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Background and Purpose: Stroke complicating acute myocardial infarction is associated with substantial morbidity and mortality. The purpose of this study was to assess the incidence, predictors, and impact on mortality of stroke/transient ischemic attacks occurring after hospital discharge in a large unselected population of acute myocardial infarction survivors., Methods: During a secondary prevention study with nifedipine (SPRINT), demographic, anamnestic, and clinical data were collected for 5839 consecutive acute myocardial infarction patients admitted to 13 coronary care units in Israel. Hospital survivors (n = 4808) were followed for a year after their discharge. Mortality was assessed for a mean follow-up of 5.5 years (range, 4.5 to 7 years)., Results: One percent (48/4808) of hospital survivors from acute myocardial infarction experienced a stroke/transient ischemic attack in the year after acute myocardial infarction. Thirty-one percent (15 of 48) of events occurred in the first month after hospital discharge. Incidence was higher among older patients (> 70 years; 1.9%), those with anterior site of myocardial infarction (1.35%), a previous history of myocardial infarction (1.8%), hypertension (1.4%), stroke in the past (4.1%), and chronic atrial fibrillation (9%). Multivariate analysis identified the following as independent predictors of stroke/transient ischemic attacks occurring in the year after hospital discharge: chronic atrial fibrillation, older age, history of previous myocardial infarction, anterior myocardial infarction site, serum glutamic oxaloacetic transaminase levels more than four times above upper normal limits, and stroke in the past. The age-adjusted 1-year and long-term mortality rates (4.5 to 7 years; mean, 5.5 years) were significantly higher in patients with (31% and 62%) than in those without stroke/transient ischemic attacks (9% and 31%, respectively; P < .01)., Conclusions: Stroke/transient ischemic attack is a relatively rare (1%) complication in the year after hospital discharge from acute myocardial infarction, though more frequent in the first month. Chronic atrial fibrillation, older age, anterior myocardial infarction site, serum glutamic oxaloacetic transaminase levels more than four times above upper normal limits, past myocardial infarction, and stroke identify high-risk patients. Patients suffering from subsequent stroke/transient ischemic attacks experienced higher mortality than counterparts who remained free from this complication.

The incidence of complete atrioventricular block (AVB) in a large group of patients with Q-wave inferior acute myocardial infarction (AMI) was 251 (11%) of 2273 patients. This incidence was significantly higher in women (14%) and patients > 70 years old (15%) than in men and patients < 70 years old (10% and 9%, respectively). Patients with complete AVB exhibited more serious arrhythmic and mechanical complications during hospitalization and included more patients with very high enzyme levels than their counterparts without AVB. The in-hospital mortality rate was 92 (37%) of 251 patients with complete AVB versus 200 (11%) of 1890 in those without AVB (p < 0.0001). After adjustment for age, gender, and important anamnestic, medical, and enzymatic findings, complete AVB emerged as an independent predictor of in-hospital mortality, yielding an odds ratio of 2.0 (90% confidence interval 1.12 to 3.57). The long-term (5-year) mortality rate in hospital survivors was slightly but not significantly higher in patients with complete AVB (28%) during hospitalization than in their counterparts with no AVB (23%). In view of these data, patients with inferior AMI in whom complete AVB develops are at increased risk and may benefit from urgent revascularization; the postdischarge management of survivors with complete AVB should be no different from that of patients without AVB.

In countries with aging populations acute myocardial infarction (MI) in the elderly is increasing rapidly and hospital and long-term mortality remain high. During 1981-83, 5839 consecutive patients with acute MI were hospitalized in 13 coronary care units in Israel. Of these, 653 (11%) were older than 75 years, 41% were women, and 70% had a first MI. The hospital mortality in these very elderly patients was 35%. The mortality rates 1 and 5 years postdischarge were 24% and 55%, respectively. In view of this high risk and the promising results obtained elsewhere with thrombolysis, particularly in the elderly, this treatment should be routinely considered in elderly patients with acute MI when there are no specific contraindications.

