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PubMed1991

The clinical presentation of acute myocardial infarction predicts the severity of the lesion in the infarct-related artery.

The purpose of this study was to correlate the clinical presentation of acute myocardial infarction with the patency rate and degree of residual stenosis of the infarct-related artery. One hundred and forty-five patients who underwent angiography after acute myocardial infarction were divided into two groups according to the time of onset of anginal pain prior to infarction. Group A comprised 119 patients, (109 men, 10 women, aged 53 +/- 9 years) who did not experience any symptoms before infarction or with anginal pain of less than 5 days preceding myocardial infarction, and group B 26 patients (all men, aged 54 +/- 12 years) with previous stable angina for greater than or equal to 1 year. Twenty-two days after acute myocardial infarction, 68 of the 145 patients (47%) had a patent infarct-related artery: 64 patients in group A (54%) and four patients in group B (15.4%) (P less than 0.006). Furthermore, 19 patients in group A (16%) and none in group B had less than 70% stenosis in the infarct-related artery (P less than 0.02). The mean residual stenosis in group A was 83.3 +/- 27% whereas in group B it was 98.1 +/- 4% (P less than 0.001). These results indicate that a long-standing history of angina before acute myocardial infarction is often related to a severe pre-existing atheromatous obstruction, which would account for the higher incidence of total coronary occlusion observed in group B. Thus angina of recent onset preceding acute myocardial infarction is associated with a higher patency rate of the infarct-related artery and frequent less than 70% residual lesions.

Adult↗
PubMed1994

Long-term function in the remote region after myocardial infarction: importance of significant coronary stenoses in the non-infarct-related artery.

BACKGROUND: Left ventricular (LV) function is the most important determinant of outcome after a myocardial infarction. Global LV function after a myocardial infarction is affected not only by wall motion in the infarct zone but also by regional function in the contralateral territory. It was hypothesised that the presence of significant stenoses in coronary arteries supplying the contralateral territory might influence the ability of this region to compensate for damaged myocardium after a myocardial infarction. METHODS AND RESULTS: 79 patients treated with thrombolysis for acute myocardial infarction had coronary and ventricular angiograms within 24 h and at a mean follow up of 12 months after myocardial infarction. Wall motion in the contralateral territory was analysed and scored by the centre line method and the change over time was correlated with the presence or absence of significant (> 70%) diameter stenoses in the non-infarct-related artery. Mean (SD) contralateral territory motion worsened, from 0.74 (1.78) to -1.55 (2.06) SD chord (p < 0.001) in 40 patients with stenoses, whereas contralateral territory motion improved from -0.02 (2.4) to 0.63 (2.21) SD chord (p < 0.05) in the 39 patients without coronary stenoses. The same pattern was present whether or not the infarct artery was patent. The global left ventricular ejection fraction at 12 months was also related to contralateral territory motion (r = 0.71, p < 0.001) and to the presence of coronary stenoses (54 (15)% in those with coronary stenoses and 62 (16)% in those without, p < 0.05). CONCLUSION: The results demonstrate that significant stenoses in arteries supplying the non-infarct territory adversely affect global and regional left ventricular function after a transmural infarction. Non-infarct artery anatomy should be considered in intervention strategies to improve left ventricular function after acute myocardial infarction.

Coronary Angiography↗
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↗
PubMed1993

Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction.

BACKGROUND: In the minutes to days after myocardial infarction, endogenous lysis of an occlusive coronary arterial thrombus occurs in most subjects. Compared with those in whom thrombolysis does not occur, those with antegrade flow in the infarct artery have improved left ventricular performance, less left ventricular dilatation, and improved survival. This study was performed to assess intrinsic hemostasis and fibrinolysis in survivors of myocardial infarction with or without antegrade perfusion of the infarct artery. METHODS AND RESULTS: In 105 survivors of infarction (75 men, 30 women; age, 30 to 80 years) not given thrombolytic therapy, coronary angiography revealed a patent (group 1, n = 52) or occluded (group 2, n = 53) infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, plasminogen activator inhibitor activity, cholesterol, triglycerides, and lipoproteins, including lipoprotein(a) (Lp[a]), were measured in blood procured 23 +/- 13 (mean +/- SD) months after infarction. Groups 1 and 2 were similar in age, sex, race, cardioactive medications, infarct artery, extent of coronary artery disease, and left ventricular performance. Of the plasma constituents assayed, the groups were similar except that Lp(a) averaged 18.5 +/- 21.7 mg/dL in group 1 and 49.1 +/- 44.8 mg/dL in group 2 (P < .001). This difference was evident in both Caucasian (n = 65) (P = .009) and African American (n = 40) (P = .01) subjects. CONCLUSIONS: Survivors of myocardial infarction who failed to recanalize the infarct artery have higher plasma Lp(a) concentrations than those with a patent infarct artery. Lp(a) may inhibit intrinsic fibrinolysis.

