Non-Q wave myocardial infarction. Recurrent myocardial infarction, unstable angina and arrhythmia in 8-year observation

The contradictory views on long term clinical course of patients after non-Q wave myocardial infarction (NQMI) as compared with those after Q wave myocardial infarction (QMI)--induced us to undertake a comparative study of both types of myocardial infarction during a 8 year follow-up. The study was carried out in 400 patients (pts) with NQMI (mean age 51) and 485 pts with QMI (mean age 53). Both groups were compared. We have analysed the following parameters: the dynamics of ischaemic heart disease (unstable angina, reinfarction, arrhythmias, mortality) and coronary arteriography. During 8 year observation unstable angina and arrhythmias, were statistically more frequent in pts after NQMI. Recurrent myocardial infarction occurred in 196 (49%) of pts after NQMI and only in 87 pts (18%) after QMI (p less than 0.001). However, the difference in mortality between both groups was not significant (37% vs 39% respectively). Coronary angiography was performed at 1-6 months after myocardial infarction. In 65% of pts after NQMI detected lesions were limited to proximal part of one or two coronary arteries. Conclusion: NQMI is characterized by unstable long-term clinical course, and that is why pts with NQMI should be recommended for early coronary angiography and revascularization.     

The prevalence and clinical significance of residual myocardial ischemia 2 weeks after uncomplicated non-Q wave infarction: a prospective natural history study

Despite having smaller infarct size and better left ventricular function, patients with non-Q wave myocardial infarction (NQMI) appear to have an unexpectedly high long-term mortality that is ultimately comparable to that of patients with Q-wave myocardial infarction (QMI). Patients with NQMI may lose their initial prognostic advantage because there is more viable tissue in the perfusion zone of the infarct-related vessel, rendering myocardium more prone to reinfarction. We tested this hypothesis in a prospective study of 241 consecutive patients 65 years of age or younger with acute uncomplicated myocardial infarction confirmed by creatine kinase levels (MB fraction). All patients received customary care and none underwent thrombolytic therapy or emergency angioplasty. Predischarge coronary angiography, radionuclide ventriculography, 24 hr Holter monitoring, and quantitative thallium-201 (201T1) scintigraphy during treadmill exercise were performed 10 +/- 3 days after infarction. Infarcts were designated as QMI (n = 154) or NQMI (n = 87) by accepted criteria applied to serial electrocardiograms obtained on days 1, 2, 3, and 10. The baseline Norris coronary prognostic index, angiographic jeopardy scores, and prevalence of Lown grade ventricular arrhythmias were similar between groups despite evidence for less necrosis with NQMI vs QMI, reflected by lower peak creatine kinase levels (520 vs 1334 IU/liter; p = .0001, 4 hr sampling), higher resting left ventricular ejection fraction (53% vs 46%; p = .0001), fewer akinetic or dyskinetic segments (1.2 vs 2.4; p = .0001), and fewer persistent 201Tl defects in the infarct zone (0.9 vs 1.9; p = .0001). Patients with NQMI also had more patent infarct-related vessels (54% vs 25%; p less than .0001) and a shorter time from onset of infarction to peak creatine kinase level (16.9 vs 22.5 hr; p = .0001). Importantly, the prevalence and extent of quantitatively determined 201Tl redistribution within the infarct zone on exercise scintigraphy was greater in patients with NQMI vs those with QMI (60% vs 36%, p = .007; and 0.98 vs 0.53 myocardial segments, p = .0003); when the two groups were stratified on the basis of the infarct-related vessel, subset analysis revealed the same findings. During 30 months median follow-up, cardiac mortality was low, 8.4% in the QMI group and 9.2% in the NQMI group (p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)     

Coronary angiographic features within 48 hours from onset of non-Q wave myocardial infarction with R wave regression and no ST segment depression

The clinical features of acute non-Q wave myocardial infarction (NQMI) with R wave regression and no ST segment depression are distinct from those of acute Q wave myocardial infarction (QMI). NQMI patients showed ST segment elevation at admission, and significantly earlier regression of the ST segment elevation and appearance of coronary T waves were observed compared to QMI patients. In addition to the significantly lower level of mean peak serum creatine kinase activity and the significantly lower incidence of pump failure during the acute phase, the incidences of in-hospital mortality and multivessel disease were significantly lower in the NQMI patients. With respect to acute-phase coronary angiographic features within 48 h after the onset, the rate of spontaneous opening of infarct-related vessels was significantly higher in the NQMI patients. Thirteen of the 19 NQMI patients responded to urokinase infusion. These facts suggest that transient, intermittent or incomplete obstruction may favor this type of NQMI over QMI, and that thrombus might be an important factor in the pathogenesis of this type of NQMI.     

