Infarct expansion versus extension: Two different complications of acute myocardial infarction

Precordial S-T segment mapping studies have suggested that extension of acute transmural myocardial infarcts occurs in up to 80 percent of patients within 6 days. To determine the morphologic nature of extension 76 consecutive acute myocardial infarcts aged 30 days or less were studied. All infarcts had been clinically diagnosed and proved at autopsy. Extension (histologically more recent foci of contraction band necrosis around an infarct) was found in only 13 infarcts (17 percent). However, “expansion” (acute dilatation and thinning of the area of infarction not explained by additional myocardial necrosis) was present in 45 infarcts (59 percent). Severe expansion did not develop until 5 days after infarction and was greater with transmural and first infarcts. Clinically diagnosed extension manifested by new pain, S-T segment elevation, rise in serum creatine kinase level and increased congestive heart failure occurred in 14 of the 76 patients (18 percent). At autopsy these clinical extensions were associated with expansion alone in three patients, with extension alone in two and with both in nine. The study shows that expansion is a common complication of acute myocardial infarction that can worsen cardiac function through left ventricular dilatation and can mimic or possibly cause infarct extension. In contrast, extension with additional myocardial necrosis is an infrequent accompaniment of acute myocardial infarction and is usually a result of hypoperfusion.     

Clinicopathologic correlates of acute ischemic heart disease syndromes

To better define the relations among acute and chronic coronary arterial lesions and different syndromes of acute ischemic heart disease, the clinicopathologic findings in 100 recent myocardial infarcts in 83 patients were reviewed and the results correlated with those of previous studies. Severe atherosclerosis (greater than 75 percent narrowing of luminal cross-sectional area) involved three or more major coronary arteries in 65 percent; two arteries in 16 percent, one artery in 15 percent, and no arteries in 4 percent of cases. The incidence rate of recent occlusive coronary arterial lesions was 61 percent, including 50 (90.2 percent) of 55 grossly apparent transmural infarcts, 9 (34.6 percent) of 26 grossly evident subendocardial infarcts and 2 (10.5 percent) of 19 multifocal microinfarcts associated with clinical episodes of acute coronary insufficiency (p <0.001). The 61 recent occlusive lesions consisted of two thromboemboli, two isolated plaque hemorrhages and 57 in situ thrombi that were associated with a high incidence rate of plaque erosion, rupture and hemorrhage. Clinical conditions predisposing to reduced coronary perfusion were identified before the onset of 26.2 percent of infarcts with recent occlusions and 61.5 percent of infarcts without recent occlusions (p <0.001). Clinical onset of infarction was followed by severe cardiac pump failure or congestive heart failure in 63.9 percent of infarcts with and 41.0 percent of infarcts without recent occlusions (p = 0.04).From this and previous studies, it is concluded that (1) acute ischemic heart disease does not have a constant relation with the severity of chronic atherosclerosis; (2) myocardial necrosis commonly occurs in the absence of acute permanent coronary occlusion, but in this setting is usually limited to subendocardial involvement of variable extent; (3) acute coronary thrombosis frequently acts as a major factor in determining the extent and distribution of an evolving infarct, as indicated by the large incidence of occlusive coronary thrombi with regional transmural infarcts; and (4) coronary thrombus formation is not dependent on a generalized impairment of coronary perfusion, either before or after the onset of infarction.     

Coronary angiography and left ventriculography in survivors of transmural and nontransmural myocardial infarction

