Cardiac arrhythmias 48 hours before, during, and 48 hours after discharge from hospital following acute myocardial infarction.

The cardiac rate and rhythm were studied by 24-hour ambulatory electrocardiographic recording in 44 patients before, during, and after being discharged from hospital following an acute myocardial infarction. The first recordings were started 48 hours before discharge, the second on the morning of the day of discharge, and the third 48 hours after discharge (at home). While in hospital and after returning home the heart rate fell during sleep but there was no diurnal variation in the frequency of ventricular extrasystoles. Daytime heart rate and both the frequency and grade (severity) of ventricular arrhythmias were significantly raised 48 hours after discharge. The frequency of ventricular extrasystoles during sleep was also increased in the 48 hours post-discharge recording. Rises in heart rate and frequency and severity of ventricular extrasystoles were observed on the morning of the day of discharge, increasing up to the time of leaving hospital, but during the journey home they all diminished. No relation was found between ventricular arrythmias during early convalescence and (i) ventricular arrhythmias during the acute phase of acute myocardial infarction (including ventricular fibrillation); (ii) peak aspartate aminotransferase; (iii) the level of anxiety; or (iv) the personality type. Six patients taking beta-blocking drugs behaved similarly. Five patients taking anxiolytic drugs has significantly raised frequency of ventricular extrasystoles during each 24-hour electrocardiogram. In spite of the above findings, at the time of leaving hospital after acute myocardial infarction there does not appear to be a serious risk from the development of major cardiac arrhythmias.

Vomiting as a diagnostic aid in acute ischaemic cardiac pain.

The incidence of vomiting before the administration of analgesics was studied in 109 patients admitted to hospital as emergencies with prolonged ischaemic cardiac pain. In transmural myocardial infarction (58 patients) the incidence was 43% (anterior infarction 58%, inferior infarction 41%). Of the 23 patients with myocardial necrosis but without transmural infarction (that is, those with diffuse or subendocardial necrosis) and the 28 with coronary insufficiency but no necrosis, only one patient in each group experienced vomiting. When vomiting occurs early in association with cardiac pain transmural infarction may be expected in 90% of patients.

The combined clinical and hemodynamic effects of trinitrin and propranolol.

The clinical and hemodynamic effects of trinitrin (nitroglycerin) have been studied in 5 patients with long-established coronary artery disease who had been receiving long-term beta blockade therapy (propranolol). 5 similar patients not on propranolol acted as controls. Patients on propranolol reported as effective relief of angina with trinitrin as patients not on this therapy. Although the patients on propranolol had an initially lower systolic blood pressure and mean ventricular rate, sublingual trinitrin caused in both groups a similar fall in aortic pressure, pulmonary wedge pressure, oxygen consumption and stroke volume, together with a similar rise in ventricular rate. It was concluded that trinitrin was as effective, both subjectively and objectively, in patients on propranolol as in those without beta blockade and promoted similar side effects.

Streptokinase in acute myocardial infarction: a controlled multicentre study in the United Kingdom.

In a multicentre trial of streptokinase in acute myocardial infarction 302 patients received an intravenous infusion of 2 500 000 IU of streptokinase over 24 hours, while 293 patients served as controls. Neither group received anticoagulants unless indicated by thromboembolic complications. No significant difference in mortality was evident during inpatient treatment nor at six-week or six-month follow-up. The inpatient death rate was 12-6% in the streptokinase group and 13-7% among controls. There was no significant difference in the peak levels or pattern of enzyme increase. The incidence of cardiac failure and reinfarction was similar in the two groups, but major arrhythmias were less common in those on streptokinase (P less than 0-05). In the streptokinase group there were 36 minor and six more serious haemorrhagic complications. Gastrointestinal haemorrhage may have contributed to the death of one patient in each group. There were 18 thromboembolic complications in the streptokinase group and 38 among the controls. Pathological examination of the hearts of 25 patients who had taken streptokinase and 24 controls showed no striking differences between the groups, but haemorrhagic infarcts were found in three patients who had received streptokinase. An infusion of streptokinase within 24 hours of the onset of acute myocardial infarction does not significantly affect the mortality or course of the illness up to six months.

Primary ventricular fibrillation and resumption of work, sexual activity, and driving after first acute myocardial infarction.

