Prognostic significance of a low peak serum creatine kinase level in acute myocardial infarction

To assess the prognostic significance of a low peak creatine kinase (CK) level, 723 consecutive patients admitted with acute myocardial infarction (AMI) within 16 hours after onset of symptoms were studied. Thrombolytic therapy was not attempted during the study. Patients were dichotomized according to their peak CK levels, determined from a cluster analysis of peak CK distribution among the population of patients who died within 3 years after hospital discharge. The 139 patients with low peak CK (less than or equal to 650 IU/liter) (group 1) were compared to the 584 patients with high peak CK (greater than 650 IU/liter) (group 2). Patients in group 1 were older and had a higher incidence of previous AMI, angina pectoris before AMI and non-Q-wave AMI. Despite a lower incidence of in-hospital complications and a nonsignificantly lower hospital mortality rate (4 vs 9%) the group 1 three-year posthospital mortality rate was higher (26 vs 17%; p less than 0.02), especially in the subgroup of patients with a Q-wave infarct (mortality 31% in group 1 vs 16% in group 2; p less than 0.001). Among the 491 patients who had a first Q-wave AMI, 55 had a peak CK less than or equal to 650 IU/liter. Compared to the 436 patients with a higher peak CK, these 55 patients had a higher incidence of early postinfarction angina (31 vs 14%; p less than 0.01), a similar hospital mortality (4 vs 7%) but a higher 3-year posthospital mortality (23 vs 12%; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Presence of angina pectoris before acute myocardial infarction and degree of residual stenosis after coronary thrombolysis

This study tested the hypothesis that the degree of residual stenosis after coronary thrombolysis reflected that of original stenosis presented by symptom of angina before acute myocardial infarction (AMI). The relation between the presence of angina before AMI and the degree of residual stenosis after coronary thrombolysis was observed in 57 patients with successful coronary thrombolysis for AMI. Patients with significant coronary artery stenoses other than the artery responsible for AMI were excluded from this study. In 22 patients with chronic angina for 2 weeks or longer before AMI, 14 patients had a residual stenosis of 75% or more and 8 patients had a residual stenosis of less than 75%. In 35 patients with angina for less than 2 weeks or not at all before AMI, 9 patients had a residual stenosis of 75% or more, and 26 patients had a residual stenosis of less than 75% (p less than 0.01). In the course of progression of coronary artery disease, some patients had AMI without severe underlying stenosis and others with severe underlying stenosis. Patients with chronic angina before AMI might tend to have AMI with acute occlusion superimposed on the severe organic stenosis. Patients without chronic angina before AMI would be more at risk for AMI caused by acute occlusion without underlying severe stenosis.     

Prognosis in acute myocardial infarction in relation to development of Q waves.

In a totally nonselected group of patients with acute myocardial infarction (AMI) (n = 921) admitted from the emergency department to the coronary care unit or other hospital ward, the occurrence of non-Q-wave AMI and the prognosis in these patients was determined and compared with those in whom Q waves were developed. Fifty-two percent had AMI without new Q waves. Patients with a non-Q-wave AMI differed from patients with Q-wave AMI, more frequently having a previous history of AMI (p less than 0.001), angina pectoris (p less than 0.01), diabetes mellitus (p less than 0.05), congestive heart failure (p less than 0.001), and a higher mean age (p less than 0.001), whereas smoking was more common in Q-wave AMI. Patients with non-Q-wave AMI had a 1-year mortality of 31% compared with 26% in Q-wave AMI (p greater than 0.2) and a reinfarction rate of 20% compared with 12% for Q-wave AMI (p less than 0.01). Among patients aged less than 75 years without a previous history of AMI, congestive heart failure, and diabetes mellitus, the 1-year mortality rate was 16% for patients with Q waves versus 15% for those without Q waves (NS). Appearance of Q waves was not independently associated with death. We conclude that in a nonselected group of patients with AMI the occurrence of a non-Q-wave AMI is much higher than previously reported. The prognosis in AMI during one year of follow-up is not associated with development of Q waves.     

