Nontransmural Myocardial Infarction Research Articles

Bypass Surgery in Acute Myocardial Infarction

During early myocardial infarction the goals of reperfusion are to limit the extent of infarction as well as to provide protection from future coronary-related events. If reperfusion can be successful, this may be reflected by reduction in the expected mortality rates as well as possible improvement in global and regional left ventricular function. The present article examines these issues in a series of 701 patients who were operated on between 1971 and 1982. Examination of mortality is divided between transmural and nontransmural myocardial infarction, and these are further divided by the presence of disease in one-, two- or three (or more than three) vessels. In the transmural group, results derived from an analysis of global and regional left ventricular function before and after reperfusion are presented. We conclude that (1) early reperfusion is associated with lower short and long-term mortality than is late reperfusion, (2) some recovery of left ventricular function is more likely with early reperfusion than with late reperfusion and (3) three-vessel disease in the presence of previous myocardial infarction is associated with much higher mortality, especially in the group with transmural myocardial infarction.

Myocardial infarction following acute occlusion and reperfusion of the septal coronary artery.

It has been demonstrated that temporary occlusion of major epicardial arteries of the dogs produces a nontransmural myocardial infarction (MI) whose size is reduced by early reperfusion. This study was undertaken to determine the location and extent of MI following acute occlusion and reperfusion of the septal artery (SA). The SA was occluded for four hours in group I (7 dogs). Occlusion time for group II (6 dogs) was 2 hours and for group III (6 dogs) was 1 hour, followed by 2 and 3 hours of reperfusion, respectively. The hearts were then removed and cut into transverse slices from base to apex. The triphenyl tetrazolium chloride technique identified the areas of infarction, which were quantitated with a microcomputer-based graphics system. To determine the extent of necrosis across the interventricular septum (IVS), the IVS was divided into 5 transverse segments of equal depth and the amount of MI was determined for each. In group I, MI involved 3.42 +/- 0.9% (mean +/- SEM) of the left ventricle (LV) and 13.49 +/- 3.4% of the IVS. In group II, 6.11 +/- 1.3% of the LV and 25.00 +/- 5.5% of the IVS were infarcted. In group III, 5.63 +/- 1.3% of the LV and 31.9 +/- 14.3% of the septum were infarcted. MI was larger on the left side of the IVS than on the right in all groups, and the extent of MI did not differ significantly between the three groups. This study showed that early reperfusion of the SA did not reduce MI as reported for other coronary beds.

Chest pain after nontransmural infarction: The absence of remediable coronary vasospasm

To assess the contribution of coronary vasospasm to chest pain in patients with nontransmural myocardial infarction, we performed a controlled trial of prophylactic antivasospastic therapy. Fifty patients with nontransmural infarction received either nifedipine or placebo in a double-blind randomized trial. Chest pain occurred in 52% of treated patients (38 episodes on 35 days) compared to 48% of control patients (42 episodes on 33 days). Concurrent therapy was comparable in the two groups. Recurrent infarction occurred in 12% and was comparable between groups. Ejection fraction was similar and was unchanged throughout the study in both groups. Logistic regression failed to identify predictors for recurrent chest discomfort. These data indicate that potent antivasospastic therapy does not reduce the incidence of recurrent chest pain or infarction. Thus, remediable coronary vasospasm is not likely to be a major cause of post infarction ischemia in patients with nontransmural infarction.

Emergency Surgery after Coronary Artery Disruption Complicating PTCA. Report of Four Cases

Four out of 150 patients having a PTCA at our institution sustained a coronary artery disruption and underwent emergency surgery. All of them presented a severe stenosis of the LAD, in 2 of them there was also a stenosis at the origin of a diagonal branch. In each case the injured vessel was a diagonal branch. Three patients had a rupture of subepicardial arteries and developed cardiac tamponade. In another patient the rupture was located intramyocardially. Severe hemodynamic derangement occurred in all 4 cases, one resulting in cardiac arrest. The latter was the only patient who died postoperatively, due to neurological damage. Two of the surviving patients sustained a non-transmural myocardial infarction in the area of the injured vessel. However, all 3 survivors recovered easily and are doing well 6 months after surgery.

Electrocardiographic effects of experimental nontransmural myocardial infarction.

