Rosano G M, Kaski J C, Arie S, Pereira W I, Horta P, Collins P, Pileggi F, Poole-Wilson P A
National Heart and Lung Institute, London, U.K.
Eur Heart J. 1996 Aug;17(8):1175-80. doi: 10.1093/oxfordjournals.eurheartj.a015034.
Whether myocardial ischaemia is the mechanism underlying chest pain in patients with angina and normal coronary arteriograms is controversial. We sought to detect the presence of transient myocardial ischaemia using continuous monitoring of coronary sinus blood pH during atrial pacing.
We studied 14 patients (eight women, six men, mean age 51 +/- 3 years) with typical exertional angina and normal coronary arteriograms and nine patients with coronary artery disease (two men, seven women, mean age 61 +/- 7 years). Of the 14 patients with normal coronary arteries, eight had a reduced coronary blood flow reserve (< 2.5-fold increase), 11 had an ischaemic-appearing response to exercise testing, six had reversible perfusion detects on exercise thallium scans and one had resting left bundle branch block. All patients underwent continuous pH monitoring of coronary sinus blood at rest and during incremental atrial pacing (up to 160 bpm). Coronary sinus oxygen saturation and myocardial lactate extraction ratio were also evaluated at rest and at peak pacing. Eleven patients with angina and normal coronary arteries and eight with coronary artery disease had angina during pacing. Both patients with angina and normal coronary arteries (n = 13) and patients with coronary artery disease (n = 9) showed a fall in coronary sinus pH (-0.02 +/- 0.02 vs -0.11 +/- 0.03 pH units, respectively, P < 0.01). Coronary sinus oxygen saturation expressed as a percentage dropped by 19 +/- 6% in patients with coronary artery disease and by 6 +/- 2% in patients with angina and normal coronary arteriograms (P < 0.05). Myocardial lactate extraction ratio decreased from 33 +/- 6% to -1.4 +/- 4% in patients with coronary artery disease and from 23 +/- 8% to 20 +/- 8% in those with angina and normal coronary arteriograms. Three patients with angina and normal coronary arteries had a drop in coronary sinus pH > 0.02 pH units (-0.043 +/- 0.006 pH units) and in coronary sinus oxygen saturation > 8% (16 +/- 3%) consistent with myocardial ischaemia.
Despite severe chest pain and reduced coronary flow reserve after pacing, most patients with angina and normal coronary arteriograms do not show metabolic evidence of myocardial ischaemia.
心肌缺血是否为心绞痛且冠状动脉造影正常患者胸痛的潜在机制存在争议。我们试图通过在心房起搏期间持续监测冠状窦血pH值来检测短暂性心肌缺血的存在。
我们研究了14例(8例女性,6例男性,平均年龄51±3岁)有典型劳力性心绞痛且冠状动脉造影正常的患者以及9例冠状动脉疾病患者(2例男性,7例女性,平均年龄61±7岁)。在14例冠状动脉正常的患者中,8例冠状动脉血流储备降低(增加<2.5倍),11例运动试验时有缺血样反应,6例运动铊扫描时有可逆性灌注缺损,1例有静息左束支传导阻滞。所有患者在静息时以及递增性心房起搏(最高至160次/分)期间均接受冠状窦血pH值的持续监测。在静息时和起搏峰值时还评估了冠状窦血氧饱和度和心肌乳酸摄取率。11例心绞痛且冠状动脉正常的患者和8例冠状动脉疾病患者在起搏期间出现心绞痛。心绞痛且冠状动脉正常的患者(n = 13)和冠状动脉疾病患者(n = 9)均出现冠状窦pH值下降(分别为-0.02±0.02对-0.11±0.03pH单位,P<0.01)。以百分比表示的冠状窦血氧饱和度在冠状动脉疾病患者中下降了19±6%,在心绞痛且冠状动脉造影正常的患者中下降了6±2%(P<0.05)。冠状动脉疾病患者的心肌乳酸摄取率从33±6%降至-1.4±4%,心绞痛且冠状动脉造影正常的患者从23±8%降至20±8%。3例心绞痛且冠状动脉正常的患者冠状窦pH值下降>0.02pH单位(-0.043±0.006pH单位)且冠状窦血氧饱和度下降>8%(16±3%),符合心肌缺血表现。
尽管起搏后出现严重胸痛且冠状动脉血流储备降低,但大多数心绞痛且冠状动脉造影正常的患者未显示心肌缺血的代谢证据。