Regional myocardial functional and electrophysiological alterations after brief coronary artery occlusion in conscious dogs.

The time relationship for recovery of mechanical function, the intramyocardial electrogram and coronary flow after brief periods of regional myocardial ischemia, was studied in conscious dogs. Total left vemtricular (LV) function was assessed with measurements of LV systolic and diastolic pressures, rate of change of LV pressure (dP/dt), and dP/dt/P. Regional LV function was assessed with measurements of regional segment length and velocity of shortening. An implanted hydraulic occluder on either the left anterior descending or circumflex coronary artery was inflated for 5- and 15-min periods on separate days. A 5-min occlusion depressed overall LV function transiently, but just before release of occlusion overall function had nearly returned to control. At this time regional function in the ischemic zone was still depressed to the point of absent shorteining or paradoxical motion during systole and was associated with marked ST segment elevation (+ 10 +/- 2.2 mV) at the site where function was measured. With release of occlusion and reperfusion the intramyocardial electrogram returned to normal within 1 min, and reactive hyperemia subsided by 5-10 min. In contrast to the rapid return to preocclusion levels for coronary flow and the electrogram, regional mechanical function remained depressed for over 3 h. A 15-min coronary occlusion resulted in an even more prolonged (greater than 6 h) derangement of function in the ischemic zone. Thus, brief periods of coronary occlusion result in prolonged impairement of regional myocardial function which could not have been predicted from the rapid return of the electrogram and coronary flow. These observations indicate that brief interruptions of coronary flow result either in a prolonged period of local ischemia or that alterations of mechanical induced by ischemia far outlast the repayment of the oxygen debt.     

早期亚低温对家兔持续性心肌梗死的影响

目的探讨早期亚低温疗法对家兔持续性心肌梗死的影响。方法36只家兔分为3h结扎组和24h结扎组,各自再随机分为常温组和亚低温组,开胸持续结扎心脏前降支建立急性心肌梗死模型。亚低温组物理降温使结扎后30min体温降到35℃以下,保持在(33~35)℃之间,24h结扎组动物3h后自然复温;常温组体温维持在38℃以上。动物处死后取心染色切片,计算梗死心肌和左室心肌重量。结果(1)3h结扎组的亚低温组梗死心肌的重量明显低于常温组[(0·33±0·06)g比(0·52±0·04)g;P<0·01],其占左室心肌重量的百分比也明显低于常温组[(6·5±1·3)比(11·3±3·7)%;P<0·01)。(2)24h结扎组的亚低温组梗死心肌重量与常温组相近[(0·57±0·05)g比(0·60±0·09)g,P>0·05],占左室心肌重量的比例也相近[(16·0%±1·3%)比(16·3%±1·1%);P>0·05]。(3)3h及24h结扎组亚低温组梗死24h血清CK-MB活力低于常温组,差异接近显著。结论亚低温可以在心肌梗死早期延缓缺血心肌坏死速度,而不能缩小最终心肌梗死面积。     

Effect of exercise on perfusion of collateral-dependent myocardium in dogs with chronic coronary artery occlusion.

Since the ability of mature intercoronary collateral channels to increase myocardial blood flow in response to drug-induced coronary vasodilation has been questioned, the present study was undertaken to evaluate the response of coronary collateral circulation to the stress of exercise. Studies were performed at rest and during two levels of treadmill exercise in six dogs a minimum of 6 mo after placement of an Ameroid constrictor on the left circumflex coronary artery. Regional myocardial blood flow was estimated in normally perfused anterior and predominantly collateral-dependent posterior left ventricular wall with left atrial injections of radio-nuclide-labeled microscheres 7-10 mum in diameter. At rest, heart rate was 87 +/- 7 beats/min and mean myocardial blood flow was comparable in control and collateral-dependent regions (0.96 +/- 0.13 and 0.97 +/- 0.14 ml/min-g, respectively). During exercise, heart rates increased to 180 +/- 13 and 228 +/- 14 beats/min and myocardial blood flow (MBF) in the anterior control region increased linearly with heart rate (HR), (MBF = 0.133 HR - 0.202, r = 0.88). MBF to the posterior collateral-dependent region was similarly augmented during exercise (MBF = 0.140 HR - 0.252, r = 0.89), so that the linear correlation between HR and MBF was similar for the control and collateral-dependent regions. In addition, the transmural distribution of MBF was uniform at rest and during exercise in both the anterior control and posterior collateral-dependent regions. Thus, not only could the mature intercoronary collateral vasculature supply adequate flow at rest, but when subjected to the natural stress of exercise, the increase in flow to the predominantly collateral-dependent area was similar to that in the normally perfused area.     

Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs.

The relationship between early and late epicardial electrocardiographic changes as well as those in regional myocardial blood flow (MBF) and the severity of myocardial damage was determined in 12 anesthetized dogs with left anterior descending coronary artery ligation. Radioactive microspheres (15 mum) were used to measure regional MBF at 15 min (early) and 24 h (late) after coronary occlusion. Severity of myocardial damage was assessed by the extent of myocardial creatine phosphokinase depletion 24 h after coronary ligation. There was a close linear correlation between myocardial creatine phosphokinase activity and regional MBF both early (r=0.93, 2P less than 0.001) and late (r=0.88, 2P less than 0.001). An inverse but less precise relationship existed between acute epicardial ST-segment elevation and early (r=-0.41, 2P less than 0.001), or late (r=0.35, 2P less than 0.05) regional MBF. Similarly, a weak correlation was found between myocardial creatine phosphokinase (IU/mg protein) at 24 h and early epicardial ST (millivolt) elevation (r=-0.36, 2P less than 0.02). In the center zones of the infarct with MBF 1/10 of normal, about 35% of the areas with normal QRS width had no epicardial ST-segment elevation 15 min after coronary occlusion. About 44% of the areas which developed pathological Q-waves in the electrocardiogram at 24 h had no ST elevation 15 min after coronary ligation. Late evolution of abnormal Q-waves occurred almost invariably in areas in which the early MBF was reduced to less than 50% of normal and in areas which subsequently had myocardial creatine phosphokinase levels reduced to less than 60% of normal. After coronary occlusion, the severity of the ultimate myocardial damage, which was directly proportional to the degree of reduction in MBF, was therefore not reliably predicted by the early epicardial ST-segment elevation. The data obtained in these studies suggest the need for caution in the use of acute ST-segment elevation as a predictive index of the extent or severity of myocardial ischemic damage.     

Effect of efonidipine, a novel dihydropyridine derivative, on myocardial metabolic changes induced by coronary artery ligation in dogs: comparison with nifedipine

Summary— Efonidipine is a dihydropyridine derivative having a vasodilating action, which is slower in onset and longer in duration than that of nifedipine. In the present study, we compared the effects of efonidipine with those of nifedipine on the ischemic myocardial metabolism in anesthetized dogs. The heart was made ischemic by ligating the left anterior descending coronary artery (LAD) completely for 3 or 30 min. Efonidipine or nifedipine was injected intravenously, 10 or 3 min, respectively, before the start of LAD occlusion. Efonidipine (0.01 or 0.03 mg/kg) decreased both blood pressure and heart rate, whereas nifedipine (0.003 mg/kg) decreased blood pressure and increased heart rate. The magnitude of decrease in mean blood pressure induced by 0.03 mg/kg efonidipine was similar to that induced by 0.003 mg/kg nifedipine. Although efonidipine did not modify the changes in myocardial carbohydrate metabolism induced by ischemia, it attenuated the ischemia-induced decrease in the myocardial level of adenosine triphosphate and energy charge potential. Nifedipine, however, did not modify the changes in both myocardial energy and carbohydrate metabolism induced by ischemia. The results suggest that efonidipine has a cardioprotective effect in the dog, probably because of its negative chronotropic effect.     

