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PubMed1995

Direct Comparison of Aspirin Plus Hirudin, Aspirin Plus Heparin, and Aspirin Alone Among 12,000 Patients with Acute Myocardial Infarction Not Receiving Thrombolysis: Rationale and Design of the First American Study of Infarct Survival (ASIS-1).

While antithrombotic therapy of acute myocardial infarction is clearly beneficial, substantial controversy exists regarding the optimal regimen. In particular, while aspirin alone has proven highly effective in reducing rates of reinfarction, stroke, and death following acute coronary occlusion, heparin has not clearly been shown to have additional benefit when added to aspirin but is associated with increased rates of hemorrhagic stroke and major bleeding. At the same time, available data for newer specific thrombin inhibitors such as hirudin suggest greater benefits than aspirin alone or aspirin plus heparin in terms of maintaining coronary flow, but possibly higher risks of hemorrhagic stroke and major bleeding. Since no completed or ongoing large-scale clinical trial has directly compared aspirin plus hirudin, aspirin plus heparin, and aspirin alone, it is not currently possible to decide which of these three antithrombotic regimens provides the optimal bmefit-to-risk ratio. The First American Study of Infarct Survival (ASIS-1) is directly comparing aspirin alone, aspirin plus heparin, and aspirin plus hirudin among 12,000 patients presenting with signs and symptoms of acute myocardial infarction who are not felt by their responsible physicians to be appropriate candidates for thrombolytic therapy. Such patients comprise almost two thirds of all U.S. subjects presenting with acute myocardial infarction and are a group at substantial risk of death, reinfarction, and stroke. Thus, the ASIS-I trial will provide importantly relevant data regarding the optimal antithrombotic regimen for the majority of patients presenting with acute myocardial infarction. In this manuscript we provide the rationale and design for the First American Study of Infarct Survival (ASIS-1), a randomized, double-blind, placebo-controlled trial directly comparing aspirin alone, aspirin plus intravenous heparin, and aspirin plus intravenous hirudin in the treatment of acute myocardial infarction patients not receiving thrombolytic therapy.

Journal Article↗
PubMed2001

Differential effect of preconditioning on post-ischaemic myocardial performance in the absence of substantial infarction and in extensively infarcted rat hearts.

OBJECTIVES: There is controversy concerning the beneficial effects of ischaemic preconditioning during short periods of ischaemia (stunning). The aim of the study was to investigate post-ischaemic myocardial performance after various periods of ischaemia in both non-preconditioned and preconditioned hearts and to compare these results with infarct volume estimation. METHODS: Isolated perfused rat hearts were subjected to various periods of sustained ischaemia (15, 20, 30, and 45 min). Haemodynamic parameters, infarct size and lactate dehydrogenase (LDH) leakage were recorded in both preconditioned and non-preconditioned hearts. RESULTS: After 15 min of ischaemia, preconditioned hearts revealed significantly lower developed pressure than non-preconditioned hearts (80+/-4.1 vs. 95+/-0.3%, P=0.02). In the 20 min ischaemia group, preconditioning resulted in non-significantly lower developed pressure (76+/-3.1% in preconditioned hearts vs. 87+/-5.3% in non-preconditioned hearts, P=0.11). In these groups infarct volume was small and not different between non-preconditioned and preconditioned hearts. After 30 min of ischaemia, preconditioning significantly improved developed pressure (66+/-3.1% in preconditioned and 44+/-5% in non-preconditioned hearts, P=0.002). LDH leakage was significantly higher in non-preconditioned hearts compared with preconditioned hearts (16+/-2.3 vs. 9.0+/-1.3, P=0.04), whereas infarct volume was not (12.5+/-0.8 and 9.8+/-1.5, respectively, P=0.1). Non-preconditioned hearts of this group, subjected to inotropic stimulation at the end of reperfusion, responded poorly. Significantly higher developed pressure was attained by preconditioned hearts (150+/-3.1 vs. 123+/-7.5%, P=0.01). After 45 min of ischaemia, preconditioning resulted in 69% limitation of infarct volume (P<0.0001) and 53% reduction in LDH release (P=0.009). Developed pressure was 57+/-8.5% in preconditioned hearts and 32+/-4.5% in non-preconditioned hearts (P=0.02). CONCLUSIONS: When ischaemic insult results in minimally lethal injuries, preconditioned hearts do not have the advantage of not being prone to stunning rather than non-preconditioned. If ischaemic insult is potentially able to produce extensive infarction, improvement in post-ischaemic myocardial function is mainly due to infarct size limitation evoked by preconditioning.