Recent studies have suggested a similar prognosis for patients with transmural myocardial infarction and nontransmural myocardial infarction despite a smaller infarct size in the latter patients estimated by creatine phosphokinase (CPK). Thirty-one patients with transmural myocardial infarction and 17 patients with nontransmural myocardial infarction as defined by electrocardiographic criteria underwent coronary angiography and left ventriculography from 10 to 24 days after they had an acute myocardial infarction. Forty-three of these 48 patients were asymptomatic following their myocardial infarction. When compared to patients with nontransmural myocardial infarction, those with transmural myocardial infarction had greater peak CPK levels, 1,090 +/- 210 versus 290 +/- 60 IU (p less than 0.01). There was no difference in prevalence of single, double or triple vessel coronary artery disease, mean number of coronary arteries 50 per cent narrowed (2.0 +/- 0.2 versus 2.0 +/- 0.2), near total or total occlusions, coronary score (Friesinger) (7.9 +/- 0.6 versus 8.2 +/- 0.7), left ventricular ejection fraction (48 +/- 2 versus 53 +/- 4), or per cent of akinetic-dyskinetic myocardial segments (66 of 242 [27 per cent] versus 32 of 132 [24 per cent]) between two groups. The similar extent of coronary artery narrowing and degree of left ventricular dysfunction may explain the similar prognosis for patients with transmural myocardial infarction and those with nontransmural myocardial infarction despite differences in enzymatically estimated acute infarct size.     

Nontransmural myocardial infarction: A comparison of hospital and late clinical course of patients with that of matched patients with transmural anterior and transmural inferior myocardial infarction

The hospital and long-term course of 67 patients with nontransmural myocardial infarction was compared with that of 66 patients with transmural anterior and 63 patients with transmural inferior infarction matched for age, sex, previous infarction and prior congestive heart failure. During their hospital stay, patients with nontransmural infarction had significantly less congestive heart failure and fewer intraventricular conduction defects than did patients with transmural anterior infarction; fewer atrial tachyarrhythmias and less sinus bradycardia and atrioventricular block than did patients with transmural inferior infarction; and an incidence of hypotension, pericarditis and ventricular irritability similar to that of patients in the other two groups. Patients with nontransmural infarction had a significantly lower coronary care unit mortality rate (9 percent) than that of patients with transmural anterior or transmural inferior infarction (20 and 19 percent, respectively). By 3 months, the mortality rate had risen to 14 percent in patients with nontransmural infarction, but was significantly higher (29 and 27 percent, respectively) in patients with transmural anterior or transmural inferior infarction. Angina was common in all three groups, occurring in more than 50 percent of patients during a mean follow-up period of 28.6 months after hospital discharge.In contrast, the incidence of subsequent myocardial infarction was significantly greater in patients with nontransmural myocardial infarction, occurring in 21 percent at 9 months compared with only 3 percent of patients with transmural anterior (p <0.01) and 2 percent of patients with transmural inferior (p <0.05) infarction. By 54 months, 57 percent of patients with nontransmural infarction had sustained a new infarction contrasted with only 12 percent of patients with transmural anterior (/p <0.001) and 22 percent of patients with transmural inferior (p <0.01) infarction. Late mortality increased in patients with nontransmural myocardial infarction and, although this group had a significantly better survival rate at 3 months, the overall late mortality of the three groups was comparable. The study suggests that nontransmural myocardial infarction is an unstable ischemic event associated with a great risk of later myocardial infarction and high late mortality rate. A more aggressive diagnostic and therapeutic approach may be warranted in patients with nontransmural myocardial infarction.     

Clinicopathologic study of abnormal Q waves in Kawasaki disease (mucocutaneous lymph node syndrome): An infantile cardiac disease with myocarditis and myocardial infarction

A correlative study of abnormal Q waves and pathologic findings was performed on 15 hearts from children with Kawasaki disease. Gross pathologic study revealed acute angiitis with pericarditis, acute myocarditis and coronary heart disease as the result of angiitis.Three hearts in infants with abnormal Q waves in leads I and aVL and chest leads had gross transmural fibrosis in the anteroseptal-lateral walls of the left ventricle. Coagulation necrosis (acute myocardial infarction) or fibrosis, or both, in more than 30 percent of the wall thickness in the posterior ventricular wall was found in four of five hearts in infants with abnormal Q waves in leads II, III and aVF. Seven of the 15 infants had no abnormal Q waves, and only 2 of the 7 had myocardial damage in over 30 percent of the wall thickness.In 9 of the 15 hearts there were 11 gross areas of fibrosis; in these hearts there was a corresponding severe stenosis of more than 90 percent due to organization in the major coronary arteries supplying these areas. In three hearts with coagulation necrosis, the coronary occlusion was caused by fresh large thrombi. In the six hearts without sizable fibrosis, the grade of stenosis due to organization was less than 75 percent in each of the major coronary arteries.Coronary aneurysm due to angiitis was seen in 12 of the 15 hearts, and at autopsy fresh large thrombi were seen in each aneurysm. Ten of the 12 hearts exhibited sizable areas of myocardial damage. Three hearts without aneurysm manifested angiitis with mild stenosis of less than 25 percent, but there were no macroscopic fresh thrombi in any of the major coronary arteries.Thus, abnormal Q waves in children with Kawasaki disease almost always reflect myocardial damage in over 30 percent of the wall thickness of the left ventricle. Electrocardiograms are useful to determine the anterior or posterior localization of the damage. Nevertheless, the possibility of transmural and nontransmural areas of damage cannot be excluded in the absence of abnormal Q waves.     

