Marcus M L, Harrison D G, Chilian W M, Koyanagi S, Inou T, Tomanek R J, Martins J B, Eastham C L, Hiratzka L F
Circulation. 1987 Jan;75(1 Pt 2):I19-25.
During the past decade our understanding of the complex interaction between cardiac muscle and coronary vascular growth has increased substantially. Some types of cardiac hypertrophy, for example, left ventricular hypertrophy secondary to hyperthyroidism, are associated with increased coronary vascular growth. However, in most animal preparations of hypertrophy and in several clinical types of hypertrophy of the left and/or right ventricles, pathologic cardiac enlargement impairs the ability of the coronary circulation to allow normal increases and perfusion in response to intense dilator stimuli. In general, clinical studies have demonstrated far more profound abnormalities than studies in experimental animals. These observations provide a plausible explanation of why patients with hypertrophied ventricles often exhibit signs and symptoms of myocardial ischemia in the absence of coronary obstructive disease. The recent observation that experimentally produced left ventricular hypertrophy secondary to renal hypertension augments infarct size and the incidence of sudden lethal arrhythmias has additional implications relevant to the interaction between cardiac hypertrophy and myocardial perfusion. Although coronary reserve is impaired in many types of pathologic hypertrophy, the anatomic or biochemical basis for these observations remains elusive.
在过去十年中，我们对心肌与冠状血管生长之间复杂相互作用的理解有了显著提高。例如，某些类型的心肌肥大，如继发于甲状腺功能亢进的左心室肥大，与冠状血管生长增加有关。然而，在大多数肥大的动物模型以及几种临床类型的左心室和/或右心室肥大中，病理性心脏增大损害了冠状循环在强烈扩张刺激下实现正常增加和灌注的能力。一般来说，临床研究显示出比实验动物研究更为严重的异常情况。这些观察结果为心室肥厚患者在无冠状动脉阻塞性疾病的情况下为何常表现出心肌缺血的体征和症状提供了一个合理的解释。最近的观察发现，实验性产生的继发于肾性高血压的左心室肥大增加了梗死面积和致命性心律失常的发生率，这对心肌肥大与心肌灌注之间的相互作用有进一步的启示。尽管在许多类型的病理性肥大中冠状动脉储备受损，但这些观察结果的解剖学或生化基础仍然难以捉摸。
