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[Patient-specific determinants of delay in goal-oriented patient behavior in acute myocardial infarct. Results of the post-infarct late potential study].

369 (63%) of 586 consecutive patients with confirmed myocardial infarction were admitted to hospital within 6 h of symptom onset. Patients' arrival to hospital followed a characteristic circadian distribution with a marked morning increase between 0600 and 1200 hours, and a corresponding decrease in the late night hours. There were no differences in the occurrence of late potentials and in ECG data between early and late arrival group. The early group (less than 5.9 h) was, however, characterized by significantly higher cardiac enzyme levels than the late group (greater than 6.0 h); they also experienced more arrhythmic events in the acute phase (16.0% vs. 9.7%; p less than 0.032). Catecholamines were significantly more often necessary (26.4% vs. 10.3%; p less than 0.0001). Six-month prognosis after AMI was markedly worse. The time between symptom onset and hospital arrival was not affected by age and risk factors. In univariate analysis, pain history and recurrent infarction also had no influence on delay of admission to hospital. The time interval was, however, significantly shorter when the acute event occurred during the night (18.4% vs. 8.3%; p less than 0.0001). Absence of prodromi in the prehospital phase (18.5% vs. 12.0%; p less than 0.04) and a higher socio-economic level (68.3% vs. 61.0%; p less than 0.077) also shortened the admission time, whereas a hyperactive behavioral pattern prolonged the delay time (21.1% vs. 28.9%; p less than 0.05).

Adult↗

[Clinical manifestations of ischemic heart disease in the subacute period of myocardial infarction and post-infarct cardiosclerosis depending on the status of coronary arteries].

Multifactor discriminant analysis was used on a computer to examine 100 patients with myocardial infarction in the subacute period (at week 4 of the disease onset) and 76 in the postinfarction period (at months 2-120 of postinfarction). A complex of clinical and coronary signs was defined, which differentiated patients with subacute myocardial infarction and postinfarct cardiosclerosis, as well as those with postinfarct stable and progressive angina pectoris.

Acute Disease↗

Secondary prevention of death and reinfarction with verapamil after an acute myocardial infarction. The Danish Study Group on Verapamil in Myocardial Infarction.

The effect of verapamil on death, reinfarctions, and major events i.e. reinfarction or death, has been investigated in two Danish double-blind, placebo-controlled verapamil infarction trials DAVIT I and II. DAVIT I, which was an early intervention trial, demonstrated that after six months there was a statistically non-significant reduction of mortality and reinfarction. DAVIT II demonstrated a non-significant reduction of mortality rate (P = 0.11, hazard ratio 0.80, 95% confidence limits 0.61-1.05), a significant reduction of reinfarction rate (P = 0.04, 0.77, 0.58-1.03), and major event rate (P = 0.03, 0.80, 0.64-0.99) in the verapamil group compared with the placebo group. Meta-analyses of DAVIT I (including only patients alive on day eight) and of DAVIT II showed a statistically significant reduction of odds ratio of mortality of 22% (P = 0.04), of reinfarctions of 27% (P = 0.02), and of major events of 21% (P = 0.02). It is concluded that long-term treatment with verapamil after an acute myocardial infarction is associated with a significant reduction in overall mortality, major events, and reinfarction rates.

Anti-Arrhythmia Agents↗

Stroke in patients treated with thrombolytic therapy for acute myocardial infarction. The thrombosis in myocardial infarction clinical trial and a review of placebo-controlled trials.

The frequency of stroke among patients in six recent placebo-controlled trials of thrombolytic therapy for acute myocardial infarction is reviewed. Three trials used streptokinase and three used tissue plasminogen activator as the thrombolytic agent. While thrombolytic therapy greatly reduces the morbidity and mortality of acute myocardial infarction, it increases the rate of intracerebral hemorrhage.

Cerebrovascular Disorders↗

[Incidence of intravenous thrombolytic therapy and fatalities in patients with acute transmural myocardial infarct (Q infarct). A study of observations from 1984 to 1987].

