Mundhenke M, Schwartzkopff B, Strauer B E
Department of Internal Medicine, Heinrich-Heine University of Düsseldorf, Germany.
Virchows Arch. 1997 Oct;431(4):265-73. doi: 10.1007/s004280050098.
Left ventricular hypertrophy is a risk factor for cardiovascular morbidity and mortality. In arterial hypertension and in hypertrophic cardiomyopathy it may be accompanied by clinical signs of myocardial ischaemia resulting from microcirculatory dysfunction in the absence of coronary macroangiopathy. Structural changes of the vascular and interstitial compartment of the heart are involved in the pathogenesis of impaired microcirculation. We investigated patients with hypertensive heart disease (HHD; n = 12) and hypertrophic cardiomyopathy (HCM; n = 19) without coronary macroangiopathy but with signs of myocardial ischaemia. Right septal endomyocardial biopsies were evaluated to quantify the structure of intramyocardial arterioles, collagen content and myocytic diameter by morphometric rules. Nine normotensive subjects served as controls. The groups differed significantly (P < 0.05) in myocytic diameter and total collagen content. The myocytic diameter correlated with the thickness of the interventricular septum. Arterioles in HHD showed a significant increase in cross-sectional medial area and in HHD patients the periarteriolar collagen area increased both in absolute terms and when standardized to medial area. Arteriolar density was significantly reduced in HCM. In a multivariate discriminant analysis the positive predictive value for differentiation of the groups by non-myocytic variables was 72.5% (P = 0.013). HHD and HCM differ in the structural alterations in the arteriolar bed. Medial hypertrophy and periarteriolar fibrosis prevail in HHD, and reduced arteriolar density is found in HCM. Different microvascular remodelling at the level of arterioles indicates distinct pathophysiologic processes that may contribute to the clinically observed disturbance of coronary microperfusion in these two diseases.
左心室肥厚是心血管疾病发病和死亡的危险因素。在动脉高血压和肥厚型心肌病中,在没有冠状动脉大血管病变的情况下,它可能伴有因微循环功能障碍导致的心肌缺血的临床症状。心脏血管和间质成分的结构变化参与了微循环受损的发病机制。我们研究了患有高血压性心脏病(HHD;n = 12)和肥厚型心肌病(HCM;n = 19)且无冠状动脉大血管病变但有心肌缺血迹象的患者。对右间隔心内膜活检组织进行评估,通过形态计量学规则量化心肌内小动脉的结构、胶原含量和心肌细胞直径。九名血压正常的受试者作为对照。这些组在心肌细胞直径和总胶原含量方面存在显著差异(P < 0.05)。心肌细胞直径与室间隔厚度相关。HHD患者的小动脉横截面积显著增加,并且在HHD患者中,小动脉周围胶原面积无论是绝对值还是相对于中膜面积标准化后均增加。HCM患者的小动脉密度显著降低。在多变量判别分析中,通过非心肌细胞变量区分这些组的阳性预测值为72.5%(P = 0.013)。HHD和HCM在小动脉床的结构改变方面存在差异。HHD以中膜肥厚和小动脉周围纤维化为特征,而HCM则表现为小动脉密度降低。小动脉水平的不同微血管重塑表明不同的病理生理过程,这可能导致这两种疾病临床上观察到的冠状动脉微灌注障碍。