Animals↗
PubMed2005

Enzyme estimates of infarct size correlate with functional and clinical outcomes in the setting of ST-segment elevation myocardial infarction.

BACKGROUND: Cardiac biomarkers are routinely obtained in the setting of suspected myocardial ischemia and infarction. Evidence suggests these markers may correlate with functional and clinical outcomes, but the strength of this correlation is unclear. The relationship between enzyme measures of myocardial necrosis and left ventricular performance and adverse clinical outcomes were explored. METHODS: Creatine kinase (CK) and CK-MB data were analyzed, as were left ventricular ejection fraction (LVEF) by angiogram, and infarct size by single-photon emission computed tomography (SPECT) imaging in patients in 2 trials: Prompt Reperfusion In Myocardial-infarction Evolution (PRIME), and Efegatran and Streptokinase to Canalize Arteries Like Accelerated Tissue plasminogen activator (ESCALAT). Both trials evaluated efegatran combined with thrombolysis for treating acute ST-segment elevation myocardial infarction (STEMI). RESULTS: Peak CK and CK area-under-the-curve (AUC) correlated significantly with SPECT-determined infarct size 5 to 10 days after enrollment. Peak CK had a statistically significant correlation with LVEF, but CK-AUC and LVEF correlation were less robust. Statistically significant correlations exist between SPECT-determined infarct size and peak CK-MB and CK-MB AUC. However, there was no correlation with LVEF for peak CK-MB and CK-MB AUC. The combined outcome of congestive heart failure and death were significantly associated with CK AUC, CK-MB AUC, peak CK, and peak CK-MB measurements. CONCLUSION: Peak CK and CK-MB values and AUC calculations have significant correlation with functional outcomes (LVEF- and SPECT-determined infarct size) and death or CHF outcomes in the setting of STEMI. Cardiac biomarkers provide prognostic information and may serve as valid endpoint measurements for phase II clinical trials.

Journal Article↗
PubMed2002

A modified infarct exclusion technique for a post-infarction ventricular septal defect.

BACKGROUND: Operative mortality for a post-infarction ventricular septal defect (VSD) remains high. The infarct exclusion technique has been producing a favorable outcome for repairing this serious defect. However, there is the technical weakness, namely running suture along the base of the necrotic septum. We sutured a pericardial patch using multiple interrupted mattress sutures in such a manner as to exclude the infarct and VSD. METHODS: Over the past seven years, nine consecutive patients with a post-infarction VSD underwent an early repair in the same manner. The VSD was anterior in eight patients and posterior in one. We sutured a xenopericardial patch to the healthy myocardium around the infarct using interrupted mattress sutures instead of running sutures as the infarct exclusion technique. In addition, on the postero-inferior margin of the patch, one or two mattress sutures passing through the full thickness of the anterior papillary muscle were used. RESULTS: Only one patient died of pneumonia 50 days after surgery. The other eight patients were followed up and were functionally classified as NYHA class I or II. CONCLUSIONS: These findings suggest that our modified infarct exclusion technique using multiple mattress sutures is an effective alternative surgical technique.

Aged↗
PubMed2003

A randomized, double-blinded, placebo-controlled, dose-ranging study measuring the effect of an adenosine agonist on infarct size reduction in patients undergoing primary percutaneous transluminal coronary angioplasty: the ADMIRE (AmP579 Delivery for Myocardial Infarction REduction) study.

