Myocardial infarction in young women with special reference to oral contraceptive practice.

Sixty-three women discharged from hospital with a diagnosis of myocardial infarction and 189 control patients were studied. All were under 45 years of age at the time of admission. Current oral contraceptive use, heavy cigarette smoking, treated hypertension and diabetes, pre-eclamptic toxaemia, and obesity were all reported by, and type II hyperlipoproteinaemia was found more often in, patients with myocardial infarction than their controls. The relationship between myocardial infarction and oral contraceptives could not be explained in terms of an association between the use of these preparations and the other factors. The combined effect of the risk factors was clearly synergistic.     

Myocardial infarction and nitric oxide

The report deals with the induction of the inducible form of nitric oxide synthase (iNOS) in infarcted heart muscle of rabbit and man. In the rabbit, nitric oxide synthase was significantly increased in the infarcted area beginning on the third day following ligation of a coronary artery. iNOS induction occured primarily in macrophages. In man, iNOS immunoreactivity was also primarily localized in macrophages on the seventh day following death from myocardial infarction. Of the specific inhibitors of iNOS in infarcted heart muscle, S-methylisothiourea (SMT) was the most potent. Its greatest effect occured in the normal non-affected area of the heart. Dexamethasone and cyclosporin A failed to inhibit NOS. Apoptosis of macrophages commenced two days following ligation of a coronary artery.     

Myocardial infarction after taking zolmitriptan

We report the case of a patient with mild non-obstructive coronary artery disease who sustained an inferior wall myocardial infarction shortly after taking zolmitriptan as abortive therapy for migraine headaches. A Medline search was performed to review all reported cases of myocardial infarction related to migraine therapy with zolmitriptan and related medications. Zolmitriptan may cause myocardial infarction (MI) even in the absence of significant coronary artery disease.     

The fate of young individuals with a history of myocardial infarction]

The fate of young individuals (to 45 years) with a history of myocardial infarction during 12 years was analysed with the aid of a questionnaire containing questions of both social and medical character. Sudden cardiac death or the second infarction were the most frequent causes of death during the first two years following myocardial infarction. Change in the physical activity mainly involved the return to work. Only 47% of young men and 29.8% of women started full-time jobs. They mainly belonged to so-called white collars. The lack of patients' physicians permission was a main cause of the abstinence of young men from the occupation. A position within the family and social activity usually remained unchanged in the majority of patients, but every third patient greatly reduced sexual activity. Every third patients continued smoking, and did not observe recommended diet despite the systematical medical check-ups. The course of the disease is unclear in the majority of young patients. It is often deformed and requires further, detailed information on young patients' style of life.     

Myocardial infarction and intramyocardial injection models in swine

Sustainable and reproducible large animal models that closely replicate the clinical sequelae of myocardial infarction (MI) are important for the translation of basic science research into bedside medicine. Swine are well accepted by the scientific community for cardiovascular research, and they represent an established animal model for preclinical trials for US Food and Drug Administration (FDA) approval of novel therapies. Here we present a protocol for using porcine models of MI created with a closed-chest coronary artery occlusion-reperfusion technique. This creates a model of MI encompassing the anteroapical, lateral and septal walls of the left ventricle. This model infarction can be easily adapted to suit individual study design and enables the investigation of a variety of possible interventions. This model is therefore a useful tool for translational research into the pathophysiology of ventricular remodeling and is an ideal testing platform for novel biological approaches targeting regenerative medicine. This model can be created in approximately 8-10 h.     

Antiphospholipid antibodies in young myocardial infarction patients

Myocardial infarction (MI) is a multi-factorial disease which claims many young lives. There are very few Indian studies that have investigated antiphospholipid antibodies (APLs) in MI patients. APLs have been implicated in arterial thrombosis including premature coronary artery and cerebrovascular thrombosis. In the present study, the prevalence of two clinically significant APLs--anticardiolipin antibody (ACA) and lupus anticoagulants (LA) in young MI patients was studied and compared with age- and sex-matched controls. Fifty healthy blood donors and 40 young MI patients (less than 45 yrs) diagnosed according to the American Heart Association guidelines were recruited for the study. The criteria for diagnosis were presence of atleast two of three classical findings including: clinical symptoms, diagnostic ECG, and presence of one or more cardiac biomarkers out of raised CK-MB isoform and T-troponin on serial measurement. LA and ACA were tested by lupus-sensitive activated partial thromboplastin time (aPTT) and ELISA respectively. Elevation of ACA was observed in 9 patients, while 6 were positive for LA. ACA of IgG isotype was detected in 8 patients. One patient had LA and raised ACA of IgG and IgM isotypes. Antiphospholipid antibodies were found to be significantly associated with MI in young patients, when considered together (p < 0.05) and in coronary thrombosis, mild elevation of ACA may be considered significant.     

Myocardial infarction size: measurement and modification

The majority of in-hospital deaths from acute myocardial infarction occur as a result of the “power failure” syndrome (severe congestive heart failure and cardiogenic shock), which results from extensive loss of myocardium. The death of myocardial cells is sequential over many hours. Surrounding the central zone of necrosis in an acute myocardial infarction is a zone of ischemic myocardium whose fate might be altered by interventions during the early phase of the infarction. ST-segment mapping, serial measurement of the serum concentration of creatine phosphokinase and myocardial imaging by means of radionuclides are being developed for the noninvasive assessment of infarct size in animals and humans. A number of interventions appear to limit infarct size in animals. There have been relatively few studies in humans to date, but preliminary results suggest that infarct size might be limited by certain interventions. The research has provided important practical benefits in terms of understanding the course of acute myocardial infarction and the potential effects of conventional therapies. For the present, interventions designed to limit infarct size remain in the realm of clinical research; routine clinical use would be inappropriate.