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At least 19 recordsLinked to original sources

PubMed1976

Experimental myocardial infarction: XII. Dynamic changes in segmental mechanical behavior of infarcted and non-infarcted myocardium.

The mechanical behavior of ischemic myocardium was studied in anesthetized open chest dogs. In each animal, a small well localized myocardial infarction was produced by ligation of a single ventricular branch of the left circumflex coronary artery. Serial in situ measurements of segment length were made by mercury-in-Silastic gauges sutured directly to the left ventricular surface. After coronary ligation, systolic aneurysmal bulging of the ischemic segment was uniformly noted. This was quantified as follows: normalized segment length change in this region, expressed in muscle lengths (where muscle lengths = phasic segment length amplitude/end-diastolic segment length), immediately increased from 0.06 +/- 0.01 (standard error of the mean) to 0.10 +/- 0.02 muscle lengths (+67 percent, P less than 0.02). Over a 6 hour period, muscle lengths progressively declined to near control values, but retained an aneurysmal contour. End-diastolic segment length increased 5 percent above control values after coronary occlusion and remained fixed at this level for 6 hours. In contrast, noninfarcted myocardium exhibited no significant changes in muscle length or end-diastolic segment length. These studies demonstrate that the degree of systolic aneurysmal bulging in infarcted myocardium, although initially great, resolves within 6 hours but retains an aneurysmal contour. These findings are consistent with either partial return of contractility or diminished local compliance, but persistence of an aneurysmal shape favors the latter mechanism. The fixed increase in end-diastolic segment length suggests that "stress-relaxation" takes place in the infarcted region. It is possible that diminished compliance in zones of infarction, previously noted after several days, begins within a few hours after the onset of ischemia.

Animals↗

PubMed1975

Surgery for impending myocardial infarction, acute evolving myocardial infarction, and complications of myocardial infarction.

Post-infarction ventricular aneurysm, ventricular septal defect, and mitral insufficiency are all potentially amenable to surgical intervention. In each instance the results of operation and the prognosis following operation depend largely on the extent of infarction, the status of the residual myocardium, and the interval between infarction and operation. When the residual myocardium exhibits good contractility, the results are usually good. When early operation is performed in the face of a deteriorating clinical course and with poorly contracting residual myocardium, the mortality rates are extremely high. In an effort to increase the efficiency of the residual myocardium, concomitant coronary bypass surgery should be performed whenever possible. In this difficult group, more recent supportive measures such as the intra-aortic balloon pump may be particularly helpful when utilized both before and after operation. The surgical indications and results of coronary bypass surgery in impending or acute evolving myocardial infarction are not as well defined, but it is evident that myocardial revascularization may be useful in carefully selected patients.

Acute Disease↗

PubMedDate not supplied

[Enzyme activity in post-infarct aneurysm and in the myocardial zone outside the infarct in experimental infarct in rats].

Activities of lactate dehydrogenase, glucose-6-phosphate dehydrogenase, transketolase and creatine phosphokinase were studied in tissue of aneurysm and in extrainfarctional part of rat heart muscle after experimental infarction. Activity of total LDH, content of its anode isoenzymes and creatine phosphokinase activity were decreased. Enzymes of pentose phosphate pathway were activated and amount of cathode LDH isoenzymes was increased. The most distinct and apparently irreversible alterations in the enzymatic activity were observed in the aneurysm tissues.

Animals↗

PubMed1978

Relationship of myocardial infarction to presence of angina pectoris in patients with coronary heart disease: lack of abolition of angina by infarction.