BACKGROUND: Evidence suggests that myocardial ischemic preconditioning and reperfusion injury may be mediated by adenosine A1 and A2 receptors. AMP579 is a mixed adenosine agonist with both A1 and A2 effects. In animal models of acute myocardial infarction (MI), AMP579 reduced infarct size at serum levels of 15 to 24 ng/mL. METHODS: The AMP579 Delivery for Myocardial Infarction REduction study evaluated AMP579 in a double-blind, multicenter, placebo-controlled trial of 311 patients undergoing primary percutaneous transluminal coronary angioplasty (PTCA) after acute ST-segment elevation MI. Patients were randomly assigned to placebo or to 3 different doses of AMP579 continuously infused over 6 hours. The primary end point was final MI size measured by technetium Tc-99m sestamibi scanning at 120 to 216 hours after PTCA. Secondary end points included myocardial salvage and salvage index at the same time interval (in a subset of patients who underwent baseline technetium Tc-99m sestamibi scan), left ventricular ejection fraction and heart failure at 4 to 6 weeks, duration of hospitalization, and cardiac events at 4 weeks and 6 months. RESULTS: Final infarct size did not differ among the placebo group and the active treatment groups for either anterior MI or nonanterior MI. In patients with anterior MI, median myocardial salvage was increasingly higher in the groups receiving ascending dosages of AMP579 plus PTCA. Serum levels approaching levels shown to reduce infarct size in animal models were achieved only in the 60-mcg/kg treatment group. CONCLUSION: AMP579 was safe at the doses tested, but it did not reduce infarct size. There was a trend toward greater myocardial salvage in treated patients with anterior MI.

Adenosine↗
PubMed2005

Evaluation of serum S100B as a surrogate marker for long-term outcome and infarct volume in acute middle cerebral artery infarction.

BACKGROUND: An easily accessible and valid surrogate marker for interventional stroke trials is needed. OBJECTIVE: To investigate the usefulness of various S100B serum measures to predict long-term outcome and infarct volume in patients with acute stroke. DESIGN: Inception cohort study. SETTING: Tertiary care university hospital. PATIENTS: Thirty-nine patients (mean +/- SD age, 69.1 +/- 11.5 years) with acute nonlacunar middle cerebral artery infarction presenting less than 6 hours after symptom onset. MAIN OUTCOME MEASURES: Functional outcome 6 months after stroke (modified Rankin scale score) and final infarct volume on day 7 by means of standardized volumetry of brain images. Serum S100B level was determined at hospital admission and 24, 48, 72, 96, 120, and 144 hours after symptom onset. RESULTS: Single S100B measures obtained 48 and 72 hours after stroke onset demonstrated the highest Spearman rank correlations with modified Rankin scale scores (rho = 0.68 and rho = 0.67, respectively; P<.001) and infarct volume (rho = 0.95 and rho = 0.94, respectively; P<.001). A 48-hour S100B value of 0.37 microg/L or less revealed a sensitivity of 0.87 and a specificity of 0.78 in predicting an independent functional outcome. In a multivariate model, S100B emerged as an outcome predictor that was independent of age, sex, stroke severity, etiology, lesion side, and risk factors. CONCLUSIONS: Single S100B values obtained 48 and 72 hours after stroke onset provide the highest predictive values with respect to functional outcome and infarct volume in nonlacunar middle cerebral artery infarction. More complex measures of the S100B kinetic (ie, area under the curve or peak value) were not superior. Therefore, these single S100B measures appear to be useful surrogate end points in acute interventional stroke trials.

Acute Disease↗
PubMed2003

Patients with large myocardial infarction gain a greater improvement in exercise capacity after exercise training than those with small to medium infarction.

BACKGROUND: It remains unclear whether patients with large-size myocardial infarction (MI) achieve the same benefit from exercise training as do those with small- to medium-size MI. HYPOTHESIS: This study was designed to determine the magnitude and mechanisms underlying improvement in exercise capacity in patients with large-size MI after cardiac rehabilitation. METHODS: In all, 296 patients who participated in a cardiac rehabilitation program after acute MI were divided into two groups according to the peak serum creatine phosphokinase (CPK) level: the group with large infarction (Group 1) (> or = 5000 U/l peak CPK, 64 patients) and the group with less extensive infarction (Group 2) (< 5000 U/I, 232 patients). Exercise capacity was assessed before and after a 3-month cardiac rehabilitation program that included exercise training. RESULTS: Before exercise training, both the peak work rate (p < 0.05) and peak oxygen uptake (VO2) (p < 0.01) were significantly lower in Group 1 than in Group 2. After exercise training, the changes in peak work rate and peak VO2 were significantly greater in Group 1 than in Group 2 (both p < 0.01). The infarction size measured by the peak CPK level correlated significantly with both the baseline exercise capacity and its improvement after exercise training, although these correlations were insignificant in a multivariate analysis. In the multivariate analysis, the improvement in exercise capacity is determined by age and baseline exercise capacity, which is determined by the duration of inactivity, minute ventilation (VE)/VCO2 slope and left ventricular end-diastolic pressure. CONCLUSIONS: Compared with patients with small- to medium-size myocardial infarction, patients with large infarction gain a greater improvement in exercise capacity after exercise training due to reversal of physical deconditioning and improvement in congestive heart failure.

