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PubMed1987

Role of myocardial perfusion imaging in evaluating thrombolytic therapy for acute myocardial infarction.

Myocardial thallium-201 scintigraphy is being increasingly employed as a method for assessing the efficacy of coronary reperfusion in acute myocardial infarction. New thallium uptake after intracoronary tracer administration after successful recanalization indicates that nutrient blood flow has been successfully restored. One may also presume that some myocardial salvage occurred if thallium administered in this manner is transported intracellularly by myocytes with intact sarcolemmal membranes. However, if one injects thallium by way of the intracoronary route immediately after reperfusion, the initial uptake of thallium in reperfused myocardium may predominantly represent hyperemic flow and regional thallium counts measured may not be proportional to the mass of viable myocytes. When thallium is injected intravenously during the occlusion phase the degree of redistribution after thrombolysis is proportional to the degree of flow restoration and myocardial viability. When thallium is injected for the first time intravenously immediately after reperfusion, an overestimation of myocardial salvage may occur because of "excess" thallium uptake in the infarct zone consequent to significant hyperemia. Another approach to myocardial thallium scintigraphy in patients undergoing thrombolytic therapy is to administer two separate intravenous injections before and 24 hours or later after treatment. Clinical studies have demonstrated that the improvement in defect size on serial images predicts improvement in regional function and patency of the infarct-related vessel. Finally, patients with acute myocardial infarction who receive intravenous thrombolytic therapy are candidates for predischarge exercise thallium-201 scintigraphy for risk stratification and detection of residual ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibrinolytic Agents↗
PubMed1987

[Tomoscintigraphy of the myocardium labelled with thallium-201. Value in the quantification and prognosis of myocardial infarction].

Myocardial thallium 201 tomography was performed in 112 patients admitted to hospital in the acute stage of a first myocardial infarction. Our quantification method for the myocardial lacuna, validated by animal studies, is described. The necrotic mass evaluated is compared with enzymatic (CPK) (r = 0.89) and angiographic (r = 0.78) quantitative assessments. Thallium 201 tomographic quantification has an unquestionable prognostic value. Thus, among patients whose infarcted mass represented more than 25% of the total myocardial mass, 71% died or developed severe heart failure. Conversely, 93% of patients with a small infarct (less than 20% of total myocardial mass) were asymptomatic on a 24-month follow-up. Myocardial thallium 201 tomography provides a reasonable quantification of the infarct. Its prognostic value seems to be satisfactory.

Adult↗
PubMed1997

Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. European Myocardial Infarct Amiodarone Trial Investigators.

BACKGROUND: Ventricular arrhythmias are a major cause of death after myocardial infarction, especially in patients with poor left-ventricular function. Previous attempts to identify and suppress arrhythmias with various antiarrhythmic drugs failed to reduce or actually increase mortality. Amiodarone is a powerful antiarrhythmic drug with several potentially beneficial actions, and has shown benefit in several small-scale studies. We postulated that this drug might reduce mortality in patients at high risk of death after myocardial infarction because of impaired ventricular function, irrespective of whether they had ventricular arrhythmias. METHODS: The European Myocardial Infarct Amiodarone Trial (EMIAT) was a randomised double-blind placebo-controlled trial to assess whether amiodarone reduced all-cause mortality (primary endpoint) and cardiac mortality and arrhythmic death (secondary endpoints) in survivors of myocardial infarction with a left-ventricular ejection fraction (LVEF) of 40% or less. Intention-to-treat and on-treatment analyses were done. FINDINGS: EMIAT enrolled 1486 patients (743 in the amiodarone group, 743 in the placebo group). Median follow-up was 21 months. All-cause mortality (103 deaths in the amiodarone group, 102 in the placebo group) and cardiac mortality did not differ between the two groups. However, in the amiodarone group, there was a 35% risk reduction (95% CI 0-58, p = 0.05) in arrhythmic deaths. INTERPRETATION: Our findings do not support the systematic prophylactic use of amiodarone in all patients with depressed left-ventricular function after myocardial infarction. However, the lack of proarrhythmia and the reduction in arrhythmic death support the use of amiodarone in patients for whom antiarrhythmic therapy is indicated.