Identification of first acute Q wave and non-Q wave myocardial infarction by multivariate analysis of body surface potential maps.

BACKGROUND. Patients with acute non-Q wave myocardial infarction (NQMI) appear to have more jeopardized residual myocardium at high risk for subsequent angina, reinfarction, or malignant arrhythmias than patients with acute Q wave myocardial infarction (QMI). Unfortunately, conventional electrocardiographic (ECG) criteria have limited utility in recognizing NQMI. METHODS AND RESULTS. The present study combines the increased information content of body surface potential maps (BSPM) over the 12-lead ECG with the power of multivariate statistical procedures to identify a practical subset of leads that would allow improved diagnosis of NQMI. Discriminant analysis was performed on 120-lead data recorded simultaneously in 159 normal subjects and 308 patients with various types of myocardial infarction (MI) by using instantaneous voltages on time-normalized P, PR, QRS, and ST-T waveforms as well as the duration of these waveforms as features. Leads and features for optimal separation of 159 normals from 183 patients with recent or old QMI (group A) were selected. A total of six features from six torso sites accounted for a specificity of 96% and a sensitivity of 94%. All lead positions were outside the conventional electrode sites and selected features were voltages at mid-P, early and mid-QRS, and before and after the peak of the T wave. The discriminant function was then tested on 57 patients with acute NQMI (group B) and 68 patients with acute QMI (group C): Rates of correct classification were 91% and 93%, respectively. Because of the possible deterioration of the results caused by ST-T abnormalities also present in other clinical entities, a second classification model including an independent group of 116 patients with left ventricular hypertrophy (LVH) but without MI was developed. Two additional measurements were required, namely, P wave duration and a mid-QRS voltage on a lead located 10 cm below V1. Testing the model on both acute MI groups produced correct classification rates of 88% for acute NQMI and 93% for acute QMI. Group mean BSPM were plotted for the three MI groups at successive instants throughout the PQRST waveform. Typical patterns for each MI group were identified during PQRST by removing the corresponding normal variability at each electrode site from sequential MI maps. These standardized maps or discriminant maps provided information on the capability of each measurement at each electrode site and at each instant to separate each class of MI from the normal group (N). Striking similarities were observed between the three MI groups, particularly at mid-QRS and throughout ST-T. The closest resemblance was between acute NQMI and old QMI. Discriminant analysis was also performed on the 12-lead ECG: The first classification model (N versus MI) produced correct classification rates of 85% for acute QMI and 70% for NQMI. With the second model (MI versus N or LVH), correct rates were 81% and 65%, respectively. CONCLUSIONS. Diagnosis of acute NQMI and QMI (also in the presence of LVH) can be improved substantially by appropriate selection of ECG leads and features. Comparison of discriminant maps from groups A, B, and C does not support the concept of acute NQMI as a distinct ECG entity but rather as a group with infarcts of smaller size. However, pathophysiological and clinical differences between acute NQMI and acute QMI influence long-term risks and may define different therapeutic approaches.     

Ischemic and viable myocardium in patients with non-Q-wave or Q-wave myocardial infarction and left ventricular dysfunction: a clinical study using positron emission tomography, echocardiography, and electrocardiography