Correlates of bundle-branch block in patients undergoing primary angioplasty for acute myocardial infarction.

BACKGROUND: Early reperfusion therapy has reduced the infarct size and mortality rate in patients with acute myocardial infarction (AMI). The occurrence of bundle-branch block in AMI is related to the amount of myocardial damage and the insult to the conduction system. HYPOTHESIS: To evaluate the clinical and angiographic factors related to the occurrence of bundle-branch block (BBB) in patients with primary percutaneous transluminal coronary angioplasty (PTCA), we investigated consecutive series of patients with their first Q-wave AMI and successful PTCA. METHODS: Coronary angiogram at the time of admission, electrocardiogram, and echocardiogram were evaluated in 279 patients with their first Q-wave AMI and successful PTCA. RESULTS: Bundle-branch block was detected in 26 patients (9%); 16 patients had transient and 10 patients had persistent block, while 16 patients had bifascicular block and 10 patients had right BBB. The patients with BBB had a significantly larger number of left ventricular asynergic segments, higher incidence of total occlusion of infarct-related artery, angiographic no reflow, and pericardial rub than those without BBB. When the multivariate analysis was performed using five clinical markers of infarct severity, angiographic no reflow (F = 20.2, p < 0.001) and total occlusion of infarct-re-lated artery (F = 4.2, p = 0.04) were found to be the significant variables related to BBB. CONCLUSIONS: Despite successful primary PTCA, absence of antegrade flow in the infarct-related artery at the onset of AMI and/or angiographic no reflow resulted in more severe transmural myocardial damage and, hence, the occurrence of BBB.     

Influence of collateral filling of the occluded infarct-related coronary artery on prognosis after acute myocardial infarction.

Previous studies showed that long-term morbidity and mortality after acute myocardial infarction (AMI) are influenced by the presence or absence of anterograde flow in the infarct artery. In comparison with patients with anterograde flow, those whose infarct artery remains occluded are more likely to have unstable angina, recurrent AMI, congestive heart failure and sudden death. This study was performed to assess the influence of collateral filling of the infarct artery on long-term morbidity and mortality in surviving patients of initial AMI in whom the infarct artery was occluded. Over a 12.5-year period, 146 subjects (108 men and 38 women, aged 25 to 76 years) with AMI, no anterograde flow in the infarct artery, and no disease of other coronary arteries were medically treated and followed for 42 +/- 28 (mean +/- standard deviation) months. Of these subjects, 120 had angiographic evidence of collateral filling of the infarct artery (group I), whereas the remaining 26 did not (group II). The groups were similar in age, sex, cardioactive medications, left ventricular performance and infarct artery. They were also similar in incidence of unstable angina (19% of group I, 31% of group II; p = not significant [NS]), recurrent AMI (12% of group I, 8% of group II; p = NS), congestive heart failure (16% of group I, 12% of group II; p = NS) and cardiac death (16% of group I, 19% of group II; p = NS). Thus, angiographic evidence of collateral filling of the infarct artery in surviving patients of AMI exerts no demonstrable influence (beneficial or detrimental) on long-term morbidity or mortality.     