Attenuation by atenolol of myocardial acidosis during ischemia in dogs: contribution of beta-1 adrenoceptors to myocardial acidosis

Coronary artery occlusion produces myocardial acidosis, which can be attenuated by propranolol or sotalol. The present study was undertaken to determine which beta adrenoceptors, beta-1 or beta-2, contribute to the ischemic myocardial acidosis. Dogs anesthetized with pentobarbital were used. In the first series of experiments, blood flow in the left anterior descending coronary artery was reduced by an occluder to about one-third of the original flow. Myocardial pH was measured by means of a micro pH electrode inserted into the left anterior descending coronary artery area at the depth of about 8 mm. The myocardial pH decreased from 7.44 to 7.55 to 6.73 to 6.89, 30 min after partial occlusion being the time immediately before an i.v. injection of drugs. Atenolol (1 mg/kg) attenuated significantly the decrease in myocardial pH that had been induced by partial occlusion, whereas IPS 339 (360 micrograms/kg) and ICI 118,551 (300 micrograms/kg) did not. The pH effect of atenolol was confirmed even in the paced heart. In the second series of experiments, the antagonistic action of these drugs on the isoproterenol-induced increase in heart rate and myocardial contractile force and the decrease in diastolic blood pressure was investigated. By this experiment, it was confirmed that atenolol has the beta-1 adrenoceptor antagonistic action, and the IPS 339 and ICI 118,551 have the beta-2 antagonistic action. These results suggest that the activation of beta-1 adrenoceptors contribute to the myocardial acidosis during ischemia.     

New conclusive data on human myocardial dysfunction induced by acidosis

Acidosis is one of the major consequences of hemodynamic instability in shock state patients directly associated with multiple organ failure evolution and death. Most studies on the hemodynamic consequences of acidosis have been experimental, nonhuman studies with severe acidosis, and thus far from the most common clinical situations. Schotola and colleagues offer a new approach to human failing myocardium where the authors highlight, ex vivo, the deleterious hemodynamic consequences of mild acidosis. Their work strengthens the current view of the urgent need to discover new efficient and nondeleterious therapy for the treatment of acidosis.During the shock state, understanding the mechanisms of acidosis, its hemodynamic and inflammatory consequences as well as the best therapeutic approach remain an ongoing debate. In the previous issue, Schotola and colleagues provide, for the first time, new and en-lightening data on the consequence of acidosis in isolated human failing myocardium [1].Over the past two decades, the mortality rate from a shock state has decreased; for instance, in septic shock from 30% to around 20% [2,3]. This improvement stems from many factors, including early management, more aggressive resuscitation with specific goals (volemic expansion, targeted main arterial pressure, blood transfusion, and so forth) and a better identification of prognostic factors such as acidosis [4]. As a major metabolic consequence of shock states, acidosis is also known to be a high predictor of in hospital mortality [5]. Both a cause and a consequence, this acidosis impairs cardiac and vascular function through various cellular and molecular mechanisms. Intracellular acidosis, which reduces myofilament sensitivity to Ca²⁺, is thus one of the crucial factors involved in myocardial dysfunction [6]. A low pH value also induces vessel hyporeactivity mediated by a number of factors such as nitric oxide, peroxynitrite, activation of K_ATP channels and modification of catecholamine signaling [7].Although it has long been known that cardiovascular function is impaired by acidosis, the bulk of the studies have been mostly experimental, and only a few human studies have been relevant on this subject [8-10]. In the present study by Schotola and colleagues, the authors obtained ventricular trabeculae from human right ventricles explanted from failing hearts. These trabeculae were mounted in a chamber in which the development of isometric force was recorded and the tissues superfused with a HEPES solution at pH 7.20 and 7.40. The response to incremental doses of isoproterenol, a B mimetic agent, was also recorded. Their major finding was a reduction in cardiac contractility at pH 7.20 and a rightward shift of the pH 7.20 curve compared with the 7.40 curve in response to increasing doses of isoproterenol. Therefore, without providing actual new pathophysiological information regarding cardiac depression in acidotic patients, this study definitely confirms the deleterious effects of a moderate and common acidosis on the failing human heart. Obviously, these experimental conditions (that is, ex vivo fragments of myocardium, artificial organic acidosis) are far from the clinical situation. However, this study confirms all other previous results. Furthermore, given that the hemodynamic consequences of common mild acidosis on altered myocardium are important, physicians should be alarmed in the presence of severe acidosis. In shock patients, hemodynamic treatment in order to treat acidosis should be a primary goal for the physician. Finally, it would be of interest, albeit ethically complex, to determine whether this mild acidosis has the same impact not only on preserved human myocardium but also on both preserved and altered arterial vessels.The management of acidosis remains a complex challenge. The main treatment must involve the correction of the underlying disease at the origin of acidosis. However, buffering severe acidosis by sodium bicarbonate is known to be associated with severe deleterious effects. One such effect is paradoxical intracellular acidosis. Bollaert and colleagues demonstrated that sodium bicarbonate infusion in acidotic rats decreases the intracellular pH [11]. Moreover, sodium bicarbonate infusion increases carbon dioxide, which is highly diffusible in cells (HCO₃^- + H⁺ <=> H₂CO₃ and H₂CO₃ <=> CO₂ + H₂O). Carbon dioxide increases dramatically and exacerbates cardiovascular dysfunction [12]. Another deleterious effect is that hypocalcemia is worsened by bicarbonate infusion, which probably also impairs cardiovascular function [9]. A final example is hydric and sodium overload, which often occurs during sodium bicarbonate infusion.Two small randomized, controlled clinical studies describe the inefficiency of this treatment in restoring the hemodynamic balance in critically ill patients [9,10]. Other treatments such as Carbicarb, an equimolar solution of sodium bicarbonate and sodium carbonate, or THAM (trometamol; tris-hydroxymethyl aminomethane), a biologically inert amino alcohol of low toxicity that buffers carbon dioxide and acids in vitro and in vivo, have also been studied for the treatment of metabolic or respiratory acidosis, although not in shock state patients [8,13].For all of these reasons, bicarbonate therapy is not recommended even with pH <7.15. In fact, the Surviving Sepsis Campaign guidelines only recommend against its use for pH ≥7.15 [4]. Currently, there are no relevant published studies regarding the effect of bicarbonate therapy for pH <7.15. Nevertheless, while the underlying disease remains the main course of treatment, there is an urgent need to research a new symptomatic approach to acidosis management.     