OBJECTIVES: We investigated whether patients with non-Q-wave myocardial infarction (NQMI) have more ischemic viable myocardium (IVM) than patients with Q-wave myocardial infarction (QMI). BACKGROUND: Non-Q-wave myocardial infarction is associated with higher incidences of cardiac events than QMI, suggesting more myocardium at risk in NQMI. METHODS: To identify myocardial ischemia, hibernation, and scar, the resting and stress (82)rubidium perfusion and F-18 fluorodeoxyglucose metabolic positron emission tomographic imaging (PET) was performed in 64 consecutive patients with NQMI (n = 21) or QMI (n = 43). Echocardiography was performed for assessment of left ventricular function and wall motion index (WMI). The relationships between PET, echocardiographic, and electrocardiographic findings were analyzed. RESULTS: There were no significant differences in left ventricular ejection fraction (LVEF) between NQMI and QMI groups (28 +/- 10% vs. 25 +/- 11%, p > 0.05). Ischemic and viable myocardium was more common in NQMI than in QMI (91% vs. 61%, p < 0.05). The total amount of IVM was significantly higher in NQMI than in QMI (6.5 +/- 5.2 vs. 2.9 +/- 2.8 segments, p < 0.001). Neither the number of Q waves, residual ST-segment depression of >or=0.5 mm or elevation of >or=1 mm, nor LVEF and WMI were significant predictors for IVM. Wall motion index correlated with scar segments (r = 0.54, p < 0.001) and LVEF (r = -0.67, p < 0.001). CONCLUSIONS: Ischemic and viable myocardium is common in patients with NQMI and left ventricular dysfunction, suggesting that aggressive approaches should be taken to salvage the myocardium at risk in such patients.     

急性Q波性和非Q波性心肌梗死后存活心肌及其对晚期血运重建术后心功能的影响

目的:比较急性Q波性心肌梗死(QMI)和非Q波性心肌梗死(NQMI)患者临床和冠状动脉病变特征以及梗死相关区域存活心肌的情况,并随访观察其对心肌梗死晚期血运重建术后心功能的影响。方法:连续收集121例急性心肌梗死(AMI)患者,分为QMI组(79例)和NQMI组(42例)。详细记录和分析所有患者的病史资料。于AMI后2周左右行经皮冠状动脉介入治疗,术前采用小剂量多巴酚丁胺超声负荷试验,检查梗死相关区域存活心肌的情况,并且于术前和术后6个月时常规超声心动图检查左室功能和室壁节段性运动障碍情况。随访6个月内主要心血管事件的发生率。结果:AMI前有心绞痛发作史者和冠状动脉病变血管的数量在NQMI组明显多于QMI组(P<0.05),而梗死相关部位平均管腔残余狭窄以NQMI组明显小于QMI组(P<0.05)。NQMI组中86%的患者有存活心肌,明显高于QMI组(61%)(P<0.01)。术后6个月随访,2组左室射血分数较术前明显提高,左室舒张末期及收缩末期容积指数、室壁运动积分均较术前明显降低(分别为P<0.05和P<0.01),以NQMI组更明显。结论:与QMI相比,NQMI患者有较多的存活心肌;心肌梗死后晚期血运重...     

Significance of Q wave disappearance in the chronic phase following transmural acute myocardial infarction

The mechanism and prognostic implications of Q wave regression following transmural acute myocardial infarction (AMI) were assessed in 54 patients. Of these subjects, 14 lost their Q waves. Exercise myocardial thallium-201 (201Tl) scintigraphy and two-dimensional echocardiography were performed before the patients were discharged from hospital. Two-dimensional echocardiography and electrocardiography were simultaneously repeated about 18 months after AMI. Both the relative 201Tl activity in the infarcted area and the improvement of echocardiographic wall motion index were higher in patients who had lost their Q waves than in those with retained Q waves (70 +/- 14% vs 58 +/- 13%, p less than 0.01; 5.2 +/- 3.0 vs 2.0 +/- 3.4, p less than 0.01, respectively). The prevalence of post-infarction angina pectoris was significantly higher in the former (29% vs 0%, p less than 0.01). We concluded that remnants of viable myocardial muscle might be responsible for Q wave regression following transmural acute myocardial infarction, and the prevalence of post-infarction angina pectoris was high among these patients.     

老年人无Q波型心肌梗死研究进展

老年人无Q波心肌梗死在病理生理、临床表现,近期和远期预后方面,均与Q波心肌梗死有重要区别,其再梗死率,梗死 后心绞痛发生率及长期死亡率均甚高,治疗很复杂。近年来由于临床重视,检测技术的普及和完善,早期溶栓疗法的应用使非Q波 心肌梗死的诊断率有逐年增加的趋势。本文就老年人无Q波心肌梗死的病理生理,临床特点.预后和治疗作一综述。     

Survival analysis within one year of first acute myocardial infarction: comparison between non-Q and Q wave myocardial infarction.