Coronary Angiography↗
PubMed1994

Open infarct artery, late potentials, and other prognostic factors in patients after acute myocardial infarction in the thrombolytic era. A prospective trial.

BACKGROUND: Successful reperfusion of the infarct-related artery in patients with acute myocardial infarction has been shown to reduce in-hospital as well as 1-year mortality. Besides the thrombolysis-induced myocardial salvage, there is increasing evidence that an open infarct-related artery results in increased electrical stability of the heart and that this effect is at least in part responsible for the favorable long-term outcome of these patients. The exact incidence of arrhythmic events during the first year after myocardial infarction and the predictive value of different risk factors for these complications, however, have not been determined in patients in the thrombolytic era. METHODS AND RESULTS: A total of 173 patients with acute myocardial infarction, 51% treated with thrombolysis, were prospectively entered into the study. At the time of hospital discharge, signal-averaged ECG, Holter monitoring, radionuclide angiography, coronary angiography, and levocardiography were performed in all patients. An open infarct-related artery was documented in 136 patients. The overall incidence of late potentials was 24% (41 patients). By multivariate analysis, an occluded infarct-related artery (P = .04) and the presence of regional wall motion abnormalities (P = .02) were the strongest independent predictors for the development of a late potential. Residual ischemia was treated by either percutaneous transluminal coronary angioplasty or surgery in 86 of 173 patients (50%). Seventy percent of the patients received beta-blocker therapy. During a mean follow-up of 12 +/- 5 months, 7 patients died suddenly or had ventricular fibrillation documented, while only 2 developed sustained monomorphic ventricular tachycardia. Overall 1-year mortality was 4.1%. Multivariate analysis revealed only an occluded infarct-related artery as an independent predictor of arrhythmic complications (P = .017). CONCLUSIONS: In patients with acute myocardial infarction treated according to contemporary therapeutic guidelines, with a large proportion of individuals undergoing coronary artery revascularization, a low incidence of arrhythmic events, particularly of ventricular tachycardia, was observed in the first year after the index infarction. The presence or absence of an open infarct-related artery was the strongest independent predictor of these events, whereas other traditional risk factors, such as late potentials, were less helpful in identifying patients prone to sudden death. These findings emphasize the importance of the open artery hypothesis in patients recovering from acute myocardial infarction.

Adult↗
PubMed1995

Aspirin enhances the benefits of late reperfusion on infarct shape. A possible mechanism of the beneficial effects of aspirin on survival after acute myocardial infarction.

