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PubMed1997

Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators.

BACKGROUND: Survivors of acute myocardial infarction with frequent or repetitive ventricular premature depolarisations (VPDs) have higher mortality 1-2 years after the event than those without VPDs. Although there is no therapy of proven efficacy for such patients, previous studies of amiodarone have been encouraging. CAMIAT was a randomised double-blind placebo-controlled trial designed to assess the effect of amiodarone on the risk of resuscitated ventricular fibrillation or arrhythmic death among survivors of myocardial infarction with frequent or repetitive VPDs (> or = 10 VPDs per h or > or = 1 run of ventricular tachycardia). METHODS: Patients from 36 Canadian hospitals were randomly assigned amiodarone or placebo; a loading dose of 10 mg/kg daily for 2 weeks, a maintenance dose of 300-400 mg daily for 3.5 months, 200-300 mg daily for 4 months, and 200 mg for 5-7 days per week for 16 months. Patients were followed up for 2 years. The primary outcome was the composite of resuscitated ventricular fibrillation or arrhythmic death. FINDINGS: We recruited 1202 patients (606 in the amiodarone group and 596 in the placebo group). The mean follow-up was 1.79 years (SD 0.44). In the efficacy analysis, resuscitated ventricular fibrillation or arrhythmic death occurred in 39 (6.9%) [corrected] patients in the placebo group and in 25 (4.5%) [corrected] in the amiodarone group (relative-risk reduction 48.5% [95% CI 4.5 to 72.2], p = 0.016). In the intention-to-treat analysis, primary outcome events occurred in 24 (6.9%) patients in the placebo group and in 15 (4.5%) in the amiodarone group (38.2% [95% CI -2.1 to 62.6], p = 0.029). The absolute-risk reductions were greatest among patients with congestive heart failure or a history of myocardial infarction. INTERPRETATION: Amiodarone reduces the incidence of ventricular fibrillation or arrhythmic death among survivors of acute myocardial infarction with frequent or repetitive VPDs. Treatment decisions for individual survivors should require an assessment of their baseline risk factors and judgments based on the synthesis of our findings with those of related trials.

Adult↗
PubMed2001

QT dispersion within the first 6 months after an acute myocardial infarction: relationship with systolic function, left ventricular volumes, infarct related artery status and clinical outcome.

INTRODUCTION: We analysed QT dispersion within the first 6 months postinfarction, its relationship with the main established risk stratifiers and its clinical value. METHODS AND RESULTS: In 55 patients with a first Q-wave myocardial infarction the 12-lead electrocardiogram was scanned and digitised for analysis of QT dispersion (QT maximum-QT minimum) at first day (72 [61-96] ms), first week (69 [47-90] ms), first month (67 [46-88] ms) and sixth month (47 [40-74] ms; P<0.0001 vs. first day). Cardiac catheterization was performed at first week and at sixth month; QT dispersion was not related to ejection fraction, left ventricular volumes, infarct related artery status or contractile reserve (improvement of the infarcted area with low-dose dobutamine); no relation was found between QT dispersion decrease from first week to sixth month with regional systolic function improvement. Finally, during a mean follow-up period of 35+/-22 months QT dispersion was not independently related to clinical events. CONCLUSION: QT dispersion decreases progressively during the first months after myocardial infarction. These changes should be taken into account to define cut-off values of clinical interest in this phase. This variable does not seem related to the classic prognosis predictors. In a nonselected postinfarction population it has a low clinical value.

Coronary Vessels↗
PubMed1997

[Differential characteristics and survival of women with acute myocardial infarction. Registry of Acute Myocardial Infarctions of the City of Valencia (RICVAL). Researchers of the RICVAL].

INTRODUCTION AND OBJECTIVES: The prevalence of women who are admitted to the hospital after acute myocardial infarction is lower to that of men and their prognosis is worse. The reason for these differences is unclear. We studied the demographic and historical variables, the evolution, treatment and early survival in 269 women included in the Register of Acute Myocardial Infarctions of the City of Valencia (RICVAL) and compared them with the 855 men included in the same Register. PATIENTS AND METHODS: Register of patients admitted into a Coronary Care Unit in the City of Valencia since December, 1st, 1993 until November 30th, 1994. RESULTS: 23.9% of the patients were women with a mean age of 71.9 +/- 9 years; 46.8% of them were diabetics, 55.4% hypertensives, and 6.7% smokers. The women arrived for treatment later than men and 34.9% of them were thrombolised. The incidence in women of severe heart failure (Killip III and IV) was 40.1% and the mortality 29.7%. In women with thrombolytic treatment the mortality was 29.8%. In the logistic regression model performed, female sex predicted a higher mortality rate (odds ratio [OR] = 1.30; confidence interval [CI], 1.05-1.61). CONCLUSIONS: Early mortality in women after acute myocardial infarction is higher than in men in the RICVAL Register. The longer delay in initiating medical care and thrombolysis might be the cause for the higher proportion of heart failure among women and explain their worse prognosis after an acute myocardial infarction compared to men.