Clinical and experimental data have documented the ability of nontransmural myocardial infarction to produce abnormal Q waves on both the epicardial and body surfaces. We undertook this study to define the anatomic determinants of such Q wave development. Thirty dogs were studied before and after occlusion-reperfusion (26 dogs) or latex embolization (four dogs) of the left circumflex coronary artery. Occlusion was maintained for 60 to 240 min before reperfusion to produce nontransmural lesions of various sizes. Electrocardiographic data were registered from 84 torso electrodes by body surface mapping techniques before and 1 week after infarction. Infarct size was quantitated by computer analysis of heart slices stained with triphenyl tetrazolium chloride. Six dogs did not develop infarction. Of the remaining 24, 10 did and 14 did not develop significant changes in body surface Q wave duration and width. The incidence of Q wave changes was not different in dogs with nontransmural and those with transmural lesions. Infarct size (expressed as a percentage of the left ventricle infarcted), the percentage of endocardium subjacent to infarction, the average depth of necrosis, the percent of the four outer fifths of the ventricular wall infarcted, and the duration of occlusion were significantly (p less than .05) greater in dogs with than in those without Q wave changes. Logistic regression modeling demonstrated that only two anatomic parameters--percentage of left ventricle infarcted and average lesion depth--significantly and independently predicted Q wave development. A model including only these two variables accurately classified all 24 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical, electrocardiographic, and ventriculographic consequences of isolated occlusion of the right coronary artery

The effects of total occlusion of the right coronary artery, a sole lesion, were evaluated In an unselected series of 45 patients. Findings ranged from no detectable consequences to massive post-infarction left ventricular scars. Patients were divided into three groups: Group I, those without clinical or ventriculographic evidence of myocardial infarction (10 patients); Group II, those with clinical or angiographic evidence of nontransmural myocardial infarction (eight patients); Group III, those with electrocardiographic evidence of transmural myocardial infarction (27 patients). The critical compensatory importance of collateral vessels was demonstrated (1) by the difference between the presence of adequate collaterals in Groups I and II (89 percent), versus 44.5 percent in Group III (p <0.005), and (2) by the fact that the three patients without demonstrable collaterals showed the most extensive wall motion abnormalities. Four patients in Group I had no clinical evidence of ischemic disease, occlusion being an incidental finding. It is concluded that the natural history of total occlusion of the right coronary artery depends largely upon the function of collateral vessels.

High mortality early reinfarction with first nontransmural myocardial infarction

Thirty-eight patients with first nontransmural myocardial infarction were studied to determine prognosis and clinical markers of a high-risk subgroup. We found a high incidence of reinfarction (18%) at a median time of 16 days post nontransmural infarction (seven patients). Reinfarction was uniformly associated with death within 24 hours. A total of 14 patients (37%) either died (eight patients) or required urgent revascularization (six patients). Predominant ST segment depression with presenting nontransmural infarction and a history of prior angina were associated with increased mortality ( p < 0.05 and p = 0.05, respectively). We conclude that patients with nontransmural infarction are at high risk for ealy recurrent infarction. Patients with history of prior angina and predominant ST segment depression may be at particularly high risk. Reinfarction in these patients is frequently extensive. We recommend that these patients be considered for early coronary angiography.

Quantitative thallium-201 imaging: Limitations in detecting pathophysiologically significant obstructive coronary artery disease

Washout of thallium-201 after stress testing has been proposed as a method of detecting abnormal zonal myocardial perfusion without relating it to a reference “normal” area. Therefore, 18 patients with single-vessel coronary artery disease, undergoing percutaneous transluminal coronary angioplasty, underwent maximum stress testing and thallium imaging. A myocardial perfusion defect was seen in the immediate postexercise images in all 19 zones (one patient studied twice) supplied by the vessel with the obstructive lesion. Delayed images showed improvement in 15 of the 19 segments. Of the four zones which did not improve, three had evidence of a prior nontransmural myocardial infarction. Quantitative analysis of washout curves showed that counts decreased in 17 of 19 zones after background subtraction and in all 19 zones if background was not subtracted. In the corresponding normal zones directionally similar decreases in counts were seen. Thus washout characteristics were similar for both diseased and normal zones. These data indicate that washout curves are limited in their ability to detect the presence of a physiologically significant lesion.

Relationship between electrocardiographically estimated infarct size and clinical findings in inferior myocardial infarction.