BACKGROUND: Non-Q wave Myocardial Infarction (non-Q AMI) is related pathophysiologically to Q wave AMI, as each represents different stages of plaque rupture and thrombosis. Post-hospital re-infarction and recurrent angina are more frequent in non-Q AMI than in Q wave AMI, offsetting the higher early risk with Q wave AMI, with one-year survival rates similar in the two types of MI. OBJECTIVES: 1--Evaluation of early (< or = 28 days) and one-year total mortality from first non-Q AMI in comparison to QMI. 2--Analysis of recurrent acute ischaemic events (non-fatal reinfarction and unstable angina) in both types of MI in the same periods of time. POPULATION AND METHODS: A retrospective study of 1146 patients, mean age 65 +/- 13 years, 65% male, admitted at CCU with a first MI, from January 1988 to December 1997 (minimum follow-up period of one year, mean follow-up 42 +/- 37 months). We compared the baseline demographics and clinical characteristics (coronary risk factors, previous angina, MI evolution, recurrent cardiac events, 28 day mortality and one year mortality) of patients with non-Q AMI (NQ group = 239) and Q wave AMI (Q group = 907). RESULTS: The NQ group patients were significantly older (mean age: 67 +/- 12.6 vs 65 +/- 12.5 years; p < 0.05), included fewer smokers (29% vs 43%; p < 0.001) and were more symptomatic before the index infarction (stable angina: 40% vs 30%; p < 0.05; unstable angina: 16% vs 6%; p < 0.001), when compared to the Q group patients. There were no significant differences in MI evolution, in Killip-Kimbal class > or = 2, recurrent angina and in-hospital mortality (Q-12% vs NQ-9%; ns), although there was a higher combined risk of arrhythmias and AV conduction disturbances in patients with QMI (Q-34% vs NQ-26%; p < 0.05). The combined risk of unstable angina and reinfarction at one year was significantly higher in group NQ (NQ-13% vs Q-8.1%; p < 0.05). The NQ group showed no significant difference in 28 day total mortality (NQ-14% vs Q-17%; ns) or at one year follow-up (NQ-24% vs Q-26%; ns) when compared to the Q group. CONCLUSION: 1--Despite a lower severity of non-Q AMI in the acute phase, 28 day and one year total mortality were similar in the two groups. 2--Patients with non-Q AMI showed a higher incidence of recurrent ischemic events at one year follow-up.     

Survival of women and men after myocardial infarction does not differ. Results of several years' observation

The contention that female gender is an independent factor that affects survival after acute myocardial infarction (AMI) is still controversial. The aim of this retrospective study was to assess whether or not early and late mortality after AMI is greater in women than in men. Data of 464 consecutive patients (130 women and 334 men) who had a documented acute myocardial infarction in our Department of Cardiology between 1990 and 1993 were eligible for the study. We excluded 48 patients from the study for the following reasons: the location of infarct could not be determined in 18 patients: 16 patients refused to take part in the study and we were not able to contact 14 patients. The remaining 416 patients were analyzed in the study. The mean follow-up period was 36 months (from 1 to 72 months). Women were significantly older than men (62.1 +/- 11.2 vs 58.1 +/- 11.6; p < 0.001), especially those who died in hospital (70.7 +/- 9.3 vs 64.4 +/- 8.7; p < 0.01). In hospital died 26 women (20%) and 39 men (11.7%)--p < 0.05. However, age-adjusted in-hospital mortality did not differ between women and men (p = 0.256). We did not find any significant difference in 3-year survival after AMI between women and men (22% vs 20.7%; NS). Total mortality was also similar (38% vs 30.2%; NS). QMI was diagnosed in 85 women and 234 men (73% vs 78%; NS), NQMI in 31 women and 66 men (27% vs 22%; NS). The rate complications of acute phase of AMI (acute heart failure and/or rhythm disturbances) was similar in women and men. Fibrinolytic treatment was introduced in 27.2% of women and in 26.4% of men. Hypercholesterolemia and hypertension were more often associated with female gender. In multivariate analysis we found that age, acute heart failure, previous MI, hypercholesterolemia and diabetes mellitus were significant factors which affects survival after AMI. Of these only age and diabetes mellitus appeared to be significant in women.     