左主干急性闭塞或狭窄所致急性心肌梗死的急诊介入治疗

目的总结左主干急性闭塞或狭窄所致急性心肌梗死(AMI)患者急诊经皮冠状动脉介入治疗(PCI)的经验,探讨急诊PCI在此类患者中的安全性和有效性。方法从1995年1月至2004年12月,在1343例急诊PCI中,共有11例梗死相关血管为左主干。11例患者均为男性,年龄43~70岁,平均(56·4±9·2)岁,其中6例(54·5%)入院时即存在严重心原性休克。所有患者均在主动脉内球囊反搏支持下接受急诊PCI治疗。结果8例急诊置入支架,余3例仅行球囊扩张,后者有2例术后接受急诊冠状动脉旁路移植术。住院期间死亡5例(45·5%),存活的6例患者均完成3个月随访,其中4例随访超过2年,1例于术后4年猝死,1例患者术后5年重复造影检查结果良好。对比分析提示术前存在良好的侧支循环可能是影响此类患者急诊PCI术后疗效的因素。结论左主干急性闭塞或严重狭窄所致的AMI患者病情凶险,急性期死亡率高。侧支循环形成与否,治疗策略和预后不同,主动脉内球囊反搏支持下急诊PCI治疗可以挽救部分患者的生命和改善预后,对于侧支循环不良的患者,部分再灌注策略可能为一种有效手段之一,值得进一步研究。     

Determinants of infarct size in reperfusion therapy for acute myocardial infarction.

BACKGROUND. Experimental animal studies have demonstrated that myocardium at risk, residual collateral flow, and duration of coronary artery occlusion are important determinants of final infarct size. The present study examined these variables in patients with acute myocardial infarction in relation to final infarct size. METHODS AND RESULTS. Myocardium at risk was assessed with hexakis(2-methoxyisobutyl isonitrile) technetium (I) (99mTc sestamibi) in 89 patients with first-time myocardial infarction (anterior, 48 patients; inferior, 41 patients). All patients had successful reperfusion therapy with either intravenous thrombolysis (32 patients) or primary coronary angioplasty (57 patients) within 24 hours of the onset of chest pain (4.7 +/- 3.9 hours; range, 0.5-21.5 hours) documented by coronary angiography. 99mTc sestamibi was injected intravenously before reperfusion therapy, and tomographic imaging was performed 1-6 hours later. Myocardium at risk was quantitated for each patient and expressed as a percentage of the left ventricle: 35 +/- 19%; range, 2-73%. Collateral flow was estimated by both invasive and noninvasive methods. Fifty-three patients with TIMI grade 0 or I flow who underwent primary coronary angioplasty had collateral flow graded angiographically (0-3) before the first balloon inflation. All patients had collateral flow estimated noninvasively from the acute sestamibi short-axis profile curve by three methods that assess the severity of the perfusion defect. Each of these three methods was significantly associated with angiographic collateral grade. Final infarct size was determined at hospital discharge by a second sestamibi study (17 +/- 17%; range, 0-59%). Myocardium at risk (r = 0.61, p less than 0.0001), angiographic collateral grade (p = 0.0003), and radionuclide estimates of collateral flow (r = 0.69-0.70, all p less than 0.0001) were all significantly associated with final infarct size. The time to reperfusion therapy was not significantly associated with final infarct size by univariate analysis (r = 0.18, p = 0.10). Two multivariate models were constructed to determine which variables were independently associated with final infarct size. In the invasive model, myocardium at risk, angiographic collateral grade with an interaction term for infarct location, and time to reperfusion were all independently significant and accounted for 70% of the variability in final infarct size. The noninvasive model, which substituted a radionuclide estimate of collateral flow for angiographic collateral grade, showed nearly identical results, accounting for 68% of the variability in infarct size in patients where the infarct artery was known to be occluded. When all patients were included (patients with and without acute angiography), the noninvasive model accounted for 59% of the variability in infarct size. CONCLUSIONS. Myocardium at risk, collateral flow, and duration of coronary occlusion are each independently associated with final infarct size and account for most of its variability. Ideally, all three parameters should be examined in evaluation of the efficacy of new treatment strategies for acute myocardial infarction.     

