non-Q Wave Infarction Research Articles

Lack of diurnal variation in the onset of non-Q wave infarction.

Data concerning the time of onset of myocardial infarction were obtained for 540 of the 544 patients with creatinine kinase (CK)-MB-confirmed non-Q wave myocardial infarction enrolled in the multicenter Diltiazem Reinfarction Study. Data were also collected for 627 patients who were screened but excluded. Among the 1,167 patients, no diurnal pattern of onset could be found at either 2- or 6-hour intervals. Among the 540 patients enrolled in the trial, no pattern could be found at these intervals either, although at 8-hour intervals, 27% of infarctions occurred between midnight and 8:00 AM, compared with 37% between 8:00 AM and 4:00 PM and 36% between 4:00 PM and 12:00 AM (p = 0.02). In contrast to the patterns previously noted for Q wave myocardial infarction, there was no preponderance of non-Q wave infarction in the late morning. Circadian rhythm was also absent among patients not treated with beta-blockers as well as among patients presenting with ST segment elevation on their enrollment electrocardiograms. Diabetics, women, and patients with first infarction were more likely to present during the afternoon hours. We conclude that the late morning preponderance seen for Q-wave myocardial infarction is not discernable in patients with non-Q wave myocardial infarction. This observation suggests that the pathogenesis of these two infarct subtypes is different or that the process of thrombotic coronary occlusion in Q wave infarction (sustained) differs from that in non-Q wave infarction (nonsustained).

Is there a different mechanism of heart failure in first non-Q wave infarction compared to first Q wave or recurrent infarction?

Is there a different mechanism of heart failure in first non-Q wave infarction compared to first Q wave or recurrent infarction?

The role of calcium antagonists in the treatment of myocardial ischemia

Calcium antagonists are often prescribed for treatment of ischemic heart disease. Therapeutic activity is achieved by reducing myocardial oxygen requirements and by increasing blood supply in ischemic heart disease associated with coronary artery spasms. The efficacy of calcium antagonists depends on the type and clinical presentation of ischemic heart disease: (1) in vasospastic angina (variant angina, short episodes of angina at rest), first-line therapy with calcium antagonists will reduce the number of ischemic episodes and improve long-term prognosis. (2) In effort angina the efficacy of calcium antagonists is comparable with that of β blockers. (3) In unstable angina the use of calcium antagonists is controversial. Large-scale studies with nifedipine showed no benefit when it was given alone but an additive effect in patients pretreated with β blockers. In contrast, diltiazem and verapamil appear to have comparable efficacy to β blockers in patients with unstable angina. (4) After myocardial infarction the results of treatment with calcium antagonists have been disappointing. Nifedipine and verapamil did not reduce mortality or the incidence of reinfarction. In one study diltiazem significantly reduced the rate of reinfarction in patients who had had a non-Q wave infarction, but in a recent large-scale multicenter trial it had no effect on mortality and cardiac events in patients with evidence of both Q- and non-Q wave infarctions. Other secondary preventative measures against reinfarction, such as the use of β-blockers and aspirin, appear to be more effective than calcium antagonists. The most frequently prescribed calcium antagonists, verapamil, diltiazem, and nifedipine, each of which represents a different chemical class, have in general similar efficacy in vasospastic and effort angina. Their different pharmacologic profile, such as the slowing of heart rate with verapamil or diltiazem and a more marked vasodilatation with nifedipine and other dihydropyridines, may become clinically relevant in individual patients. The new dihydropyridine derivatives have a pharmacologic profile comparable to that of nifedipine but some of these compounds, especially amiodipine, have more favorable pharmacokinetics, such as a prolonged elimination half-life. These agents may offer the advantage of a more practical dosage regimen for long-term treatment in patients with ischemic heart disease.

Risk stratification of patients with non-Q wave myocardial infarction. The critical role of ST segment depression. The Diltiazem Reinfarction Study Research Group.