Aged↗
PubMedDate not supplied

Emergency department management of acute myocardial infarction.

Myocardial infarction-remains one of the leading causes of death among adults in the United States despite the significant advances in therapy made during the past three decades. However, a significant reduction in mortality following acute myocardial infarction has been accomplished through an aggressive strategy directed toward early recognition and intervention. This approach requires that the emergency physician act promptly and choose appropriately from the ever-expanding therapeutic options. This paper summarizes the recent progress and treatment options in the management of acute myocardial infarction with regard to prehospital care, diagnostic challenges in the emergency department, conventional therapy and pharmacologic advances, newer interventional measures, and future trends.

Adult↗
PubMed1990

[Site and type of acute myocardial infarct in relation to myocardial infarct size--dynamics of global ejection fraction in acute myocardial infarct].

By the ejection fraction global (EFg) statements concerning the remaining function of the myocardium in acute myocardial infarction and thus individually concerning the prognosis (classification of risk groups) become possible. For the valuation of the dynamics of the EFg in a period up to 6 months after an acute myocardial infarction the EFg was multifariously controlled. Only patients with first myocardial infarction in localization on the anterior wall and Q-wave showed a significant dynamics of the EFg between the measurements acute and third week as well as acute and 6th month (absolutely 5.2%). --In re-infarction/Q-wave this could be confirmed also for the localization of the posterior wall in the period acute till third week. For the localization on anterior and posterior wall a dynamics of the EFg could also be calculated for the period acute and 6th month. Thereby the absolute increase of the EFg was between 4.0 and 4.6%. The dynamics of the EFg in the region of the anterior wall was 5.2% for the first infarction and only 4% for the reinfarction. Thus it is below the dynamics of the EFg in an effective thrombolytic therapy.

Angina Pectoris↗
PubMed2005

Relation of T-wave inversion in Q-wave acute myocardial infarction to myocardial viability on resting rubidium-82 and 18-fluoro-deoxyglucose positron emission tomography imaging.

T-wave inversion in areas of Q-wave myocardial infarction has been advocated as a predictor of myocardial viability. However, the predictive value of this electrocardiographic finding in distinguishing viable from nonviable muscle is not fully defined. Thus, we correlated electrocardiographic Q waves and a measure of T-wave inversion with the results of rubidium-82 (Rb-82) and 18-fluoro-deoxyglucose-positron emission tomography (FDG-PET) imaging at rest. We analyzed 35 Q-wave myocardial infarct regions in 25 patients. Nineteen of the 35 (54%) were judged viable by Rb-82/FDG-PET. Using the Novacode T-wave score, T-wave inversion was present in 11 of 19 regions (58%) with viability and 5 of 16 regions (31%) without viability. Thus, neither Q waves nor T-wave inversion can accurately predict myocardial viability in patients with Q-wave myocardial infarction.

Acute Disease↗
PubMed1993

Ventricular arrhythmias in patients recovering from myocardial infarction: do residual myocardial ischemia and anti-ischemic medical intervention influence the one-month prevalence? The Danish Study Group on Verapamil in Myocardial Infarction.

The relationship between myocardial ischemia revealed by exercise testing and ventricular arrhythmias on Holter monitoring, and the effect of anti-ischemic intervention on the incidence of ventricular arrhythmias in patients with residual ischemia were studied in 125 patients recovering from myocardial infarction. Prior to discharge exercise testing and 24-h Holter monitoring were carried out. In patients with ST-segment depression (n = 34), ventricular arrhythmias on Holter monitoring were seen in 7 (21%) compared with 20 (22%) patients without ST-segment depression (NS). Patients were hereafter double-blindly randomized to intervention with verapamil (n = 63) or placebo (n = 62). One month after discharge, 24-h Holter monitoring was repeated. In the verapamil group ventricular arrhythmias increased from 25 to 33% (NS). In the placebo group the figures were 18 and 27%, respectively (NS). In patients with ST-segment depression and verapamil treatment, the prevalence increased from 25 to 38% (NS). In the placebo group the figures were 17 and 22%, respectively (NS). The differences between the groups were not significant. A significantly increased prevalence of ventricular arrhythmias was found in patients with either heart failure or non-Q-wave infarct. In these patients myocardial ischemia during exercise did not correlate with ventricular arrhythmias either. ST-segment depression during pre-discharge exercise testing correlated with neither the prevalence nor the incidence of ventricular arrhythmias, and anti-ischemic intervention with verapamil did not influence the incidence of ventricular arrhythmias in both patients with and without myocardial ischemia.