Left ventricular functional alterations at rest and during submaximal exercise in patients with recent myocardial infarction

Submaximal exercise testing with radionuclide ventriculography was performed in 117 patients prior to hospital discharge 16.7 ± 6.7 days (SD) following acute myocardial infarction. The hypothesis tested in this study was that patients with different locations and types of infarction have different functional responses to submaximal exercise prior to discharge. The distribution of the myocardial infarctions were anterior transmural in 33, Inferior transmural in 39, anterior nontransmural in 23, inferior nontransmural in 19, and indeterminant in three. Patients with transmural infarction generally had significantly larger resting left ventricular volumes at enddiastole and end-systole and lower ejection fractions and systolic blood pressure/end-systolic volume Indexes than patients with nontransmural infarctions (p < 0.05). During submaximal exercise, the change in end-systolic volume was significantly different in these two groups. When patients were separated further into anterior and inferior transmural subgroups, the patients with anterior transmural infarction had significantly lower left ventricular ejection fractions and higher right ventricular ejection fractions than the group with inferior transmural Infarction (p < 0.05). In response to exercise, the group with anterior transmural infarction had a significant decrease in left ventricular ejection fraction and a blunted systolic blood pressure/left ventricular end-systolic volume index, in comparison to patients with inferior myocardial infarction (p < 0.05); this was the only group to have a significant increase in end-systolic volume. The group variance for the parameters studied was large, particularly during exercise when the individual responses were frequently directionally opposite from the group means. The group with anterior transmural infarction was the most homogenous, with 26 of 33 having a directionally abnormal response to submaximal exercise. It was concluded that the group with anterior transmural infarction generally displayed the most abnormal left ventricular function. However, despite significant group differences in resting ventricular function with different infarcts, the intragroup variability at rest and in response to exercise was too great to permit an accurate prediction of the subject's resting ventricular performance or to permit a prediction of exercise response based solely on location of the infarct.     

Preponderance of acute proximal left anterior descending coronary arterial lesions in fatal myocardial infarction: A clinicopathologic study

To determine whether an acute lesion in a specific segment of the cororiary tree is more likely than other obstructions to cause fatal myocardial infarction, 77 autopsy patients Who died of acute myocardial infarction were studied. Multiple coronary stenoses were present in 92 percent of these patients, arid the proximal left anterior descending coronary artery before the first septal perforator accounted for only 23 percent of the critical narrowings (greater than 70 percent of luminal diameter). In contrast, acute thrombotic coronary events associated with fatal myocardial infarction occurred most often in the proximal left anterior descending artery, accounting for 61 percent of acute lesions; this rate compared with 8 percent of acute lesions occurring in the mid or distal left anterior descending artery, 18 percent of those in the right, 6 percent of those in the left circumflex and 7 percent of those in the left main coronary artery. Of the autopsy patients, 32 (40 percent) had 77 prior nonfatal myocardial infarcts of which only 17 (22 percent) were anteroseptal infarcts related to occlusion of the proximal left anterior descending coronary artery. The amount of infarcted myocardium in the hearts with acute proximal left anterior descending coronary arterial lesions was somewhat more extensive but not significantly different from that of hearts with other acute coronary lesions.