Alpha-adrenoceptor subtypes and regional myocardial blood flow distribution during coronary occlusion in dogs

The involvement of postsynaptic alpha-adrenoceptors in the distribution of regional myocardial blood flows (RMBFs, microsphere technique) within the left ventricle has been investigated during intermittent coronary artery occlusion in open-chest anesthetized dogs. Two types of RMBFs distribution were assessed: (1) between endocardial (endo) and epicardial (epi) layers (endo/epi ratio) and (2) between nonischemic (NIZ) and ischemic zones (IZ) (IZ/NIZ ratio). Equipressor does of selective alpha 1-(cirazoline after rauwolscine) and alpha 2-(UK-14,304 after prazosin) adrenoceptor agonists were infused in dogs previously submitted to ganglionic and muscarinic blockade. In a control group, aortic pressure was mechanically raised by aortic stenosis to levels similar to those reached with both alpha-adrenoceptor agonists. Cirazoline and aortic stenosis increased RMBFs in IZ and NIZ but did not alter the calculated coronary resistance in NIZ and did not affect endo/epi and IZ/NIZ ratios. In contrast, UK-14,304 preferentially augmented coronary resistance in NIZ, increased IZ/NIZ ratio (both P less than 0.05) but did not affect endo/epi ratio in IZ and NIZ. Thus, we conclude that if transmural distribution of RMBFs (endo/epi ratio) is not preferentially controlled by any alpha-adrenoceptor subtype, postsynaptic alpha 2-adrenoceptors are of importance during coronary occlusion in promoting a favorable redistribution of RMBFs from NIZ towards IZ by inducing a selective NIZ coronary vasoconstriction (ie a "reverse coronary steal").     