One-year follow-up data on 515 patients who survived hospitalization with MB-creatine kinase-confirmed, acute non-Q wave myocardial infarction were analyzed for factors related to mortality (n = 57) and late reinfarction (n = 64). Twelve of 24 analyzed variables were significantly associated with mortality. Those factors, which were independently predictive of mortality by Cox regression analysis, were persistent ST depression (p = 0.0009), a history of congestive heart failure (CHF) (p = 0.0069), older age (p = 0.0128), and ST elevation at hospital discharge (p = 0.0173). In-hospital reinfarction achieved borderline significance (p = 0.0512). Mortality during the follow-up period was 5.5% in patients with no ST depression, 10.1% in those with ST depression at baseline or discharge, and 22.2% in patients with ST depression at baseline and discharge (i.e., "persistent" ST depression). The age-adjusted risk of mortality for patients with persistent ST depression, discharge-ST elevation, and CHF was 13.99 times as high as was the risk for patients with no ST depression, no discharge-ST elevation, and no CHF. Of the 483 patients with complete electrocardiographic data at both baseline and discharge, 203 (42%) could be stratified into a high risk population with a risk ratio for 1-year mortality more than sevenfold that of patients with no risk factors. Although persistent ST depression was significantly associated with several measures of structural left ventricular damage, the independent significance of ST depression persisted even after adjusting for these factors. The independent predictors of late reinfarction (persistent ST depression, p = 0.0058; Killip class II or III, p = 0.0106; and left ventricular hypertrophy, p = 0.0470) permitted a similar risk stratification. We conclude that 1) easily identified clinical and electrocardiographic factors permit stratification of patients with non-Q wave infarction into high-risk subsets who may benefit from aggressive therapy; 2) ST depression is a highly significant and independent predictor of poor prognosis; and 3) the powerful predictive value of persistent ST depression suggests that non-Q wave myocardial infarction patients with this depression should be viewed as potentially high-risk patients who may be candidates for additional noninvasive testing or early coronary angiography.

Functional significance of hypertrophy of the noninfarcted myocardium after myocardial infarction in humans.

Hypertrophy of the noninfarcted left ventricle as a chronic response to myocardial infarction has been demonstrated in animals and at autopsy in humans. However, the functional significance of postmyocardial infarction hypertrophy is a subject of dispute. The purpose of this study was to determine the time course of development of postmyocardial infarction hypertrophy of the noninfarcted myocardium in humans and to assess its functional significance. Subcostal view, two-dimensional echocardiograms were recorded at rest and during peak exercise, 6 and 40 weeks postmyocardial infarction in 45 patients (16 anterior, 20 inferior, nine non-Q wave infarcts), for measurement of left ventricular mass and ejection fraction. The left ventricular mass index increased from 94 +/- 30 to 118 +/- 27 g/m2 (p less than 0.01) during the time of the two studies. There was a significant correlation between the change in left ventricular mass index and improved resting ejection fraction (r = 0.48, p less than 0.001) and exercise ejection fraction (r = 0.48, p less than 0.001) at the follow-up study. Of the 32 patients who increased their left ventricular mass index greater than 7%, 18 improved their rest ejection fraction greater than 0.05 units and 17 improved their exercise ejection fraction greater than 0.05 units. Conversely, of the 13 patients who failed to increase their left ventricular mass index, only three improved their rest ejection fraction and one improved the exercise ejection fraction (Fisher's exact test, p less than 0.05). We reached three conclusions. First, in humans, significant hypertrophy of the noninfarcted myocardium can be detected by two-dimensional echocardiography, 9 months postmyocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Non-Q Wave Cocaine-related Myocardial Infarction

Since our initial report in 1984 of six patients with AMI temporally related to cocaine use, we have observed 19 additional patients in whom ischemic chest pain syndromes occurred shortly after intranasal or IV use of cocaine or after smoking the drug. Seventeen patients (89 percent) developed non-Q wave infarction and two had Q-wave infarction. One patient manifested angina with striking ST-segment elevation. None of the patients had diabetes or hypertension, and all but one were cigarette smokers. The serum cholesterol level was 162 +/- 7 mg/dl. Four of the five patients who consented to coronary angiographic studies displayed normal coronary arteries, and one showed proximal stenosis of the right coronary artery. The cold pressor test was performed in seven patients; none had angina or ECG changes induced by cold stimulation. We conclude that T-wave infarction is a common form of an acute cardiac event related to cocaine abuse, and its pathogenesis may involve that of the cocaine-induced coronary vasospasm.