Aged↗
PubMed2002

Influence of prehospital administration of aspirin and heparin on initial patency of the infarct-related artery in patients with acute ST elevation myocardial infarction.

OBJECTIVES: The aim of this study was to investigate the influence of prehospital administration of aspirin and heparin on the initial patency of the infarct-related artery (IRA) in patients with acute myocardial infarction (MI). BACKGROUND: Prehospital diagnosis of acute MI facilitates early pharmacologic intervention on the way to the catheterization laboratory for primary angioplasty. METHODS: We studied the angiographic data and 30-day clinical outcome of 1,702 patients treated with primary angioplasty; 860 received aspirin and heparin before transportation to our hospital and 842 received aspirin and heparin in our hospital. RESULTS: The Thrombolysis In Myocardial Infarction (TIMI) 2 or 3 flow in the IRA was higher in the prehospital treated group (31% vs. 20%, relative risk 0.65, 95% confidence interval 0.55 to 0.78, p < 0.001). Patients with TIMI 2 or 3 flow on the initial angiogram had a higher angioplasty success rate (94% vs. 89%, p < 0.001), a smaller enzymatic infarct size, a higher left ventricular ejection fraction and a lower 30-day mortality (1.6% vs. 3.4%, p = 0.04). CONCLUSIONS: Prehospital administration of aspirin and heparin results in a higher initial patency of the IRA in patients with acute MI.

Angioplasty, Balloon, Coronary↗
PubMed2003

Thrombolysis in myocardial infarction myocardial perfusion grade in angiography correlates with myocardial salvage in patients with acute myocardial infarction treated with stenting or thrombolysis.

OBJECTIVES: We sought to assess the relationship between the Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion (TMP) grade and myocardial salvage as well as the usefulness of TMP grade in comparing two different reperfusion strategies. BACKGROUND: The angiographic index of TMP grade correlates with infarct size and mortality after thrombolysis for acute myocardial infarction (AMI). Its relationship to myocardial salvage and its usefulness in comparing different reperfusion strategies are not known. METHODS: We analyzed the TMP grade on angiograms obtained at one to two weeks after treatment in 267 patients enrolled in two randomized trials that compared stenting with thrombolysis in AMI. Patients were classified into two groups: 159 patients with TMP grade 2/3 and 108 patients with TMP grade 0/1. Two scintigraphic studies were performed: before and one to two weeks after reperfusion. The salvage index was calculated as the proportion of the area at risk salvaged by reperfusion. RESULTS: Patients with TMP grade 2/3 had a higher salvage index (0.49 +/- 0.42 vs. 0.34 +/- 0.49, p = 0.01), a smaller final infarct size (15.4 +/- 15.5% vs. 22.1 +/- 16.2% of the left ventricle, p = 0.001), and a trend toward lower one-year mortality (3.8% vs. 8.3%, p = 0.11) than patients with TMP grade 0/1. The relationship between TMP and salvage index was independent of the form of reperfusion therapy. The proportion of patients with TMP grade 2/3 was significantly higher after stenting than after thrombolysis (70.9% vs. 48.1%, p = 0.001). CONCLUSIONS: These findings show that the TMP grade is a useful marker of the degree of myocardial salvage achieved with reperfusion and a sensitive indicator of the efficacy of reperfusion strategies in patients with AMI.

Abciximab↗
PubMed1984

Patterns of creatine kinase release during acute myocardial infarction after nonsurgical reperfusion: comparison with conventional treatment and correlation with infarct size.