Fifty survivors of myocardial infarction who underwent cardiac catheterization were studied for comparison. In those patients, proximal left anterior descending coronary disease accounted for 17 percent of critical narrowings and only 22 percent of nonfatal infarcts. These findings suggest that an acute proximal left anterior descending coronary arterial lesion is more likely to result in fatal myocardial infarction than are critical obstructions elsewhere in the coronary arterial tree. Because the quantity of the infarct does not appear to be sufficient to explain these differences, qualitative differences in anteroseptal myocardium are suggested.     

Clinical characteristics,electrocardiographic and enzyme correlations,and long-term prognosis of patients with chest pain associated with ST depression and/or T wave inversion

The clinical characteristics, electrocardiographic changes, and long-term prognosis were studied in 50 patients suffering nontransmural myocardial infarctions. It is concluded that nontransmural myocardial infarcts tend to occur in older patients with known coronary atherosclerosis and these infarctions are frequently preceded by a period of unstable angina. The clinical course is often complicated with congestive heart failure and other major management problems. Three different groups of electrocardiographic changes were noted and all four in-hospital deaths showed the same pattern of electrocardiographic changes. The prognosis of patients suffering nontransmural myocardial infarctions is not good, as evidenced by a death rate similar to reported patients suffering transmural myocardial infarction and a significant incidence of cardiovascular disability in those who survive.     

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 less than 0.005) and left ventricular end-systolic volume lower (29 +/- 11 vs 42 +/- 20 ml/m2, 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.(ABSTRACT TRUNCATED AT 250 WORDS)     

The short- and long-term prognosis of patients with transmural and nontransmural myocardial infarctio

To compare the long-term prognosis in patients surviving transmural with patients surviving nontransmural myocardial infarctions, the records of 188 consecutive patients with clinical histories and enzyme elevations consistent with acute infarction were reviewed. According to standard electrocardiographic criteria the patients were divided into two groups: 148 with transmural myocardial infarction (group 1) and 40 with nontransmural myocardial infarction (group 2). Of the patients who survived hospitalization, follow-up data were obtained on 119 of 124 patients in group 1 and 36 of 37 patients in group 2 at a mean follow-up period of 36 months. In group 2, the patients had a high incidence of sudden death after discharge (33 per cent in group 2 versus 15 per cent in group 1, p < 0.02) as well as a significantly higher incidence of death from all cardiac causes (41.6 per cent in group 2 versus 24.3 per cent in group 1, p < 0.05). Furthermore, the patients in group 2 still alive at the end of the follow-up period had an increased incidence of angina pectoris and of recurrent infarction. The data suggest that patients with nontransmural myocardial infarction carry a particularly guarded prognosis.     

Survival of patients with nontransmural myocardial infarction: A population-based study

A population-based study was conducted in metropolitan Baltimore in which the short- and long-term prognosis of 283 patients with nontransmural myocardial infarction was compared with that of 953 patients with transmural infarction. After simultaneous adjustment for several variables, the in-hospital case fatality rate was greater for patients with transmural (30.1 percent) than with nontransmural (18.3 percent) infarction (P < 0.01). However, for patients discharged alive from the hospital and followed up for as long as 10 years, no significant differences in survival were found between the groups with transmural and nontransmural infarction. A multiple adjustment procedure yielded 3 year case fatality rates of 27.1 percent and 28.3 percent, respectively, for patients with transmural and nontransmural myocardial infarction surviving the acute phase.These results suggest that the long-term prognosis of patients with nontransmural infarction is as guarded as that of patients with transmural infarction and that attempts to prevent subsequent mortality should be diligently pursued in both groups of patients.     

Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis,coagulation necrosis,hemorrhage, and infarct size

Summary In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. Autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. Autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%–26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67±20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86±14% of the infarcted area) and/or hemorrhage. The findings suggested that MI associated with normal coronary arteries was caused by transient coronary arterial occlusion due to spasm and/or thromboembolism, with the CBN seen in these hearts representing reperfusion injury.     

Selective inhibition of the contractile apparatus. A new approach to modification of infarct size, infarct composition, and infarct geometry during coronary artery occlusion and reperfusion.