Aged↗
PubMed1989

Qualitative and quantitative comparison of amounts of narrowing by atherosclerotic plaques in the major epicardial coronary arteries at necropsy in sudden coronary death, transmural acute myocardial infarction, transmural healed myocardial infarction and unstable angina pectoris.

The amounts of narrowing of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaques were compared in 4 subsets of coronary patients. Of the 129 patients studied at necropsy, an average of 2.7 of the 4 arteries was narrowed greater than 75% in cross-sectional area at some point (0.7/4 in controls), and the group with unstable angina pectoris (3.2/4) had more narrowing than did the groups with sudden coronary death (2.8/4), acute myocardial infarction (2.7/4) and healed myocardial infarction (2.3/4). Each of the 4 major epicardial coronary arteries was divided into 5-mm long segments and a histologic section was prepared and stained by the Movat method of each of the 6,461 segments in the 129 patients and in the 1,849 segments in the 40 control subjects. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (3% in controls) and the group with unstable angina had the highest percent (48%) of segments severely narrowed compared to the groups with sudden coronary death (36%), acute myocardial infarction (34%) and healed myocardial infarction (31%). Thus, of the 4 subsets of patients with fatal coronary artery disease studied at necropsy, those with unstable angina pectoris had the most severe and extensive coronary atherosclerosis.

Angina Pectoris↗
PubMed1982

Comparative investigation of the effects of metoprolol, propranolol, practolol, and verapamil in the acute phase of experimental myocardial infarction.

Myocardial infarction in rats was produced by ligation of the left coronary artery. To ensure exact comparison of drug effect, the extent of the myocardial zone excluded from the coronary circulation was determined in each animal, and the experimental data were related to it. For this purpose, the hearts were perfused with Evans blue, and after the photometric determination of the dye content of the hearts the percentage of ischemic myocardium was calculated. With metoprolol, propranolol, and verapamil a significant increase of the survival times was obtained (min/% of non-ischemic myocardium). Metoprolol and propranolol also significantly increased the survival rates. None of the beta-blockers exerted an antiarrhythmic effect. The arrhythmias were prevented by higher doses of the calcium antagonist verapamil which, however, decreased the survival times. All beta-blocking agents delayed the typical elevation of the ST-segment in the electrocardiogram, and reduced the increase of the activity of the serum creatine kinase. Propranolol and metoprolol antagonized the blood pH decrease obtained after coronary occlusion. Results concerning heart rate, and arterial and central venous pressures are also reported. - The findings with metoprolol, especially, indicate that the essential mechanism in the therapeutic action of beta-blockers is their ability to block the cardiac beta 1-receptors.

Adrenergic beta-Antagonists↗
PubMed1995

Prognostic value of N-terminal proatrial natriuretic factor plasma levels measured within the first 12 hours after myocardial infarction. Thrombolysis in Myocardial Infarction (TIMI) II Investigators.

OBJECTIVES: The aim of the present study was to examine the relation between the plasma levels of the atrial peptide N-terminal proatrial natriuretic factor (proANF) measured during the 1st 12 h after myocardial infarction and 1-year mortality. BACKGROUND: The atrial peptides atrial natriuretic factor and N-terminal proANF are released from cardiac atria secondary to increased atrial pressures. The plasma levels of both peptides have been found to be related to long-term prognosis when measured in the subacute phase of myocardial infarction. METHODS: The study was of a retrospective case-control design studying patients enrolled in the Thrombolysis in Myocardial Infarction (TIMI) II trial. Seventy-six patients who died within the 1st year of enrollment in the trial were matched with another 76 patients who survived. N-terminal proANF was analyzed by radioimmunoassay at enrollment (no later than 4 h after the start of chest pain) and at 50 min, 5 h and 8 h after enrollment. RESULTS: At all studied time points the peptide levels were significantly higher in the case group than in the control group. At 8 h after enrollment, an N-terminal proANF value above a cutoff point of 1,500 pmol/liter was associated with an odds ratio for death of 3.9. CONCLUSIONS: The plasma level of N-terminal proANF, when measured during the 1st 12 h after the onset of chest pain, is related to 1-year mortality after myocardial infarction. Together with previous findings, these results suggest that N-terminal proANF measurements represent a valuable supplement to currently used prognostic indicators after myocardial infarction.

