Heart Rate in Coronary Artery Disease: Should We Lower It?
- PDF / 270,896 Bytes
- 11 Pages / 595.276 x 790.866 pts Page_size
- 15 Downloads / 173 Views
Coronary Artery Disease (PG Steg, Section Editor)
Heart Rate in Coronary Artery Disease: Should We Lower It? Kelly Axsom, MD Sripal Bangalore, MD, MHA, FACC, FSCAI* Address *The Leon H. Charney Division of Cardiology, New York University School of Medicine, New York, NY 10016, USA Email: [email protected] Published online: 27 October 2012 * Springer Science+Business Media New York 2012
Keywords Coronary artery disease
I
Heart rate
I
Prognosis
I
Reduction
Opinion statement Elevated resting heart rate is an independent risk factor for cardiovascular morbidity and mortality in patients with and without coronary artery disease. In patients with known coronary artery disease, elevated heart rate reduces diastolic filling time and increases cardiac workload, resulting in supply demand mismatch with consequent ischemia and angina. While lower heart rate is associated with better prognosis, it is not known if pharmacological reduction in heart rate is beneficial and if heart rate is merely a marker for increased risk and worse outcomes. Certainly, physiologically lower resting heart rate as attained by exercise improves morbidity and mortality. While physiological reduction in heart rate is mainly a manifestation of increased parasympathetic drive, pharmacological reduction of heart rate with beta-blockers is mediated via the sympathetic pathway and associated with mixed outcomes. In addition, betablockers have other cardiovascular effects (lowering blood pressure), are metabolically active, and it is unknown if the beneficial effects (if any) are mediated via reduction in heart rate versus other cardiovascular effects. Ivabradine is a new medication that lowers heart rate selectively by inhibiting the If current without other cardiovascular effects, offering for the first time a therapeutic agent that selectively targets heart rate. The medication has shown promise in early trials in patients with heart failure, but it is unclear if this agent will be beneficial in patients with stable coronary artery disease without heart failure.
Introduction In 1997, Levine described an inverse relationship between heart rate, body size and life expectancy across mammalians, such that a higher resting heart rate (RHR) was associated with a lower life expectancy. For example, a mouse has a RHR of 580 beats per minute (bpm) and a life expectancy of 2 years, whereas an
elephant with a heart rate of 28 bpm has a life expectancy of 50 years [1]. Despite extreme differences in body size and heart rate, the total number of heartbeats per lifetime remains remarkably constant within one order of magnitude [1]. In addition, slowing heart rate in mice from 563 bpm to 266 bpm with digoxin
Heart Rate in CAD Axsom and Bangalore was associated with increased life span of 850 days versus 700 days (pG0.001) [2]. Levine hypothesized that if we are predisposed to have ∼1 billion heart beats per lifetime, we might extend life with therapies that slow average heart rate [1]. Coronary artery disease (CAD) is the leading cause of death wor
Data Loading...