To evaluate the relationship between myocardial infarction and angina pectoris, history of symptomatic coronary heart disease was analyzed in 146 patients who had had documented myocardial infarction. There were 126 males and 70 females of mean age 55 years (range 32 to 70 years). Infarction had occurred 6 to 63 months prior to the study (mean: 30 months). Angina pectoris occurred at some time during the clinical course of 75 patients (51%), and 71 patients (49%) had not experienced angina. In the majority of the group with angina (n = 39; 52%) the symptom had not been present before infarction, appearing initially thereafter. Angina was present both before and after infarction in 31 patients (41%). In only 5 patients (7%) was precedent angina lost after infarction. Angina was, therefore, present in 70 of 146 patients (48%) after, compared to 36 patients (25%) before, infarction and in 86% (31/36) of patients with angina before infarction it persisted following the attack. Prior angina following myocardial infarction was not related to increased activity since in the majority of patients activity level was less after than before infarction. Post-infarction cardiac failure, which developed in 9 patients who had prior angina, was not associated with abolition of angina in any of this group. It is concluded that: 1. angina is frequent after myocardial infarction, 2. when present before infarction it usually persists thereafter, 3. angina commonly appears as a new symptom after infarction when not previously present and 4. disappearance of angina after infarction is distinctly uncommon.

Adult↗

PubMed1977

Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction: retrospective study of patients with typical anterior and posterior infarcts.

This retrospective study correlates electrocardiographic and histopathologic findings in 24 patients with single well-circumscribed infarcts to determine 1) whether ECG terms commonly used to describe the location of myocardial infarcts are significant, and 2) whether the extent of infarct can be determined using QRS characteristics. Transverse sections of the hearts were photographed. Based on histologic sections, the infarct was outlined on the photograph and each section was planimetered via a sonic digitizer into a computer that was programmed to divide the left ventricle into 8 radial sectors and also into basal, mesial, and apical thirds. The percentage of infarct in each of these areas was then calculated. Of the 24 hearts evaluated 12 had posterior infarcts and 12 had anterior infarcts. Posterior infarcts principally involved the basal and mesial levels, whereas the anterior infarcts were more extensive in the apical and mesial thirds, with relative or total sparing of the base. Posterior infarcts were associated with Q waves in leads II, III and aVF in 11 instances. The other posterior infarct was associated with markedly diminished R waves in leads II, III and aVf in the presence of a horizontal axis. All anterior infarcts were associated with Q waves or markedly diminished R waves in the right precordial leads. Eight of the anterior infarcts exhibited circumferential apical involvement and all eight were associated with Q waves or markedly diminished R waves in the left precordial leads. This study documents the electrocardiographic identification of anterior, posterior, and apical infarcts by correlation with pathologic anatomy.

Adult↗

PubMed1978

Myocardial infarction size from serial CPK: variability of CPK serum entry ratio with size and model of infarction.

To study the variability of the fraction of CPK released from the infarcted heart which enters the serum (serum entry ratio, or SER) with size and model of infarction, nine dogs underwent homogeneous infarctions (LAD ligation) of varying sizes, and 10 dogs underwent scattered infarctions (left coronary embolization). In homogeneous infarcts there was an inverse linear relationship of SER to infarct size (IS) (SER = -0.8514% LV + 0.345, r = 0.98). No such relationship was found for scattered infarcts. CPK Kd (exponential disappearance constant for CPK) was not significantly different in homogeneous (-0.00178 min-1) vs scattered infarcts (-0.00195 min-1). Although similar IS was produced in each (homogeneous 19.9% LV, scattered 18.4% LV) cumulative CPK serum entry (CPKr) was much lower in homogeneous (4175 mlU/ml) vs scattered infarcts (7,296 mlU/ml). SER was also much lower in homogeneous (17.7%) vs scattered infarcts (29.0%) (P less than 0.025). Cumulative CPK plateau occurred significantly later in homogeneous (15.8 hours) vs scattered infarcts (11.7 hours) (P less than 0.01). Further corrections to the serial CPK equations for IS determination are indicated. The method may not be applicable in some infarct situations, e.g., scattered infarction.

Animals↗

PubMed1977

Infarct sizing with technetium-99m stannous pyrophosphate scintigraphy in dogs and man; relationship between scintigraphic and praecordial mapping estimates of infarct size in patients.