Coronary arteriography and biplane ventriculography were performed in 51 patients during the acute (mean of 6.6 hours after onset of symptoms) and chronic (1 to 3 months after admission) phase of myocardial infarction. Twenty-four patients were treated in a conventional manner. In 27 patients, reperfusion was achieved with intracoronary streptokinase after 24 +/- 20 minutes of infusion. Peak creatine kinase and cumulative creatine kinase release were derived from serial creatine kinase measurements. Ejection fraction and the length of the akinetic or dyskinetic segments were calculated in the chronic phase. The time interval between onset of symptoms and peak creatine kinase was significantly shorter for the streptokinase-treated patients as compared with the conventionally treated patients (13.5 +/- 5.3 versus 22.9 +/- 7.4 hours, p = 0.0001). Significant linear correlations were obtained for both streptokinase-treated and control patients, relating: 1) peak creatine kinase value to both length of the noncontracting segment and ejection fraction in the chronic phase, and 2) cumulative creatine kinase release to both length of the noncontracting segment and ejection fraction in the chronic phase. Patients treated with streptokinase experienced a relatively greater release of enzyme for a given infarct size as compared with those treated in a conventional manner. The difference in enzyme release between the two groups increased as infarct size increased. These observations may be explained by enhanced washout of enzyme from the infarct zone, secondary to reperfusion after intracoronary streptokinase therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Circulation↗
PubMed1998

Use of angiotensin-converting enzyme inhibitors at discharge in patients with acute myocardial infarction in the United States: data from the National Registry of Myocardial Infarction 2.

OBJECTIVES: This study was undertaken to examine recent trends in the use of angiotensin-converting enzyme (ACE) inhibitor therapy in patients discharged after acute myocardial infarction (AMI) and to identify clinical factors associated with ACE inhibitor prescribing patterns. BACKGROUND: Clinical trials have demonstrated a significant mortality benefit in patients treated with ACE inhibitors after AMI. Numerous studies have demonstrated underuse of other beneficial treatments for patients with AMI, such as beta-adrenergic blocking agents, aspirin and immediate reperfusion therapy. METHODS: Demographic, procedural and discharge medication data from 190,015 patients with AMI were collected at 1,470 U.S. hospitals participating in the National Registry of Myocardial Infarction 2. RESULTS: Prescriptions for ACE inhibitor therapy at hospital discharge increased from 25.0% in 1994 to 30.7% in 1996. Patients with a left ventricular ejection fraction < or =40% or evidence of congestive heart failure while in the hospital were discharged with ACE inhibitor treatment 42.6% of the time. Of patients experiencing an anterior wall myocardial infarction and no evidence of heart failure, 26.1% of patients were discharged with this treatment. Of the remaining patients, 15.6% received ACE inhibitors at discharge. ACE inhibitors were prescribed more often to elderly and diabetic patients as well as those requiring intraaortic balloon pump placement. This therapy was given less often to patients who underwent revascularization with coronary angioplasty or coronary artery bypass graft surgery or were treated with calcium channel blocking agents. CONCLUSIONS: Physicians are prescribing ACE inhibitors in patients with myocardial infarction with increasing frequency. Those patients with the greatest expected benefit receive ACE inhibitor treatment most often. However, the majority of even these high risk patients were not discharged with this life-saving therapy.

Adrenergic beta-Antagonists↗
PubMed2000

Treatment and outcome of myocardial infarction in hospitals with and without invasive capability. Investigators in the National Registry of Myocardial Infarction.