心肌肌钙蛋白I在急性冠状动脉综合征中的应用

急性冠状动脉综合征(ACS)是指不稳定型心绞痛(UA)、Q波型心肌梗死(QMI)、非Q波型心肌梗死(NQMI)和心源性猝死这样一组临床病征。心肌肌钙蛋白I(cTnI)是新近发展的心肌组织所特有的心肌酶学标志物。本文对cTnI的生物化学特点、检测方法、cTnI与ACS的联系进行评价。cTnI在诊断心肌损害方面敏感性高,特异性强,诊断时间窗口宽,明显优于传统心肌酶,对ACS可进行危险度分层及预后评价,并可预测UA患者复杂冠状动脉形态,值得推广使用。     

Post-myocardial infarction exercise testing. Non-Q wave versus Q wave correlation with coronary angiography and long-term prognosis

BACKGROUND. The presence or absence of baseline diagnostic Q waves has been believed to compromise the accuracy of standard exercise electrocardiography in identifying severe coronary artery disease (three-vessel and/or left main disease); therefore, a retrospective analysis was performed using a personal computer data base of exercise test responses and cardiac catheterization results to evaluate this premise, and follow-up was performed to observe how Q waves and/or severe coronary disease impacted on survival. METHODS AND RESULTS. Two hundred fifty-three male patients who had survived a myocardial infarction were studied. Patients on digitalis, those with left bundle branch block or left ventricular hypertrophy on their baseline electrocardiogram, those with previous revascularization procedures, and those with significant valvular or congenital heart disease were excluded. All patients performed either a low-level predischarge or a sign/symptom limited exercise test and underwent diagnostic coronary angiography within 32 days of each test (range, 0-90 days). Long-term follow-up on patients was performed for an average of 45 months (+/- 17 months). Group NQMI comprised 103 post-myocardial infarction patients lacking Q waves at the time of exercise testing and group QMI comprised 150 patients who developed Q waves with their myocardial infarction. The cut points of greater than or equal to 1 mm (chi 2 = 14.39, p less than 0.001) and greater than or equal to 2 mm (chi 2 = 26.11, p less than 0.001) of exercise-induced ST segment depression were reliable markers of severe coronary disease in Q wave infarct survivors. This was also true for non-Q wave infarct survivors as greater than or equal to 1 mm (chi 2 = 6.02, p = 0.01) and greater than or equal to 2 mm (chi 2 = 4.37, p = 0.04) of ST segment depression were reliable markers of severe coronary disease. Receiver operating characteristic curve analysis revealed that exercise-induced ST segment depression had discriminating power for the identification of severe coronary artery disease in both the Q wave myocardial infarction patients (area = 0.735, z = 4.47, p less than 0.001) and the non-Q wave infarct patients (area = 0.700, z = 3.20, p less than 0.001). After 4.4 years of cumulative follow-up, patients with severe coronary disease had an infarct-free survival rate of 72% (95%, CI, 50.0-86.0%), whereas those without severe disease had an 86% (95% CI, 76.5-91.5%) infarct-free survival rate (Cox chi 2 = 4.00, p = 0.045). Non-Q wave patients had an infarct-free survival rate of 81% (95% CI, 66.0-89.5%), whereas those with Q waves had an infarct-free survival rate of 85% (95% CI, 73.9-91.3%) (Cox chi 2 = 0.0005, p = NS). CONCLUSIONS. The presence or absence of diagnostic Q waves has no significant effect on the ability of the exercise electrocardiogram to identify severe coronary artery disease in survivors of myocardial infarction. Long-term infarct-free survival of patients with myocardial infarction is more related to the presence of severe coronary disease rather than if they suffered a non-Q wave or Q wave infarction.     

非Q波与Q波心肌梗死的临床分析

本组急性心肌梗死１１２１例中，非Ｑ波心肌梗死３９２例（３５％），Ｑ波心肌梗死７２９例（６５％）。既往有心绞痛及心肌梗死者，在非Ｑ波心肌梗死组分别有７６．８％及３８．８％，显著地多于Ｑ波心肌梗死组的６１．２％及３０．６％。有高血压、糖尿病史及吸烟者，两组间比较无差别。并发泵衰竭、室性心动过速和（或）心室颤动及Ⅱ～Ⅲ度房室传导阻滞者，在非Ｑ波心肌梗死组分别有１０．２％、１０％及１．５％，显著地少于Ｑ波心肌梗死组的１９．３％、２０．６％及１３．６％。梗死后心绞痛者，在非Ｑ波心肌梗死组有４５．２％，显著地多于Ｑ波心肌梗死组的２８．９％。４周病死率，在非Ｑ波心肌梗死组为２．８％，显著地低于Ｑ波心肌梗死组的８．２％。非Ｑ波与Ｑ波心肌梗死比较，患者在急性期并发症较少，病死率较低；而梗死后早期心绞痛较多。     