Significance of Q-wave regression after transmural acute myocardial infarction

A total of 313 consecutive patients was studied to assess the prevalence and prognostic implications of Q-wave loss after transmural acute myocardial infarction. Heart catheterization, including single-plane left ventriculography and selective coronary arteriography, was performed before hospital discharge. After a mean follow-up of 65 (1 to 100) months, 34 patients (11%) lost their Q waves. The time interval from the acute event to the first electrocardiogram showing Q-wave disappearance was 14 (1 to 32) months. Peak creatine kinase value was significantly higher in patients who retained their Q waves than in those who lost them (1,121 +/- 813 vs 779 +/- 464 IU, respectively, p less than 0.05). Severity of coronary artery disease, as judged by the number of diseased arteries and the number of arteries with total or subtotal occlusion, was similar in both groups. However, patients showing Q-wave regression had lower left ventricular end-diastolic pressure, higher ejection fraction and fewer abnormally contracting segments than their counterparts (12 +/- 6 vs 15 +/- 7 mm Hg, p less than 0.05; 53 +/- 11 vs 44 +/- 14%, p less than 0.001; 1 +/- 1 vs 2 +/- 1 segments, p less than 0.001, respectively). In addition, no patient with normalized electrocardiogram presented with left ventricular aneurysm. Although differences in mortality, nonfatal reinfarction and new onset of angina between the 2 groups were not significant, congestive heart failure was prevalent among patients with permanent Q waves (23 vs 6%, p less than 0.05). Our findings suggest that Q-wave loss after AMI may be related to a smaller infarct size.     

Mechanism of acute myocardial infarction in patients with prior coronary artery bypass grafting and therapeutic implications

Although acute myocardial infarction (AMI) is usually due to thrombotic occlusion when involving a native coronary artery, the mechanism responsible for AMI in patients with previous coronary artery bypass grafting (CABG) is not well understood. Since knowledge of pathophysiology of AMI may alter subsequent management, angiograms obtained between 1 hour and 7 days of AMI (median 1 day) were reviewed in 50 patients greater than 1 year after CABG. The culprit vessel was identified by the presence of residual stenosis and/or thrombus in the vessel supplying the infarct zone or by reviewing previous angiograms. The infarct vessel was identified as a vein graft in 38 (76%) patients, the native vessel in 8 patients (16%) and could not be accurately determined in 4 patients (8%). Among the 38 vein grafts suspected as the infarct vessel, unequivocal angiographic evidence of residual thrombus (filling defect/persistent staining) was present in 31 (82%) and was greater than 2 cm in length in 15 patients. Successful reperfusion occurred in only 2 of 8 (25%) grafts after intravenous thrombolytic therapy. Intragraft thrombolysis with or without additional angioplasty was successful at restoring flow in 8 of 10 (80%) grafts. Data indicate that in patients who have undergone previous CABG, AMI is usually caused by thrombotic occlusion of a saphenous vein graft and that conventional intravenous thrombolytic therapy may be inadequate to restore flow. The large mass of thrombus and absent flow in the graft may require subselective drug infusion, a higher thrombolytic dose or a mechanical means of recanalization.     

Prognostic importance of delayed Q-wave evolution 3 to 24 hours after initiation of thrombolytic therapy for acute myocardial infarction

The timing of Q-wave evolution and its prognostic significance was studied in 201 patients who received thrombolytic therapy for a first acute myocardial infarction (AMI). One hundred forty-one patients (70%) had evidence of a Q-wave AMI within 3 hours of the initiation of thrombolytic therapy, 31 (16%) developed Q waves after 3 hours but before hospital discharge, and 29 (14%) were discharged with a non-Q-wave AMI. Laboratory indicators of myocardial damage and in-hospital morbidity and mortality were greater among patients with Q-wave AMIs than with non-Q-wave AMIs. When these indexes were examined with respect to the timing of Q-wave evolution, the prognosis of patients with delayed Q-wave development was similar to that of patients with non-Q-wave AMIs. Thus, compared to patients with early (less than or equal to 3 hours) Q-wave evolution, patients with delayed Q-wave evolution or with a non-Q-wave AMI had a smaller creatine kinase peak (mean 661 to 1,081 vs 1,251 to 1,541 IU; p = 0.005), better preservation of left ventricular function as measured by radionuclide ventriculography before discharge (mean +/- standard deviation 54 +/- 11% vs 47 +/- 13%; p less than 0.01), and a lower incidence of congestive heart failure at discharge (3 vs 15%; p = 0.02). In-hospital mortality was lower among patients with delayed Q-wave evolution or with a non-Q-wave AMI (5 of 141 vs 0 of 60; difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)     

