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At least 19 recordsLinked to original sources
PubMed1992

Early diagnosis of the site of infarction and the infarct-related coronary artery in patients with acute inferior myocardial infarction.

We evaluated the relationship between the site of infarction and the infarct-related coronary arteries from electrocardiograms (ECGs) recorded early after the onset of chest pain in patients with an initial acute inferior myocardial infarction (IMI). The subjects were 80 patients (mean age 57 +/- 12 years) with IMI admitted within 6 hours from the onset of chest pain. This was prior to the thrombolytic era. We analyzed the ECGs on admission, at 24 hours and at 4 weeks. All patients underwent left ventriculography and coronary angiography at 4-6 weeks from the onset of the IMI. Left ventricular ejection fraction (EF) and regional area changes were measured. The infarct-related coronary artery was determined by the site of the asynergy. Patients were allocated into 2 groups according to the infarct-related artery, i.e. right (RCA, n = 52) and left circumflex (LCX, n = 28). Parameters measured were ST elevation, amplitude and width of R wave and R/S ratio in leads V1 and V2, and amplitude of U waves in leads V1 to V3. We defined the U wave as a prominent positive U wave (PPU) if it was > 0.5 mm (50 microV) in height. A significantly greater number of patients with PPU showed asynergy in posterolateral segments compared to those without PPU. The EF was significantly lower in patients with PPU than in those without (46 +/- 12% vs 54 +/- 13%, p < 0.05). Patients with PPUs eventually showed ECG evidence of posterior infarction (increased R wave duration and R/S ratio > or = 1 in lead V1 or V2) by 4 weeks compared to those without PPUs. Also a significantly greater number of patients with PPUs developed posterior infarction shown by left ventriculograms than those without PPUs. As to the infarct-related coronary arteries, a significantly greater number of patients with LCX disease showed concomitant posterior infarction than those with RCA disease. Also, a significantly greater number of LCX patients showed PPUs and ST elevations in leads V5 and V6 than those with RCA disease. The sensitivity of PPUs and ST elevations in leads V5 and V6 suggesting LCX disease was 60% and the specificity was 98% with a predictive accuracy of 87%. Therefore, we conclude that PPUs in leads V1-3 and ST elevations in leads V5 and V6 are specific markers for the diagnosis of LCX-related infarction in the setting of evolving IMI.

Adult↗
PubMed1992

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.

Actins↗
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↗
PubMed1992

Modifiers of timing and possible triggers of acute myocardial infarction in the Thrombolysis in Myocardial Infarction Phase II (TIMI II) Study Group.

OBJECTIVES: The aim of this study was to provide insight into the mechanism of acute myocardial infarction by determining the modifiers of timing and possible triggers of onset of infarction. BACKGROUND: A higher frequency of onset of acute myocardial infarction has been reported in the morning with a peak in the 1st 3 h after awakening. This observation suggests that the onset of infarction may be triggered by activity in the morning and at other times of the day. METHODS: The clinical history of the 3,339 patients entered into the Thrombolysis in Myocardial Infarction phase II study was analyzed to determine characteristics predicting a higher frequency of infarction between 6 AM and noon, and onset of infarction during exertion. RESULTS: A higher proportion (34.4%) of infarctions began in the morning (6 AM to noon) compared with other times of the day. Characteristics independently predicting a higher frequency between 6 AM to noon were no beta-adrenergic blocking agent use in the 24 h before infarction, no discomfort other than the index pain in the preceding 48 h, occurrence of the infarction on a weekday and no history of current smoking. In 18.7% of patients, infarction occurred during moderate or marked physical activity. Independent predictors of exertion-related infarction included male gender, no history of current smoking, white race, no use of calcium channel blocking agents or nitrates in the preceding 24 h, the absence of either chest pain at rest in the 3 weeks before infarction or any pain in the preceding 48 h, the absence of new onset angina and the presence of exertional pain in the preceding 3 weeks. Compared with patients whose infarction occurred at rest or during mild activity, those with exertion-related infarction had fewer coronary vessels with > or = 60% stenosis (p = 0.002) and were more likely to have an occluded infarct-related vessel after thrombolytic therapy (p = 0.01). CONCLUSIONS: Further study of the timing and activity at onset of infarction may provide insight into the pathophysiologic mechanisms causing acute myocardial infarction and provide clues to preventive measures.

Analysis of Variance↗
PubMed1992

Effects of amlodipine on myocardial infarction, infarct expansion, and ventricular geometry in the rat.

