Background Despite anecdotal evidence suggesting that heavy physical exertion can trigger the onset of acute myocardial infarction, there have been no controlled studies of the risk of myocardial infarction during and after heavy exertion, the length of time between heavy exertion and the onset of symptoms (induction time), and whether the risk can be modified by regular physical exertion. To address these questions, we collected data from patients with confirmed myocardial infarction on their activities one hour before the onset of myocardial infarction and during control periods. Methods Interviews with 1228 patients conducted an average of four days after myocardial infarction provided data on their usual annual frequency of physical activity and the time, type, and intensity of physical exertion in the 26 hours before the onset of myocardial infarction. We compared the observed frequency of heavy exertion (6 or more metabolic equivalents) with the expected values using two types of self-matched analys...

https://www.nejm.org/doi/pdf/10.1056/NEJM199312023292301

Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators

Background Many anecdotes and several uncontrolled case series have suggested that emotionally stressful events, and more specifically, anger, immediately precede and appear to trigger the onset of acute myocardial infarction. However, controlled studies to determine the relative risk of myocardial infarction after episodes of anger have not been reported. Methods and Results We interviewed 1623 patients (501 women) an average of 4 days after myocardial infarction. The interview identified the time, place, and quality of myocardial infarction pain and other symptoms, the estimated usual frequency of anger during the previous year, and the intensity and timing of anger and other potentially triggering factors during the 26 hours before the onset of myocardial infarction. Anger was assessed by the onset anger scale, a single-item, seven-level, self-report scale, and the state anger subscale of the State-Trait Personality Inventory. Occurrence of anger in the 2 hours preceding the onset of myocardial infarct...

Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators.

Background It is controversial whether the onset of myocardial infarction occurs randomly or is precipitated by identifiable stimuli. Previous studies have suggested a higher risk of cardiac events in association with exertion. Methods Consecutive patients with acute myocardial infarction were identified by recording all admissions to our hospital in Berlin and by monitoring a general population of 330,000 residents in Augsburg, Germany. Information on the circumstances of each infarction was obtained by means of standardized interviews. The data analysis included a comparison of patients with matched controls and a case-crossover comparison (one in which each patient serves as his or her own control) of the patient's usual frequency of exertion with the last episode of exertion before the onset of myocardial infarction. Results From January 1989 through December 1991, 1194 patients (74 percent of whom were men; mean age [±SD], 61 ±9 years) completed the interview 13 ±6 days after infarction. We found tha...

https://www.nejm.org/doi/pdf/10.1056/NEJM199312023292302

Physical Exertion as a Trigger of Acute Myocardial Infarction

Objective: To examine the incidence of cardiovascular diseases and cancer from published clinical trials that studied other outcomes of postmenopausal hormone therapy as some surveys have suggested that it may decrease the incidence of cardiovascular diseases and increase the incidence of hormone dependent cancers. Design: Trials that compared hormone therapy with placebo, no therapy, or vitamins and minerals in comparable groups of postmenopausal women and reported cardiovascular or cancer outcomes were searched from the literature. Subjects: 22 trials with 4124 women were identified. In each group, the numbers of women with cardiovascular and cancer events were summed and divided by the numbers of women originally allocated to the groups. Results: Data on cardiovascular events and cancer were usually given incidentally, either as a reason for dropping out of a study or in a list of adverse effects. The calculated odds ratios for women taking hormones versus those not taking hormones was 1.39 (95% confidence interval 0.48 to 3.95) for cardiovascular events without pulmonary embolus and deep vein thrombosis and 1.64 (0.65 to 4.18) with them. It is unlikely that such results would have occurred if the true odds ratio were 0.7 or less. For cancers, the numbers of reported events were too low for a useful conclusion. Conclusions: The results of these pooled data do not support the notion that postmenopausal hormone therapy prevents cardiovascular events. Key messages The results of these pooled data do not support the notion that postmenopausal hormone therapy prevents cardiovascular events These results concern only short term effects of postmenopausal hormone therapy, and long term effects may be different There have been hundreds of trials studying the impact of hormones on various physiological phenomena, laboratory values, osteoporosis, symptoms, or various health problems but few fully report adverse effects. Small trials would be useful in studying unintended effects if they were more systematically reported