All patients admitted to the ICU with acute myocardial infarction (MI) were treated by the same protocol since 1984. We report the results in Q-wave-MI of 1987 compared to 1984. Age (67.2 +/- 12.4 vs. 66.8 +/- 11.4 years), sex distribution (70.1% vs. 71.9% male), time elapse between begin of symptoms and admittance to the hospital (15.5 +/- 27.0 vs. 15.0 +/- 32.5 hours) were similar in both years, but the total number of definite Q-MI decreased by 22% from 135 (1984) to 105 (1987). Inhospital mortality (20% vs. 23%) and ICU mortality (14% vs. 20%) tended to decrease, although differences did not reach statistical significance. This was paralleled by an increase in the rate of i.v. thrombolytic therapy from 17% (1984) to 28% (1987) of all patients with Q-MI. The percentage of patients who definitely received i.v. thrombolysis when all indication criteria were present and all contraindicatory factors excluded increased from 47% (1984) to 97% (1987). We conclude, that the performance of i.v. thrombolysis in all patients, who fulfill the general accepted criteria for thrombolysis may improve clinical course and outcome in a given population of patients with acute Q-wave-infarction.

Aged↗

[Ultrastructure of the peri-infarction zone during treatment of experimental myocardial infarct with cardiolin].

Cardiolin therapy influence on the periinfarction zone cardiomyocyte ultrastructure, sarcolemma permeability for colloidal lantan, myocardium energy level were studied in 25 white noninbred rats with experimental myocardial infarction. 6 hours after coronary occlusion ultrastructural damage in treated rats was less pronounced and mitochondria energy efficiency ratio was higher than those in the control group. 24 hours after the occlusion the tendency to normalization of the cardiomyocyte damage in treated rat myocardium was demonstrated, while in non-treated animals ischemic damage becomes irreversible, this being confirmed by the test with colloidal lantan. Cardiolin therapy prevents the infarction zone expansion by decreasing ischemic damage of periinfarction cardiomyocytes and by stimulating regeneration processes in these cells.

Animals↗

Cigarette smoking and the risk of myocardial infarction, and acute non-infarct coronary events among Malaysian women.

In a prospective case-control study over a two-year period involving 1006 women, 264 women with acute myocardial infarction (AMI), 305 with non-infarct acute coronary syndromes (CAD) were compared with 437 women with no coronary heart disease (Controls), to determine the relationship between cigarette smoking and other risks factors with coronary heart disease. A history of current cigarette smoking was strongly associated with the risk of coronary events for both AMI And CAD (p less than 0.001). 23.9% of patients with acute coronary syndromes were current smokers, compared with only 12.8% among controls. Overall, women smokers had about a two-fold increase in risk for all coronary events. Younger women smokers (less than 40 years) and those between 61-70 years had particularly higher risks (10.3 and 2.7 times respectively (p less than 0.01, p less than 0.02). A dose-response pattern of increased AMI risks (from 2.0 to 2.9 times) among women smokers was also found, corresponding to the number of cigarettes smoked per day (p less than 0.05). Other significant coronary risk factors established were: postmenopausal status (OR 6.5), diabetes mellitus (OR 5.1), hypertension (OR 1.6), family history of premature coronary heart disease less than 50 years (OR 1.3) and use of oral contraceptive pills (OR 1.4). Our results thus emphasize that cigarette smoking is an important determinant of acute coronary events even among Malaysian women.

Acute Disease↗

The interaction between diltiazem and left ventricular function after myocardial infarction. Multicenter Diltiazem Post-Infarction Research Group.

The interactions between diltiazem and three parameters of left ventricular function using cardiac death as the end point were investigated in 2,466 patients, aged 25-75 years, who were involved in the long-term diltiazem postinfarction trial. Indexes of left ventricular function included pulmonary congestion on chest x-ray, acute anterolateral Q wave myocardial infarction on electrocardiogram, and radionuclide ejection fraction. Pulmonary congestion and acute anterolateral infarction had significant (p less than 0.01) interactions with treatment allocation, and the third variable, ejection fraction, showed a similar trend (p less than 0.1). There was a diltiazem-related reduction in cardiac death (Cox hazard ratio, 0.76-0.86) for each of the parameters reflecting good ventricular function, and a significant diltiazem-related increase in cardiac death (Cox hazard ratio, 1.52-1.85) for each of the parameters associated with impaired function. Three-factor interactions highlighted the extremes of the favorable and adverse effects of diltiazem in subsets with unimpaired and impaired left ventricular function. These findings permit more appropriate selection of patients for the safe and effective administration of diltiazem to postinfarction patients.

Adult↗

[Infarct size and left ventricular function in patients after thrombolytic therapy of acute myocardial infarct].