Purpose: To determine whether a circadian pattern in onset of symptoms existed and possible external triggers were implicated in the precipitation of acute myocardial infarction (AMI)., Patients and Methods: One thousand eight hundred eighteen consecutive patients with AMI hospitalized in 14 of the 21 existing coronary care units in Israel during the study period were assessed., Results: The frequency of onset of symptoms by 6-hour intervals showed a predominant morning peak (6 AM to noon) (32%, p < 0.01) in comparison with the other three 6-hour intervals of the day. The preponderance of the morning peak persisted for subgroup analysis by gender (males 32%, females 31%); age (less than or equal to 65 years--32%; greater than 65 years--33%); diabetes mellitus (present or absent, 32%). However, patients with peripheral vascular disease and those with stroke in the past had a predominant evening peak. Possible external triggers of onset of AMI were present in 10% of patients. Exceptional heavy physical work, violent quarrel at work or at home, and unusual mental stress were the three most frequent possible external triggers reported immediately before or within the 24 hours preceding pain onset. Patients with possible external triggers were more likely to be males (85%) and were somewhat but not significantly younger (63.1 years) in comparison with patients without external triggers (73% and 64.3 years respectively)., Conclusions: In a large group of consecutive patients with AMI, a predominant cyclic morning peak of pain onset was found in comparison with the other hours of the day. Possible external triggers precipitating AMI were involved in a minority of cases, suggesting that endogenous changes occurring in the morning hours are generally responsible for the increased rate of myocardial infarction occurring after awakening.

Background: The administration of nifedipine, 30 mg/d, between 7 and 22 days after hospitalization for an acute myocardial infarction (Secondary Prevention Reinfarction Israel Nifedipine Trial study) showed no effect on subsequent mortality and morbidity. Since a possible indication of benefit was observed in patients with a second- or higher-order infarction, a second trial was conducted with a higher dose (60 mg/d), early administration (usually within 3 hours of hospital admission), and in high-risk patients only., Methods: A total of 1358 men and women with suspected acute myocardial infarction (MI), judged not to require calcium antagonist therapy, were randomized to receive nifedipine, 60 mg/d, or placebo between November 1985 and July 1986. Study medication was discontinued in 352 patients because they did not exhibit study criteria for MI or lacked high-risk criteria, or because they decided to discontinue the study. Thus, the treated high-risk group included 1006 patients, of whom 826 were successfully titrated to the target dose of 60 mg/d and were treated for up to 6 months., Results: In the 1006 patients, mortality was 18.7% among those randomized to nifedipine and 15.6% in the patients randomized to placebo. This reflected an increased mortality of 7.8% as compared with 5.5% during the first 6 days in the nifedipine and placebo groups, respectively (adjusted mortality odds ratio by logistic regression, 1.60; 95% confidence interval, 0.86 to 3.00). Among the 826 patients who continued treatment, mortality was equal in the nifedipine (9.3%) and placebo (9.5%) groups. No differences in the rates of nonfatal MI (5.1% and 4.2% in the nifedipine and placebo groups, respectively), hospitalization due to unstable angina, and frequency of chest pain reported during follow-up were observed. An increased rate of sudden death (4.9%) in the placebo group in comparison with the nifedipine group (2.3%) was not statistically significant on post hoc testing, nor was an effect of nifedipine demonstrable in post hoc analyses by congestive heart failure status of randomized patients., Conclusion: Nifedipine as a prophylactic treatment in patients immediately after acute MI or in survivors recovering 1 week or longer after acute MI appears ineffective. Early routine administration of nifedipine in acute MI, other than to patients in whom it may be specifically indicated (eg, those with Prinzmetal's variant angina or severe hypertension) may be hazardous and seems to be contraindicated.