OBJECTIVES: We sought to determine the extent to which the capability of a hospital to perform invasive cardiovascular procedures influences treatment and outcome of patients admitted with acute myocardial infarction (AMI). BACKGROUND: Patients with AMI are usually transported to the closest hospital. However, relatively few hospitals have the capability for immediate coronary arteriography, percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft surgery (CABG), should these interventions be needed. METHODS: The 1,506 hospitals participating in the National Registry of Myocardial Infarction 2 were classified according to their highest level of invasive capability: 1) none (noninvasive, 28.1%); 2) coronary arteriography (cath-capable, 25.2%); 3) coronary angioplasty (PTCA-capable, 7.4%); and 4) bypass surgery (CABG-capable, 39.2%). Treatment and in-hospital outcomes were assessed for 305,812 patients admitted from June 1994 through October 1996. Follow-up through 90 days was ascertained in a subset of 30,402 patients enrolled simultaneously in both the National Registry of Myocardial Infarction (NRMI) 2 and the Cooperative Cardiovascular Project (CCP). RESULTS: The proportion of patients receiving initial reperfusion intervention was only slightly higher at the more invasive hospitals (noninvasive 32.5%, cath-capable 31.2%, PTCA-capable 32.9% and CABG-capable 35.9%, p < 0.001 by chi-square statistic). Among thrombolytic recipients, median door-to-drug time interval differed little among hospital types and ranged from 42 to 45 minutes. At cath-capable, PTCA-capable and CABG-capable hospitals, coronary arteriography was performed in 32.9%, 37.4% and 64.9%, respectively, and PTCA in 0.0%, 5.1% and 31.4%, both p < 0.001 by chi-square statistic. The proportion of patients transferred out to other facilities was 51.0%, 42.2%, 39.9% and 4.4% (p < 0.0001) among noninvasive, cath-capable, PTCA-capable and CABG-capable hospitals, respectively. Among patients in the combined NRMI and CCP data set, mortality at 90 days postinfarction was similar among patients initially admitted to each of the four hospital types. CONCLUSIONS: Although patients with AMI admitted to hospitals without invasive cardiac facilities have a high likelihood of subsequent transfer to other facilities, their likelihood of receiving a reperfusion intervention at the first hospital, their door to thrombolytic drug intervals and their 90-day survival rates are similar to those of patients initially admitted to more invasively equipped hospitals. These data suggest that a policy of initial treatment of myocardial infarction at the closest medical facility is appropriate medical practice.

Aged↗
PubMed2003

Infarct size limiting effect of apstatin alone and in combination with enalapril, lisinopril and ramipril in rats with experimental myocardial infarction.

Bradykinin is a potent vasoactive peptide that is known to elicit a number of biological responses. A number of peptidases have been identified to possess kininase activity, the inhibition of which increases the availability and effectiveness of kinins. We wished to determine the cardioprotective actions of an aminopeptidase P inhibitor, apstatin alone and in combination with enalapril/lisinopril/ramipril in an in vivo rat model of acute ischemia (30 min) and reperfusion (4 h). Myocardial infarction was produced by occlusion of the left anterior descending coronary artery for 30 min followed by 4 h of reperfusion. Infarct size was measured by using the staining agent 2,3,5-triphenyl tetrazolium chloride (TTC). Lipid peroxide levels in serum and in heart tissue were estimated spectrophotometrically. A lead II electrocardiogram was monitored at various intervals throughout the experiment. Infarct size was reduced to a greater extent with apstatin and with combined inhibition it was further reduced. Infarct size reduction obtained with the combined inhibition came to normal with the prior administration of B2 bradykinin antagonist HOE140 suggests the involvement of bradykinin in the cardioprotective actions of apstatin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Accuracy of detection of myocardial viability and residual infarct vessel stenoses with rest Tl-201 and adenosine Tc-99m sestamibi imaging after coronary reperfusion in dogs with experimental acute myocardial infarction.

BACKGROUND: We sought to determine whether a dual-isotope imaging strategy (rest thallium 201/stress technetium 99m sestamibi) might be useful for assessing myocardial viability and residual ischemia in the infarct zone very early after reperfusion. METHODS AND RESULTS: Fifteen open-chest dogs had left anterior descending coronary artery occlusion for 60 minutes, followed by full reperfusion (group 1, n = 8) or reperfusion through a residual critical stenosis (group 2, n = 7). Tl-201 was injected at rest 45 minutes after reperfusion, and initial and 2-hour redistribution images were acquired. Tc-99m sestamibi was then injected during vasodilator stress, followed by imaging. Infarct size was similar in both groups (risk area, 21% +/- 4% vs 22% +/- 3%). Rest Tl-201 defect count ratios (left anterior descending coronary artery/left circumflex artery) were comparable (0.71 +/- 0.03 vs 0.74 +/- 0.02) and reflected infarct size. With vasodilation, Tc-99m sestamibi defect count ratio in group 1 (0.71 +/- 0.02) was comparable to rest Tl-201 and was significantly greater than in group 2 (0.62 +/- 0.02) with residual stenoses (P <.01). Although vasodilator Tc-99m sestamibi imaging unmasked the presence of residual stenoses, Tc-99m sestamibi uptake underestimated their functional severity (flow ratio, 0.38 +/- 0.03). CONCLUSIONS: Dual-isotope imaging very early after reperfusion may have limited utility for detecting residual stenoses in the infarct zone. Underestimation of the flow disparity by Tc-99m sestamibi may make the detection of stenoses more difficult, and impaired flow reserve after ischemic insult may complicate the detection of fully reperfused segments.