The resumption of work, sexual activity, and driving were studied in 32 patients who had suffered primary ventricular fibrillation after their first myocardial infarction. They were compared with 95 patients whose myocardial infarction was not so complicated. Though initially slowing rehabilitation, primary ventricular fibrillation did not affect ultimately either the return to work or the resumption of normal sexual activity and driving.

Prognostic significance of acute systolic hypertension after myocardial infarction.

The clinical behaviour and mean peak serum aspartate aminotransferase (SGOT) values of 106 patients admitted to a coronary care unit with acute myocardial infarction who displayed acute systolic hypertension were studied. Another 106 normotensive patients with acute myocardial infarction acted as controls. Neither group had established hypertension. The mortality rate, incidence of cardiac failure, major arrhythmias, and mean peak SGOT were significantly greater in the hypertensive group, within which the duration of hypertension was correlated with mean peak SGOT levels--through there was no definite relation between the height of systolic or diastolic pressure and SGOT. Transient systolic hypertension after acute myocardial infarction was therefore associated with a relatively poor prognosis, but our observations suggest that patients with a systolic blood pressure of at least 170 mm Hg might benefit from early hypotensive treatment.

Low voltage electrocardiogram after acute myocardial infarction.

In a retrospective study of patients with acute myocardial infarction admitted to a coronary monitoring unit in 1971 12 per cent (39 patients) had low voltage electrocardiograms within 72 hours of admission. Of these, 7 patients (18%) died while in hospital and a further 9 (23%) died within one year of their infarction. Of the 23 patients who survived, 16 were severely incapacitated by their symptoms at the one-year follow-up. A low voltage electrocardiogram in association with acute myocardial infarction appears to imply a poor prognosis in terms of both mortality and morbidity, independently of other prognostic indices.

Long-term beta blockade: possible protection from myocardial infarction.

The clinical behaviour of 90 patients on beta-blocking drugs for established coronary heart disease who were admitted to a coronary care unit with prolonged ischaemic myocardial pain was compared with that of 90 similar patients not on this therapy. Transmural myocardial infarction was confirmed in 30 of the patients on beta-blockers and in 62 controls. A diagnosis of myocardial necrosis without infarction was made in 20 patients on beta-blockers and in 14 controls. Coronary insufficiency was diagnosed in 40 patients on beta-blockers and in 14 controls. The incidence of simus bradycardia, hypotension, syncope, and radiological pulmonary oedema was similar in the two groups. Established beta-blockade, therefore, has not been shown to prejudice the outcome of patients with coronary heart disease admitted to hospital with prolonged ischaemic myocardial pain. On the contrary, it may protect some patients from the development of a myocardial infarction.

The influence of psychological factors and an early hospital follow-up on return to work after first myocardial infarction.

The factors influencing the return to work following first myocardial infarction were studied in 112 male patients, all of whom had previously been fully employed. Delay in return to work within 4 months of discharge from hospital was seen in patients who were not given an early hospital follow-up appointment and in those who attibuted their illness to aspects of their work. Encouragement by the General Practitioner to resume employment was found to be essential if an unnecessary delay was to be avoided. Positive advice of this nature was given more frequently by General Practitioners whose patients had been seen at early hospital review. Age, a tendency to neuroticism, personal knowledge of how others had fared following a similar illness, and apparent benefit from sick payments did not appear to influence the rate of return to work.

Lignocaine therapy for ventricular ectopic activity after acute myocardial infarction: a double-blind trial.

The effectiveness of intravenous lignocaine in suppressing ventricular ectopic activity after acute myocardial infarction was examined in a double-blind trial in 82 patients. Whereas suppression of unifocal ventricular ectopics was achieved by lignocaine in 90% of patients, other forms of potentially more dangerous ectopic activity (multifocal or R-on-T ectopics) seemed more resistant to therapy. Cessation of ectopic activity was also observed in about one-third of the patients in the control group. The incidence of ventricular tachycardia and fibrillation and the mortality during and after the trial period were similar in the lignocaine-treated and control groups, whether or not the initial ventricular ectopics had been suppressed.This study provides no evidence to support the routine use of intravenous lignocaine in the management of ventricular ectopic activity after acute myocardial infarction.