Aged↗
PubMed1999

C-reactive protein and complement are important mediators of tissue damage in acute myocardial infarction.

Myocardial infarction in humans provokes an acute phase response, and C-reactive protein (CRP), the classical acute phase plasma protein, is deposited together with complement within the infarct. The peak plasma CRP value is strongly associated with postinfarct morbidity and mortality. Human CRP binds to damaged cells and activates complement, but rat CRP does not activate complement. Here we show that injection of human CRP into rats after ligation of the coronary artery reproducibly enhanced infarct size by approximately 40%. In vivo complement depletion, produced by cobra venom factor, completely abrogated this effect. Complement depletion also markedly reduced infarct size, even when initiated up to 2 h after coronary ligation. These observations demonstrate that human CRP and complement activation are major mediators of ischemic myocardial injury and identify them as therapeutic targets in coronary heart disease.

Acute Disease↗
PubMed1996

Acute myocardial infarction and myocardial bridging: a case report.

The present report describes a 55-year-old man who presented an anterior myocardial infarction in association with myocardial bridge of the left anterior descending artery (LAD). We discuss the pathophysiology of myocardial infarction occurring with myocardial bridge.

Anistreplase↗
PubMed2001

Effect of a selective aldosterone receptor antagonist in myocardial infarction.

Myocardial infarction (MI) initiates adaptive tissue remodeling, which is essential for heart function (such as infarct healing) but is also important for maladaptive remodeling (for example, reactive fibrosis and left ventricular dilation). The effect of aldosterone receptor antagonism on these processes was evaluated in Sprague-Dawley rats using eplerenone, a selective aldosterone receptor antagonist. Infarct healing and left ventricular remodeling were evaluated at 3, 7, and 28 days after MI by determination of the diastolic pressure-volume relationship of the left ventricle, the infarct-thinning ratio, and the collagen-volume fraction. Eplerenone did not affect reparative collagen deposition as was evidenced by a similar collagen volume fraction in the infarcted myocardium between eplerenone and vehicle-treated groups at 7 and 28 days post-MI. In addition, the thinning ratio, which is an index of infarct expansion, was comparable between the eplerenone and vehicle-treated animals at 7 and 28 days post-MI. A protective effect of eplerenone was demonstrated at 28 days post-MI, where reactive fibrosis in the viable myocardium was reduced in eplerenone-treated animals compared with vehicle-treated animals. Thus aldosterone receptor antagonism does not retard infarct healing but rather protects against maladaptive responses after MI.

Animals↗
PubMed2006

Identification of mast cells in the cellular response to myocardial infarction.

Myocardial infarction is associated with an acute inflammatory response, leading to replacement of injured cardiomyocytes with granulation tissue. Mast cells are actively involved in postinfarction inflammation by releasing histamine and tumor necrosis factor-alpha, triggering a cytokine cascade. During the proliferative phase of healing, mast cells accumulate in the infarct and may regulate fibrous tissue deposition and angiogenesis by releasing growth factors, angiogenic mediators, and proteases. This chapter describes simple and reliable methods used to identify mast cells in control and infarcted canine hearts. Toluidine blue staining, labeling with conjugated avidin, and tryptase histochemistry are useful in the detection of mast cells in canine tissues. In the healing infarct, mast cells are associated with other cell types that are important for granulation tissue formation. We present immunohistochemical methods identifying monocytes, neutrophils, macrophages, endothelial cells, myofibroblasts, and smooth muscle cells in dog infarcts. These techniques are useful tools for pathological studies in canine models.

Animals↗
PubMed1976

Scan analysis in myocardial infarction.

