McCutcheon Keir, Manga Pravin
Division of Cardiology, Department of Internal Medicine, Charlotte Maxeke Johannesburg Academic Hospital and University of the Witwatersrand, Johannesburg, South Africa. Email:
Division of Cardiology, Department of Internal Medicine, Charlotte Maxeke Johannesburg Academic Hospital and University of the Witwatersrand, Johannesburg, South Africa.
Cardiovasc J Afr. 2018 Jan/Feb;29(1):51-65. doi: 10.5830/CVJA-2017-009.
Surgical repair or replacement of the mitral valve is currently the only recommended therapy for severe primary mitral regurgitation. The chronic elevation of wall stress caused by the resulting volume overload leads to structural remodelling of the muscular, vascular and extracellular matrix components of the myocardium. These changes are initially compensatory but in the long term have detrimental effects, which ultimately result in heart failure. Understanding the changes that occur in the myocardium due to volume overload at the molecular and cellular level may lead to medical interventions, which potentially could delay or prevent the adverse left ventricular remodelling associated with primary mitral regurgitation. The pathophysiological changes involved in left ventricular remodelling in response to chronic primary mitral regurgitation and the evidence for potential medical therapy, in particular beta-adrenergic blockers, are the focus of this review.
目前,手术修复或置换二尖瓣是重度原发性二尖瓣反流唯一推荐的治疗方法。由此产生的容量超负荷导致的壁应力长期升高,会引起心肌的肌肉、血管和细胞外基质成分发生结构重塑。这些变化最初具有代偿作用,但长期来看会产生有害影响,最终导致心力衰竭。在分子和细胞水平上了解容量超负荷导致的心肌变化,可能会带来医学干预措施,这有可能延缓或预防与原发性二尖瓣反流相关的不良左心室重塑。本文综述的重点是慢性原发性二尖瓣反流引起的左心室重塑所涉及的病理生理变化,以及潜在药物治疗(特别是β-肾上腺素能阻滞剂)的证据。