Co-morbidity (HFrEF and HFpEF): hypertension

Francesco Paneni, Massimo Volpe
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Abstract

Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.
合并症(HFrEF和HFpEF):高血压
高血压性心脏病是导致心力衰竭和死亡的主要原因。在75%的病例中,高血压先于心衰,与非高血压个体相比,高血压的风险增加了6倍。最重要的是,少数患者在高血压性心衰发病后能存活5年。在高血压患者中,心脏可能呈现不同的适应性重构模式:同心重构、同心肥厚和偏心肥厚。虽然大多数高血压患者都有发生同心肥厚的高风险,但越来越多的受试者表现出从同心到偏心的进展,最终导致左心室扩张和收缩功能障碍。包括心肌缺血、种族、遗传背景、糖尿病史和血压模式在内的几个因素可能显著影响高血压到左室扩张的途径。同心型肥厚患者通常发展为HF并保留射血分数(HFpEF),而偏心型(扩张型)患者发展为HF并降低射血分数(HFrEF)。降低血压对降低心衰的风险有显著的效果。虽然现有的降压药都能有效降低血压,但血管紧张素转换酶抑制剂、血管紧张素受体阻滞剂(ARBs)和利尿剂在预防心衰方面比其他药物更有效。neprilysin抑制剂sacubitril与ARB缬沙坦(LCZ696)的联合用药最近被证明在降低高血压患者的hf相关结局方面非常有效。考虑到血压水平、HF类型(HFpEF或HFrEF)以及相关合并症(如肾脏疾病、糖尿病)的个体化治疗方案是目前改善高血压合并HF患者发病率和死亡率的最佳方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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