BACKGROUND. Myocardial reperfusion is associated with calcium overload and cell contracture, mechanisms that may precipitate cell death. In this study, we tested the hypothesis that in vivo inhibition of this contracture could lead to cell preservation in an open-chest large animal model. METHODS AND RESULTS. Regional myocardium function was measured during a selective intracoronary infusion of 2,3-butanedione monoxime (BDM), a specific inhibitor of actin-myosin coupling, in the control state (10 pigs) and in a protocol of a 51-minute coronary occlusion followed by reperfusion (40 pigs). The effects on coronary artery blood flow in the basal state were also studied (seven pigs). Intramyocardial distribution of the infusate during coronary occlusion, myocardial water content after 30 minutes of reperfusion and area at risk, infarct size, type of histological necrosis, and infarct geometry after 24 hours of reperfusion were assessed. Methods used included electromagnetic flowmeter, radiolabeled microspheres, subendocardial sonomicrometers, fluorescein, triphenyl tetrazolium chloride and Masson's trichrome staining, and computer quantification of infarct edges. In the absence of ischemia, BDM infusion inhibited regional shortening in a dose-dependent manner up to full systolic bulging while producing marked regional increase in coronary blood flow. During early reperfusion, BDM reduced end-diastolic length 76% more than the control infusion (p less than 0.05) and increased systolic bulging by 420% compared with no change in control animals. The ratio of infarct size/area at risk was reduced by 31% with BDM (p less than 0.05), with striking modifications of infarct histology and infarct geometry; specifically, the extent of contraction band necrosis was reduced by 63% from 105.5 +/- 18.2 to 39.2 +/- 13.6 mm2 (p less than 0.02), and more patches of necrosis (6.5 +/- 2.1 versus 1.6 +/- 0.4, p less than 0.05) and higher contour (7.7 +/- 1.2 versus 5.03 +/- 0.2, p less than 0.05) and fractal (12.1 +/- 1.3 versus 7.8 +/- 0.2, p less than 0.05) indexes were found. CONCLUSIONS. Selective intracoronary infusion of BDM at doses inhibiting regional wall motion decreased infarct size after reperfusion. The effects of BDM on regional function, the reduction in contraction band necrosis at histology, and the peculiar configuration of these infarcts all suggest that inhibition of contracture can interfere with cell-to-cell progression of myocardial necrosis, supporting a role for contracture in reperfusion-induced cell death.     

Pathological changes after intravenous streptokinase treatment in eight patients with acute myocardial infarction.

At necropsy five of eight patients (mean age 57 years) who died after intravenous streptokinase treatment for severe acute myocardial infarction (mean Peel index = 18) were found to have a patent infarct related coronary artery. Coronary artery stenoses were caused by fibrofatty atheromatous plaques; there were no residual thrombi in the lumen or acute intimal lesions. Three of these infarcts were of partial thickness (less than two thirds wall width) with sparing of the outer third of the myocardium and subendocardial zones. In the other three patients the infarct related coronary arteries remained histologically closed with residual lumen thrombi and underlying intimal lesions. Two infarcts were transmural. Six of the eight infarcts were noticeably haemorrhagic. Myocardial haemorrhage was confined to areas of necrotic myocardium and did not affect viable regions. These findings suggest that thrombus overlying a complex lesion may be more difficult to lyse than thrombus overlying a simple fibrofatty plaque. They also suggest that myocardial haemorrhage outside the infarct area, which might lead to cardiac rupture or delayed healing, does not usually occur.     

Pathological changes after intravenous streptokinase treatment in eight patients with acute myocardial infarction

At necropsy five of eight patients (mean age 57 years) who died after intravenous streptokinase treatment for severe acute myocardial infarction (mean Peel index = 18) were found to have a patent infarct related coronary artery. Coronary artery stenoses were caused by fibrofatty atheromatous plaques; there were no residual thrombi in the lumen or acute intimal lesions. Three of these infarcts were of partial thickness (less than two thirds wall width) with sparing of the outer third of the myocardium and subendocardial zones. In the other three patients the infarct related coronary arteries remained histologically closed with residual lumen thrombi and underlying intimal lesions. Two infarcts were transmural. Six of the eight infarcts were noticeably haemorrhagic. Myocardial haemorrhage was confined to areas of necrotic myocardium and did not affect viable regions. These findings suggest that thrombus overlying a complex lesion may be more difficult to lyse than thrombus overlying a simple fibrofatty plaque. They also suggest that myocardial haemorrhage outside the infarct area, which might lead to cardiac rupture or delayed healing, does not usually occur.     