老年人急性心肌梗死的临床特征分析

目的　探讨老年人急性心肌梗死 (AMI)的临床特点。方法　对住院的 AMI患者的临床资料进行统计 ,分析年龄≥ 6 0岁的老年 AMI患者 (老年组 )及年龄 <6 0岁 (非老年组 )患者的临床特点。结果　本研究包括 2 5 8例老年AMI患者 (平均年龄 6 8.5± 6 .6岁 )及 117例非老年 AMI患者 (平均年龄 5 1.2± 6 .8岁 )。与非老年患者比较 ,老年AMI患者更多患有心绞痛或陈旧性心肌梗死 (7.8%与 18.2 % ,P <0 .0 2 )及高血压病 (43.6 %与 5 8.1% ,P <0 .0 1)。表现为无 Q波心肌梗死 (NQMI)的老年患者明显高于非老年组 (13.1%与 6 .0 % ,P<0 .0 5 ) ,肌酸激酶 (CK)峰值在老年组则显著低于非老年组 (1198.7± 132 2 .1U /L与 15 70 .4± 15 0 7.0 U /L ,P<0 .0 2 )。老年组较非老年组中有更多的患者伴有心力衰竭 (8.5 %与 2 .6 % ,P<0 .0 2 ) ,心房颤动 (14 .7%与 5 .1% ,P<0 .0 1)及右束支传导阻滞 (RBBB) (8.9%及 0 % ,P<0 .0 0 1) ,死亡率也显著增高 (13.5 %与 5 .1% ,P<0 .0 2 ) ,但老年患者却较少接受静脉溶栓治疗 (2 0 .1%及 4 1.9% ,P<0 .0 0 1)及择期经皮腔内冠状动脉成形术 (PTCA) (13.5 %与 33.3% ,P<0 .0 0 1)。结论　本研究提示老年 AMI患者较非老年患者更多表现为 NQMI,更多伴有心房颤动、心力衰竭及 RBBB等     

Evidence of prolonged inflammation in unstable angina and non-Q wave myocardial infarction

OBJECTIVES: This study was designed to document the inflammatory response up to one year after acute presentation with unstable angina (UA) and non-Q wave infarction (NQMI) as reflected by the expression of soluble cell adhesion molecules (CAMs). BACKGROUND: Coronary plaque inflammation is a key component in the pathogenesis of acute coronary syndromes. Cell adhesion molecules are critical mediators of the inflammatory process. Soluble forms of these molecules are detectable in serum and are elevated acutely in patients with UA and NQMI. METHODS: Patients presenting with UA and NQMI had serum samples taken at presentation and then after three, six and 12 months. A control group of similar age and gender distribution was used for comparison. Levels of soluble inter-cellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial-selectin and platelet-selectin were measured using an ELISA technique. RESULTS: We studied 91 patients (M/F = 73/18, mean age 62 +/- 11 years, 56 UA and 35 NQMI) and 24 controls (M/F = 18/6, mean age 56 +/- 12 years). Levels of all four soluble CAMs were significantly elevated in both UA and NQMI patients at presentation, three and six months in comparison with controls. Levels in UA and NQMI groups fell between six and 12 months after initial presentation. CONCLUSIONS: The results suggest that the inflammatory stimulus triggering expression of CAMs is sustained for up to six months after presentation with either UA or NQMI and then returns toward control values over the following six months.     

