Smucker M L, Tedesco C L, Manning S B, Owen R M, Feldman M D
Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville.
Circulation. 1988 Sep;78(3):573-82. doi: 10.1161/01.cir.78.3.573.
Patients with aortic stenosis are susceptible to myocardial ischemia during hemodynamic stress, which may be caused by two mechanisms. First, vascular abnormalities inherent in myocardial hypertrophy may impair coronary vasodilation, limiting the ability to increase coronary blood flow to meet increased metabolic demands. Second, aortic stenosis itself may cause an imbalance between oxygen supply and demand during hemodynamic stress by decreasing aortic pressure (decreasing coronary perfusion or oxygen supply) and increasing left ventricular pressure (increasing oxygen demand). By decreasing aortic valve gradient without immediately altering ventricular hypertrophy, aortic balloon valvuloplasty offers the opportunity to distinguish these mechanisms. We hypothesized that aortic valvuloplasty would improve the balance between myocardial oxygen supply and demand, especially during isoproterenol infusion. Nine patients undergoing aortic balloon valvuloplasty were assessed at baseline and during isoproterenol infusion (5 +/- 2 micrograms/min, mean +/- SD) before and after valvuloplasty. Valvuloplasty increased myocardial oxygen supply. After valvuloplasty, isoproterenol decreased diastolic pressure time index (DPTI) less and increased coronary sinus blood flow more than before valvuloplasty (-630 +/- 367 vs. -292 +/- 224 mm Hg.sec/min, p = 0.02 and 53 +/- 137 vs. 179 +/- 145 ml/min, p = 0.001, respectively). Valvuloplasty also decreased oxygen demand, decreasing systolic pressure time index (SPTI) from 4,135 +/- 511 to 3,021 +/- 492 mm Hg.sec/min (p = 0.0002). Valvuloplasty improved the balance between myocardial oxygen supply and demand, increasing baseline DPTI:SPTI, decreasing aortocoronary sinus oxygen content difference (0.51 +/- 0.15 to 0.68 +/- 0.14, p = 0.005 and 96 +/- 14 to 78 +/- 15 ml O2/l, p = 0.002, respectively), and decreasing myocardial lactate production during isoproterenol infusion (mean lactate extraction fraction, -0.26 +/- 0.40 to 0.14 +/- 0.17; p = 0.01). We conclude that aortic valvuloplasty improves the balance between myocardial oxygen supply and demand during hemodynamic stress induced by isoproterenol infusion. We speculate that the clinical improvement, which often occurs in these patients after valvuloplasty despite persistence of hemodynamically "critical" aortic stenosis, is in part attributable to immediate improvement in the myocardial oxygen supply:demand ratio.
主动脉瓣狭窄患者在血流动力学应激期间易发生心肌缺血，这可能由两种机制引起。首先，心肌肥厚固有的血管异常可能损害冠状动脉舒张功能，限制增加冠状动脉血流量以满足增加的代谢需求的能力。其次，主动脉瓣狭窄本身可能在血流动力学应激期间通过降低主动脉压（降低冠状动脉灌注或氧气供应）和增加左心室压力（增加氧气需求）导致氧气供需失衡。通过降低主动脉瓣梯度而不立即改变心室肥厚，主动脉球囊瓣膜成形术提供了区分这些机制的机会。我们假设主动脉瓣膜成形术将改善心肌氧供需平衡，尤其是在异丙肾上腺素输注期间。对9例行主动脉球囊瓣膜成形术的患者在基线时以及瓣膜成形术前、后异丙肾上腺素输注期间（5±2微克/分钟，平均值±标准差）进行评估。瓣膜成形术增加了心肌氧供应。瓣膜成形术后，异丙肾上腺素降低舒张压时间指数（DPTI）的幅度小于术前，增加冠状窦血流量的幅度大于术前（分别为-630±367与-292±-±224mmHg·秒/分钟，p = 0.02；53±137与179±145毫升/分钟，p = 0.001）。瓣膜成形术还降低了氧需求，使收缩压时间指数（SPTI）从4135±511降至3021±492mmHg·秒/分钟（p = 0.0002）。瓣膜成形术改善了心肌氧供需平衡，增加了基线DPTI:SPTI，降低了主动脉-冠状窦氧含量差（分别从0.51±0.15降至0.68±0.14，p = 0.005；96±14降至78±15毫升O2/升，p = 0.002），并在异丙肾上腺素输注期间降低了心肌乳酸生成（平均乳酸摄取分数，从-0.26±0.40降至0.14±0.17；p = 0.01）。我们得出结论，主动脉瓣膜成形术改善了异丙肾上腺素输注诱导的血流动力学应激期间的心肌氧供需平衡。我们推测，这些患者在瓣膜成形术后尽管血流动力学上仍存在“严重”主动脉瓣狭窄但临床症状常有所改善，部分原因是心肌氧供需比立即得到改善。