Differing circadian patterns of symptom onset in subgroups of patients with acute myocardial infarction.

Circadian variation of the onset of acute myocardial infarction has been noted in many studies and may carry important pathophysiologic implications. However, only a few previous studies have attempted subgroup analyses. In 4,796 patients with documented acute myocardial infarction, the time of symptom onset was recorded. As in other studies, the peak of onset occurred in the morning from 6:01 AM to 12:00 noon, and 28% of the population (1.16 times the average percentage for the other time periods) experienced symptom onset in that period (p less than 0.001). There was a second, lower peak (25%) in the evening between 6:01 PM and 12:00 midnight, which was also observed in some previous studies. We sought to determine whether or not the presence of subgroups with specific clinical characteristics would exhibit different patterns and thereby contribute to these peaks in the overall population. In patients with a history of congestive heart failure (n = 606) or with non-Q wave infarction (n = 832), a pronounced peak (29%) occurred only in the evening. Two nearly equal peaks were observed in patients older than 70 years of age (n = 1,422), smokers (n = 2,057), diabetics (n = 767), women (n = 1,213), and patients taking beta-blocking drugs (n = 847). Finally, in patients with a previous myocardial infarction (n = 1,104), no peaks were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Specific platelet mediators and unstable coronary artery lesions. Experimental evidence and potential clinical implications.

We have speculated previously that the abrupt conversion from chronic stable to unstable angina and the continuum to acute myocardial infarction may result from myocardial ischemia caused by progressive platelet aggregation and dynamic vasoconstriction themselves caused by local increases in thromboxane and serotonin at sites of coronary artery stenosis and endothelial injury. Platelet aggregation and dynamic coronary artery vasoconstriction probably result from the local accumulation of thromboxane and serotonin and also relative decreases in the local concentrations of endothelially derived vasodilators and inhibitors of platelet aggregation, such as endothelium-derived relaxing factor (EDRF) and prostacyclin. With severe reductions in coronary blood flow caused by these mechanisms, platelet aggregates may increase, and an occlusive thrombus composed of platelets and white and red blood cells in a fibrin mesh may develop. When coronary arteries are occluded or narrowed for a sufficient period of time by these mechanisms, myocardial necrosis, electrical instability, or sudden death may occur. We believe that unstable angina and acute myocardial infarction are a continuum in relation to the process of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary artery stenosis is brief, unstable angina or non-Q wave infarction may occur. However, when the coronary artery obstruction by these mechanisms is prolonged for several hours, Q wave myocardial infarction results. Chronic endothelial injury and coronary artery stenosis are probably associated with the accumulation of platelets, white and red blood cells, and a fibrin mesh at the site of stenosis and endothelial injury.

Unexpected sudden death during acute myocardial infarction: role of primary electromechanical dissociation

The causes of death during the acute phase of myocardial infarction were studied in 128 patients. Forty-three of these, who had no clear signs of cardiocirculatory failure, were considered to be cases of sudden and unexpected death. Thirty-two of these patients (74%) had electromechanical dissociation, defined as a sudden disappearance of an effective arterial pressure in the presence of adequate electrocardiographic complexes. Twenty-three patients who had been given this diagnosis were males and 9 females; 53% presented with anterior infarction, 31% with infero-posterior infarction, 3.5% with both anterior and infero-posterior and 12.5% with non-Q wave infarction. A previous episode of infarction was recorded in 31.2% of patients with electromechanical dissociation. Autopsy was performed in 84 patients, 23 of whom died with electromechanical dissociation. Half of the latter cases revealed cardiac rupture (secondary electromechanical dissociation), whereas in the other half death was due to primary electromechanical dissociation. The study stresses the relatively high incidence of this cause of death and the need to differentiate between the two different forms. Although at present the pathophysiology of primary electromechanical dissociation is not completely understood, we believe that recurrence of global or local ischemia may play a more important role than cardiovascular inhibitory reflexes.