/pdf/impact-of-postmenopausal-hormone-therapy-on-cardiovascular-34atvef6w0.pdf

Impact of postmenopausal hormone therapy on cardiovascular events and cancer: pooled data from clinical trials

Recent documentation of a circadian variation in acute myocardial infarction (AMI) suggests that AMI is not a random event, but may frequently result from identifiable triggering activities. The possible triggers reported by 849 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size were analyzed. Possible triggers were identified by 48.5% of the population; the most common were emotional upset (18.4%) and moderate physical activity (14.1%). Multiple possible triggers were reported by 13% of the population. Younger patients, men and those without diabetes mellitus were more likely to report a possible trigger than were older patients, women and those with diabetes. The likelihood of reporting a trigger was not affected by infarct size. This study suggests that potentially identifiable triggers may play an important role in AMI. Because potential triggering activities are common in persons with coronary artery disease, yet infrequently result in AMI, further studies are needed to identify (1) the circumstances in which a potential trigger may cause an event, (2) the specific nature of potential triggering activites, (3) the frequency of such activities in individuals who do not develop AMI and (4) the presence or absence of identifiable triggers in various subgroups of patients with infarction.

Analysis of possible triggers of acute myocardial infarction (the MILIS study).

In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.

Evaluation of clinical factors involved in onset of myocardial infarction.

Comparison of clinical features of non-Q wave and Q wave myocardial infarction

The characteristics of 93 patients in whom electrocardiographic recordings were obtained within 12 hours of the onset of non-Q-wave myocardial infarction were studied. Patients were divided into the three groups according to what electrocardiographic changes were seen. Forty nine patients had ST segment depression, 35 had ST segment elevation, and nine had T wave changes. Patients with ST segment depression had a higher rate of pump failure and multivessel disease than the other two groups. There were no significant differences in peak serum creatine kinase activity among the three groups. Twelve of 13 patients who died of non-Q-wave myocardial infarction in hospital had ST segment depression. Furthermore nine of them had attacks of non-Q-wave myocardial infarction with severe ST segment depression in many leads. At necropsy five of six patients who had shown severe ST segment depressions in many leads at the onset of non-Q-wave myocardial infarction were found to have circumferential subendocardial lesions with triple vessel disease. This study suggests there are electrocardiographic subtypes of non-Q-wave myocardial infarction that are associated with specific patient characteristics.

https://heart.bmj.com/content/heartjnl/54/5/473.full.pdf

Classification of non-Q-wave myocardial infarction according to electrocardiographic changes.

Determination of intracardiac shunts in patients with congenital heart disease by means of analog simulation of radiocardiogram.

(1) ECG-gated RCG were performed in 127 cases, among them 30 were normal controls, 35 were hypertensives, 16 were ischemic heart diseases, 8 were cardiomyopathies and the rest of 38 cases were of miscellaneous cardiac diseases. (2) ECG-gated RCG were performed consecutively after the preceding RCG. Parameters calculated from RCG and ECG-gated RCG were evaluated together in terms of the sensitivity to discriminate the ischemic heart diseases from the control subjects. Among those parameters evaluated, peak diastolic dV/dt was the most sensitive index to discriminate the ischemic heart group from the control group. PDdV/dt of 20 ml/100 msec/m2 was considered to be a borderline between two groups. (3) Principal component analysis of 12 variables in 127 cases demonstrated that the peak diastolic dV/dt was closely correlated with the cardiac pump function, but was also well related to the ischemic heart factor. (4) ECG-gated RCG following the preceding RCG is a sensitive method to discriminate the ischemic heart disease from the control group.

Decreased Early Diastolic dV/dt in Ischemic Heart Disease Observed by ECG-gated Radiocardiography : SYMPOSIUM ON EVALUATION OF CARDIAC FUNCTIONS THROUGH NON-INVASIVE TECHNIQUES

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