Editorial Commentary: The success of heart rate control in the treatment of chronic heart failure

Abstract

Heart rate control in patients in sinus rhythm became possible with the introduction of beta blockers in the 1960s. Initially this approach was used in patients with hypertension. In patients with chronic systolic heart failure an elevated heart rate was considered caused by sympathetic activation, which was important to the support of the failing myocardial function. Using a beta blocker in this situation was therefore considered contraindicated. However, if a chronic sympathetic activation was thought to be harmful to a failing myocardium, heart rate reduction could be favorable. After an observation by Waagstein et al. [1] in 1975 that a few patients with idiopathic dilated cardiomyopathy improved after the initiation of beta-blocker therapy, I was assigned by Ake Hjalmarson to explore this possibility when I started my cardiology training in 1974. We reported beneficial effects on survival in 1979 [2] and on myocardial function the following year [3] .I n this report, we also presented some relationship between the degree of heart rate reduction and improvement of myocardial function. Our findings were of course very controversial and it took another 20 years before the use of beta blockers became accepted for the treatment of systolic heart failure. In this issue of TCM, Borer and Tavazzi [4] make a comprehensive review of agents and devices for the treatment of systolic heart failure. They state that “while RAASmanipulation was under study, exploration of beta blockade for heart failure also began.” As you can realize the opposite was actually the case but the acceptance of new treatments was different and RAAS blockade came earlier into clinical practise. Their summary is followed by a more detailed review of the beneficial effects of lowering heart rate by ivabradine, an agent with no direct effects on the sympathetic nervous system but instead ivabradine lowers heart rate by a completely different mechanism, blockade of the iF channels. With this approach, the importance of heart rate can be explored separate from the sympathetic activation. It is obvious that elevated heart rate in patients with systolic heart failure is associated with increased mortality and morbidity. This relationship was reported from meta-analyses of beta-blocker trials [5] .I n SHIFT, the magnitude of the heart rate reduction by ivabradine was associated with a reduction in cardiovascular risk [6] .F urther, and in contrast to the experience after beta-blockade, the degree of heart rate reduction was associated with the level of improvement of health related quality of life (HQoL) [7] .A s HQoL was associated with mortality e.g., lower QoL and higher risk, improved QoL might translate into reduced risk. The experience from SHIFT emphasizes the importance in measuring and controlling heart rate when examining patients with systolic heart failure. To explore this further, we pooled the “SHIFT-type” patients from BEAUTIFUL with SHIFT and checked the last heart rate prior to an event [8] .W e could then see that for the time-updated heart rate every 5 beats/min increase in heart rate increased the risk for subsequent hospitalization by 22%. Importantly, this finding underscores the need for measuring and controlling heart rate every time a patient with systolic heart failure is examined. I agree with Borer and Tavazzi that the possibilities to better control heart rate have now been expanded also for patients in USA with the addition of ivabradine. In Europe this option has been available for patients with chronic systolic heart failure since 2012.