Correlation of electrocardiologic and pathologic findings in 100 cases of Q wave and non-Q wave myocardial infarction

Of 100 cases of acute myocardial infarction as shown on autopsy, 55 cases were transmural infarcts and 45 were subendocardial. Pathologic Q waves appeared in 67% of the cases of transmural infarct and in 30% of subendocardial infarct. In transmural infarcts, Q wave infarcts occurred twice as frequently as non-Q wave infarcts. In the cases of subendocardial infarcts just the opposite was observed: non-Q wave infarcts had double the frequency of Q wave infarcts. In spite of this, when a myocardial infarct is characterized strictly by electrocardiology, it should be described by only the accurate terminology of Q wave infarct or non-Q wave infarct. To distinguish with certitude between subendocardial infarct and transmural myocardial infarct on the basis of the ECG does not seem possible. Q wave infarct as "transmural" and non-Q wave infarct as "subendocardial" does not correspond to the pathologic evidence.     

Topographic changes in the left ventricle after experimentally induced myocardial infarction in the rat

The factors that determine the thickness of transmural myocardial infarcts are unknown. Therefore, the relation between the size and thickness of transmural infarcts in 67 rats 21 days after occlusion of the left main coronary artery was studied. On examination of histologic sections, infarct size was determined by planimetry and expressed as a percentage of the left ventricular (LV) area, and thickness was expressed as a percentage of noninfarcted ventricular septal wall thickness. The circumferential length of the infarcted ventricle was measured in millimeters, as well as the circumferential length of the noninfarcted ventricular septum. Septal wall thickness was similar in rats with transmural infarcts and in sham-operated rats. No significant correlation was observed between infarct size and thickness (r = 0.10) or between circumferential length of the infarct and infarct thickness (r = 0.17). However, large (greater than or equal to 20% of the left ventricle, n = 37) and small (less than 20% of the left ventricle, n = 30) infarcts which were similarly thin (37 +/- 1% and 34 +/- 2% of septal wall thickness, respectively) affected LV topography differently. Large infarcts resulted in a 23% greater loss of myocardium (p less than 0.001), greater expansion of the LV cavity (18 +/- 9 mm2 compared with 14 +/- 1 mm2 in small infarcts, p less than 0.005), and lengthening of the septal wall (7.2 +/- 1.1 mm and 6.7 +/- 1.0 mm in large and small infarcts, respectively [p less than 0.05], and 6.3 +/- 0.1 mm in shams). Increase in cavity area and septal length in infarcted ventricles suggested a volume overload hypertrophy, which at 3 weeks was nonetheless inadequate to provide as much normal muscle as was present in sham-operated rats. In an additional 9 rats with subendocardial infarctions (involving less than 75% of the LV wall from endocardium to epicardium), the LV walls were thicker (94 +/- 5% of septal wall thickness, compared with 35 +/- 1% for transmural infarcts, p less than 0.001) and an inverse correlation was observed between infarct size and thickness. In conclusion, neither the size of a transmural infarct in rat nor the circumferential length of infarction determines the thickness of the infarct; however, infarct size does affect LV topography by increasing LV cavity area and the length of the noninfarcted septal wall. Subendocardial infarcts result in less myocardial thinning than do transmural infarcts.     