Animals↗
PubMed1998

Effect of verapamil on heart rate variability after an acute myocardial infarction. Danish Verapamil Infarction Trial II.

Because decreased heart rate variability measured after an acute myocardial infarction (AMI) has been demonstrated to predict subsequent mortality and sudden death, and an efficacy analysis of the Danish Verapamil Infarction Trial II (DAVIT II) demonstrated that long-term postinfarction treatment with verapamil significantly reduced sudden death, the aim of the present substudy was to evaluate the effect of verapamil on heart-rate variability in the time and frequency domain, measured in two 5-minute segments during the day and night. Thirty-eight patients were examined by Holter monitoring, at 1 week, that is, before randomization, and at 1 month after infarction; 22 of the patients were examined 12-16 months after infarction as well. In both treatment groups (verapamil and placebo) no significant alteration of heart rate variability during the day-time was demonstrated from before to after 1 and 12-16 months of treatment. In accord with the known reduction of overall heart rate by verapamil, a significant increase of mean NN interval from before to after 1 (P = 0.0004) and 12-16 months (P = 0.004) of treatment was seen in the verapamil, but not in the placebo, group at night. Parameters generally interpreted as an index of parasympathetic modulation, that is, RMSSD, pNN50, and high-frequency power, increased significantly at 1 month (P = 0.04, P = 0.03, NS, respectively) and 12-16 months (P = 0.03, P = 0.04, P < 0.05) after AMI in the verapamil, but not in the placebo, group. In conclusion, the present study indicates that verapamil shifts the autonomic balance to a vagal preponderance or sympathetic attenuation in the postinfarction period.

Aged↗
PubMed1998

The Cardiac Infarction Injury Score as a predictor for long-term mortality in survivors of a myocardial infarction.

AIMS: The Cardiac Infarction Injury Score (CIIS) is an electrocardiographic classification system that was developed as a diagnostic tool to assess the extent of cardiac injury in acute myocardial infarction. We investigated the prognostic value of the CIIS in post-myocardial infarction patients. METHODS AND RESULTS: The prognostic values of the CIIS for total and cardiac mortality was assessed in a large series (n = 3395) of patients who were enrolled in the ASPECT trial. Standard 12-lead electrocardiograms, recorded prior to hospital discharge were coded according to the CIIS and the Minnesota Code. Mean CIIS was 26 (range--8 to 59). After adjustment for other baseline characteristics, the CIIS was directly related to the risk of total mortality and cardiac mortality. At one-year follow-up the relative risks of CIIS > or = 40, CIIS 30-40 and CIIS 20-30 were significantly higher than in those with a CIIS < 20. The relative risks were, respectively, 2.3 (1.2-4.4), 2.2 (1.3-3.9) and 1.6 (0.9-2.9). At 3 year follow-up, the relative risks were, respectively, 2.1 (1.4-3.2), 1.7 (1.2-2.4) and 1.5 (1.0-2.1). The relative risks for total mortality were similar. When patients with major ECG abnormalities, as defined by the Minnesota code, were excluded, the associations were still significant in the CIIS classes 30-40 and > 40. CONCLUSION: The CIIS ECG scoring system is an important predictor for long-term cardiac mortality in post myocardial infarction patients. It can easily be automated and is efficient for classifying cardiac injury in epidemiological studies.

Adult↗
PubMed2002

Myocardial ischemia adjacent to infarction enhances the magnitude of exercise-induced ST-segment elevation one month after myocardial infarction.

The aims of this study were to compare exercise-induced ST-segment elevation with and without ischemia and to examine the relation between exercise-induced ST-segment elevation and the location of myocardial ischemia. Seventy-nine patients with first anterior myocardial infarction underwent thallium-201 exercise myocardial scintigraphy test one month after myocardial infarction. There were 37 patients showing no reversible defect (non ischemia group), 33 with reversible defect in the territory of the left descending coronary artery (homozonal ischemia group) and 9 with a reversible defect in the territory of the left circumflex or right coronary artery (remote ischemia group). There were no significant differences among the three groups with respect to infarct size, presence of dyskinesis and exercise endurance time. Patients with homozonal ischemia had the highest degree of ST-segment elevation (0.22 +/- 0.09 mV) followed by patients without ischemia (0.13 +/- 0.07 mV) and those with remote ischemia (0.09 +/- 0.08 mV, P <.01). In conclusion, Myocardial ischemia adjacent to infarction amplifies exercise-induced ST-segment elevation.

