Pathophysiological role of heart rate: from ischaemia to left ventricular dysfunction

Myocardial ischaemia results from imbalance between myocardial oxygen demand and supply. An increase in heart rate (HR) will raise both demand and supply. HR is the most important determinant of myocardial oxygen consumption and of cardiac energy demand. HR reduction improves myocardial perfusion by increasing the fraction of the cardiac cycle occupied by diastole, which accounts for 80% of coronary flow. Besides these physiological characteristics, HR is also linked to the progression of atherosclerosis, at least in animals, and an increase in HR is associated with plaque rupture in humans. The symptom of chest pain in stable angina is almost always triggered by elevated HR owing to physical or emotional stress. Equally, an increased HR precedes an episode of asymptomatic or silent myocardial ischaemia. Therefore, it is not surprising that the efficacy of some anti-anginal drugs such as beta-blockers and non-dihydropyridine calcium antagonists has been related to their effectiveness in reducing HR. In many studies, multivariate analysis has shown HR to be an independent predictor of mortality and of hospitalization for heart failure. A relationship has been found between HR reduction and mortality in patients with congestive heart failure treated with beta-blockers. Thus HR is an important therapeutic target for ischaemia and left ventricular dysfunction or congestive heart failure, and it seems likely that relatively high HR is both causative and indicative of important pathophysiological processes: HR is a risk factor for cardiovascular morbidity and mortality throughout the cardiovascular continuum.