Adaptation, Physiological↗
PubMed1994

Management of myocardial infarction patients with an occluded infarct-related artery.

Based on the foregoing data it is not unreasonable to hypothesize that restoration of flow in the infarct-related artery at a later date might decrease mortality. If that is the case, then a strong argument can be made for coronary angiography in patients surviving acute myocardial infarction. Of course, the ideal way to investigate this problem is to perform a large-scale prospective trial in which patients who have an occluded infarct-related artery are randomized to a revascularization procedure or continued on nonsurgical therapy. The specific management strategy for the patient with an occluded infarct-related artery after myocardial infarction depends on several features that the patient exhibits. For example, the presence or absence of LV dilatation, arrhythmias, recurrent ischemia, or clinical heart failure may dictate one form of therapy or another. There is no generic postinfarction patient with an infarct-related artery occlusion. Choices of drugs to use in these patients include the vasodilators, such as nitrates and ACE inhibitors, as well as aspirin and beta blockers. The use of calcium antagonists, chronic anticoagulants, and antiarrhythmics should have specific indications. Antithrombin agents are still experimental.

Adrenergic beta-Antagonists↗
PubMed1997

Neuronal nitric oxide synthase mutant mice show smaller infarcts and attenuated apparent diffusion coefficient changes in the peri-infarct zone during focal cerebral ischemia.

Diffusion-weighted MRI at 2 T was used to monitor and assess tissue damage after permanent middle cerebral artery occlusion (MCAO) in wild-type (WT) and mice deficient in nitric oxide synthase gene expression (nNOS-). The ischemic lesion was evaluated 3 h after occlusion and subdivided into the lesion core and peri-infarct zone based on the magnitude of the apparent diffusion coefficient (ADC) change. Infarct volume, measured by using histochemical staining 24 h after MCA occlusion, correlated best with MRI infarct volume as assessed by an ADC threshold of 25% decrease from baseline at 3 h. For ADC thresholds of greater than 25% decrease, lesion size was not significantly different in nNOS- and WT mice. However, brain tissue showing ADC decreases of 10-25% was significantly smaller in the ipsilateral hemisphere of mutants (27 +/- 2% and 21 +/- 2% in WT and nNOS-, respectively; P < 0.05). These findings occurred independently of infarct volume and are consistent with a smaller peri-infarct zone in nNOS- mice. We postulate that the smaller peri-infarct zone is a reflection of less severe metabolic disturbance after ischemia in nNOS- mice, possibly related to diminished production of nitric oxide (NO) or a related product. We conclude that magnetic resonance techniques previously used to assess ischemic damage in larger animals can be extended to the mouse, raising the possibility that the molecular mechanisms leading to ischemic damage can be examined by using genetically engineered mice.

Animals↗
PubMed1995

Computer-assisted mapping of infarcted and viable regions of gross cardiac sections following experimental myocardial infarction.

We have developed a computer-assisted method that creates digital maps of the viable and infarcted regions of tetrazolium-stained gross cardiac sections. Here we describe and test the method, using a canine occlusion-reperfusion infarction model. Quantitative image analysis showed that the method accurately recorded differences between infarcted and viable regions at a spatial resolution of 5-20 pixels per mm2. Microscopic analysis of tissue samples taken from the sections showed that the maps were accurate. In 15 of 15 cases the histology of the samples matched that predicted by the maps. A comparison of infarct area measurements derived from the maps showed that the method was reproducible. The average intraoperator standard deviation was +/- 8% of a slice's infarcted area and the average interoperator standard deviation was +/- 20%. We conclude that the method creates accurate, detailed, and reproducible maps of the infarcted and viable regions of tetrazolium-stained cardiac sections.