Catecholamines↗
PubMed2006

C1-INH and its effect on infarct size and ventricular function in an acute pig model of infarction, cardiopulmonary bypass, and reperfusion.

BACKGROUND: Recent studies suggest that complement inhibition reduces reperfusion injury. A clinical setting with local application of a C1 esterase inhibitor (C1-INH) has been modeled in an animal study in order to further investigate these findings. METHODS: In 21 pigs, the left anterior descending coronary artery (LAD) was occluded distally to the first diagonal branch for 2 hours (h), including 1 h of cardioplegic arrest during CPB. After release of the coronary snare, C1-INH or NaCl (control) was applied to the aortic root. Thereafter, the aortic cross-clamp was removed and the heart was reperfused for 30 minutes before weaning from CPB. Left ventricular pressure volume analysis was performed by a multielectrode conductance catheter and the area at risk and infarct size were determined from excised hearts. RESULTS: The following data were observed (mean+/-SEM) for the control group and the C1-INH group, respectively, after 1-h ligation of the LAD: heart rate (HR) 86+/-3 and 93+/-6 beats/min, stroke volume (SV) 1.2+/-0.1 and 1.2+/-0.1 ml/kg, aortic pressure (AoP) 83+/-6 and 87+/-5 mmHg, left ventricular end-diastolic pressure (LVedP) 12+/-1 and 11+/-2 mmHg; two hours after weaning from CPB: HR 106+/-9 and 123+/-4 beats/min, SV 0.9+/-0.1 and 0.9+/-0.1 ml/kg, AoP 65+/-5 and 79+/-7 mmHg, LVedP 9+/-1 and 8+/-1 mmHg. Conductance catheter measurements showed no improved left ventricular performance after C1-INH application. Infarct size to area at risk ratio was 61.5+/-4.2% for controls and 61.4+/-4.8% for C1-INH. CONCLUSIONS: Intracoronary application of complement inhibitor in an acute infarction model, which mimicked a clinical setting of urgent coronary bypass grafting after ischemia, has been shown to neither influence the area of infarction, nor the ventricular function.

Animals↗
PubMed1992

[Captopril in acute myocardial infarct: its effect on infarct size and arrhythmias].

The effect of captopril on infarct size and arrhythmias was determined in a prospective, randomized, placebo-controlled double-blind study of 46 patients (9 women, 37 men; mean age 61 [38-86] years). Within 2-18 hours of entry into the study these patients received either a slow intravenous bolus injection of 2.5 or 5.0 mg captopril followed by a continuous infusion of 1.5-2.0 mg/h for a period of 48 hours (n = 22), or of a placebo by the same mode of administration (n = 24). The two groups were comparable as to age, infarct site and time of intervention. All patients, except one in each group, also received nitroglycerin (1.2-6.0 mg/h intravenously). QRS complexes were measured to provide a necrosis index. Q-wave amplitudes decreased under captopril (-0.08 +/- 0.04 mV) while increasing under placebo (+0.15 +/- 0.04 mV; P less than 0.05). The number of ventricular extrasystoles in the first 24 hours after onset of treatment or on placebo was 25/h and 9/h, respectively (P less than 0.02). Ventricular fibrillation occurred in 7 patients of the placebo group, in none of the captopril group. Creatine-kinase infarct weight was 59 and 45 gram-equivalents, respectively (placebo vs treated group: not significant). The mean arterial blood pressure fell by 14 mm Hg during the first hour in the captopril group, but by only 3 mm Hg on placebo (P less than 0.01). These results indicate that captopril has a favourable influence on infarct size and electrical stability which is additional to that provided by standard nitroglycerin treatment.

Adult↗
PubMed1991

[Prognostic significance of prehospital phase in acute myocardial infarct. Results of the Augsburg Myocardial Infarct Registry, 1985-1988].

Data collected by the Augsburg Infarct Register during 1985-1988 were analysed. There were 3,729 cases of acute myocardial infarct (2,672 men and 1,057 women; mean age 62.8 [25-74] years). Before hospitalization cardiac arrest had occurred in 1,401 persons (38%); resuscitation attempts were made in 494 of them (34%). A doctor witnessed the arrest in 243 persons, 13 of whom survived the subsequent 28 days. But none of 640 persons who had a cardiac arrest when only lay people were present survived the first day: resuscitation had been attempted in 39. 518 persons died before hospitalization without anyone present. In the first hour after infarction 30% died, within 4 hours 38% of the total group. The median pre-hospitalization time was 3.11 (range 1.67-8.05) hours. 42% of the patients first called their doctor, 26% went to him (her). This caused decisive delays. The thrombolysis rate was 24%, if the pre-hospital interval was under 6 hours (mortality rate 6% with, 12% without thrombolysis). The prognosis of acute myocardial infarction could be improved by specific instructions to high-risk patients and their relatives and by widening emergency care provisions.