In 270 patients with acute inferior wall myocardial infarction (MI) and no previous MI, Q- and R-wave changes in leads II, III, and aVF in a 12-lead standard ECG were related to the clinical course during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI showed a higher incidence of tachycardia, high degree of AV block, congestive heart failure (CHF), and pericarditis than patients with nontransmural MI. In a subgroup including 226 patients, the series was divided into quartiles according to the sum of Q- and R-wave changes in leads II, III, and aVF 4 days after arrival in hospital. A weak correlation between ECG-determined infarct size and the incidence of complications such as congestive heart failure (CHF), need for furosemide, and pericarditis, as well as the duration of hospitalization was observed. It is concluded that ECG-determined infarct size from leads II, III, and aVF in inferior MI is associated with the clinical course, although it cannot predict the outcome in the individual patient.

Relationship between electrocardiographically estimated infarct size and clinical findings in anterior myocardial infarction.

In 292 patients with anterior myocardial infarction (MI) and no previous MI the electrocardiographically estimated infarct size was correlated with clinical findings during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI had a higher incidence of different types of complications, such as congestive heart failure (CHF), hypotension, pericarditis, and a longer duration of hospitalization than patients with nontransmural MI. In a subgroup including 182 patients of the total series, a precordial map containing 24 electrodes was used. The sum of R waves (sigma R), the sum of Q waves (sigma Q), the number of Q waves, and sigma R - sigma Q were calculated 4 days after arrival in hospital to estimate the size of infarction. There was generally a correlation between these ECG variables and different clinical findings, such as incidence of CHF, hypotension, pericarditis, and the duration of hospitalization. It is concluded that the ECG determined infarct size in anterior MI in a majority of patients correlates with the incidence of different types of complications in acute myocardial infarction. In the individual patient, however, the risk of developing complications cannot be predicted by ECG changes.

Comparison of the influence of acute transmural and nontransmural myocardial infarction on ventricular function

In order to assess the relative impact on left and right ventricular function of nontransmural and transmural acute myocardial infarction (AMI), we performed radionuclide ventriculography in 86 patients (54 men and 32 women) within 16 hours after a first infarct. Nontransmural infarction was present in 19 patients (11 anterior and 8 inferior). Transmural infarction was found in 67 patients (30 anterior and 37 inferior). Left ventricular ejection fractions were higher (0.57 ± .014 vs 0.46 ± 0.14, p < 0.005) and left ventricular end-systolic volume lower (29 ± 11 vs 42 ± 20 ml/m 2, p = 0.013) in patients with nontransmural infarction compared to those with transmural infarction. Right ventricular ejection fraction also may have been different in the two groups (0.63 ± 0.15 vs 0.55 ± 0.13, p = 0.057). In patients with inferior infarction, left and right ventricular ejection fractions were similar in patients with nontransmural and transmural infarction (0.60 ± 0.09 vs 0.55 ± 0.10, p = 0.119 and 0.58 ± 0.14 vs 0.51 ± 12, p = 0.226). On the other hand, patients with anterior transmural infarction had lower left ventricular ejection fractions (0.36 ± 0.12 vs 0.54 ± 0.17, p = 0.003) but similar right ventricular ejection fractions (0.60 ± 0.13 vs 0.66 ± 0.14, p = 0.14) compared to those with nontransmural anterior infarction. In 29 additional patients with a history of previous infarction, no differences in any of the parameters studied were found between those with transmural and those with nontransmural infarcts. Thus, left ventricular function is better preserved in patients with a first nontransmural infarct compared to those with a first transmural anterior infarct. However, this difference is not seen in patients with a history of a previous infarction.

Quantitative computer-assisted analysis of left ventricular wall thickening and motion by 2-dimensional echocardiography in acute myocardial infarction

Quantitative regional wall motion analyses of 2-dimensional echocardiograms (2-D echo) have usually focused on large arcs (>45 °) of the left ventricular (LV) perimeter rather than on small LV zones. Few studies have assessed changes in wall thickness. To determine normal ranges of regional LV function, the endocardial and epicardial contours of short-axis 2-D echoes obtained at the papillary muscle level of 10 normal subjects were manually traced. Then, 15 patients with acute myocardial infarction (MI) were studied, comparing their contours at admission with ranges determined from the normal subjects. In all patients with MI, 2-D echoes located abnormal wall motion involving at least the region identified as abnormal by the electrocardiogram and often extending into adjacent regions. All 9 patients with transmural MI had either decreased wall thickening or abnormal endocardial wall motion; all except 1 had focal thinning in the region of the MI. Of the 6 patients with nontransmural MI, 2 had abnormal endocardial wall motion, and all had decreased wall thickening. Evaluating regional wall motion at multiple points around the LV circumference should permit more precise delineation of LV function in health and disease than has been heretofore possible.