Non-Q-wave acute myocardial infarction: Body surface potential map and ventriculographic patterns

Day 5 body surface map and radionuclide angiographic patterns were compared among 56 patients with first non-Q-wave or Q-wave acute myocardial infarction (AMI). Three radionuclide angiographic patterns were recognized in patients with non-Q infarction: no wall motion abnormalities (n = 8), single-segment wall motion abnormalities (n = 10) and multiple-segment wall motion abnormalities (n = 9). In contrast, only 2 radionuclide angiographic patterns were identified in patients with Q-wave infarction: multiple-segment wall motion abnormalities (n = 25) and single-segment wall motion abnormalities (n = 4). The Q-wave distributions of 14 of 18 patients with non-Q infarction with 0 or 1 wall motion abnormalities were normal; 2 patients had “missed” anterior; 1 patient had inferior; and 1 had posterior AMI patterns. Of 9 patients with non-Q infarction who had multiple-segment wall motion abnormalities, 8 had infarct Q waves on the posterior torso. Q-wave patterns in patients with anterior (n = 17) and inferior (n = 12) Q-wave infarctions were typical and homogeneous for each group. Quantitative analysis of minimum Q-zone integral, ΣQ-wave integrals, ST-integral maximum, wall motion abnormality score and ejection fraction revealed no differences between patients with non-Q-wave and those with inferior Q-wave infarction. In contrast, patients with anterior AMI had significantly more abnormal values of all variables than either of the other groups. Overall, the data support the concept of non-Q-wave AMI as a distinct, if heterogeneous, pathophysiologic entity. The variable body surface potential map and radionuclide angiographic patterns of the non-Q-wave AMI subgroups further suggest a variable prognosis. It remains to be determined, however, which patients are at greatest risk and why.     

Coronary anatomy and left ventricular function in the first 12 hours of acute myocardial infarction: the Western Washington Randomized Intracoronary Streptokinase Trial

The relationships among clinical variables, coronary anatomy, and left ventricular function during the early hours of acute myocardial infarction (AMI) were evaluated from data acquired in the Western Washington Intracoronary Streptokinase Trial. All patients had symptoms and electrocardiographic changes typical of AMI. All data were obtained before treatment with streptokinase. Mean time to catheterization was 4.1 hr after onset of symptoms. Coronary angiograms (n = 245) were analyzed for location of infarct-related occlusion and collateral flow to the infarct bed. Left ventricular ejection fraction and regional left ventricular function were quantitated in 227. Sixty-two percent of occlusions were in the most proximal segment of the involved coronary artery. Collateral circulation was seen in 42% overall, in 31% with left anterior descending artery (LAD) occlusion, and in 52% with right coronary artery (RCA) occlusion (p less than .005). Left ventricular ejection fraction was lowest and regional function was most abnormal in the group with proximal LAD occlusion. Hyperkinesis was present in 32%; in those with hyperkinesis, hyperkinetic segment length was longest in those with RCA or circumflex occlusion. Multivariate analysis identified proximal LAD occlusion as the factor most closely associated with left ventricular ejection fraction and with measures of left ventricular regional hypofunction. We conclude that (1) AMI is usually caused by occlusion or subtotal occlusion in the most proximal portion of the involved coronary artery, (2) collateral circulation is more frequent with RCA than with LAD occlusion, and (3) location of the infarct-related occlusion is the most important determinant of global and regional left ventricular function in the early hours of AMI.     