Animals↗
PubMed2003

Additional ST-segment elevation during thrombolytic therapy in patients with acute ST-elevation myocardial infarction: impact on myocardial salvage and final infarct size.

The aim of the study was to investigate the clinical significance of additional ST-segment elevation that occurs during thrombolytic therapy. Therefore, we classified 153 patients with a first acute myocardial infarction (MI) into two groups: Group A, 55 patients with additional ST-segment elevation > or = 1 mm above the initial ST elevation during thrombolytic therapy and Group B, 98 patients without this electrocardiographic pattern. Among the patients with anterior MI, Group A (n = 33) had no reduction from ST-predicted to final QRS-estimated infarct size (+12% versus -27%; p = 0.0005) and a larger final infarct size (QRS-score: 18% versus 12%; p = 0.0002) than Group B (n = 41). Among the patients with inferior MI, Group A (n = 22) had a smaller reduction from ST-predicted to final QRS-estimated infarct size (-30% versus -53%; p = 0.03) and a larger final infarct size (QRS-score: 15% versus 9%; p = 0.03) than Group B (n = 57). The area under the curve (AUC) of CK and CK-MB was higher in patients from Group A compared with those from Group B (anterior MI: AUC-CK: 22,048 versus 19,490 U.h.l-1; p = 0.07; AUC-MB: 2227 versus 2016 U.h.l-1; p = 0.11; inferior MI: AUC-CK: 17,206 versus 11,004 U.h.l-1; p = 0.01; AUC-MB: 2193 versus 1046 U.h.l-1; p = 0.007). Both global left ventricular function and ST-segment elevation resolution were significantly better in Group B. Two and three vessel disease was observed more frequently in Group A. Additional ST-segment elevation during thrombolytic therapy suggests reduced myocardial salvage by thrombolytic therapy and thus may result in larger final infarct size.

Aged↗
PubMed1993

Autonomic correlates of late infarct artery patency after first myocardial infarction.

Occlusion of the infarct-related artery has recently been associated with an increased risk of sudden death, particularly in patients with poor left ventricular function. Depressed heart rate variability (HRV) also identifies postinfarction patients at an increased risk of sudden death. The correlation between infarct artery patency, left ventricular function, and HRV was therefore examined in 186 survivors of a first myocardial infarction. Predischarge coronary angiography and Holter monitoring were carried out in 186 patients with a first acute myocardial infarction. Coronary angiography was performed because of abnormal predischarge exercise test findings. Mean age (56 +/- 9 years) and the proportions of type and site of infarction did not differ between patients with occluded or patent arteries or between patients who did or did not undergo coronary angiography. The mean left ventricular ejection fraction (EF) was 55 +/- 15% in patients with patent and 49 +/- 14% in those with occluded infarct arteries (p < 0.001), and the EF was < 40% in 17% and 28% of the respective groups (p < 0.05). HRV was < 20 U in 7 (18%) of the 39 patients with an EF < 40% but in only 7 (5%) of the 147 patients with an EF > 40% (p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Reperfusion reduces left ventricular dilatation by preventing infarct expansion in the acute and chronic phases of myocardial infarction.

