Almost six million people in the United States suffer from heart failure (HF). Often stemming from acute trauma such as myocardial infarction, HF is a chronic condition in which the contractility and resulting efficiency of the heart tissue vastly decreases, leading to poor circulation that results in systemic problems. As such, HF contributes to almost 300,000 deaths per year in the US alone. Fortunately, a number of cardiovascular drugs and devices have reduced the overall morbidity of heart failure by improving cardiac output, either by directly stimulating the myocardium to contract more vigorously (e.g. inotropy, which alters the ion composition in the cytoplasm of muscle cells) or by improving the timing and efficiency of contractions (e.g. pacemakers).
One of the most successful interventions for HF is called cardiac resynchronization therapy (CRT) and involves placing two pacemaker leads on the heart walls – one on both the right and left ventricles – to synchronize heart contractions. This improves the mechanical performance of the heart as well as its efficiency, so energy is not unduly wasted. Since it was approved by the FDA ten years ago, CRT has saved or improved tens of thousands of lives. It has remained a hot area of research because soon after approval it became apparent that its clinical benefits did not simply stem from device-based electromechanical stimulation; rather, CRT was inducing actual molecular changes in the heart tissue that augmented its benefits. Just this month a paper in Science Translational Medicine was published that elucidates some of the molecular mechanisms by which CRT improves cardiac efficiency.
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