BACKGROUND: The time window of the benefits of late reperfusion on infarct shape is limited. In rats, these benefits diminish in a wave front over time, with minimal benefits when reperfusion follows 16 hours of coronary occlusion. The mechanism of the benefits of aspirin on survival after acute myocardial infarction is unknown. The purpose of this study was to test the ability of aspirin to enhance the benefits of late coronary artery reperfusion on infarct shape and to examine the mechanism of the benefits of aspirin on infarct shape. METHODS AND RESULTS: Rats were entered into two different protocols, the morphometric and the histological protocols. In the morphometric protocol, rats were randomized into two groups: the aspirin group, in which rats underwent left coronary artery occlusion followed by treatment with aspirin (12 mg/kg i.v.), and the control group, in which rats underwent left coronary artery occlusion followed by treatment with placebo. Rats in both groups were reperfused 8 hours after coronary occlusion. Rats in the aspirin group received aspirin in the drinking water (12 +/- 2 mg/kg daily). Morphometric analysis was performed 2 weeks after acute myocardial infarction. In the histological protocol, rats underwent the same randomization, coronary occlusion, and reperfusion protocols. Hearts were removed 24 hours after coronary occlusion, and microvessels were assessed for patency. Infarct size expressed as a percent of circumference was similar in the aspirin and placebo treatment groups (28 +/- 2% versus 33 +/- 3%, P = NS). Septal thickness was also similar in both groups (1.8 +/- 0.1 versus 2.1 +/- 0.1 mm, P = NS for aspirin versus placebo). The aspirin-treated group had thicker infarcts compared with the placebo-treated group (0.8 +/- 0.1 versus 0.5 +/- 0.1 mm, P < .05) and less expanded infarcts (expansion index, 1.2 +/- 0.1 versus 2.0 +/- 0.2, P < .05). Aspirin was associated with increased patency of the microvessels in the infarcted area compared with the placebo group (96% versus 64% of microvessels patent, P < .001). CONCLUSIONS: Aspirin enhances the benefit of late coronary artery reperfusion on infarct shape after 8 hours of coronary occlusion. The benefits of aspirin on infarct shape after late reperfusion are related to increased patency of the microvessels in the infarcted area.

Animals↗
PubMed2003

Subcortical white matter infarcts: comparison of superficial perforating artery and internal border-zone infarcts using diffusion-weighted magnetic resonance imaging.

BACKGROUND AND PURPOSE: Because of difficulty in distinguishing between superficial perforator (SP) and internal border-zone (IB) infarcts, some studies lumped SP and IB infarcts together as so-called subcortical white matter infarcts, which might complicate the classification of infarct type and its pathogenesis. Using diffusion-weighted MRI (DWI), we made comparative analyses of clinical and neuroradiological characteristics between IB and SP infarcts to clarify the difference in underlying pathogenesis. METHODS: We selected SP and IB infarcts on DWI using templates for the identification of subcortical vascular territories. Sex, age, neurological symptoms, clinical course, risk factors, concomitant cortical spotty lesions, and degree and location of arterial occlusive disease were compared between the 2 groups. RESULTS: Among the 720 consecutive patients, 54 and 29 patients met the criteria for SP and IB infarcts, respectively. The SP group had lower initial National Institutes of Health Stroke Scale scores (2.4+/-2.1 versus 4.4+/-3.1; P=0.001), favorable clinical outcomes (P=0.001), and more frequent potential cardioembolic sources (14.8% versus 0%; P=0.046) than the IB group. Cortical spotty lesions were more frequently accompanied by SP than IB infarcts (72.2% versus 24.1%; P<0.001). IB infarcts were larger (24.2+/-10.2 versus 11.4+/-8.5 mm; P<0.001), appeared in a chainlike fashion (72.4% versus 33.3%; P=0.001), and had a higher degree of stenosis or occlusion (86.2% versus 46.3%; P=0.001) compared with SP infarcts. CONCLUSIONS: Our present study suggests that embolic pathogenesis makes a greater contribution to SP infarcts than IB infarcts. This finding may explain the difference in clinical and neuroradiological characteristics between the 2 groups.

Acute Disease↗
PubMed2006

Large subcortical infarcts: clinical features, risk factors, and long-term prognosis compared with cortical and small deep infarcts.

BACKGROUND AND PURPOSE: In this study we compared risk factors, clinical features, and stroke recurrence in a large series of patients with large subcortical, cortical, or small deep infarcts. METHODS: Patients with a transient or minor ischemic attack (modified Rankin Scale grade of < or =3) who had a single relevant supratentorial infarct of presumed noncardioembolic origin on CT were classified as suffering from a large subcortical (n=120), small deep (n=324), or cortical (n=211) infarct. Mean follow-up was 8 years. Rates of recurrent stroke were compared with Cox regression. RESULTS: The clinical deficits caused by large subcortical infarcts resembled either those of a cortical or those of a small deep infarct. Risk factor profiles were similar in the 3 groups. The rate of recurrent stroke in patients with a large subcortical infarct (25/120; 21%) did not differ from that of patients with a cortical infarct (46/211; 22%) or with a small deep infarct (60/324; 19%). After adjustment for age, sex, and vascular risk factors, hazard ratios for recurrent stroke of large subcortical and cortical infarcts were 1.05 (95% CI, 0.65 to 1.70) and 1.17 (95% CI, 0.79 to 1.73), respectively, compared with small deep infarcts. CONCLUSIONS: Clinical features, risk factor profiles, and stroke recurrence rate in patients with a large subcortical infarct only differ slightly from those in patients with small deep or cortical infarcts.