Adult↗
PubMed1995

The effect of the angiotensin-converting-enzyme inhibitor zofenopril on mortality and morbidity after anterior myocardial infarction. The Survival of Myocardial Infarction Long-Term Evaluation (SMILE) Study Investigators.

BACKGROUND: Left ventricular dilatation and neuroendocrine activation are common after acute anterior myocardial infarction. Long-term treatment with an angiotensin-converting-enzyme (ACE) inhibitor may improve outcome by attenuating these processes. We investigated whether the ACE inhibitor zofenopril, administered for six weeks after anterior myocardial infarction, could improve both short-term and long-term outcome. METHODS: A total of 1556 patients were enrolled within 24 hours after the onset of symptoms of acute anterior myocardial infarction, and they were randomly assigned in a double-blind fashion to receive either placebo (784 patients) or zofenopril (772 patients) for six weeks. At this time we assessed the incidence of death or severe congestive heart failure. The patients were reexamined after one year to assess survival. RESULTS: The incidence of death or severe congestive heart failure at six weeks was significantly reduced in the zofenopril group (55 patients, 7.1 percent), as compared with the placebo group (83 patients, 10.6 percent); the cumulative reduction in the risk of death or severe congestive heart failure was 34 percent (95 percent confidence interval, 8 to 54 percent; P = 0.018). The reduction in risk was 46 percent (95 percent confidence interval, 11 to 71 percent; P = 0.018) for severe congestive heart failure and 25 percent (95 percent confidence interval, -11 to 60 percent; P = 0.19) for death. After one year of observation, the mortality rate was significantly lower in the zofenopril group (10.0 percent) than in the placebo group (14.1 percent); the reduction in risk was 29 percent (95 percent confidence interval, 6 to 51 percent; P = 0.011). CONCLUSIONS: Treatment with zofenopril significantly improved both short-term and long-term outcome when this drug was started within 24 hours after the onset of acute anterior myocardial infarction and continued for six weeks.

Aged↗
PubMed1996

A comparison of thrombolytic therapy with primary coronary angioplasty for acute myocardial infarction. Myocardial Infarction Triage and Intervention Investigators.

BACKGROUND: Several relatively small randomized trials have shown that primary angioplasty results in a better short-term outcome than thrombolytic therapy in patients with acute myocardial infarction. These results, however, have not been duplicated other than in investigational trials. METHODS: We compared mortality during hospitalization and long-term mortality, as well as the use of resources, among 1050 patients in a primary-angioplasty group and 2095 patients in a thrombolytic-therapy group. Patients were selected from the Myocardial Infarction Triage and Intervention Project Registry cohort of 12,331 consecutive patients admitted with acute myocardial infarction to 19 Seattle hospitals between 1988 and 1994. Because of the potential for selection bias, several subgroup analyses were performed that included patients eligible for thrombolysis, high-risk patients, and patients in the primary-angioplasty group who were treated at hospitals with high volumes of angioplasty. RESULTS: There was no significant difference in mortality during hospitalization or long-term follow-up between patients in the thrombolytic-therapy group and those in the primary-angioplasty group (mortality during hospitalization, 5.6 percent and 5.5 percent, respectively; P=0.93; adjusted hazard ratio for the risk of death within three years after primary angioplasty, 0.95; 95 percent confidence interval, 0.8 to 1.2). There was also no significant difference in mortality between high-risk subgroups of patients in the two treatment groups. The rates of procedures and costs were lower among patients in the thrombolytic-therapy group both at the time of hospital discharge and after three years of follow-up (30 percent fewer coronary angiograms, 15 percent fewer coronary angioplasties, and 13 percent lower costs after three years of follow-up). CONCLUSIONS: In a community setting, we observed no benefit in terms of either mortality or the use of resources with a strategy of primary angioplasty rather than thrombolytic therapy in a large cohort of patients with acute myocardial infarction.

Angioplasty, Balloon, Coronary↗