Measurement of acute Q-wave myocardial infarct size with single photon emission computed tomography imaging of indium-111 antimyosin

Myocardial infarct size was measured by single photon emission computed tomography (SPECT) following injection of indium-111 antimyosin in 27 patients (18 male and 9 female; mean age 57.4 +/- 10.5 years, range 37 to 75) who had acute transmural myocardial infarction (MI). These 27 patients represent 27 of 35 (77%) consecutive patients with acute Q-wave infarctions who were injected with indium-111 antimyosin. In the remaining 8 patients either tracer uptake was too faint or the scans were technically inadequate to permit infarct sizing from SPECT reconstructions. In the 27 patients studied, infarct location by electrocardiogram was anterior in 15 and inferoposterior in 12. Nine patients had a history of prior infarction. Each patient received 2 mCi of indium-111 antimyosin followed by SPECT imaging 48 hours later. Infarct mass was determined from coronal slices using a threshold value obtained from a human torso/cardiac phantom. Infarct size ranged from 11 to 87 g mean 48.5 +/- 24). Anterior infarcts were significantly (p less than 0.01) larger (60 +/- 20 g) than inferoposterior infarcts (34 +/- 21 g). For patients without prior MI, there were significant inverse correlations between infarct size and ejection fraction (r = 0.71, p less than 0.01) and wall motion score (r = 0.58, p less than 0.01) obtained from predischarge gated blood pool scans. Peak creatine kinase-MB correlated significantly with infarct size for patients without either reperfusion or right ventricular infarction (r = 0.66). Seven patients without prior infarcts had additional simultaneous indium-111/thallium-201 SPECT studies using dual energy windows.(ABSTRACT TRUNCATED AT 250 WORDS)     

颈内动脉颅外段严重狭窄和闭塞所致脑梗死病灶分布模式特征分析

目的 分析颈内动脉颅外段(extracranial internal carotid artery,EICA)严重狭窄和闭塞所致脑梗死的病灶分布模式,进而探讨两者导致脑梗死机制的差异,为个体化防治策略提供依据.方法 回顾性分析61例EICA粥样硬化性严重狭窄(狭窄程度70%～99%)或闭塞所致急性脑梗死患者的临床和影像...     

Usefulness of myocardial contrast echocardiography in predicting collateral blood flow in the presence of a persistently occluded acute myocardial infarction-related coronary artery

Adequate collateral blood flow at rest can sustain myocardial viability despite persistent occlusion of the infarct-related artery (IRA) in acute myocardial infarction (AMI). This has therapeutic and prognostic implications. Studies addressing the value of intravenous myocardial contrast echocardiography (MCE) to detect collateral blood flow after AMI in humans are limited. Accordingly, 70 consecutive patients with AMI underwent low-power intravenous MCE using a Sonovue infusion 7 to 10 days after thrombolysis. Myocardial perfusion detected by MCE was analyzed (qualitatively and quantitatively) in the akinetic segments in 20 patients (29%) with an occluded IRA who subsequently underwent revascularization. Contractile reserve, which is a marker of myocardial viability, was assessed with low-dose dobutamine 12 weeks after mechanical revascularization. Of the 102 akinetic segments (32%), 37 (36%) showed contractile reserve. Contractile reserve was present in 24 of the 29 segments (83%) with homogenous contrast opacification and absent in 60 of the 73 segments (82%) with reduced/absent opacification. Quantitative peak contrast intensity, microbubble velocity, and myocardial blood flow were significantly higher (p <0.0001) in the segments with contractile reserve than in those without contractile reserve. Multiple logistic regression analysis using electrocardiographic, biochemical, and myocardial contrast echocardiographic markers of collateral blood flow showed that MCE (odds ratio 26.0, 95% confidence interval 6.3 to 108.0, p <0.001) was the only independent predictor of collateral blood flow as demonstrated by the presence of contractile reserve. MCE may thus be used as a reliable bedside technique for the accurate evaluation of collateral blood flow in the presence of an occluded IRA after AMI.     