The present study was performed in order to evaluate the ability of technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigrams to size infarcts in experimental animals and man. In 10 dogs with proximal left anterior descending coronary artery occlusion and acute anterior myocardial infarcts, there was a significant correlation between scintigraphic infarct size and histological infarct weight (P less than 0.01). In 25 patients with acute anterior or anterolateral myocardial infarcts, there was a significant correlation between relatively large infarct size determined scintigraphically and the acute development of left ventricular failure. There was some overlap, however, in 99mTc-PYP scintigraphic infarct size between patients who did and did not develop left ventricular failure with infarction. Presumably this is explained by some patients having had earlier myocardial damage and thus developing left ventricular failure with relatively small new infarcts. There was also a statistically significant, but weak, correlation in patients between scintigraphic infarct size and precordial ST segment mapping including peak ST segment elevation (P less than 0.05) and the number of praecordial sites with ST segment elevation equal to or greater than 2 mm (P less than 0.01). The data suggest that 99mTc-PYP scintigrams and praecordial mapping measure some similar but some dissimilar aspects of infarct size in patients, and that 99mTc-PYP scintigraphy does size acute anterior and anterolateral infarcts in experimental animals and patients.

Animals↗

PubMed1979

Imaging experimental myocardial infarction with indium-111-labeled autologous leukocytes: effects of infarct age and residual regional myocardial blood flow.

The external imaging patterns and the kinetics of infiltration of indium-111 labeled polymorphonuclear leukocytes (PMNs) occurring in the course of the inflammatory response associated with myocardial infarction were studied in dogs subjected to closed-chest anterior wall infarction. The effects of infarct age and regional residual myocardial blood flow upon PMN infiltration were investigated and quantified, and the capacity of indium-111 PMNs to image the experimental infarction was evaluated qualitatively. The epicardial accumulation of indium-111 PMNs occurred primarily in infarct zones with residual blood flow of 0.6 times normal and was maximal (14.8 +/- 3.8 times normal) in the lowest blood flow zone (less than 0.1 times normal). PMN accumulation in the endocardial infarct zones occurred in the regions with blood flow less than 0.6 times normal and was maximal (26.8 +/- 4.9 times normal) in the lowest blood flow zone. However, contrary to the maximal epicardial infiltration period, which occurred within the first 24 hours after infarction, the maximal endocardial infiltration occurred at 72 hours after infarction. In both endocardium and epicardium, PMN uptake was minimal at 120 hours after infarction. In vivo cardiac images were abnormal and revealed discrete, anatomically distinct areas of increased myocardial radioactivity uptake in the anterior wall of all dogs studied within 24--96 hours after infarction. All images obtained 120 hours after infarction were negative. Thus, indium-111 PMNs provide a noninvasive means of in vivo imaging of the inflammatory response to myocardial infarction and allow quantification of this response at a tissue level.

Animals↗

PubMed1992

[A clinicopathologic study of atrial infarction complicating left ventricular posterior myocardial infarction].

Among a series of 400 consecutive autopsy cases we performed a clinicopathologic study of atrial infarction in 46 autopsy-proven cases, which had acute or old left ventricular (LV) myocardial infarction. We used blocks taken from both atrial appendages, the region of the sinus-node, the lateral wall of the right atrium, the posterior wall of the right atrium, and the posterolateral wall of the left atrium. Atrial infarction was identified in 13 (28%) of 46 cases with LV posterior infarction which was caused by lesions of the right coronary artery; 10 cases were right atrial infarction and 3 were both right and left atrial infarction. Among 13 cases in which the acute phase of ventricular infarction could be followed, 3 cases exhibited transient atrial fibrillation. Of these 3 cases, 2 had atrial infarction. The mean stenotic index of the proximal right coronary artery was 4.3/5 in the 13 cases of atrial infarction, 3.2/5 in 17 cases of acute necrosis or scar and 3.1/5 in 16 cases without ischemic atrial lesions. Most of the atrial infarction was found in the right atrium; 10 in the right atrial appendage, 8 in the right atrial lateral wall, 3 in the region of the sinus node and the left atrial posterolateral wall, 2 in the right atrial posterior wall, and one in the left atrial appendage. In conclusion, the incidence of atrial infarction was unexpectedly high (28%) in LV posterior infarction caused by lesions of the proximal right coronary artery, particularly in severe stenosis or obstruction.

Aged↗

PubMed1976

[Heart muscle after heart infarct. Function of surviving heart muscle following acute myocardial infarct].