Myocardial scans with 99mTc-labelled phosphates are reported to be useful in the diagnosis of acute myocardial infarction. A retrospective survey of 205 patients referred for 99mTc-phosphate bone scanning and with no evidence of recent heart disease revealed an occurrence of 10% of false positive images, that is to say, uptake of phosphate in non-infarcted myocardium. These striking findings stress the need for critical assessment of the usefulness of this diagnostic technique.

Etidronic Acid↗
PubMed1998

Impact of diabetes on mortality after the first myocardial infarction. The FINMONICA Myocardial Infarction Register Study Group.

OBJECTIVE: To study diabetic and nondiabetic patients with their first myocardial infarction to determine overall 1-year mortality, out-of-hospital mortality, 28-day mortality of hospitalized patients, and 1-year mortality of 28-day survivors. RESEARCH DESIGN AND METHODS: This study--based on the FINMONICA Myocardial Infarction Register, a part of the Finnish contribution to the WHO MONICA Project (World Health Organization Multinational Monitoring of Trends and Determinants of Cardiovascular Disease)--covered coronary heart disease (CHD) deaths and acute CHD events occurring during hospitalization among residents of Finland aged 25-64 years in three geographically defined areas. The study population comprised 620 diabetic and 3,445 nondiabetic patients who had their first myocardial infarction during the years 1988-1992. RESULTS: The age- and area-adjusted mortality rates and hazard ratios (HRs) for diabetic versus nondiabetic patients (95% CI) were as follows: The 1-year mortality rate was 44.2% in diabetic men and 32.6% in nondiabetic men (HR, 1.38; 1.18-1.61) and 36.9% in diabetic women and 20.2% in nondiabetic women (HR, 1.86; 1.40-2.46); the out-of-hospital mortality rate was 28.3% in diabetic men and 22.4% in nondiabetic men (HR, 1.25; 1.03-1.52) and 10.4% in diabetic women and 11.0% in nondiabetic women (HR, 0.95; 0.58-1.54); the 28-day mortality rate of hospitalized patients was 14.4% in diabetic men and 8.8% in nondiabetic men (HR, 1.58; 1.15-2.18) and 21.7% in diabetic women and 7.8% in nondiabetic women (HR, 2.60; 1.71-3.95); and the 1-year mortality rate of 28-day survivors was 9.6% in diabetic men and 5.0% in nondiabetic men (HR, 1.97; 1.25-3.12) and 10.7% in diabetic women and 2.5% in nondiabetic women (HR, 4.17; 2.05-8.51). CONCLUSIONS: The high mortality rate of diabetic patients after their first myocardial infarction and the high proportion of out-of-hospital deaths in this group imply that vigorous primary and secondary preventive measures should become an integral part of their medical care.

Adult↗
PubMed2005

S100A1 gene therapy preserves in vivo cardiac function after myocardial infarction.

Myocardial infarction (MI) represents an enormous clinical challenge as loss of myocardium due to ischemic injury is associated with compromised left ventricular (LV) function often leading to acute cardiac decompensation or chronic heart failure. S100A1 was recently identified as a positive inotropic regulator of myocardial contractility in vitro and in vivo. Here, we explore the strategy of myocardial S100A1 gene therapy either at the time of, or 2 h after, MI to preserve global heart function. Rats underwent cryothermia-induced MI and in vivo intracoronary delivery of adenoviral transgenes (4 x 10(10) pfu). Animals received saline (MI), the S100A1 adenovirus (MI/AdS100A1), a control adenovirus (MI/AdGFP), or a sham operation. S100A1 gene delivery preserved global in vivo LV function 1 week after MI. Preservation of LV function was due mainly to S100A1-mediated gain of contractility of the remaining, viable myocardium since contractile parameters and Ca(2+) transients of isolated MI/AdS100A1 myocytes were significantly enhanced compared to myocytes isolated from both MI/AdGFP and sham groups. Moreover, S100A1 gene therapy preserved the cardiac beta-adrenergic inotropic reserve, which was associated with the attenuation of GRK2 up-regulation. Also, S100A1 overexpression reduced cardiac hypertrophy 1 week post-MI. Overall, our data indicate that S100A1 gene therapy provides a potential novel treatment strategy to maintain contractile performance of the post-MI heart.

Adenoviridae↗