Right ventricular infarction: role of the moderator band artery in determining infarct size

We studied 19 patients with proximal right coronary artery occlusions associated with acute myocardial infarcts less than 30 days old. Right ventricular infarct size, determined as a percentage of right ventricular surface area, ranged from 0% to 29%. Correlation of 24 variables measuring infarct size, chamber size and coronary artery disease failed to demonstrate a significant correlation with the extent of right ventricular infarction. However, estimates of the degree of obstruction to potential collateral flow into the right coronary arterial system from the left anterior descending coronary artery, especially through the moderator band artery, showed a significant positive correlation with infarct size (p less than 0.02). Among the five patients with massive (greater than 25%) right ventricular infarction, four had significant (greater than 75%) obstruction of the left anterior descending system, resulting in potentially impaired collateral blood flow; the other patient had normal coronary arteries and embolic occlusion of the proximal right coronary artery with contraction band necrosis. The study suggests that collateral flow to the right ventricular myocardium, especially through the moderator band artery, protects against massive infarction in the presence of proximal right coronary artery occlusion.     

Salvage of ischaemic myocardium by reperfusion: importance of collateral blood flow and myocardial oxygen demand during occlusion

Early reperfusion after coronary artery occlusion is used to treat acute myocardial infarction, but the factors that determine whether salvage of ischaemic myocardium actually occurs remain poorly defined. Differences in collateral blood flow to the region at risk, and haemodynamic variables during occlusion, may contribute to uncertainty as to the time beyond which reperfusion no longer reduces infarct size. To clarify this issue, open chest anaesthetised dogs underwent 1, 2, 3, 4, or 6 hours of left anterior descending coronary artery occlusion followed by reperfusion or permanent occlusion (n = 8 per group). Microspheres were injected before occlusion and 15 minutes after occlusion for regional myocardial blood flow determination, and heart rate and arterial blood pressure were measured before occlusion and 10 minutes and 30 minutes after occlusion. At 96 hours after occlusion haemodynamic variables were again measured; the animals were then killed, and occluded bed size was determined by in vitro dye perfusion. The area of necrosis was quantified from histological sections and expressed as a percentage of occluded bed size (AN/OB). If duration of occlusion is considered alone, reperfusion beyond two hours did not salvage ischaemic myocardium in this model. If the results for occlusion equal to and greater than two hours are combined, the mean area of necrosis (27(2)%) was significantly greater than that produced by one hour of occlusion followed by reperfusion (10(4)%). For the animals undergoing occlusion for two or more hours or permanent occlusion, collateral blood flow significantly influenced the area of necrosis. When epicardial flow during occlusion was high (greater than 0.30 ml X min-1 X g-1 tissue) 13 out of 14 dogs undergoing occlusion for two or more hours or permanent occlusion developed small (AN/OB less than 27%) infarcts (mean AN/OB 17(2)%). In contrast, when epicardial collateral flow was low (less than 0.30 ml X min-1 X g-1) 14 out of 23 animals had large (AN/OB greater than 27%) infarcts (mean AN/OB 34(3)%). For the 23 dogs in which epicardial flow was low, heart rate during occlusion significantly influenced infarct size: the 14 dogs that developed large infarcts (AN/OB greater than 27%) had a higher mean heart rate (152(6) beats X min-1) than the nine that developed small infarcts (AN/OB less than 27%) (130(5) beats X min-1; p less than 0.025). Thus reperfusion at one hour after occlusion salvaged ischaemic myocardium.(ABSTRACT TRUNCATED AT 400 WORDS)     

Prognostic significance of angina pectoris before first acute myocardial infarction