Angiographic study of the infarct-related coronary artery in the chronic stage of acute myocardial infarction

We and others have demonstrated a high prevalence of total coronary occlusiion during the acute phase of myocardial infarction (MI). This study reports the angiographic appearance of the infarct-related artery (IRA) in 130 patients with a history of MI, who underwent cardiac catheterization 2 weeks to more than 12 months afterwards. The IRA was the left anterior descending in 47%, the right coronary artery in 50%, and the circumflex in 3% of cases. Total coronary occulusion was found in 80% of patients studied 2 to 4 weeks after MI, and decreased gradually reaching 40% of those studied after 12 months of MI. In those patients with a patent IRA, severe stenosis remained: 99% obstruction at 2 to 4 weeks, decreasing to 85.9% obstruction after 12 months ( p < 0.005). The prevalence of total coronary occlusion (TCO) and the severity of stenosis in those without TCO was similar in those with transmural or nontransmural MI and in those with one-, two- or three-vessel disease. This study suggests that endogenous lysis is probably a slow process, and that severe coronary narrowing persists in those with recanalization.

Long-term prognosis after first Q-wave (transmural) or non-Q-wave (nontransmural) myocardial infarction: Analysis of 593 patients

Follow-up results in 593 patients ≤7 years (mean 4.7) after hospital discharge for their first myocardial infarction (MI) are presented. Patients were grouped according to the presence or absence of Q waves on electrocardiograms after the MI and by peak serum glutamic oxalacetic transaminase (SGOT) level during hospitalization. Cardiac mortality varied. Patients with Q-wave infarcts and an SGOT level ≤240 IU/liter had a cardiac mortality of 3.1% per year, whereas patients with Q-wave MI and an SGOT level > 240 IU/liter had an 11% 6-month mortality and a 3.8% per year cardiac mortality thereafter. However, patients with non-Q-wave (nontransmural) MI had a excellent survival rate for 2 years (96.8%) which continued in patients aged ≤60 years thereafter. However, patients with non-Q-wave infarcts aged > 60 years had a 12% per year cardiac mortality in the third post-MI year and an additional 12% died each year thereafter. Early mortality was related to enzyme level, whereas late mortality was a function of type (Q-wave or non-Q-wave) and age.

Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris

Although intracoronary thrombus formation plays a major role in acute transmural myocardial infarction (MI), its occurrence in unstable angina (UA) and nontransmural MI has not clearly been established. To determine whether intracoronary thrombus does occur in these syndromes, coronary arteriography was performed before, during, and after intracoronary nitroglycerin and streptokinase infusion in 17 patients. None of the 8 patients with nontransmural MI and 1 of the 9 patients with UA responded to intracoronary nitroglycerin. Seven of 8 patients with nontransmural MI and 4 of 9 patients with UA responded to streptokinase infusion with opening of an occluded vessel, an increase in stenotic diameter, dissolution of an intracoronary filling defect, or a combination of these. Serial opening and closing of ischemia-related vessels occurred spontaneously and in response to streptokinase in some patients in whom thrombolysis was demonstrated. Evidence of thrombolysis was not seen in any patient studied longer than 1 week from the onset of the rest pain syndrome. The finding of thrombolysis in several patients with nontransmural MI and UA suggests that intracoronary thrombus formation plays a pathogenetic role in some patients with these ischemic syndromes.

Prevalence and prognosis after a first nontransmural myocardial infarction

Prevalence, prognosis, and coronary anatomy associated with nontransmural myocardial infarction (MI) were prospectively assessed in 458 consecutive men admitted to our coronary care unit with a first MI. Cardiac catheterization was performed in 402 of the 436 survivors within 1 month of the acute event. Mean follow-up was 33 months (range 5 to 72). Nontransmural MI was diagnosed in 28 patients (6%). These patients were younger (46 ± 10 versus 51 ± 7 years, p < 0.001) and had lower peak creatine kinase values (601 ± 319 versus 1,141 ± 923 U, p < 0.01) and better ejection fraction (63 ± 8 versus 46 ± 14, p < 0.001) than did their counterparts. Survivors of nontransmural MI also had fewer affected arteries (p < 0.001) and a lower prevalence of total or subtotal occlusion (> 90%) in the involved artery (p < 0.01). Mortality in the acute phase and long-term survival at 4 years (Kaplan-Meier) in patients with nontransmural MI (94%) were similar to those in patients with transmural MI (90%). The occurrence of new nonfatal coronary events was also similar in both groups of MI survivors. Thus, in the absence of symptoms, more aggressive management to improve survival does not seem warranted after nontransmural MI.