急性左主干闭塞所致急性心肌梗死的临床特点

目的 回顾性分析急性左主干（LM）闭塞所致急性心肌梗死（AMI）患者的临床表现,总结此类患者的临床特点。方法 从1995年1月至2006年5月,首都医科大学附属北京朝阳医院共完成1793例AMI患者的急诊经皮介入治疗（PCI）,其中共有15例患者的梗死相关血管为左主干。15例患者均为男性,年龄（43—85）（60．6±10．4）岁。回顾性分析这15位患者的临床资料、造影和介入治疗情况、以及临床随访结果。结果 1例患者表现为aVR导联以外的广泛导联ST段压低,其余14例均表现为急性广泛前壁心肌梗死。10例（66．7％）患者术前存在严重心源性休克,所有患者均在主动脉内球囊反搏（IABP）支持下接受急诊PCI治疗。急性期死亡9例（60．0％）,存活的6例患者均完成3个月随访,其中1例于术后4年猝死。对比分析的结果,提示术前存在良好的侧支循环可能是影响此类患者近期预后的影响因素。结论 LM急性闭塞所致的AMI患者病情凶险,心源性休克发生率及急性期死亡率高。IABP支持下急诊PCI治疗可以挽救部分病人的生命和改善预后。     

The effects of fructose-1,6-diphosphate on myocardial damage in acute coronary artery occlusion.

Acute myocardial infarction can result from thrombosis of a coronary artery. The purpose of this study was to evaluate the ability of fructose-1,6-diphosphate (FDP; Esafosfina) to reduce myocardial necrosis during acute thrombosis of a coronary artery. A canine model of acute myocardial infarction was used to produce intraluminal thrombosis by placement of a coil of wire in a coronary artery. After developing a coronary thrombosis of the left anterior descending artery, dogs were injected intravenously with 90 mg/kg, 175 mg/kg, or 350 mg/kg of FDP or normal saline (controls). Hemodynamic, biochemical and electrocardiographic parameters were evaluated before, and 30 min and 4 h after occlusion. Four hours after acute coronary occlusion, the animals were sacrificed, and the weights of ischemic and necrotic myocardial tissue were quantified using a histologic-staining method. There were no significant differences between control and treated animals in biochemical or hemodynamic parameters. All animal groups treated with FDP demonstrated significant reductions in the amount of necrotic and ischemic tissue compared to controls (P less than 0.05). However, only the 175 mg/kg group had a significant reduction compared to controls in necrotic tissue weight as a percentage of ischemic myocardium (24 +/- 15% vs. 72 +/- 22%, respectively, P less than 0.01). These data suggest that FDP may have a role in limiting the amount of myocardial damage after an acute coronary artery occlusion.     

声学造影实时三维超声心动图评价犬急性冠状动脉闭塞的侧支循环

目的 应用声学造影实时三维超声心动图评价急性冠状动脉闭塞犬的侧支循环.方法 结扎12只健康杂种犬左前降支,分别于结扎前、结扎后即刻、结扎后30 min及结扎后180 min时行心肌声学造影观察,并计算供血区心肌重量. 结果左前降支结扎后所有实验犬均有不同程度的侧支循环建立.结扎后30 min,侧支循环供血区心肌重量为(9.65±2.90)g;结扎后180 min,侧支循环供血区心肌重量为(12.58±3.98)g;二者之间差异有统计学意义. 结论 应用声学造影实时三维超声心动图可以很好地显示冠状动脉侧支循环的形成,并获得全面准确的侧支循环区心肌重量.     

Local myocardial function following coronary occlusion in cats,Effect on non-ischaemic regions

Summary. The mechanical function and perfusion in ischaemic and non-ischaemic myocardium after coronary occlusion was studied in 10 cats using pressure-length loop analysis and radiolabeled microspheres. Measurements in three regions—ischaemic, adjacent normal and remote normal myocardium—all showed different responses to coronary occlusion. In the ischaemic region loop area, segment shortening and tissue flow were markedly reduced. In the adjacent normal region, both loop area and segment shortening as well as flow increased. In the remote normal region, neither loop area, segment shortening nor flow showed consistent changes. End-diastolic segment length increased in all regions, most in the ischaemic region and least in the remote region. The increased end-diastolic segment length in all regions after coronary occlusion indicates activation of the Frank-Starling mechanism as an attempt to maintain stroke volume. However, the end-diasolic segment length did not increase uniformly for all normal myocardium: it depended on the proximity to the ischaemic region. Increased contractile function in the adjacent normal myocardium due to non-uniform distribution of the Frank-Starling effect is the most likely mechanism behind the left ventricle's ability to partially compensate for loss of contractile mass during acute regional ischaemia in anaesthetized cats.     