The authors give an account of factors which influence left ventricular function after thrombolytic treatment of an occluded coronary artery. They found that improvement of left ventricular function following a three-week interval after recanalization of the artery the occlusion of which led to myocardial infarction, depends on the size of the necrotic focus. Improvement of global left ventricular function and above all of the regional function of the infarction segment can be expected if the size of the focus is such that less than 40 gram-equivalent of total creatine kinase are liberated from it.

Humans↗

Mechanisms for the early mortality reduction produced by beta-blockade started early in acute myocardial infarction: ISIS-1. ISIS-1 (First International Study of Infarct Survival) Collaborative Group.

In a large randomised trial of early beta-blockade in acute myocardial infarction (ISIS-1), almost all the reduction in mortality associated with the use of atenolol occurred on the day of admission or on the subsequent day. To help determine the mechanisms that might be responsible for this retrospective observation, case notes were obtained for British, Irish, and Scandinavian patients who died during this early period. Of 217 early deaths adequate records were available for 193 (79 allocated atenolol and 114 allocated control). In the atenolol group, necropsy had shown cardiac rupture in 5 patients, and a further 15 in whom necropsy had not been done had had electro-mechanical dissociation (total, 20 early deaths from these causes); among control patients the corresponding numbers were 17 and 37 (total, 54 such deaths). Electro-mechanical dissociation was probably a manifestation of acute rupture, and the observed difference in the numbers with this complication was responsible for much of the difference in early mortality. There was a slightly higher incidence of fatal ventricular fibrillation and aortic dissection in the control group, and of bradycardia/asystole in the atenolol group. The data did not indicate any substantial contribution from mechanisms such as limitation of infarct size or prevention of reinfarction or cardiac arrest.

Atenolol↗

Factors influencing the infarct: the place of beta-blockade in limiting infarct size.

The mechanisms whereby myocardial infarction in man is precipitated are not understood--largely because the event is usually well established by the time medical help is called, but also because the techniques available have not yet permitted analysis of the earliest changes. On the other hand, the consequences of myocardial infarction for the heart and circulation are now well understood, and the need for therapy better appreciated.

Adrenergic beta-Antagonists↗

Myocardial infarction and water hardness in the WHO myocardial infarction registry network.

The negative association between water hardness and cardiovascular disease found by several authors in different countries has also been found in the present investigation. All cases of myocardial infarction were registered in a standardized way at 15 WHO Collaborating Centres in Europe; information on the hardness of drinking water used by the population studied was also collected. Higher rates of myocardial infarction were usually found in towns served by softer water.

Aged↗

[The myocardial infarct status of a South German population: results of the Augsburg myocardial infarct register l985].

The Augsburg Myocardial Infarction Register recorded in 1985, 999 coronary events (734 men, 265 women) occurring in 25-74-year-old residents of the city of Augsburg and the counties of Augsburg and Aichach-Friedberg (study population: 156,489 men and 171,093 women). On average, 444 men and 138 women per 100,000 of the population suffered an acute myocardial infarction (AMI) in 1985. The risk of morbidity increased with age in both men and women, but gained significance for women only after their 55th year of life. The 28-day case fatality was 54% for male AMI cases and 66% for females; 34% of the AMI patients died without ever reaching a hospital. Cardiopulmonary resuscitation (CPR) was attempted by a physician in one-in-three of these out-of-hospital deaths. Although one of two out-of-hospital deaths occurred in the presence of a medical lay person; lay CPR was the exception. Broader population education in CPR techniques may thus constitute one method of reducing the number of early AMI deaths. The median prehospital time for interviewed hospital patients (66%) was 5 h, and approximately 2 h for patients with systemic thrombolysis (n = 71). The combination of fatal coronary events from the official cause-of-death statistics and the results from the Augsburg register were used to estimate AMI morbidity for the whole of the FRG in 1985. This leads to an expected morbidity of 210,000 AMI, of which 141,000 AMI will be fatal (both sexes).

Adult↗

Seasonal variation in the incidence of unstable angina and acute myocardial infarction: effect of dry hot climate on the occurrence of complications following acute myocardial infarction.

The incidence of unstable angina (UA) and acute myocardial infarction (AMI), and the occurrence of complications following AMI were studied retrospectively by utilizing data of 7859 patients admitted during three consecutive winter and summer periods from 1979 to 1982. In all patients, UA was more frequent during summer than in winter: 58 out of 3819 (1.5%) versus 37 out of 4040 (0.9%) respectively (P less than 0.05). A similar difference was observed for the incidence of AMI: 183 out of 3819 (4.8%) in summer versus 157 out of 4040 (3.9%) in winter (P less than 0.05). This seasonal variation in the incidence of UA and AMI was significant only in male patients (P less than 0.05). Shock and mortality were higher during summer than in winter in all, and in male AMI patients with or without previous infarction. It is suggested that a hot dry summer is an important risk factor for the occurrence of UA and AMI, and the associated serious complications following the latter in males.