In the initial phase of the infarction, there is a decrease of ventricular function due to loss of contractile activity. In addition, a negative effect of the paradoxical movement of the infarcted area on the hemodynamics of the ventricle is noted. The stiffening of the infarcted area in the early stage has a favorable influence on ventricular function, leading to a change in the elastic properties of the ventricle. The loss of ventricular compliance persists after the infarction, and its severity depends on the extent of myocardial destruction. In the non-compliant ventricle, the end-diastolic pressure rises without a proportionate increase in volume. Consequently, the ventricular function curve shows a shift downward and to the right, making it difficult to distinguish between the loss of contractile function or compliance in the heart in situ. Evaluation of the contractile properties of the surviving cardiac muscle in situ is, however, hardly possible due to the changed geometry and the additonal elastic elements functioning in series with the surviving muscle. To exclude these factors, a study of the contractile properties of the surviving cardiac muscle in the isolated state was carried out following experimental myocardial infarction in cats. By ligating several coronary branches, infarctions in the area of the left ventricle were caused; to avoid the ischaemic border zone of the infarction, right ventricular papillary muscles were studied. Haemodynamic investigations showed an increase in right ventricular end-diastolic pressure which persisted 6 weeks after infarction. As early as 48 hours but, more significantly 1 week after infarction, there was a decrease of actively developed force in the surviving cardiac muscle due to a lower rate of force development. The resting length tension curve of the surviving cardiac muscle after infarction showed no alterations; and 6 weeks following infarction, almost normal contractility parameters were observed. As a result of the infarction, a decrease in contractility in the surviving cardiac muscle is observed during the early stage, which regresses after complete recuperation.

Acute Disease↗

PubMed1976

A comparative study of the coronary arterial structure in the left ventricular free wall in infarcted and non-infarcted human hearts.

The structure and anastomoses of the coronary arteries were studied using coronary arteriography with barium sulfate (Micropaque) and gelatin as well as "cleared preparations" with tetralin. This was done in a total of 50 human autopsied hearts either with or without infarction and the patients had ranged from one to 84 years of age. Special emphasis was placed on the quantitative studies of the coronary anastomoses in the left ventricular free wall of 32 hearts including ten infarcted hearts. In addition histologic investigations were performed on 168 anastomotic channels selected arbitrarily from both the infarcted and non-infarcted hearts. The following results were obtained. 1. In the non-infarcted hearts, three different types of vessels, Type I, Type II and Type III respectively, were recognized in the left ventricular free wall. The number of anastomotic channels did not correlate with age, sex or weight of the heart. The number of anastomoses was closely related to the degree of coronary arterial narrowing and increased in the cases of severe narrowing. Anastomotic channels tended to be more frequent in the intracoronary and in the subendocardial layer and anastomoses of less than 150m in calibre were more numerous. 2. In the infarcted hearts the three types of vessels were changed as follows: localized increase of tree-like branching in the terminal portion of Type I vessels. Intercommunications between Type II vessels coursing parallel to the endocardial surface and between Type I and Type II vessels were found in the region of the endocardial layer up to the middle layer. Elongation of Type III vessels and an increase in their intercommunications were evident. Anastomoses in intercoronary and in the middle layer were found to have increased significantly. The percentage of anastomotic channels with large calibres, especially over 201 mu was increased, as compared with the non-infarcted hearts. 3. The wall thickness of anastomotic channels tended to be thinner in the infarcted hearts than in the non-infarcted ones. In the region adjacent to the infarction foci, attenuation of walls of the vessels was pronounced as compared with the wall thickness in anastomotic channels of similar size in the non-infarcted heats.

Adolescent↗

PubMed1977

Comparison of different noninvasive methods of infarct sizing during experimental myocardial infarction.