Reperfusion reduces left ventricular dilatation in patients with acute myocardial infarction, but it is unclear to what extent this is a primary effect or only a consequence of the limiting effect of reperfusion on infarct size. To address this issue, 56 consecutive patients were examined by means of two-dimensional echocardiography on day 1, on day 3, before discharge, and at 6 months after an acute myocardial infarction. From this population two groups of 12 patients each, perfectly matched for site of myocardial infarction, extent of ventricular asynergy at two-dimensional echocardiography (akinesis + dyskinesis), and clinical characteristics were identified according to the creatine kinase (CK) time to peak, which was regarded as a marker of spontaneous or induced reperfusion: (1) CK time to peak of 12 hours or less (reperfused patients, n = 12), and (2) CK time to peak of more than 12 hours (nonreperfused patients, n = 12). In these two groups of patients end-diastolic and end-systolic left ventricular volumes and endocardial lengths of asynergic and normal ventricular segments, imaged in a cross-sectional view at the level of the papillary muscles, were then computed. At the first examination end-diastolic volume, end-systolic volume, and endocardial segment lengths of normal and asynergic segments were similar in the two groups of patients. Patients with late CK time to peak, however, showed a progressive increase in left ventricular systolic volumes and in asynergic endocardial segment lengths between the first and third (predischarge) examinations (p < 0.05 for both), with no change in systolic length of the normal myocardium. The left ventricular end-systolic volume and the asynergic endocardial segment length of patients with early CK time to peak, however, did not increase during hospitalization. The increment in end-systolic volume and in systolic infarct segment length from the first to the third examinations was higher in nonreperfused patients (p = 0.018 and p = 0.04, respectively). Changes similar to those detected in systole were found for diastolic volume and diastolic infarcted and noninfarcted segment length in both groups, but they did not reach statistical significance. After 6 months, an increases in volume and endocardial length were found in both groups of patients. Relative to the first examination, however, the increase in systolic volume and in asynergic systolic endocardial lengths remained greater for nonreperfused patients (p = 0.077 and p = 0.01, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

Usefulness of residual ischemic myocardium within prior infarct zone for identifying patients at high risk late after acute myocardial infarction.

This study examines the prognostic implications of ischemia within the territory of a prior acute myocardial infarction (AMI) vs ischemia at a distance, which develops late after AMI. Sixty-one consecutive patients who underwent both exercise thallium-201 (TI-201) imaging and cardiac catheterization for evaluation of chest pain that developed after discharge from the hospital for AMI form the study group. Mean interval between infarction to the TI-201 study was 10 +/- 17 months. Initial and 2-hour delay TI-201 images were analyzed quantitatively to determine the presence and location (within vs outside the prior infarct zone) of TI-201 redistribution, a marker of ischemic viable myocardium. TI-201 imaging results were separated into 3 groups based on presence and location of TI-201 redistribution: no significant TI-201 redistribution was found in 16 patients; in 29, TI-201 redistribution was confined to the infarct zone; and in 16, TI-201 redistribution was outside the infarct zone. Stepwise multivariate logistic regression analysis was used to examine the comparative ability of TI-201 results and other patient variables to predict cardiac events. For total cardiac events (cardiac death, recurrent nonfatal AMI, unstable angina and coronary revascularization), both the presence of any TI-201 redistribution and multivessel angiographic coronary artery disease were significant predictors. However, when coronary revascularization was excluded as an endpoint, TI-201 redistribution limited to the prior infarct zone was the only significant predictor of cardiac events. All 8 cardiac events occurred in patients with T1-201 redistribution limited to the infart zone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of early intervention with low-dose aspirin (100 mg) on infarct size, reinfarction and mortality in anterior wall acute myocardial infarction.

Recently, it was shown that aspirin given early in acute myocardial infarction (AMI) improves hospital survival, but the mechanisms involved are unclear. In a prospective, randomized placebo-controlled trial, the influence of early intervention with low-dose aspirin (100 mg/day) on infarct size and clinical outcome was studied in 100 consecutive patients with first anterior wall AMI. Infarct size was calculated by cumulative lactate dehydrogenase release in the first 72 hours after admission and was found to be (mean +/- standard deviation) 1,431 +/- 782 U/liter in the aspirin group (n = 50) and 1,592 +/- 1,082 U/liter in the placebo group (n = 50, p = 0.35). The study medication was given for 3 months, during which mortality was 10 (20%) in the aspirin patients and 12 (24%) in the placebo patients (p = 0.65). However, reinfarction occurred in 2 patients (4%) in the aspirin group and in 9 (18%) in the placebo group (p less than 0.03). Early intervention with low-dose aspirin showed, in comparison to placebo, a 10% decrease of infarct size, but this difference was not statistically significant. However, early low-dose aspirin effectively decreased the risk of reinfarction. Therefore, the favor able results of early aspirin on mortality in acute myocardial infarction are probably due more to prevention of reinfarction than to decrease of infarct size.

Adult↗
PubMed1977

Serum myoglobin in myocardial infarction: the "staccato phenomenon." Is acute myocardial infarction in man an intermittent event?