Risk stratification in patients with first non-q wave infarction: Limited value of the early low level exercise test after uncomplicated infarcts

Risk stratification using clinical and historical variables plus early low level exercise testing was performed in 141 patients with a first non-Q wave myocardial infarction. The 111 patients who performed the exercise test had a 3.6% cardiac mortality rate in the first year compared with 13.3% in the 30 patients who could not exercise (p = 0.063), and a 1 year incidence rate of recurrent cardiac events (cardiac death or recurrent nonfatal myocardial infarction) of 10.8% compared with 23.3% (p = 0.127). Patients who developed ischemia (ST depression or angina) during the test had an increased incidence of cardiac events in the year after the infarction (odds ratio >3, p < 0.05).When patients were subgrouped by the presence or absence of pulmonary congestion, the discriminatory value of the exercise test was seen to reside primarily in the cohort with pulmonary congestion. For example, ST depression during exercise in this group identified patients with a 71 % incidence of cardiac events in the year after the infarction compared with 5.3% for those without ST depression (odds ratio 45, p = 0.002). In the patients without pulmonary congestion, the exercise test had no discriminatory value.It is concluded that early low level exercise testing has a limited role after an uncomplicated non-Q wave infarction, but is useful in patients with clinical markers of higher risk.

Favourable long term prognosis in patients with non-Q wave acute myocardial infarction not associated with specific electrocardiographic changes. Diltiazem Reinfarction Study Research Group.

Electrocardiograms obtained serially from 544 patients with non-Q wave infarction in the Diltiazem Reinfarction Study were analysed to compare the short term (less than or equal to 14 days) and long term (one year) follow up of 105 patients (19%) whose admission electrocardiogram showed no localisable repolarisation abnormalities (group 1) with the outcome in 439 patients (81%) who had ST-T wave abnormalities (group 2) localised to two or more contiguous leads within an anterior, inferior, or lateral lead group. There were no major between group differences in baseline clinical variables, concomitant medications, or treatment allocation (diltiazem v placebo). Group 2 patients, in the first year, had a higher incidence of early recurrent ischaemia (angina greater than or equal to 24 hours after myocardial infarction associated with ischaemic repolarisation changes), reinfarction, and readmission for chest pain than group 1 patients, despite comparable creatine kinase and creatine kinase MB activities in both groups. About 20% of patients with acute non-Q wave myocardial infarction did not have definable ST-T wave abnormalities. These patients had a similar clinical and enzymatic profile as patients with non-Q wave infarction with definable ST-T wave abnormalities and they were more likely to have a favourable short term and long term outcome.

ST segment shifts are poor predictors of subsequent Q wave evolution in acute myocardial infarction. A natural history study of early non-Q wave infarction.