Adult↗
PubMed2006

Evaluation of electrocardiographic algorithms in the assessment of the infarct-related artery in acute myocardial infarction.

OBJECTIVES: In acute myocardial infarction, it is of great value to identify the infarct-related artery and the site of occlusion in a coronary artery (proximal versus distal). This study assessed the diagnostic value of two previously published electrocardiographic algorithms to identify the infarct-related artery and the site of occlusion in anterior and inferior acute myocardial infarction. METHODS AND RESULTS: We studied retrospectively a group of 88 patients with a first myocardial infarction. We determined the infarct-related artery using the electrocardiographic algorithms on the electrocardiogram at the time of admission and compared these results with the angiographically determined infarct-related artery. The best electrocardiographic algorithm could determine the infarct-related artery in an inferior myocardial infarction as the left circumflex coronary artery and as the proximal and distal right coronary artery with a sensitivity of 63%, 67% and 80%, respectively, and a specificity of 100%, 82% and 69%, respectively. One algorithm was unable to diagnose a left circumflex coronary artery occlusion. In an anterior myocardial infarction the best electrocardiographic algorithm could determine the infarct-related artery as the proximal and distal left anterior descending coronary artery with a sensitivity of 85% and 80%, respectively, and with a specificity of 77% and 82%, respectively. CONCLUSION: In acute myocardial infarction the use of electrocardiographic algorithms is helpful to predict the site of occlusion and can play a crucial role in the care of patients.

Aged↗
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↗
PubMed1998

Expression of the alpha 1 and alpha 2 chains of type IV collagen in the infarct zone of rat myocardial infarction.

Healing processes affect ventricular remodeling, an important prognostic factor in acute myocardial infarction (AMI). Type IV collagen, a major component of the basement membrane, has been demonstrated to appear in the infarct zone. Six type IV alpha chains, alpha 1 to alpha 6 [alpha 1(IV) to alpha 6(IV)], have been identified. We examined the expression of the alpha 1(IV), alpha 2(IV), alpha 3(IV) and alpha 5(IV) in experimental rat AMI induced by permanent ligation of the left coronary artery in male Sprague-Dawley rats. Neonatal cardiac fibroblasts cultured to reach confluency were also used to examine the hypoxic induction of the expression of these chains. Northern blotting, in situ hybridization, and immunohistochemical staining were employed to examine the alpha chain expression. With the in situ hybridization, alpha 1(IV) and alpha 2(IV) mRNA signals were observed in spindle-shaped mesenchymal cells in the intercellular spaces, in the vascular endothelial cells and in some myocytes in the normal myocardium. Signals for both alpha 1(IV) and alpha 2(IV) mRNA appeared in the spindle-shaped mesenchymal cells located between the surviving myocytes in the infarct peripheral zone at 24 h after the ligation. These signals extended into the central zone and reached the center point of the infarct 5 days after the ligation. Neither alpha 3(IV) nor alpha 5(IV) mRNA signals were observed in the infarct zone. Northern blotting demonstrated increased expressions of alpha 1(IV) and alpha 2(IV) mRNA in the infarct zone compared to the sham-operated hearts. The expression of alpha 5(IV) mRNA was weak in the sham-operated hearts but was not detected in the infarct zone. alpha 3(IV) mRNA was not expressed in the infarct zones or sham-operated hearts. In the cultured cardiac fibroblasts, a hypoxic induction of the expression of both alpha 1(IV) and alpha 2(IV) mRNA was demonstrated by Northern hybridization. Immunohistochemistry revealed alpha 1(IV) and alpha 2(IV) staining in the infarct lesion. The findings demonstrate that among the type IV collagen alpha chains examined, alpha 1(IV) and alpha 2(IV) produced by mesenchymal cells appeared in the infarct zone, suggesting that type IV collagen composed by alpha 1 and alpha 2 chains contributes to the pathological course of myocardial infarction.