To delineate the clinical significance and prognostic importance of a history of chronic or new onset angina pectoris before acute myocardial infarction (AMI), 732 consecutive patients admitted for a first AMI were studied and divided into 3 groups. Two hundred patients (27%) had chronic angina before AMI (greater than 1 month); 247 patients (34%) had new onset angina before AMI (less than 1 month) and the 285 remaining patients (39%) never had angina before AMI. All clinical characteristics were similar in the group of patients with chronic angina and in the group of patients with new onset angina, including in-hospital mortality (10 vs 9%) and 3-year post-hospital mortality (16 vs 16%). Compared to the 285 patients without angina, the 447 patients with angina before AMI were older, more likely to be women, and had a higher frequency of anterior AMI and early post-infarction angina. Both groups had a similar in-hospital mortality (10 vs 8%, not significant), but patients with angina had a higher 3-year post-hospital mortality (16 vs 7%, p less than 0.001). In the group of patients with angina before AMI who were discharged from the hospital, the comparison of nonsurvivors and survivors showed that the patients who died were older, presented more frequently with a non-Q-wave myocardial infarct and more often had left ventricular failure and complete bundle branch block during hospital stay. Chronic and new onset angina before AMI have the same clinical characteristics and deleterious long-term prognostic significance.     

Reliability of Q-wave formation and QRS score in predicting regional and global left ventricular performance in acute myocardial infarction with successful reperfusion

The frequency of electrocardiographic Q-wave formation and the relation of Q wave and QRS score to regional and global left ventricular (LV) performance were determined in 131 patients with acute myocardial infarction (AMI) receiving thrombolytic therapy. Thrombolytic therapy was successful in reperfusing the occluded infarct artery in 100 patients and was unsuccessful in 31. The number of patients who had 1 or more Q waves (88 vs 87%) and 2 or more Q waves (70 vs 74%) was similar. In contrast, normal wall motion was significantly more common in the infarct area in patients in whom reperfusion was successful (42 vs 15%, p less than 0.05). Total QRS scores were similar in patients in whom reperfusion was successful and in those in whom it was not (6.0 +/- 3.2 vs 6.4 +/- 4.2). Despite similar QRS scores, successfully treated patients had significantly higher LV ejection fraction (53 +/- 13% vs 46 +/- 15%, p less than 0.05). Thus, Q-wave formation after successful thrombolytic therapy for AMI is common but does not faithfully reflect regional or global LV performance. Electrocardiographic analysis alone is not a reliable method to assess efficacy of reperfusion therapy.     

The functional reserve of collaterals supplying long-term chronic total coronary occlusions in patients without prior myocardial infarction.

AIMS: Chronic total coronary occlusions (CTOs) with angiographically well-developed collaterals may be considered to provide sufficient blood supply to the occluded segment, and the indication for revascularization may be questioned. Therefore, the collateral function and functional reserve in patients with a CTO without a prior Q-wave myocardial infarction (MI) were assessed. METHODS AND RESULTS: Invasive assessment of collateral function was done during successful percutaneous coronary intervention in 107 patients with a CTO and no prior Q-wave MI. Intracoronary Doppler flow velocity and pressure recordings were obtained distal to the occlusion before the first balloon inflation and collateral function indexes calculated. In 62 patients, additional pharmacological stress testing was done by intravenous adenosine (140 microg/kg/min) to assess the collateral flow reserve. Patients with normal and impaired regional dysfunction were compared. Collateral function was similar in patients with and without regional left ventricular (LV) dysfunction. In both groups, 78% collaterals provided a collateral pressure index at baseline > 0.3, sufficient to prevent ischaemia during a balloon occlusion, with a minimum of 0.2 in those with preserved LV function. A Doppler-derived function index showed a wider variation due to the high prevalence of microvascular dysfunction in CTOs. Only 7% of patients had an increase in collateral flow reserve > 2.0 during pharmacological stress, whereas coronary steal occurred in one-third independent of regional LV function. CONCLUSION: A limited increase in collateral flow and the high prevalence of coronary steal during stress underscore the functional limitation of collaterals in CTOs without prior Q-wave MI. Even presumably 'well-collateralized' CTOs may benefit from a revascularization.