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Biomedical subjects

K M Fox

Publications and source records attributed to K M Fox.

At least 217 records · Page 12Linked to original sources
PubMed1978

Plasma lysosomal enzyme activity in acute myocardial infarction.

N-acetyl-beta-glucosaminidase (EC 3.2.1.30, recommended name beta-N-Acetylglucosaminidase) was found to be a constituent of human cardiac lysosomes. beta-glucuronidase was also found in this tissue, while lysozyme, an enzyme present in leucocyte lysosomes, was not detectable in the heart. The activities of both N-acetyl-beta-glucosaminidase and beta-glucuronidase were elevated in plasma during the first 24 h after the onset of chest pain in patients with acute myocardial infarction and the peak levels of N-acetyl-beta-glucosaminidase correlated well with those of creatine kinase. N-acetyl-beta-glucosaminidase showed a further rise in plasma activity which gave a peak at 72 h after the onset of chest pain and this was accompanied by a rise in lysozyme activity. It is suggested that lysosome disruption caused by myocardial cell necrosis was responsible for the initial rise in plasma lysosomal enzyme activity and that the subsequent inflammatory reaction gave rise to the second peak.

Acetylglucosaminidase↗
PubMed1978

A method for praecordial surface mapping of the exercise electrocardiogram.

A technique for praecordial surface mapping of the exercise electrocardiogram is described. This showed the area, time course, and severity of ST segment depression as projected onto the front of the chest after exercise. Twenty normal volunteers and 20 patients with coronary artery disease have been studied. No changes were seen after exercise in the normal subjects but areas of ST segment depression appeared in all 20 patients with angina pectoris. In 5 of the 20 patients with coronary artery disease, the exercise test was repeated on a later date. There were no significant differences in the area of severity of electrocardiographic abnormalities recorded during the two tests. This technique may prove to be useful for diagnosis and assessing medical and surgical treatments in patients with ischaemic heart disease.

Adult↗
PubMed1978

Electrocardiographic precordial mapping in anterior myocardial infarction. The critical period for interventions as exemplified by methylprednisolone.

Serial 72-point precordial mapping of ECG has been recorded to describe the natural history of changes in the precordial areas of ST segment elevation and the development of Q waves in 51 patients with acute uncomplicated anterior myocardial infarction. Eight patients have been studied in the same way but received 25 mg/kg of methylprednisolone sodium succinate as a single intravenous injection within 6 hours from the onset of chest pain. There was a linear relationship between the stable precordial area of Q waves at 24 hours and the rapidly changing precordial areas of ST segment elevation at 2--3 hours, 5--6 hours and 12 hours after the onset of pain in the untreated patients. When methylprednisolone was given, the treated patients developed a smaller precordial area of Q waves at 24 hours than was predicted from the precordial area of ST elevation recorded before the drug was given. This study has introduced a technique that can provide a qualitative assessment of the relationship between ECG evidence of ischemia and infarction in each patient.

Adult↗
PubMed1978

The relationship between myocardial ischaemia and cell death during acute myocardial infarction.

Praecordial mapping of the electrocardiogram (ECG) demonstrated the natural history of ST segment elevation, loss of R and appearance of Q waves in 50 patients suffering uncomplicated anterior myocardial infarction. The results showed that ST segment elevation has a complicated natural history. The loss of R wave electromotive force and development of Q waves were complete by 12 h following the onset of chest pain. This evidence for the loss of viable myocardium was complete before the MB-isoenzyme of creatine kinase (MBCK) was detected in the plasma. Regression analysis of these results showed a direct relationship between the praecordial area of ST segment elevation at 2 h (myocardial ischaemia) and the praecordial area of Q waves at 24 h after the onset of symptoms (cell death). The efficacy of interventions on the natural history of myocardial infarction might be assessed by their effects on the relationship between myocardial ischaemia and cell death.

Acute Disease↗
PubMed1978

The relationship between posture, blood pressure and electrophysiological properties in patients with paroxysmal supraventricular tachycardia.

In 9 patients with paroxysmal supraventricular tachycardia the effects of tilting the body on the blood pressure and on responses during tachycardia or pacing revealed important effects that could influence the clinical presentation and the treatment required. Assessment of these reflex responses adds a major dimension to the understanding of the patient with supraventricular tachycardia.

Atrioventricular Node↗
PubMed1978

Effects of nifedipine on creatine kinase release during myocardial ischemia in dogs.

25 anesthetized mongrel dogs underwent a left thoracotomy. Creatine kinase (CK) activity was measured in serial blood samples drawn simultaneously from the aorta and a coronary vein. The distribution of myocardial perfusion was determined by a continuous infusion of krypton-81m (half-life 13 sec) into the aortic sinuses. Heart rate and arterial blood pressure were also measured throughout the procedure. In 20 dogs regional myocardial ischemia was produced by ligation of a major branch of the left anterior descending coronary artery. Five of these dogs received 1 microgram.kg-1 nifedipine i.v. and a further 5 received 13 microgram.kg-1. Thoracotomy alone produced a slight rise in plasma CK activity but the arteriovenous difference (AV) across the segment of the heart remained positive over 5 h. Myocardial ischemia in the untreated dogs caused a considerable increase in CK activity and the AV difference became negative at 90 min. Treatment with the lower dose of nifedipine considerably reduced the plasma CK activity and the AV difference did not become negative until 3 h. Regional myocardial perfusion showed a significant improvement. Conversely, the higher dose of nifedipine produced a marked increase in the area of ischemia and an acceleration of CK release from the heart. This was associated with a decrease in arterial pressure and an increase in heart rate. These results show that nifedipine can be beneficial in experimental myocardial infarction but care must be taken to avoid hypotension and increases in heart rate.

Animals↗
PubMed1977

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.

Adult↗
PubMed1977

Safe amounts of contrast medium for angiocardiography in neonates and infants.

The results were analysed of 485 (biplane) cineangiocardiograms performed in 200 consecutive cardiac investigations on neonates (under 4 wk) and infants (4 wk to 1 yr). 10 deaths occurred during or within 24 h of cardiac catheterization, all in patients who were profoundly acidemic because of their hemodynamic disturbance. A total dose of Cardio-Conray at any one investigation of 4-5 ml/kg body weight was satisfactory and without undue risk. Single injections of 1.5-2.0 ml/kg body weight were safe whilst providing optimal diagnostic information. The interval between multiple injections did not appear to affect the risk to the patients.

Angiocardiography↗
PubMed1976

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.

Aged↗
PubMed1975

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.

Age Factors↗
PubMed1975

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.

Aged↗
PubMed1975

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.

Adrenergic beta-Antagonists↗
PubMed1975

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.

Acute Disease↗
PubMed1975

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.

Acute Disease↗