This study evaluated the accuracy of several noninvasive infarct-sizing techniques in 12 awake, unsedated dogs with multivessel coronary obstructions and acute anterior myocardial infarcts. Estimations of infarct size by scintigraphy with technetium-99m Sn pyrophosphate (Tc-PP), serum creatine phosphokinase (CPK) release, peak serum myoglobin levels by radioimmunoassay, and precordial ECG mapping were compared and correlated with histologic measurements of infarct size. The comparisons indicate that precordial ST segments mapping, serum CPK release measurements and peak serum CPK, peak serum myoglobin, and Tc-PPi myocardial scintigraphy all provide approximate estimates of infarct size in this model. Each technique also has certain important limitations, however, including: (A) precordial mapping is relatively insensitive in the identification of small anterior infarcts, (B) serial serum CPK release measurements when obtained for only 24 hr after infarction tend to underestimate large anterior infarct size, and (C) Tc-PPi myocardial scintigrams may fail to recognize anterior infarcts less than 3 gm in size and may overestimate the size of small predominantly subendocardial infarcts. The findings also show that the closest estimate of histologic infarct size in this model was provided by combining two of the noninvasive techniques (precordial mapping to identify sites with 2 or more millimeters of ST segments elevation and Tc-PPi myocardial scintigrams) rather than by relying exclusively on any one technique alone.

Animals↗

PubMed1976

Superimposition of transmural infarction following acute subendocardial infarction; how frequent?

Thirty-five consecutive patients with acute subendocardial infarction admitted to the coronary care unit during a 15-month period were identified and analyzed for location of infarction, and for the in-hospital course in terms of recurrent chest pain, the occurrence of a second infarction, and the clinical status at the end of hospitalization. Thirteen patients developed a transmural infarction sometime between 3 and 21 days (average, ten days) after the initial subendocardial infarction. The transmural infarction was defined by a separate episode of severe and prolonged chest pain, late development of QRS alteration, and an appropriate elevation of the creatine phosphokinase concentration. Our experience with acute subendocardial infarction, hertofore regarded as a relatively benign event, indicates that the immediate prognosis of the patient who sustains his first episode of subendocardial infarction is not at all benign, and, indeed, subendocardial infarction frequently heralds transmural infarction within the acute phase of the disease.

Aged↗

PubMed1978

[Restricted myocardial infarction. Coronary angiographic and ventriculographic findings. Comparison with acute coronary insufficiency and transmural infarction].

The findings at coronary arteriography and ventricular angiography in 52 patients with a restricted myocardial infarct were compared with those of 106 patients with acute coronary insufficiency and 100 with transmural infarcts. Certain features place restricted myocardial infarction in an intermediate category when compared with the two other syndromes. The percentage of coronary occlusions was significantly higher in transmural infarction (23.5%) and in restricted infarction (16.6%) than in acute coronary insufficiency 6.8%). Study of the vessel beyond a tight stenosis (greater than or equal to 75% was particularly effective in clearly separating the three groups. As a result, 63% of patients with coronary insufficiency, 40% of these with restricted infarcts, and only 23% of patients with a transmural infarct could be referred for surgery. Ventricular angiography showed a close relationship between restricted infarction and acute coronary insufficiency because ventricular function appeared normal or subnormal (localised hypokinesia) in 69% and 81% of cases respectively, compared with 4% of cases of transmural infarction. Restricted myocardial infarction appears to resemble coronary insufficiency, but shows elevation of enzymes and often more marked disease of distal vessels.

Acute Disease↗

PubMed1978

[Coronary atherosclerosis, coronary thrombosis and myocardial infarction in autopsy cases. 9th communication: relationship of coronary thrombosis and myocardial infarction (author's transl)].

The autopsy reports of the Pathological Institute Erfurt of the period from 1.1.1951 until 31.12.1969 were scored for cases of myocardial infarction and coronary thrombosis. Among 2,393 morphologically analysed myocardial infarctions 454 coronary thromboses (18.97 per cent) were found. Males were significantly more affected than females. Fresh infarcts showed significantly more thromboses than callous infarcts. We found fresh and occluding vessel thromboses more frequently in fresh infarctions. The analysis of age distribution yielded an increase of the rate of thrombosis in cases with myocardial infarction. On the other hand, the frequency of infarctions in cases with a coronary thrombosis was decreasing. It is suggested that the risk for infarctions is larger in younger people with coronary thrombosis than in older ones. No infarctions were detected in 165 cases of thrombosis. Preferably this group includes those cases in which the patients deceased within 6 to 8 hours and, therefore, the infarction was not morphologically detectable.

