Search

Purpose: The aim of the study was to assess the prevalence and the prognostic impact of concomitant peripheral vascular disease (PVD) in patients developing acute myocardial infarction (AMI)., Patients and Methods: Four thousand two hundred fifty-eight consecutive patients with a first AMI hospitalized in 13 of 21 operating coronary care units in Israel were screened. Anamnestic, demographic, and medical data were collected from hospitalization charts, and all patients were followed clinically 1 year after discharge and up to 7 years (mean: 5.5 years) for mortality., Results: The prevalence of clinically diagnosed PVD in patients with a first AMI was 6.3% (269 of 4,258), with no difference between men and women. Patients with PVD were older (66.2 years) and included more hypertensive subjects (47.2%), diabetic persons (26.4%), and individuals with a previous history of cerebrovascular accident (CVA) (11.5%) in comparison to counterparts without PVD (61.7 years; 39.4%, 19.9%, and 3.3%, respectively; p < 0.01 for each). On admission to the coronary care units, 36.5% of patients with PVD were in Killip class II, III, or IV versus only 18.0% in the reference group (p < 0.001). During hospitalization, patients with PVD exhibited a significantly higher rate of paroxysmal atrial fibrillation (17.5%), advanced atrioventricular block (15.2%), and cardiogenic shock (11.9%) in comparison to patients without PVD (11.9%, 10.2%, and 5.3%, respectively; p < 0.01 for each). After adjustment for age, gender, hypertension, history of angina, diabetes mellitus, history of CVA, site of infarction, and congestive heart failure on admission, the odds ratio for in-hospital mortality associated with PVD was 1.37 (90% confidence interval 1.01 to 1.83). There was no independent contribution of PVD to long-term (mean: 5.5 years) postdischarge mortality; the odds ratio was 1.02., Conclusion: PVD in patients with a first AMI independently increases the risk of in-hospital death but does not affect long-term mortality in survivors.

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.

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.

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.