Dynamic changes of QT interval and QT dispersion in non-Q-wave and Q-wave myocardial infarction

QT interval and QT dispersion both prolong early postinfarction. Non-Q wave (NQMI) and Q-wave myocardial infarction (QMI) differ in the extent of transmural necrosis, which may influence these measures of myocardial repolarization. This study compared dynamic changes in QT interval and QT dispersion early postinfarction between NQMI and QMI. In 40 patients with NQMI and 69 patients with QMI, maximum QTc (QTc(max)) and QT dispersion (QTD) were measured during the first 4 days postinfarction. Infarct size was assessed daily by using the Selvester QRS score. In both infarct types, QTc(max) and QTD were prolonged on day 1 of infarction, peaking over the next 2 days before returning toward baseline by day 4. NQMI patients had significantly longer QTc(max) and QTD by days 2 to 3 when compared with QMI patients. Multivariable linear regression identified "infarct type x QRS score" as the only independent predictor of QTc(max) (R(2) =.32, P <.0001) and QTD (R(2) =.19, P <.0001) on day 2. In conclusion, dynamic changes of QTc(max) and QTD occur in both infarct types. Large NQMI is associated with greater prolongation of QTc(max) and QTD, which may be due to greater M cell uncoupling and exposure when compared with QMI.     

The appearance of giant negative T waves in anterior acute myocardial infarct with a Q wave is associated with minor myocardial damage and a minor extension of coronary disease]

INTRODUCTION AND OBJECTIVE: The early inversion of T waves in patients with acute myocardial infarction has recently been related to a better left ventricular function and a more favourable evolution, contrary to what happens in the unstable angina. On the other hand, the significance of the appearance of deep negative T waves in the early phase of some acute myocardial infarction is not known. The aim of this study is to evaluate its relation with the existing myocardial damage and the underlying coronary artery disease extension in anterior some with Q wave. METHODS: 48 patients with a first anterior Q-wave acute myocardial infarction, thrombolized or not, admitted to hospital with an evolution of less than 24 hours, and with a coronariography performed before discharge were analyzed. Giant negative T waves were defined as those which were 8 mm or more from baseline. RESULTS: 17 of the 48 patients presented giant negative T waves (T-group) and 31 did not (N-group). In the T-group patients, the size of the negative T wave was 11.29 +/- 2.86 mm and the number of precordial leads with negative T waves was 4.35 +/- 1.57. There were no differences between both groups in variables such as sex, coronary risk factors, and other basal characteristics. The T-group patients were younger, had lower peak-CK, CK-MB and LDH levels and presented greater recovery of R waves during the follow-up, the differences being significant with the N-group patients. The left ventricular ejection fraction was higher (56.3 +/- 13.4 vs 42 +/- 12%; p < 0.001) and the number of affected coronary vessels was lower in the T-group (1.12 vs 1.64; p < 0.01); there were no differences in the localization or severity of coronary lesions, nor in the frequency of postinfarction myocardial angina. None of the patients in the T-group were Killip > I, while this situation occurred in 38.7% of the N-group patients. CONCLUSIONS: The appearance of giant negative T waves in the acute or early phase of Q-wave anterior acute myocardial infarction is associated with a smaller infarct size, lower functional deterioration and less extension of the underlying coronary disease.     

Head-to-head comparison of two different low-molecular-weight heparins in acute coronary syndrome: a single center experience

Low-molecular-weight heparins (LMWH) of different types have yielded different results when used in the setting of unstable angina (UA) or non Q-wave myocardial infarction (NQMI). We compared the safety and therapeutic efficacy of two different LMWHs, namely dalteparin (Dalt.) and enoxaparin (Enox.), in the acute phase (first 5 days) of UA or NQMI. One hundred and forty-two patients with UA/NQMI were randomly assigned to treatment with either Dalt. [120 IU/kg twice daily by subcutaneous (SC) injection] or Enox. [1 mg/kg twice daily by SC injection]. The occurrence of any one of death, myocardial infarction, or angina recurrence within 5 days of the first LMWH injection was the endpoint of the study. There were 69 patients in the Enox. group (53 males, 16 females, mean age: 60.3+/-11.9) and 73 patients in the Dalt. group (54 males, 19 females, mean age: 59.6 +/-10.3). The baseline characteristics of the patients in the two groups were similar. There were no deaths in either group. Myocardial infarction occurred in two patients in the Dalt. group (4%). Angina recurrence was seen in 11 patients in the Enox. group (16%) and in 11 patients in the Dalt. group (15%). Overall, any of the events that made up the endpoint occurred in 11 (16%) and 14 (19%) patients in the Enox. and Dalt. groups, respectively (P>0.05). The time to occurrence of the first event, however, was significantly longer in the Enox. group (82.3+/-33.2 versus 37.6+/-23.4 hours, P=0.007). Thrombocytopenia and allergic reactions were not detected in any patient. Major bleeding was seen in I patient in the Enox. group. Minor bleeding occurred in 17 (25%) and 21 (29%) patients in the Enox. and Dalt. groups, respectively (P>0.05). Enoxaparin and dalteparin were found to be equally safe and effective for the early management of UA/NQMI, but enoxaparin appeared to delay the occurrence of MI or angina recurrence as compared to dalteparin in this setting.     

