non-Q Wave Acute Myocardial Infarction Research Articles

Comparison of clinical features of non-Q wave and Q wave myocardial infarction

The clinical spectrum and outcome of 119 patients with acute non-Q wave myocardial infarction (NQMI) were studied, in comparison with those of 354 patients with acute Q wave myocardial infarction (QMI). The patients with NQMI had a significantly higher incidence of preinfarction angina (73% vs 63%), previous myocardial infarction (43% vs 22%), multivessel disease (73% vs 51%), postinfarction angina (55% vs 21%), and recurrent myocardial infarction during follow-up for an average of 25 months (17% vs 8%). NQMI patients also had a lower rate of complication of pump fallure and smaller infarct size estimated by peak creatine phosphokinase (CPK) levels (1361 ± 1243 vs 2711 ± 1684 IU/L) than those with QMI. There was no difference in in-hospital mortality between the two groups (17% vs 17%). However, death due to cardiac rupture was exclusively noted in the QMI group. The present study suggests that NQMI is more unstable than QMI in the clinical course.

Two-dimensional echocardiography versus surface electrocardiography for the diagnosis of acute non-Q wave myocardial infarction

The initial two-dimensional echocardiogram (2DE) and electrocardiogram (ECG) of 50 consecutive patients with chest pain and a possible acute non-Q wave myocardial infarction (MI) were compared to each other to determine the value of 2DE in this type of acute MI. The ECG markers for a non-Q wave MI were (1) ≥0.15 mV ST segment depression, (2) ST segment elevations with reciprocal ST segment depression, and (3) new symmetrical deep T wave changes as compared to a recent preadmission ECG. The 2DE was considered positive for MI if akinesia, dyskinesia, or severe hypokinesia was seen in one or more left ventricular segments. The sensitivity, specificity, and predictive value of the 2DE as compared to the ECG was 66% and 52%, respectively (sensitivity); 91% and 95%, respectivity (specificity); and 91% and 94%, respectively (predictive value). Statistically, there were no differences in the proportion of patients who had a positive 2DE as compared to the proportion of patients who had a positive ECG ( p > 0.2). The ECG and 2DE results were combined and the sensitivity increased to 76% but the specificity decreased to 86%. Myocardial infarction size was not significantly different in infarcted subjects who had a positive 2DE (395 ± 125 IU/L) as compared to those who had a negative 2DE (727 ± 187 IU/L, p > 0.1).

The influence of location and extent of myocardial infarction on long-term ventricular dysrhythmia and mortality.

SUMMARY Although theextent ofenzymatically estimated infarct size appearstobeanimportant determinant ofmorbidity andmortality early after infarction, itsinfluences on long-term survival andlate ventricular dysrhythmia havenotyetbeencharacterized. Accordingly, we prospectively studied 173patients youngerthan66yearsofagewithout evidence ofprior myocardial infarction, whosurvived acutemyocardial infarction foratleast 24hours. Infarct size was estimated enzymatically anddysrhythmia quantified bycomputerfromtwo-channel, 24-hour ambulatory ECGs.Themean infarct size index (ISI) ofthose whodied was significantly larger thanthat ofsurvivors (46.5 ± 5.8(SEM) vs21.1i 1.4CK-g-Eq/m2, p < 0.001). Overall survival was significantly better after small (ISI < 15CK-g-Eq/m2) ormodest infarcts (15< ISI< 30)than after large infarcts (ISI30)(p< 0.01, p < 0.05, respectively). Regardless ofthelocus oftheinfarction, patients withsmall infarcts hada better prognosis thanthose withlarger infarcts. Latemortality was comparable after transmural andsubendocardial infarction, buthigher after anterior thanafter inferior infarction (15%vs 6%;p < 0.05). Amongthe10clinical andhemodynamic variables evaluated withmultivariate analysis, ISI(but notinfarct locus), peakplasma creatine kinase, congestive failure atthetimeofadmission, ageandgender weresignificantly related tomortality. Premature ventricular complexes were more frequent among patients withmodest orlarge infarcts (ISI15)throughout thefollow-up (p< 0.05), regardless ofinfarct locus. Thus, theextent ofinfarction isa strong determinant ofbothventricular dysrhythmia andmortality, late aswell asearly after acutemyocardial infarction. MORTALITY EARLY after acutemyocardial infarction isrelated toage,thepresence orabsence of oldmyocardial infarction, andthesite andextent of myocardial infarction sustained.1-5 Inaddition, theincidence andseverity ofventricular dysrhythmia during thefirst 24hours after infarction reflect theamountof myocardium damaged.6 7Long-term survival appears toreflect inpart theseverity oftheinfarct based onindirect criteria, such asthepresence ofcongestive heart failure, depressed ejection fraction anddyskinesis. Further, late ventricular dysrhythmia appears tocorrelate notonly with theseverity ofcoronary artery diseasebutalsowithleft ventricular contraction abnormalities, which inturnreflect theextent ofinjury.'2' 13 Thisstudy wasdesigned todetermine whether the extent ofinfarction isanimportant determinant ofthe incidence andseverity ofventricular dysrhythmia and mortality lateafter infarction. Becausepotential relationships might beobscured byadvanced ageor oldinfarcts,3 onlypatients aged65years oryounger andwithout historical or electrocardiographic evidence ofprevious myocardial infarction were studied.