Infarct expansion remains an important sequela of myocardial infarction. Both angiotensin converting enzyme inhibitors and intravenous nitrates reduce early infarct expansion in humans. This is believed to be caused by the reduction in left ventricular systolic wall stress that results from the arteriolar vasodilatation they produce. Patients are frequently already receiving calcium channel blockers at the time of infarction or these drugs are sometimes administered in the perimyocardial infarction period. The calcium blockers of the dihydropyridine class might be expected to modify infarct expansion. However, their effect on this process has not been studied. We therefore evaluated the effect of early treatment with the calcium blocker amlodipine, a potent arteriolar vasodilator with minimal negative inotropic properties, on chronic myocardial infarction in the rat. Permanent left coronary occlusion was created after pretreatment with amlodipine, 0.25 mg/kg (low dose) or 1.0 mg/kg (high dose), or placebo, intravenously twice a day, and continued for 7 days after infarction. Hearts (n = 50) were perfusion fixed 21 days after infarction and analyzed for infarct extent, scar thickness, left ventricular shape and size, and expansion index. Both doses decreased mean blood pressure (119 +/- 3 to 99 +/- 5 mm Hg low dose, p = 0.004; 110 +/- 5 to 84 +/- 4 mm Hg high dose, p = 0.0003), with reflex tachycardia only after the high dose (heart rate 395 +/- 9 to 434 +/- 11, p = 0.001). Infarct extent was equal in the three groups (39 +/- 2%, 41 +/- 2%, and 41 +/- 3% of left ventricular circumference for control, low, and high doses, respectively). The three groups did not differ significantly with regard to left ventricular cavity cross-sectional area (80 +/- 4, 77 +/- 3, and 87 +/- 3 mm2, control, low, and high doses, respectively; p = 0.07 high dose vs control), mean scar thickness (0.74 +/- 0.06, 0.73 +/- 0.05, and 0.65 +/- 0.06 mm, control, low, and high doses, respectively; p = NS), and expansion index (1.52 +/- 0.10, 1.58 +/- 0.12, and 1.95 +/- 0.19, control, low, and high doses, respectively; p = 0.08 high dose vs control). In the subgroup with larger infarcts (infarct extent greater than 0.39 of left ventricle), the expansion index was higher in the high-dose group (2.37 +/- 0.23 vs 1.64 +/- 0.17 control; p = 0.04). In this model, treatment with amlodipine does not limit infarct extent or reduce early infarct expansion and left ventricular dilatation, even when initiated before infarction.(ABSTRACT TRUNCATED AT 400 WORDS)

Amlodipine↗
PubMed1992

Quantification of antimyosin uptake and infarct size at various stages of myocardial infarction.

We studied with quantitative techniques the clinical efficacy of indium-111 antimyosin at a later stage of myocardial infarction in 18 patients at various stages after infarction. Antimyosin accumulation was detected irrespective of infarct age and size and quantified as an infarct weight with a tomographic technique. Higher intensities in a planar image were observed in anterior Q wave infarct group (36 +/- 5 g) but not in inferior and non-Q wave anterior infarct groups because of the smaller infarct weights (8 +/- 3 g, 13 +/- 6 g, respectively). Infarct area calculated from thallium-201 tomography significantly correlated with left ventricular ejection fraction in both recent (less than 2 weeks) and older (2-week- to 6-month-old) infarct groups (r = -0.969, P less than 0.001; r = -0.860, P less than 0.001, respectively), whereas there was a significant negative correlation between infarct weight and left ventricular ejection fraction in the recent infarct group (r = -0.731, P less than 0.05) but not in the older infarct group. Thus, antimyosin tomography can detect myocardial necrosis with a high sensitivity regardless of infarct age, size, and location. However, the accumulation might be affected by infarct age and correspond to necrotic mass but not necessarily to infarct volume itself at a later stage probably because of the presence of necrosed and scarred tissues in infarcted myocardium.

Aged↗
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↗
PubMedDate not supplied

Prognosis after first myocardial infarction. Comparison of Q-wave and non-Q-wave myocardial infarction in the Framingham Heart Study.

OBJECTIVE: To compare the short- and long-term prognosis following a first Q-wave or non-Q-wave myocardial infarction. DESIGN: Cohort study with a mean follow-up period of 5.1 +/- 4.9 years. SETTING: Population-based. PARTICIPANTS: Framingham (Mass) Heart Study subjects with an initial recognized myocardial infarction during a 17-year period were studied, including 227 men and 136 women with a mean age of 67.2 years. Seventy-seven percent of first infarctions were Q-wave infarctions and 23% were non-Q-wave infarctions. MAIN OUTCOME MEASURES: Reinfarction and death from coronary heart disease. RESULTS: During the follow-up period, subjects with non-Q-wave infarctions had a significantly higher rate of reinfarction than subjects in the Q-wave group (P = .02 for the entire follow-up). The 10-year reinfarction rates were 44.8% vs 27.4%. When analyzed separately by age and sex, differences in reinfarction rates were only noted in men and in those under the age of 65 years. There were no differences in coronary heart disease death rates based on Q-wave status, even when examined separately by age and sex. Multivariate analysis revealed a 1.8-fold higher risk of reinfarction in the non-Q-wave group (95% confidence interval, 1.1 to 3.1), and also demonstrated that baseline hypertension was an independent risk factor for predicting reinfarction (relative risk, 1.8; 95% confidence interval, 1.1 to 3.2). There were no differences in the rates of sudden death or all-cause mortality following the two types of myocardial infarction. Additionally, subjects with a first Q-wave infarction had a higher rate of subsequent congestive heart failure, while those with non-Q-wave infarctions had a significantly higher rate of coronary insufficiency (unstable angina with transient ST-T wave abnormalities). CONCLUSIONS: These results confirm and extend findings from prior studies that have identified patients with first non-Q-wave myocardial infarctions as potentially unstable, with greater subsequent morbidity and similar mortality to their counterparts with Q-wave infarctions.

Adult↗
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↗