Aged↗

A new physiologic model for dynamic process of creatine kinase activity after acute myocardial infarction and estimation of infarct size.

A new physiologic model for dynamic process of Creatine Kinase (CK) after acute myocardial infarction is proposed. The fundamental hypotheses are tested. The new model is better than the log-normal model in goodness of fit. With this new model, the infarct size of complicated cases with double or multiple peak CK curve can be estimated as well as that of uncomplicated cases. To estimate parameters, a nomographic algorithm and a computer program have been designed. In most cases, the initial values for parameters estimated with Marquardt's method can be determined from individual CK data.

Creatine Kinase↗

Metoprolol in acute myocardial infarction. Enzymatic estimation of infarct size. The MIAMI Trial Research Group.

The maximum serum activity for aspartate aminotransferase (s-ASAT) during the first 3 days was recorded in 5,507 patients with suspected or definite acute myocardial infarction. The s-ASAT activity was corrected for the normal range from each center. The median s-ASAT activity was 4.9 arbitrary units in the placebo group versus 4.6 arbitrary units in the metoprolol group (p = 0.072). Univariate analyses indicated that the delay time between onset of symptoms and randomization and sympathetic activity at entry significantly influenced the effect of metoprolol. A similar decrease in serum enzyme activity after metoprolol treatment was observed independent of signs of infarct localization on the entry electrocardiogram.

Aspartate Aminotransferases↗

Reduction of coagulation factor XIII concentration in patients with myocardial infarction, cerebral infarction, and other thromboembolic disorders.

Coagulation factor XIII and plasma fibrinogen chromatographic assays have been performed serially in patients suffering from acute myocardial and cerebral infarction, and in others with disseminated intravascular coagulation. The findings were compared with 2 groups of "controls"; normal clinically-well subjects and hospitalized patients with cerebral infarction who exhibited minimal, stable, or improving neurological deficits. Substantial depression of factor XIII concentrations developed in the 3 patient groups, together with concomitant significant increases in the proportion and concentration of plasma high molecular weight fibrin(ogen) complexes (HMWFC). An inverse correlation (p less than 0.05) between coagulation factor XIII concentration and percentage of HMWFC was demonstrated in the early stages of the illness. These findings suggest that depression of coagulation factor XIII concentration in these states, is secondary to extravascular or intravascular coagulation and may reflect its degree.

Adult↗

European Infarction Study (E.I.S.). A secondary prevention study with slow release oxprenolol after myocardial infarction: morbidity and mortality.

A multicentre, double-blind, randomized study was carried out to compare the effect on survival, cardiac mortality and non-fatal cardiac events of oxprenolol slow release 160 mg b.i.d. compared with placebo in 1741 patients 35 to 69 years of age who had survived acute myocardial infarction. The patients were entered 14-36 days after infarction and were followed for one year. Recruitment was discontinued before the scheduled 4000 patients had been entered. There were 57 deaths (6.6%) in patients randomized with respect to oxprenolol as compared with 45 deaths (5.1%) in patients randomized with respect to placebo. The difference in cumulative mortality rates (30.4%) is not statistically significant. 275 patients from each treatment group discontinued trial medication. The proportion of deaths was noted to be higher in patients who discontinued trial medication (oxprenolol 13.1%; placebo 7.6%) and in patients 65-69 years (oxprenolol 16.7%; placebo 5.6%). In the 1472 patients less than 65 years of age there was a tendency to a lower mortality in 478 'high risk' patients on beta-blockade [oxprenolol 16 patients (6.9%); placebo 25 patients (10.2%)] as compared with a somewhat higher mortality in the corresponding low risk group (oxprenolol 20 patients [4.0%]; placebo 12 patients [2.4%]). In the 1010 patients under 65 years of age who continued on trial medication, 15 patients (3%) in the oxprenolol group and 22 patients (4.3%) in the placebo group died. The overall results in our trial failed to confirm apparently positive effects in other secondary prevention trials. Debate especially concerns patients older than 65 years of age, patients at relatively low risk, and patients who discontinued oxprenolol treatment.

Adult↗