rate recovery, like other measures of autonomic tone, is an independent predictor of mortality in a wide spectrum of patients. 2,4 Patients with an attenuated heart rate recovery are at increased risk for cardiovascular events and even death, even after exercise capacity, 5,6 stress-induced myocardial perfusion defects, 2 left ventricular systolic function, 7 and extent of angiographic coronary artery disease have been taken into account. 5
An obvious question with regard to the clinical use of heart rate recovery is whether it is a modifiable risk factor. Poor functional capacity, perhaps the strongest exercise predictor of risk currently available, 8 may be a modifiable risk factor. Exercise training has been shown, for example, to reduce the risk of diabetes, 9 and possibly the risk of death as well, in patients with established cardiovascular disease. 10
It is logical to hypothesize that one potential benefit of exercise training is an improvement in autonomic tone, which may be reflected by an improvement in heart rate recovery. In this issue of JCR, Tiukinhoy et al 11 demonstrate that cardiac rehabilitation may well lead to an improvement in heart rate recovery. They compare 34 patients who underwent phase 2 cardiac rehabilitation with 35 control subjects. Among the control patients, two exercise tests scheduled 9 months apart showed little difference in resting heart rate, peak heart rate, total treadmill time, and heart rate recovery. In contrast, the patients enrolled in the cardiac rehabilitation program demonstrated substantial improvements. Their resting heart rate decreased, and their peak heart rate, treadmill time, and heart rate recovery increased. These changes are consistent with a training-induced increase in vagal tone.
Although not a prospective, randomized trial, the work of Tiukinhoy et al 11 represents an important contribution to the exercise and cardiac rehabilitation literature. It is consistent with another recent report demonstrating an improvement of heart rate recovery after exercise training. 12 The next clear question is whether an improvement in heart rate recovery during exercise identifies people likely to benefit from cardiac rehabilitation programs. What also is not clear is whether this improvement in heart rate recovery is an entity physiologically and prognostically distinct from an improvement in functional capacity, or whether the two really go together.
Heart rate recovery may be a treatable risk marker without it necessarily being modified. If the connection between heart rate recovery and adverse outcome in fact results from autonomic imbalance, then pharmacologic interventions that improve sympathetic-parasympathetic balance may well improve outcomes. Perhaps the best existing example of this phenomenon is heart failure caused by left ventricular systolic dysfunction. This condition is associated with marked autonomic imbalance, and its associated mortality rate can be reduced substantially by beta-blockers. 13 Future study could include trials of beta-blockers or other autonomic nervous system modulating agents in patients with an abnormal heart rate recovery.
Another important question is whether heart rate recovery might identify patients who would experience greater benefits from revascularization. Although the association between heart rate recovery and angiographic severity of coronary disease is weak, 5 there is a precedent for a relation between functional exercise test abnormalities and outcomes after revascularization. Data from the Coronary Artery Surgery Study and Registry have shown that functional capacity is closely correlated with survival benefit after coronary bypass surgery. 14 Thus, although revascularization may not specifically attack the autonomic derangements underling an abnormal heart rate recovery, it is conceivable that its survival benefits may be closely related.
The work of Tiukinhoy et al 11 raises the tantalizing possibility that heart rate recovery may be more than a risk marker. It may be a target for therapy as well. Clearly, much work is needed to determine how best to incorporate heart rate recovery into the risk stratification and management of patients with known or suspected cardiovascular disease.
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