When serum was sampled frequently and soon after acute myocardial infarction, myoglobinemia was extremely common, occurring in 12 of 13 selected patients. Myoglobin first appeared in the serum within a few hours after infarction, but not consistently earlier than creatine phosphokinase. The peak level of serum myoglobin was reached appreciably earlier than the peak values of serum creatine phosphokinase activity. Time of earliest myoglobin appearance in the serum, peak level of myoglobin measured, and duration of detectable myoglobin release all correlated poorly with clinical and biochemical estimates of severity of myocardial infarction. There was no correlation between myoglobin levels and infarct size as estimated from creatine phosphokinase kinetics. Myoglobin appeared in the serum in multiple short "staccato" bursts, or episodes, often lasting only one to two hours. The hypothesis is suggested that the pattern of myoglobin appearance is a reflection of the episodic nature of acute myocardial infarction. Although isolated myoglobin determination may not be useful at present, for quantification of total myocardial damage, its pattern of release may be a sensitive marker for studying the time course of infarction, and may be useful to evaluate therapeutic interventions designed to interrupt an ongoing syndrome of myocardial necrosis.

Acute Disease↗
PubMed1984

Relationship between infarct size and incidence of severe ventricular arrhythmias in a double-blind trial with metoprolol in acute myocardial infarction.

In 585 patients having an acute myocardial infarction for the first time the relationship was investigated between estimated infarct size and the incidence of ventricular fibrillation and treated ventricular tachycardia during hospitalization. The size of the infarct was estimated from analyses of heat stable lactate dehydrogenase (LD) (EC 1.1.1.27.) in serum collected every 12 hr for 48-108 hr. All patients participated in a double-blind comparison of the beta 1-selective blocker metoprolol with placebo in suspected acute myocardial infarction. A correlation was observed between the enzymatically estimated infarct size and the incidence of ventricular fibrillation and treated ventricular tachycardia in patients on placebo (P less than 0.001), while this could not be demonstrated in patients on the beta-blocker (P greater than 0.2). In placebo treated patients there was a correlation between the maximum heat stable LD activity and early ventricular fibrillation (P = 0.034), late ventricular fibrillation (P less than 0.001), primary ventricular fibrillation (P = 0.002) as well as secondary ventricular fibrillation (P = 0.034). It is concluded that there seems to be a relatively strong correlation between the final size of the infarction and the occurrence of severe ventricular arrhythmias. Treatment with beta-blockade appeared to disturb this correlation.

Adult↗
PubMed1993

Clinical course and left ventricular function in patients with acute myocardial infarction following delayed recanalization of infarct-related artery.

The effect of delayed recanalisation of the infarct related artery on clinical course and left ventricular functions was studied in 23 patients with acute myocardial infarction (Group 2). Another 82 patients with acute myocardial infarction served as controls: 48 patients with immediate recanalisation of the infarct related artery following intracoronary thrombolytic therapy (Group 1) and 34 patients with unsuccessful thrombolysis with the artery remaining occluded on repeat angiography (Group 3). Baseline clinical characteristics and left ventricular ejection fractions in the three groups did not differ statistically. Following intracoronary thrombolysis the clinical features and left ventricular functions in the three groups, respectively were as follows: post infarction angina--45.8%, 13.1% and 11.8% (1 vs. 2 and 3, P < 0.05); reinfarction--29.2%, 8.7% and 11.8% (1 vs. 2 and 3, P < 0.05); mortality--0%, 0% and 11.8% (1 and 2 vs. 3; P < 0.05); aneurysm--16.7%, 21.7% and 52.9% (1 and 2 vs. 3, P < 0.05); heart failure--20.8%, 21.7% and 47.1% (1 and 2 vs. 3, P < 0.05). Left ventricular ejection fractions on the second and on days 10-14 were, respectively, 47.6 +/- 1.1%, 42.8 +/- 1.1% and 39.2 +/- 1.6% (1 vs. 2 and 3, P < 0.05) and --52.1 +/- 1.0%, 48.9 +/- 1.1% and 44.3 +/- 1.5% (1 and 2 vs. 3, P < 0.05). Thus following delayed recanalisation of the infarct related artery the clinical course and left ventricular function improved significantly in comparison to patients without recanalisation.

Adult↗