Animals↗
PubMed1985

Right ventricular infarction with shock but without significant left ventricular infarction: a new clinical syndrome.

Right ventricular infarction has been described as concurrent with infarction involving the inferior (posterior) aspect of the left ventricular free wall and adjacent interventricular septum. Patients with right ventricular infarction typically show the ECG changes of inferior infarction in leads II, III, and aVF. This report describes two patients with right ventricular infarction but without changes in the QRS complex of the ECG, indicating an inferior infarct of the left ventricle. An autopsy-proven infarct of the right ventricular free wall with neither QRS nor other clinical evidence of left ventricular involvement was responsible for cardiogenic shock and death in one patient. This observation led to a review of a computerized data bank containing records of patients who had undergone cardiac catheterization to determine if there were other patients with clinical criteria suggesting right ventricular infarction without QRS changes of left ventricular infarction. One of the 167 patients with a history of a myocardial infarction also met the following clinical criteria: (1) transiently elevated total creatine kinase and creatine kinase myocardial band; (2) diffuse ST segment elevation without QRS changes indicative of left ventricular infarction on the ECG; (3) normal left ventricular function; (4) hemodynamic evidence of right ventricular dysfunction; and (5) cardiogenic shock.

Aged↗
PubMed1987

Five-year mortality rate in relation to enzyme-estimated infarct size in acute myocardial infarction.

In 727 patients with acute myocardial infarction, different enzyme variables reflecting infarct size were related to the 5-year mortality rate. The maximum activity of serum heat-stable lactate dehydrogenase (LD), analyzed every 12 hours for 48 to 108 hours, was significantly associated with the 5-year mortality rate when patients with a first myocardial infarction were evaluated (p less than 0.001), and similarly (p less than 0.001) when patients with a previous myocardial infarction were included in the analyses. Very similar results were found when the maximum activity of aspartate aminotransferase (ASAT) analyzed once daily for 3 days was related to the mortality rate over 5 years, whereas the maximum activity of creatine kinase (CK) and CK subunit B analyzed every 6 hours for 48 hours in a subset of patients did not predict the outcome to the same extent. The results from LD and ASAT analyses clearly indicated that the association between infarct size and 5-year mortality rate was caused by the much higher mortality rate in patients with larger infarcts during the first year after onset of infarction, whereas after the first year, incidence of death appeared to be independent of the original infarct size. Thus we conclude that although a highly significant relationship between infarct size and overall 5-year survival was found, the mortality rate seemed to be higher in patients with larger infarcts, particularly during the first year after infarction.

Adult↗
PubMed1988

Relationship of QRS scoring system to enzymatic and pathologic infarct size: the role of infarct location.

A method for estimating infarct size from 12-lead ECGs has been developed but not extensively validated. To assess its accuracy, ECG scores from 62 patients admitted to the coronary care unit at Barnes Hospital were compared to infarct size calculated from plasma MB creatine kinase (MB-CK) activity. A second cohort of 29 patients enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS) was evaluated as a test set and to provide pathologic correlates. Patients with conduction system disease, ventricular hypertrophy, or multiple infarctions were excluded, as were those in the Barnes group who had undergone thrombolytic therapy. ECGs obtained early (days 3 to 7 in the Barnes group and day 3 in the MILIS group) or late (days 8 to 14 in the Barnes group) were scored manually and by computer. QRS scores from early ECGs of patients with anterior infarctions correlated closely with MB-CK estimates of infarct size (r = 0.71 [Barnes] and 0.85 [MILIS] and with anatomic data (r = 0.78). Enzymatic and pathologic infarct size also correlated well (r = 0.85). Correcting for body surface area by means of total CK-derived infarct size or use of QRS scores from late ECGs did not alter the correlation coefficients. Among patients with inferior infarctions QRS scores corresponded poorly with MB-CK infarct size (r = 0.28 [Barnes] and r = -0.42 [MILIS]) and pathologic infarct size (r = -0.20), despite a significant relationship between pathologic and MB-CK estimates (r = 0.62).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of metoprolol on early infarct expansion after acute myocardial infarction.

