Harrison D G, Barnes D H, Hiratzka L F, Eastham C L, Kerber R E, Marcus M L
Circulation. 1985 Jun;71(6):1135-45. doi: 10.1161/01.cir.71.6.1135.
We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)
我们之前已经表明，患有肾性高血压和左心室肥厚的犬类，其梗死面积（相对于风险区域大小）比对照动物更大。对此的一个潜在解释是，这些犬类的侧支循环阻力更高。矛盾的是，先前对患有左心室肥厚的人类心脏进行的尸检研究表明，在这种情况下冠状动脉侧支实际上是增加的。为了验证左心室肥厚与冠状动脉侧支循环阻力改变相关的假设，我们对患有肾性高血压和左心室肥厚的犬类以及心脏手术时患有主动脉瓣疾病的患者进行了研究。通过放射性微球，在9只患有肾性高血压和左心室肥厚的犬类以及17只对照犬类中，利用孤立的、腺苷扩张的、血液灌注的心脏标本，建立了侧支循环和正常区域的压力 - 流量关系。根据这些压力 - 流量关系计算出的侧支循环阻力在两组中相似（患有肾性高血压和左心室肥厚的犬类为4.0±0.7，对照组为3.9±0.4 mmHg/ml/min/100 g）。此外，两组之间正常区域阻力没有差异（对照组的跨壁阻力为0.17±0.01，患有肾性高血压和左心室肥厚的犬类为0.18±0.02）。在5例患有主动脉瓣疾病、左心室肥厚且冠状动脉正常的患者以及6例左心室无肥厚且左前降支冠状动脉正常的患者中，在心脏手术时，使用7 MHz吸附式超声换能器在短暂阻断左前降支动脉期间监测收缩期室壁增厚情况。由于未形成侧支循环的心肌在冠状动脉闭塞后会迅速停止收缩，这种方法提供了侧支循环灌注的间接指标。冠状动脉闭塞开始20秒后，两组的收缩期增厚均显著降低（非肥厚心脏为对照值的15±10%，左心室肥厚心脏为10±10%；两组之间p值无统计学意义）。因此，这两组患者在短暂冠状动脉闭塞期间诱发的收缩异常严重程度相似，表明两组之间缺血的严重程度相当。我们得出结论，高血压和左心室肥厚不会改变侧支循环阻力，患者的左心室肥厚与侧支循环增强的功能证据无关。（摘要截短至400字）