Acute ST segment elevation is regarded generally as the sine qua non of evolving Q wave myocardial infarction (MI) because such electrocardiographic (ECG) injury is believed to be a marker of transmural ischemia and a forerunner of transmural necrosis. Alternatively, ST segment depression with or without T wave inversion is viewed as the dominant ECG feature of non-Q wave MI. However, this hypothesis has not been assessed prospectively in an acute MI population. We analyzed 2,304 serial ECGs at study entry (admission), day 2, day 3, and predischarge (mean, 10.2 +/- 2 days) from 576 patients with creatine kinase MB confirmed acute non-Q wave MI to determine what percentage of patients with early ST segment elevation culminated in subsequent Q wave development. Of this group, 187 patients (32%) exhibited 1 mm or greater ST segment elevation in two or more contiguous entry ECG leads. Of those patients whose non-Q wave MI could be localized on the basis of diagnostic admission ST segment shifts, the prevalence of early ST segment elevation was 43% (187 of 439). The sum total mean (+/- SD) peak ST segment elevation by lead group (anterior, inferior, lateral) was 4.0 +/- 2.4, 4.5 +/- 2.4, and 2.5 +/- 0.6 mm, respectively. Despite this, only 20% of patients with ST segment elevation (37 of 187) developed Q waves. Of 252 patients who exhibited early ST segment depression or T wave inversion or both, 39 (15%) evolved subsequent Q waves. Thus, while the prevalence of early ST segment elevation in acute evolving non-Q wave MI was higher than previously reported, 80% of patients with and 85% of patients without ST segment elevation and absent Q waves on the admission ECG did not develop subsequent Q waves during a 2-week period of observation (p = NS). In addition, when patients with ST segment elevation were compared with patients with ST segment depression or T wave inversions or both, there were no between-group differences in log peak creatine kinase (404 vs. 383 IU), reinfarction (6% vs. 8%), postinfarction angina (50% vs. 42%), or early recurrent ischemia (49% vs. 45%), defined as postinfarction angina with transient ECG changes. Thus, in patients who present with initial acute non-Q wave MI, ST segment shifts on admission are unreliable predictors of subsequent Q wave evolution and do not discriminate significant differences in postinfarction outcome. In particular, ST segment elevation during the early hours of evolving infarction is not an invariable harbinger of subsequent Q wave development.

β-Adrenergic Blockade and Calcium Channel Blockade in Myocardial Infarction

Because of their hemodynamic and antiarrhythmic actions, beta-adrenergic blockers and calcium-entry blockers have been suggested for use in patients with myocardial infarction (MI) for reducing infarct size, preventing ventricular ectopy, and for prolonging life in survivors of acute MI. Experimental studies have suggested their usefulness in these areas. Clinical studies have demonstrated a role for beta-blockers in the hyperacute phase of MI, and in longterm treatment of infarct survivors. Calcium channel blockers appear to have somewhat less utility in patients with Q wave MIs, but may have an important role in therapy of the non-Q wave infarct.

Pericarditis in acute myocardial infarction: Characterization and clinical significance

To determine the significance of pericarditis following acute myocardial infarction, the hospital course and 12-month follow-up were analyzed in 703 patients enrolled in the Multicenter investigation of the Limitation of infarct Size (MILIS). Pericarditis, defined by the detection of a pericardial rub, occurred in 20% of the patients (n = 141) and was more likely to follow Q wave than non-Q wave infarction (25% vs 9%, p < 0.001). Patients with pericarditis experienced more serious myocardial damage compared to those without pericarditis, as evidenced by a larger infarct size (25 ± 1 vs 17 ± 1 MB-CK gm-Eq/m 2, p < 0.001), a lower admission left ventricular ejection fraction (42 ± 1% vs 48 ± 1%, p < 0.001), and a higher incidence of congestive heart failure (47% vs 26%, p < 0.001) and atrial tachyarrhythmias (16% vs 10%, p < 0.05). When patients were classified by the presence of Q or non-Q wave infarction, these differences persisted although statistical significance was not always achieved due to smaller sample size. Mortality at 12-month follow-up for patients with pericarditis was 18% compared with 12% for patients without pericarditis ( p = 0.055). This mortality difference could be accounted for in part by the lower ventricular ejection fraction in patients with pericarditis ( p = 0.20 after adjustment).

Measurement of regional myocardial blood flow: Application of the electrolytic hydrogen clearance method in man