The effects of metoprolol on early infarct expansion after acute myocardial infarction were studied in rats (n = 54) that underwent either left coronary artery ligation (MI) or sham operation. Immediately after surgery, the rats received either metoprolol (M) by mouth, which had been dissolved in drinking water, for 72 hours supplemented with three intraperitoneal doses over the first 24 hours or no treatment (H2O). Three days after the initial surgery, hemodynamic measurements were made before and after volume loading. The rats were killed, the hearts were removed, and passive pressure-volume curves were obtained. The hearts were then fixed at a constant pressure and analyzed morphometrically. Infarct size was nonsignificantly lower in the metoprolol-treated group compared with the untreated group (38% +/- 5% MI-M vs 48% +/- 3% MI-H2O, p = 0.10) Compared with infarcted untreated rats, infarcted metoprolol-treated rats had a lower heart rate (322 +/- 13 beats/min MI-M vs 452 +/- 19 beats/min MI-H2O, p < 0.001), lower left ventricular systolic pressure (63 +/- 4 mm Hg MI-M vs 90 +/- 6 mm Hg MI-H2O, p = 0.004), and lower +dp/dt (1340 +/- 169 mm Hg/sec MI-M vs 2872 +/- 273 mm Hg/sec MI-H2O, p < 0.001), but left ventricular end-diastolic pressure and cardiac index did not differ between the two groups. Left ventricular weight corrected for body weight was higher in infarcted rats treated with metoprolol compared with infarcted untreated rats (2.76 +/- 0.07 gm/kg MI-M vs 2.41 +/- 0.09 gm/kg MI-H2O, p < 0.05). The initial slope of the pressure-volume relationship Ki, an index of operative volume stiffness, was lower in infarcted rats treated with metoprolol compared with infarcted untreated rats (p = 0.03). There were, however, no significant differences in the expansion index, thinning ratio, or left ventricular volume between the two infarcted groups. Thus metoprolol therapy begun in the immediate postinfarction period promotes an increase in left ventricular weight and reduces operative volume stiffness but has no significant effect on indexes of early infarct expansion.

Animals↗
PubMed1988

Ventricular function and infarct size: the Western Washington Intravenous Streptokinase in Myocardial Infarction Trial.

The Western Washington Intravenous Streptokinase in Acute Myocardial Infarction Trial randomized 368 patients with symptoms and signs of acute myocardial infarction of less than 6 h duration to either conventional care or 1.5 million units of intravenous streptokinase. The mean time to randomization was 209 min and 52% of patients were randomized within 3 h of symptom onset. Quantitative, tomographic thallium-201 infarct size and radionuclide ejection fraction were measured at 8.2 +/- 7.5 weeks in 207 survivors who lived within a 100 mile radius of a centralized laboratory. Overall, infarct size as a percent of the left ventricle was 19 +/- 13% for control subjects and 15 +/- 13% for treatment patients (p = 0.03). For anterior infarction in patients entered within 3 h of symptom onset, infarct size was 28 +/- 13% in the control group versus 19 +/- 15% for the treatment group (p = 0.09). Left ventricular ejection fraction was 47 +/- 15% in the control versus 51 +/- 15% in the treatment group (p = 0.08). For anterior infarction of less than 3 h duration, the ejection fraction was 38 +/- 16% in the control versus 48 +/- 20% in the treatment group (p = 0.13). By statistical analysis incorporating the nonsurvivors, p values for all of these variables were less than or equal to 0.08. There was no benefit for patients with inferior infarction or for anterior infarction of greater than 3 h duration. It is concluded that intravenous streptokinase, when given within 3 h of symptom onset to patients with anterior infarction, reduces infarct size and improves ventricular function.

Clinical Trials as Topic↗