医学
内科学
心脏病学
射血分数
心室
射血分数保留的心力衰竭
心肌梗塞
肥厚性心肌病
肌肉肥大
心力衰竭
心肌病
左心室肥大
冠状动脉血流储备
压力过载
心肌肥大
内皮功能障碍
作者
Paolo G. Camici,Carsten Tschöpe,Marcelo F. Di Carli,Ornella Rimoldi,Sophie Van Linthout
出处
期刊:Cardiovascular Research
[Oxford University Press]
日期:2020-01-30
卷期号:116 (4): 806-816
被引量:90
摘要
Abstract Left ventricular (LV) hypertrophy (LVH) is a growth in left myocardial mass mainly caused by increased cardiomyocyte size. LVH can be a physiological adaptation to physical exercise or a pathological condition either primary, i.e. genetic, or secondary to LV overload. Patients with both primary and secondary LVH have evidence of coronary microvascular dysfunction (CMD). The latter is mainly due to capillary rarefaction and adverse remodelling of intramural coronary arterioles due to medial wall thickening with an increased wall/lumen ratio. An important feature of this phenomenon is the diffuse nature of this remodelling, which generally affects the coronary microvessels in the whole of the left ventricle. Patients with LVH secondary to arterial hypertension can develop both heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). These patients can develop HFrEF via a ‘direct pathway’ with an interval myocardial infarction and also in its absence. On the other hand, patients can develop HFpEF that can then progress to HFrEF with or without interval myocardial infarction. A similar evolution towards LV dysfunction and both HFpEF and HFrEF can occur in patients with hypertrophic cardiomyopathy, the most common genetic cardiomyopathy with a phenotype characterized by massive LVH. In this review article, we will discuss both the experimental and clinical studies explaining the mechanisms responsible for CMD in LVH as well as the evidence linking CMD with HFpEF and HFrEF.
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