To assess myocardial perfusion intraoperatively and to evaluate the adequacy of coronary bypass grafting, we measured regional myocardial blood flow by the electrolytic hydrogen clearance method in 49 patients. Group I comprised 10 patients with nonischemic heart disease and group II, 39 patients with ischemic heart disease undergoing coronary bypass grafting. Group II was subdivided according to the percent stenosis of the coronary arteries supplying the ventricular regions: group IIa, less than 75% stenosis; group IIb, greater than or equal to 75% stenosis. Mean myocardial blood flows were 154 +/- 7, 145 +/- 5, and 98 +/- 9 ml/min/100 gm in groups I, IIa, and IIb, respectively (p less than 0.01, group IIb versus groups I and IIa). Mean blood flows were 161 +/- 19, 159 +/- 12, 78 +/- 12, and 59 +/- 15 ml/min/100 gm in areas of the left anterior descending coronary artery with less than 50%, 75%, 90%, and 99% stenosis in group II. In areas with a totally occluded left anterior descending coronary artery with collaterals, mean flow was 90 +/- 15 ml/min/100 gm. The mean myocardial blood flows were 40 +/- 7 and 100 +/- 14 ml/min/100 gm in areas with anterior Q wave and non-Q wave infarction, respectively (p less than 0.01). After cardiopulmonary bypass, the mean flow increased from 99 +/- 11 to 150 +/- 7 ml/min/100 gm in the grafted areas in group IIb (p less than 0.01), but it did not change in group I or IIa. The electrolytic hydrogen clearance method provided quantitative evaluation of myocardial perfusion and recovery from hypoperfusion by coronary bypass grafting. This method was especially useful in patients undergoing mammary artery grafting.

Early peak of creatine kinase-MB in acute myocardial infarction with a nondiagnostic electrocardiogram

This study compared the time from the onset of symptoms to the peak of the creatine kinase-myocardial band (CK-MB) in 34 consecutive patients with acute myocardial infarction. Patients were separated into two groups: group 1 (n = 21) had diagnostic (≥0.1 mV) ST segment elevation on the initial ECG, and group 2 (n = 13) did not have diagnostic ST segment elevation on the initial ECG. In group 1 the time to the peak CK-MB was 16.2 ± 50 hours vs 10.0 ± 2.0 hours for group 2 ( p = 0.0001). Peak CK-MB was 331 ± 276 IU/L in group 1 vs 81 ± 54 IU/L in group 2 ( p < 0.005). In group 1 there were 16 patients who subsequently had a Q wave myocardial infarction as opposed to one patient in group 2 ( p = 0.0001). Patients who do not have diagnostic ST segment elevation on the initial ECG have an early but low peak of CK-MB and typically have a non-Q wave infarction. These findings are consistent with early spontaneous restoration of blood flow during the infarction process in these patients. This early restoration of blood flow may provide the substrate for the high incidence of recurrent ischemic events noted in patients with non-Q wave myocardial infarction.

The ECG in acute myocardial infarction

The initial ECG is the most rapid and readily available tool in the emergency department for the evaluation of patients presenting with suspected myocardial infarction. However, studies have shown that the initial ECG is diagnostic of acute myocardial infarction in only a minority of patients. This paper discusses the importance of the initial ECG and other information in aiding the disposition of patients with suspected myocardial infarction. Classic electrocardiographic descriptions are discussed as well as the newer terminology of Q wave versus non-Q wave infarction and ST segment versus T wave infarction. A brief review is made of the electrophysiology of the ECG changes seen in myocardial infarction. Finally, clinical studies are presented that establish a definite role for the use of the initial ECG.

Non-Q wave versus Q wave myocardial infarction: Regional myocardial metabolism and blood flow assessed by positron emission tomography

This study compared regional myocardial blood flow at rest and during supine exercise as well as regional myocardial glucose utilization in the fasting condition in 22 patients, 11 with antecedent non-Q wave and 11 with antecedent Q wave infarction. With use of N-13 (nitrogen-13) ammonia and F-18 (fluorine-18) deoxyglucose as tracers of blood flow and exogenous glucose utilization and positron emission tomography, hypoperfused areas were noted at rest and during exercise in all 11 patients (100%) with Q wave infarction. Among the 11 patients with non-Q wave infarction such areas were noted in only 5 (45%) at rest and in 8 (73%) during exercise. Furthermore, segmentally enhanced F-18 deoxyglucose uptake corresponding to the infarcted areas (identified electrocardiographically) was seen in 10 (91%) of the 11 patients with non-Q wave infarction but in only 4 (36%) of the 11 patients with Q wave infarction (p < 0.01).In conclusion, segmental F-18 deoxyglucose uptake as a possible sign of myocardial viability was seen more frequently in non-Q wave than in Q wave infarction and, importantly, regionally enhanced F-18 deoxyglucose uptake occurred even in the absence of segmental rest or exercise blood flow abnormalities, or both, in 5 (45%) of 11 patients with non-Q wave infarction.