Quantitative comparison of extent of coronary narrowing and size of healed myocardial infarct in 33 necropsy patients with clinically recognized and in 28 with clinically unrecognized (“silent”) previous acute myocardial infarction

Clinical and necropsy observations are described in 61 patients with a healed transmural myocardial infarction, 33 with and 28 without a clinical history of acute myocardial infarction. There were no significant differences between the 2 groups of patients in mean age, sex, or frequency of angina pectoris, chronic congestive heart failure, systemic hypertension, sudden coronary death, or fatal acute myocardial infarction. Compared with the patients with clinically recognized acute myocardial infarction, the patients with clinically unrecognized (silent) infarction had a significantly (p < 0.05) higher incidence of diabetes mellitus (43 versus 15%), death from noncardiac causes (39 versus 9%), posterior (inferior) wall infarcts (82 versus 55%), and smaller infarcts (mean size 7 versus 17% of left ventricular wall). The patients with and without clinically recognized infarction had similar numbers of the 4 major coronary arteries severely (76 to 100% in cross-sectional area) narrowed (mean 2.8 versus $\text{2.9}\text{4.0}$ per patient), insignificant differences in incidence of severe narrowing of the left main coronary artery (18 versus 29%), similar overall percents of 5 mm segments of the 4 major coronary arteries severely narrowed (43 versus 42%), and similar percents of severely narrowed 5 mm segments of the right (46 versus 55%), left anterior descending (39 versus 33%), and left circumflex (41 versus 41%) coronary arteries.     

Cardiac Ruptures in Northern Norway

Abstract. In 4649 autopsies performed, in 1972–1985, 824 cases of acute myocardial infarction were found. Of these, 104 (12.6%) had cardiac rupture. Ten cases had rupture of the interventricular septum. The clinical and pathological records were reviewed, and the rupture group was compared with a control group of 100 patients who died from acute myocardial infarction without rupture. Of the patients with rupture, 85% died during the first week after the onset of myocardial infarction; three patients with rupture died suddenly without previous clinical evidence of myocardial infarction. Rupture occurred only in hearts with transmural infarcts, and predominantly in the anteroseptal wall. Patients with rupture had significantly higher blood pressure, fewer previous infarcts, higher frequency of coronary thrombi, less myocardial scar tissue and lower heart weight compared to the control group. There were no significant differences regarding age and sex distribution, physical effort at the symptom debut or death, medication, previous and present diseases other than infarcts, complications or the degree of atherosclerosis in the coronary arteries or aorta.     

Transmural contractile reserve after reperfused myocardial infarction in dogs

OBJECTIVES

The goal of this study was to characterize detailed transmural left ventricular (LV) function at rest and during dobutamine stimulation in subendocardial and transmural experimental infarcts.

BACKGROUND

The relation between segmental LV function and the transmural extent of myocardial necrosis is complex. However, its detailed understanding is crucial for the diagnosis of myocardial viability as assessed by inotropic stimulation.

METHODS

Short-axis tagged magnetic resonance images were acquired at five to seven levels encompassing the LV from base to apex in seven dogs 2 days after a 90-min closed-chest left anterior descending coronary occlusion, followed by reflow. Myocardial strains were measured transmurally in the entire LV by harmonic phase imaging at rest and 5 ig.kg⁻¹.min⁻¹ dobutamine. Risk regions were assessed by radioactive microspheres, and the transmural extent of the infarct was assessed by 2,3,5 triphenyltetrazolium chloride staining.

RESULTS

Circumferential shortening (Ecc), radial thickening (Err) and maximal shortening at rest were greater in segments with subendocardial versus transmural infarcts, both in subepicardium (−1.1 ± 1.0 vs. 2.5 ± 0.6% for Ecc, −0.5 ± 1.9 vs. −1.8 ± 1.0% for Err, p < 0.05) and subendocardium (−2.0 ± 1.4 vs. 2.8 ± 0.8%, 2.4 ± 1.7 vs. 0.0 ± 0.9%, respectively, p < 0.05). Under inotropic stimulation, risk regions retained maximal contractile reserve. Recruitable deformation was found in outer layers of subendocardial infarcts (p < 0.01 for Ecc and Err) but also in inner layers (p < 0.01). Conversely, no contractile reserve was observed in segments with transmural infarcts.

CONCLUSIONS

Under dobutamine challenge, recruitment of myofiber shortening and thickening was observed in inner layers of segments with subendocardial infarcts. These results may have important clinical implications for the detection of myocardial viability.