64层螺旋CT冠状动脉成像对心肌桥-壁冠状动脉的评价

目的 探讨心肌桥-壁冠状动脉(MB-MCA)形态学特征及其与冠状动脉粥样硬化病变关系.方法 回顾性分析6729例可疑或确诊冠心病(CHD)患者64层螺旋CT冠状动脉血管成像(CTA)结果,由2位心血管CT诊断医师独立判断MB-MCA的存在,结果一致时诊断为MB-MCA.测量MB厚度、MCA长度及管径,记录MB-MCA位置、包绕情况、MCA两端成角情况,并记录MCA本身以及其近、远段冠状动脉粥样硬化病变情况,应用卡方检验,分析心肌桥近段、远段冠状动脉及壁冠状动脉自身动脉粥样硬化病变发生率有无差异.结果 6729例患者中发现MB-MCA总计1214例(18.0%),1262处.MB-MCA位于LAD者占90.7%(1145例).MSCT显示MCA可被心肌完全包绕(39.3%,496/1262)或不完全包绕(60.7%,766/1262).MCA长度为(18.6±9.0) mm.MB厚度为(2.2±1.7) mm.77.3%的MCA近端或(和)远端成角.MB-MCA近段和远段冠状动脉粥样硬化病变发生率分别为53.3%和2.3%,MCA本身粥样硬化病变发生率为0.5%,各组间有显著的统计学差异(P＜0.05).结论 64层螺旋CT能够清楚显示载MB-MCA冠状动脉全程和MB-MCA本身,并用于评价MB-MCA形态学特征.心肌桥近段冠状动脉易发生粥样硬化病变.     

Effect of hypoxemia on pharmacokinetics of endotracheal lidocaine in dogs

Endotracheal administration is an effective alternative method for giving drugs in the many clinical situations in which it is difficult or impossible to quickly obtain an intravenous line. Yet whether various clinical conditions such as hypoxemia have any effect on endotracheal drug therapy is not known. Sixteen sets of plasma lidocaine levels were measured at 5, 15, 30, and 60 min after endotracheal lidocaine administration in eight dogs. Each dog was given the same dose of endotracheal lidocaine by the same technique of administration while in both a normal control state (Group I = 'Non-hypoxemia', mean Po2 = 98) and during hypoxemia (Group II = "Hypoxemia", mean Po2 = 36). Significantly higher plasma lidocaine levels occurred in the hypoxemic state (Group II) at time = 5 min while there was no significant difference in plasma lidocaine levels at time = 15, 30, and 60 min. Mean plasma lidocaine levels (micrograms/ml) at 5 min were: Group I = 1.38, Group II = 2.36 (significant at P less than 0.05). Plasma lidocaine levels were: Group I = 1.61 vs. Group II = 1.63 at time = 15 min, Group I = 1.11 vs. Group II = 1.10 at time = 30 min, and Group I = 0.54 vs. Group II = 0.51 at time = 60 min. Thus, there was a higher peak plasma lidocaine level and a shorter time to peak plasma lidocaine levels in the hypoxemic dogs.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性乳酸酸中毒对实验犬心室收缩功能影响的研究

目的：观察实验性乳酸酸中毒对犬心室收缩功能的影响。方法：应用超声心动图和血流动力学监测技术,观察９只经静脉麻醉、气管插管、连续静脉滴注０．５ｍｏｌ／Ｌ的ＤＬ乳酸液后,健康杂种犬心室收缩功能变化;每３０分钟采血液、心室、主动脉压力及超声心动图数据１次。结果：主动脉瓣血流平均加速度、左室射血分数、左室周边缩短速率、肺动脉瓣血流平均加速度、右室面积变化率和右室射血分数均降低（Ｐ均＜０．０５）,心室收缩末径较舒张末径增大更明显（Ｐ均＜０．０５）。结论：乳酸酸中毒降低心室收缩功能,尤其降低心肌收缩力。     

Predictors of exercise induced myocardial ischemia in patients with isolated coronary artery ectasia