Angiographic progression of coronary artery disease and the development of myocardial infarction

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction.In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p < 0.05). In the infarctrelated artery in Group I, only 5 (22%) of 23 lesions were initially >70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially >70% (p < 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p < 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions ≥ 50% to infarction.This irrespective study suggests that myocardial infarction frequently develops from previously nonsevere lesions. In addition, it is often difficult to predict the location of a subsequent infarct from analysis of the first coronary angiogram. Non-Q wave infarction is usually preceded by a more severe pre-existing stenosis than is a Q wave infarction, perhaps indicating some degree of prior myocardial protection. A prospective evaluation will be necessary to confirm these findings.

Prognostic significance of location and type of myocardial infarction: Independent adverse outcome associated with anterior location

To determine the relative prognostic significance of location (anterior or inferior) and type (Q wave or non-Q wave) of infarction, the hospital course and follow-up outcome (mean duration 30.8 months) of 471 patients with a first infarction were analyzed. Analyses were performed grouping the patients according to infarct location (anterior, n = 253; inferior, n = 218), infarct type (Q wave, n = 323; non-Q wave, n = 148), and both location andtype (inferior non-Q wave, n = 85; inferior Q wave, n = 133; anterior non-Q wave, n = 63; and anterior Q wave, n = 190).Patients with anterior infarction had a substantially worse in-hospital and follow-up clinical course compared with those with interior infarction, evidenced by a larger infarct size (21.2 versus 14.9 g Eq/m2creatine kinase, MB fraction [MB CK], p < 0.001), lower admission left ventricular ejection fraction (38.1 versus 55.3%, p < 0.001) and higher incidence of heart failure (40.7 versus 14.7%, p < 0.001), serious ventricular ectopic activity (70.2 versus 58.9%, p < 0.05), in-hospital death (11.9 versus 2.8%, p < 0.001) and total cumulative cardiac mortality (27 versus 11%, p < 0.001). Patients with Q wave infarction similarly experienced a worse in-hospital course compared with patients with non-Q wave infarction, evidenced by a larger infarct size (20.7 versus 12.7 MB CK g Eq/m2, p < 0.001), lower admission left ventricular ejection fraction (43.7 versus 50.6%, p < 0.001), and a hight, incidence of heart failure (31.9 versus 21.6%, p < 0.05) and in-hospital death (9.3 versus 4.1% p < 0.05). However, there was no increased rate of reinfarction or mortality in hospital survivors with non-Q wave infarction compared with those with Q wave infarction, and total cardiac mortality was similar (16 versus 21%, p = NS).To evaluate the role of infarct location and type independent of infarct size, patients were grouped according to quartile of infarct size, and outcome was reanalyzed within each group. Patients with anterior infarction demonstrated a lower left ventricular ejection fraction on admission and after 10 days than did patients with inferior infarction, even after adjustment for infarct size, as well as a higher incidence of congestive heart failure and cumulative cardiac mortality. When patients were evaluated on the basis of both location andtype of infarction, those with anterior infarction exhibited a worse hospital course and cumulative cardiac mortality than did those with inferior infarction, whether the infarction was non-Q wave or Q wave in type. Life-table analysis of cardiac mortality using the Cox proportional hazards regression model demonstrated that location, but not type, of infarction exerted an independent prognostic effect.Thus, patients with anterior infarction experience a more complicated hospital and follow-up course than do patients with inferior infarction despite adjustment for infarct size and regardless of type of infarction (Q wave or non-Q wave). The disparity between outcomes in patients with anterior as opposed to inferior infarction may be due to coexistent right ventricular infarction in patients with inferior infarction, resulting in less left ventricular impairment relative to the total MB CK released, as well as to differences in topographic responses to infarction between the two sites.