Coxsackie B virus infection in coronary care unit patients.

It has been suggested that Coxsackie B virus infections may play a part in causing or triggering myocardial infarction. This study was designed to compare the incidence of such infections in Coronary Care Unit patients and normal controls. The choice of a suitable criterion for diagnosis of Coxsackie infection is discussed fully. Two hundred and fifty admissions to a Coronary Care Unit and 100 control subjects had a serum sample tested by microneutralisation for Coxsackie B antibodies. The incidence of infection among 130 patients diagnosed as acute myocardial infarction was 5% compared with 4% in the control group. In a subgroup classified as non-transmural myocardial infarction, the incidence of infection was 14%. The sex ratio of this group differed from the myocardial infarction group as a whole suggesting that the non-transmural group may not have been homogeneous. Normal coronary arteriograms were subsequently found in three patients who were diagnosed as non-transmural myocardial infarction but who had serological evidence of recent Coxsackie infection. This study does not demonstrate an association between Coxsackie infection and myocardial infarction as a whole and does not support the view that Coxsackie infection causes or provokes myocardial infarction. It does, however, suggest that myocarditis may simulate non-transmural infarction.

Termination of Ventricular Tachycardia by Carotid Sinus Massage

The patient was a 73-year-old man admitted because of two hours of chest pain. Serial ECGs and enzyme studies confirmed the diagnosis of nontransmural myocardial infarction. For unclear reaSons, the patient had been taking digoxin 0.25 mg daily; admission serum digoxin level was 0.3 ng/ml. The arrhythmia in Figure 1 was seen upon the patient’s arrival in the emergency room. Figure LA shows a 12 lead ECG of the tachycardiawith a rate ofll5/min, QRS duration of0.12 second, and 1:1 retrograde conduction. A QS pattern is present in leads aVL, V1. ,

Implications of increased myocardial isoenzyme level in the presence of normal serum creatine kinase activity

Although increased serum creatine kinase (CK) activity in the presence of an increased level of myocardial-specific isoenzymes (CKMB) has been strongly associated with acute myocardial infarction, the significance of an increased serum CKMB level in the presence of a normal total CK level is uncertain. In 335 consecutive patients suspected of having an acute myocardial infarction and 71 control subjects, peak serum CKMB and CK levels were correlated with the presence of other clinical criteria for acute myocardial infarction: (1) typical chest pain, (2) increased myocardial lactate dehydrogenase (LDH1/LDH2), (3) acute electrocardiographic changes (new or ST-T wave changes with evolution), and (4) an elevated CKMB level on 2 or more determinations or a typical CK curve. No control subject had an increase in CK or CKMB or any of the 4 criteria for myocardial infarction. Of the 176 subjects with normal CK and normal CKMB (Group 1), only 11% had more than a single criterion, and none had more than 2 criteria consistent with myocardial injury. In contrast, of the 83 with elevated CK and CKMB levels (Group 2), 93% had 2 or more and 81% had 3 or more of the 4 criteria. Of the 63 patients with elevated CKMB but a persistently normal CK (Group 3), 65% had 2 or more criteria for acute myocardial infarction and 77% had subendocardial electrocardiographic changes; these patients resembled those with both elevated CK and MB. The phenomenon of elevated CKMB with normal CK occurred in 20% of the patients aged greater than or equal to 70 years but in only 10% of the younger group (p less than 0.01). These findings suggest that elevated CKMB with normal CK likely represents definite myocardial injury, is more likely represents definite myocardial injury, is more common in the elderly, and should be considered part of the spectrum of nontransmural myocardial infarction.

Myocardial Infarction in a National-Class Swimmer

MYOCARDIAL infarction (MI) and sudden death are periodically reported in previously healthy young adults during strenuous exercise or athletic competition. The majority of these cases are explained by latent coronary atherosclerosis, anomalous coronary morphological conditions, or hypertrophic cardiomyopathy. 1 However, exercise-related MI may also occur in young persons without apparent abnormalities of coronary or myocardial structure. 2-4 A nontransmural MI occurred in a national-caliber swimmer during intense training. Subsequent cardiac catheterization and radionuclide angiographic studies disclosed patent coronary arteries and normal ventricular function. Report of a Case A 20-year-old man, who was a varsity swimmer, complained of severe substernal chest pain while performing a routine 15-km training session. The pain was unaffected by his position or breathing movements are gradually resolved after one hour of rest. He remained asymptomatic until 3 AM the following morning, when he was awakened by similar pain that prompted medical attention. He denied having a