The aim of this study was to investigate the angiographic predictors of exercise induced ischemia in patients with isolated coronary ectasia. We have prospectively analysed coronary angiograms of 1521 consecutive patients undergoing cardiac catheterisation. The overall incidence of coronary ectasia was 6.7% (102 patients). Forty-six patients (3%) with non-obstructive, diffuse or segmental coronary ectasia (i.e. isolated coronary ectasia) constituted the main study group. Coronary angiograms were reviewed for stigmata of an impaired coronary blood flow such as 'slow flow', 'segmental backflow phenomenon' and stasis. 'Slow flow' was quantified with frame counting. An ectasia-jeopardy score was also described in order to assess the effect of the extent of coronary ectasia on exercise induced ischemia. Exercise induced ischemia was observed in 24 patients (52%). Exercise test was abnormal in 70% of the patients with diffuse ectasia and 26% of patients with segmental ectasia (p = 0.003). The frame count of the arteries of the study group was higher than the control group but the correlation between the frame count of the ectatic vessels and exercise induced ischemia was not significant. Stasis of the dye also did not correlate with ischemia. There was a significant correlation between exercise induced ischemia and backflow phenomenon in left anterior descending artery (LAD) (r = 0.56, p = 0.0001). Exercise induced ischemia was best correlated with the ectasia-jeopardy score (r = 0.77, p = 0.0001) and a score of > or =4 identified the patients at risk with 90% sensitivity and 80% specificity. In conclusion, the extent of the ectasia within the coronary tree, diffuse ectasia and backflow-phenomenon in LAD were identified as the most important predictors of exercise induced ischemia.     

Cardiac function in open-chest dogs after left to right ventricular shunting and right coronary artery occlusion

Summary. Patients with acquired ventricular septal defect (VSD) after myocardial infarction have a particularly bad prognosis if right ventricular function is severely impaired. The significance of an ischaemic right ventricular free wall on cardiac function during interventricular shunting was examined in open-chest dogs. An external interventricular shunt could be opened and closed at will, and by occlusion of the right coronary artery (RCA), a part of the right ventricular free wall was rendered ischaemic. Aortic flow decreased by 8±2% when the shunt was opened in the presence of a normal right ventricle, and by 16±2% (difference: P<0.05) in the presence of right ventricular ischaemia. Aortic flow fell by 19±3% when the RCA was occluded. Right ventricular dyskinesia was demonstrated after occlusion of RCA, by recording segment lengths in the right ventricular free wall. The dyskinesia was aggravated when the shunt was opened. The left ventricle exerted a ‘negative’ work on the ischaemic right ventricular free wall. Retention of blood in the right ventricle, with a subsequent decline in left ventricular filling and an almost unchanged interventricular shunting of blood, explain why aortic flow fell more when the shunt was opened in the presence of right ventricular ischaemia.     

Asymptomatic occlusion of the left main coronary artery by an aortic pseudoaneurysm

Extrinsic compression of the left main coronary artery is a rare cause of coronary ischemia. We describe a 35-year-old Asian woman with complete asymptomatic occlusion of the left main coronary artery by a large aortic pseudoaneurysm. She underwent repair of the pseudoaneurysm and coronary artery bypass grafting at the Mayo Clinic in Rochester, Minn. The differential diagnosis is discussed. Based on this patient's age and associated vascular lesions, we conclude that Takayasu arteritis was the most likely cause of her condition.     

Rupture of pulmonary artery induced by balloon occlusion pulmonary angiography

A case of pulmonary artery rupture induced by balloon occlusion pulmonary angiography (BOPA) is reported. A flow-directed pulmonary artery catheter had been inserted for hemodynamic monitoring in a septic shock patient complicated by acute respiratory distress syndrome. To check for pulmonary damage, BOPA was performed immediately after hemodynamic measurement. Just as the hand injection of contrast medium was ending, the patient began to cough and a small amount of hemoptysis was observed. The angiogram showed the extravasation of contrast medium from the distal pulmonary artery to the situation of catheter tip. Pulmonary hemorrhage was controlled with mechanical ventilatory support with 10 cmH₂O positive end-expiratory pressure and no specific therapy was required. This complication should be kept in mind and using a power injector to avoid injurious transient high pressure pulse is recommended.