Arrhythmias and heart failure (HF) are common causes of morbidity and premature death worldwide, and patients who present with both conditions have particularly poor outcomes. Arrhythmia-induced cardiomyopathy (AIC) is a condition in which arrhythmias, often atrial fibrillation (AF), but also frequent atrial or ventricular ectopic beats, cause or aggravate HF. The hallmark of this condition is partial or complete reversibility of left ventricular systolic dysfunction after restoration of normal sinus rhythm. Differentiation between HF that causes arrhythmias and arrhythmias that cause HF remains challenging, leads to the underuse of rhythm-control therapy and, consequently, to the under-diagnosis of AIC. In this Review, we describe the various pathophysiological mechanisms of AIC, with a focus on AF as the underlying arrhythmia. We then discuss the epidemiology, clinical presentation and assessment of patients with AIC, with consideration of the complex interactions between AF and left ventricular dysfunction. We also present the therapeutic approach taken in patients presenting with suspected AIC, including restoration of sinus rhythm to unmask a diagnosis of AIC and treatment of HF. We conclude with a discussion of priorities for future research and the observation that there is an urgent need for objective, easily quantifiable parameters to identify patients with AIC.
Growing evidence from the past seven decades indicates that atherosclerosis begins in youth and progresses in response to exposure to cardiovascular risk factors, which contribute to the development of cardiovascular disease in later life. A long-term randomized clinical trial lasting at least 50 years and involving screening and follow-up of children across their lifespan would provide the highest level of evidence to determine the lifelong influence of cardiovascular risk factors on cardiovascular disease risk but such an approach is not feasible. However, much can be learned from observing patients with familial hypercholesterolaemia. Those patients who were treated at a young age remained event-free into adulthood, beyond the ages at which their affected parent, who initiated treatment at a much later age, experienced their first cardiovascular event. The evidence is less certain for other types of dyslipidaemia and other cardiovascular risk factors, including high blood pressure. Nonetheless, the strategy of waiting until later in adulthood to screen and intervene, often after a non-fatal cardiovascular disease event has already occurred, might no longer seem prudent. In this Review, we summarize the growing body of evidence supporting intensified efforts to identify cardiovascular risk factors in children and young adults, and to identify knowledge gaps among this cohort such as the optimal timing and strategy for blood lipid screening.
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