Purpose: The purpose of this study was to report the prevalence and the clinical significance of clinically recognized chronic obstructive pulmonary disease (COPD) during acute myocardial infarction., Patients and Methods: During 1981 to 1983, a secondary prevention study with nifedipine (SPRINT) was conducted in Israel among 2,276 survivors of acute myocardial infarction. During the study, demographic, historical, and medical data were collected on special forms for all patients with diagnosed acute myocardial infarction in 13 hospitals (the SPRINT Registry, n = 5,839). Mortality follow-up was completed for 99% of hospital survivors for a mean follow-up of 5.5 years (range: 4.5 to 7 years)., Results: The prevalence of COPD was 7% (406 of 5,839). The latter rate increased significantly in men (7.6%), smokers (9.7%), and older patients (70 years or older, 10.0%). Patients with COPD exhibited a complicated hospital course with an in-hospital mortality rate of 23.9%. Subsequent mortality rates in survivors at 1 and 5 years were 12.3% and 35.9%, respectively. Rates at the same time periods in patients without COPD were 17.2%, 9.2%, and 26.9% (p < 0.005 for in-hospital and 5 years). In a multivariate analysis that included age, gender, and history of myocardial infarction and congestive heart failure, COPD was not independently associated with either in-hospital or postdischarge excess fatality rates., Conclusion: In this large cohort of consecutive patients with myocardial infarction, the prevalence of COPD was 7% and higher among smokers, men, and elderly patients. Although in-hospital and postdischarge mortality rates were higher among patients with COPD, this condition did not independently increase either the risk of early death or the risk of long-term mortality among survivors of acute myocardial infarction.

In a controlled, prospective, randomized study of the effects of diuretic therapy on serum, lymphocyte, and erythrocyte potassium, magnesium, and calcium concentrations, 155 patients were followed up for six months after experiencing acute myocardial infarction. Of these, 48 patients received furosemide and potassium; 37 patients received hydrochlorothiazide and amiloride hydrochloride; and 70 patients did not require diuretics. Lymphocyte and erythrocyte cation concentrations were all statistically significantly lower in the furosemide-treated patients when compared with the patients in the nondiuretic-therapy group or the hydrochlorothiazide-amiloride-treated group, with no change in serum levels. Since the combination of low intracellular potassium and magnesium concentrations in patients with recent myocardial infarction may be of importance in the cause of arrhythmias, we suggest that potassium- (and magnesium-) sparing diuretics be used in the treatment of patients, when necessary, unless their diuretic needs cannot be met by such agents.

Serum, lymphocyte, and erythrocyte potassium, magnesium, and calcium levels were measured in 215 patients during the five days following acute myocardial infarction. Serum potassium fell from 4.25 +/- 0.05 to 4.08 +/- 0.06 mmol/liter (p less than 0.001), magnesium from 0.93 +/- 0.01 to 0.85 +/- 0.01 mmol/liter (p less than 0.001), and calcium from 2.4 +/- 0.02 to 2.2 +/- 0.08 mmol/liter (p less than 0.001). Lymphocyte potassium increased from 18.1 +/- 1.5 to 51.6 +/- 4.3 pmol/100 cells (p less than 0.001) and magnesium from 2.0 +/- 0.1 to 8.2 +/- 0.8 pmol/100 cells (p less than 0.001), whereas calcium decreased from 2.9 +/- 0.27 to 1.4 +/- 0.25 pmol/100 cells (p less than 0.001). Erythrocyte cations remained constant. There was a larger increase in lymphocyte potassium in patients with tachyarrhythmias than in patients without (70.4 and 46.9 pmol/100 cells, respectively, p less than 0.001), whereas the presence of a high lymphocyte magnesium level was associated with a significant decrease in the development of tachyarrhythmias, despite high potassium concentrations. It is suggested that lymphocyte cation concentrations mirror myocardial interstitial concentrations and that a high interstitial magnesium level has a protective effect on the increased cell excitability due to, and despite, a high interstitial potassium level.