Decreased no-reflow in patients with anterior myocardial infarction and pre-infarction angina.

AIMS: Pre-infarction angina is associated with better outcome after myocardial infarction. The aim of this study was to assess whether pre-infarction angina is associated with decreased no-reflow after coronary recanalization. METHODS AND RESULTS: Twenty-three patients underwent intracoronary myocardial contrast echocardiography during the acute phase of anterior myocardial infarction after successful recanalization, and before hospital discharge. Myocardial perfusion was graded semi-quantitatively in the area at risk (dyssynergic segments). Global left ventricular function was assessed by radionuclide angiography on days 8 and 42 and regional wall motion was assessed by 2D echocardiography on days 0 and 42. Fourteen patients had pre-infarction angina (angina less than 7 days before myocardial infarction) and nine did not. Baseline characteristics were similar in the two groups. The myocardial contrast echocardiography perfusion score in the area at risk after recanalization was higher in the patients with pre-infarction angina than in those without (0.72 +/- 0.19 vs 0.53 +/- 0.22, P=0.04), and the incidence of no-reflow (myocardial contrast echocardiography perfusion score < or =0.5) was lower (14% vs 56%, P=0.04). This difference persisted 8 +/- 2 days after myocardial infarction (0. 87 +/- 0.11 vs 0.69 +/- 0.26, P=0.04), and was associated with greater mid-term (day 42) improvement in left ventricular function in patients with pre-infarction angina than in those without, as assessed by changes in radionuclide left ventricular ejection fraction (+5.8 +/- 8.1% vs -3.3 +/- 4.6%, respectively;P=0.01) and by changes in regional wall motion score on 2D echocardiography (-0. 61 +/- 0.39 vs -0.24 +/- 0.17, respectively;P=0.04). CONCLUSION: Pre-infarction angina is associated with preservation of the microvasculature, reflected by reduced no-reflow. This may be a mechanism underlying greater recovery of left ventricular function in patients with pre-infarction angina.     

Independent prognostic value of C-reactive protein and troponin I in patients with unstable angina or non-Q-wave myocardial infarction.

OBJECTIVES: Elevated concentrations of C-reactive protein (CRP), a non-specific acute phase reactant, and troponin I (TnI), a cardiac-specific marker of myocardial damage, have been found to be associated with a higher risk for cardiac events in patients with an acute coronary syndrome. We evaluated CRP alone and in combination with TnI for predicting the incidence of major cardiac complications within 6 months in patients with unstable angina or non-Q-wave infarction (NQMI). METHODS: CRP and TnI was measured on admission in patients with unstable angina or NQMI, but results were kept blinded. Patients were treated according to a conservative management strategy, and the incidence of major cardiac events within 6 months was assessed. RESULTS: An abnormal CRP (> 5 mg/l) and an abnormal TnI (> 0.4 microgram/l) were more frequent in patients that suffered a major cardiac event (CRP: 93 vs. 35%, P < 0.0001; TnI: 73 vs. 26%, P < 0.001). The incidence of major cardiac events was higher in patients with an abnormal CRP than in patients with a normal CRP, both when TnI was abnormal (42 vs. 4.5%, P = 0.003) and when TnI was normal (11 vs. 0%, P = 0.014). Mean event-free survival was excellent in patients with both a normal CRP and TnI, whereas survival was poorest in patients with both an abnormal CRP and TnI (121 +/- 16 vs. 180 days, P < 0.0001). CONCLUSIONS: An abnormal CRP on admission in patients with unstable angina or NQMI is associated with increased incidence of major cardiac events within 6 months, both in patients with normal and abnormal TnI. CRP and TnI have independent and additive prognostic value in this patient group, and the combination may be useful for early risk stratification.