Bayes-Genis Antoni, Bisbal Felipe, Núñez Julio, Santas Enrique, Lupón Josep, Rossignol Patrick, Paulus Walter
Heart Institute, Hospital Universitari Germans Trias i Pujol, 08916 Badalona, Spain.
CIBERCV, Instituto de Salud Carlos III, Madrid, Spain.
J Clin Med. 2020 Apr 13;9(4):1110. doi: 10.3390/jcm9041110.
To better understand heart failure with preserved ejection fraction (HFpEF), we need to better characterize the transition from asymptomatic pre-HFpEF to symptomatic HFpEF. The current emphasis on left ventricular diastolic dysfunction must be redirected to microvascular inflammation and endothelial dysfunction that leads to cardiomyocyte remodeling and enhanced interstitial collagen deposition. A pre-HFpEF patient lacks signs or symptoms of heart failure (HF), has preserved left ventricular ejection fraction (LVEF) with incipient structural changes similar to HFpEF, and possesses elevated biomarkers of cardiac dysfunction. The transition from pre-HFpEF to symptomatic HFpEF also involves left atrial failure, pulmonary hypertension and right ventricular dysfunction, and renal failure. This review focuses on the non-left ventricular mechanisms in this transition, involving the atria, right heart cavities, kidneys, and ultimately the currently accepted driver-systemic inflammation. Impaired atrial function may decrease ventricular hemodynamics and significantly increase left atrial and pulmonary pressure, leading to HF symptoms, irrespective of left ventricle (LV) systolic function. Pulmonary hypertension and low right-ventricular function are associated with the incidence of HF. Interstitial fibrosis in the heart, large arteries, and kidneys is key to the pathophysiology of the cardiorenal syndrome continuum. By understanding each of these processes, we may be able to halt disease progression and eventually extend the time a patient remains in the asymptomatic pre-HFpEF stage.
为了更好地理解射血分数保留的心力衰竭（HFpEF），我们需要更好地描述从无症状的HFpEF前期到有症状的HFpEF的转变过程。目前对左心室舒张功能障碍的关注必须转向微血管炎症和内皮功能障碍，这些会导致心肌细胞重塑和间质胶原沉积增加。HFpEF前期患者没有心力衰竭（HF）的体征或症状，左心室射血分数（LVEF）保留，但存在与HFpEF相似的早期结构变化，且心脏功能障碍的生物标志物升高。从HFpEF前期到有症状的HFpEF的转变还涉及左心房衰竭、肺动脉高压和右心室功能障碍以及肾衰竭。本综述重点关注这一转变过程中的非左心室机制，包括心房、右心腔、肾脏，以及最终目前公认的驱动因素——全身炎症。心房功能受损可能会降低心室血流动力学，并显著增加左心房和肺压力，从而导致HF症状，而与左心室（LV）收缩功能无关。肺动脉高压和右心室功能低下与HF的发生率相关。心脏、大动脉和肾脏的间质纤维化是心肾综合征连续体病理生理学的关键。通过了解这些过程中的每一个，我们或许能够阻止疾病进展，并最终延长患者处于无症状HFpEF前期阶段的时间。