Adult↗

PubMedDate not supplied

Temporal changes in sequential quantitative thallium-201 imaging following myocardial infarction in dogs: comparison of four- and twenty-four-hour infarct images.

Thallium-201 ((201)T1) myocardial perfusion imaging allows definition of zones of myocardial infarction and ischemia. The temporal changes in sequential quantitative (201)T1 infarct imaging was studied 4 and 24 hours in dogs subjected to closed-chest anterior wall myocardial infarction. A temporal decrease in (201)T1 imaged infarct areas was noted in 10 of 13 animals. In no animal did the infarct area increase. The imaged infarct area decreased by an average of 30% from 12.9 ± 6.2 cm(2) at 4 hours to 9.1 ± 5.1 cm(2) at 24 hours (p < 0.001), and involved 34 ± 16% of the total (201)T1 left ventricular distribution at 4 hours and 22 ± 14% at 24 hours (p < 0.001). The magnitude of temporal change in imaged infarct area was not predicted by initial image defect or final histopathologic infarct size. Thus, the results of (201)T1 infarct imaging in the early period of infarction are clearly dependent upon the time at which the procedure is performed.

Animals↗

PubMed1976

Effect of reperfusion on myocardial infarct, and the accuracy of estimating infarct size from serum creatine phosphokinase in the dog.

This study was designed to determine the effect of coronary reperfusion on (1) myocardial infarct size and (2) the accuracy of previously reported methods for estimation of infarct size serum creatine phosphokinase (CPK) values. Thirty mongrel dogs, chronically prepared, were studied in the awake state, and were divided into four groups according to the period or left circumflex coronary artery (LCCA) occlusion. Group 1: permanent occlusion (24 h) in nine dogs; group 2: 45 min occlusion (eight dogs); group 3: 1 h occlusion (five dogs); and group 4: 3 h occlusion (eight dogs). Serial blood samples were drawn for 24 h following the beginning of occlusion and were used to determine total and isoenzyme levels of CPK, and lactic dehydrogenase isoenzymes. All dogs were sacrified 24 h after the beginning of occlusion and were anatomically examined. The extent of anatomical myocardial infarction was determined and compared with the extent of myocardial infarction as estimated from serial serum CPK values. Total serum CPK increased significantly in all groups and was associated with the appearance of CPK-MB isoenzyme and an increase in LDH1,2 (LDH1 greater than LDH2) in most dogs. Total serum CPK increased within an hour after reperfusion and the mean values in groups 2, 3, and 4 were significantly high (P less than 0.05) than serum CPK values in group 1 in the period from 110 min to 4 after occlusion. These data demonstrate that reperfusion after 45 min to 3 h of coronary occlusion results in an earlier appearance of total serum CPK. The anatomical infarction in group 1 averaged 28% +/- 3% (SEM) of the total heart and was significantly larger than infarct size in all groups with reperfusion. In contrast, estimated infarction calculated from total CPK in group 1 was not significantly different from the reperfused groups. Although there was correlation between estimated and anatomical infarction, the data in each group showed that anatomical infarct size could not be accurately estimated from total serum CPK.

Animals↗

PubMed1979

Evaluation of praecordial ST segment mapping as an index of infarct size in patients with acute myocardial infarction.

We evaluated the usefulness and limitations of praecordial ST segment mapping as a clinical means of assessing the size of acute myocardial infarction in 14 patients with anterior myocardial infarction and 13 patients with inferior myocardial infarction. sigma ST, the sum of ST segment elevations, and nST, the number of leads showing ST segment elevation, were obtained from serial electrocardiograms recorded through 39 praecordial leads. The infarct size and period of the evolution of myocardial infarction were estimated respectively from the total creatine kinase (CK) released and the serial changes of the CK releasing rate. sigma ST and nST obtained at the time when the CK release had ceased correlated closely with the total CK released. Peak sigma ST and nST, and values 48 hours after the onset of myocardial infarction, also correlated well with the total CK released; but those on admission or 12 hours after the onset correlated poorly. These results suggest that sigma ST and nST at the end of evolution of myocardial infarction or 48 hours after the onset may be two useful indices for the assessment of infarct size in patients with either anterior or inferior myocardial infarction.

Adult↗