Myocardial ischaemia in patients with frequent angina pectoris.

One hundred patients with angina pectoris underwent 16-point electrocardiographic (ECG) mapping of the left hemithorax during a standardised exercise test. Forty-five patients had maximum ST-segment depression at position V5, while 35 had no ECG signs of ischaemia at this position. In 20 V5 was on the edge of the precordial area, which showed less severe ST-depression than the central positions. An Oxford ECG recorder and highspeed analyser were modified and used in 50 of the patients with daily angina for recording ST-segment changes over 24 hours. Serial 24-hour ambulatory recordings from the edge of the precordial area of ischaemia identified during exercise detected a mean of only 14 +/- SD 3% of the episodes of ST-segment changes recorded from the centre of the same area. Only 16 +/- 2% of the episodes detected by ECG were accompanied by chest pain. More episodes occurred between 4 am and 6 am than at any other time during the night. This study shows the importance of recording ECG evidence of ischaemia from the precordial position showing maximum changes during exercise. ECG evidence of ischaemia occurs more frequently than anginal pain. These objective measurements add important information to the frequency of chest pain reported by patients with ischaemic heart disease.     

Myocardial abscess complicating healed myocardial infarction.

An isolated myocardial abscess due to Bacteroides fragilis developed in the scar of a myocardial infarction. Fever, chills and signs of pericarditis were the main clinical features. Mild enteritis 1 week prior to the onset of symptoms related to the abscess was the most likely cause of the bacteremia. The diagnosis was established at thoracotomy, performed because of cardiac tamponade. Thirteen other cases of isolated bacterial myocardial abscess accompanying myocardial infarction have been reported, but all the infarctions were recent. Surgical resection for a suspected myocardial abscess should be considered in view of the high mortality, largely from cardiac rupture.     

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.     

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.