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Biomedical subjects

K M Fox

Publications and source records attributed to K M Fox.

At least 199 records · Page 11Linked to original sources
PubMed1981

The use of propranolol and nifedipine in the medical management of angina pectoris.

This study investigates the use of propranolol and nifedipine in the treatment of angina pectoris. The clinical response and the effects on the precordial 16-lead electrocardiogram before and after exercise were studied in 52 patients with frequent angina pectoris. Relief of chest pain and abolition of exercise-induced ST-segment depression was achieved in 16 patients on treatment with propranolol alone (mean dose, 300 mg/d). Of the remaining 36 patients, the precordial area and severity of exercise-induced ST-segment depression were unchanged in 8 patients, of whom 2 reported they were free from chest pain, improved in 10 patients of whom 4 reported they were free of chest pain, and abolished in 14 patients, all of whom were free from chest pain following treatment with both propranolol and nifedipine (mean dose, 50 mg/d). Four patients were unable to tolerate this combination. This study has shown that in patients who do not respond to treatment with propranolol alone the combination of propranolol and nifedipine can be used to control not only anginal pain, but also the precordial electrocardiographic manifestations of ischemia.

Angina Pectoris↗
PubMed1981

Treatment of angina pectoris with propranolol: the harmful effects of cigarette smoking.

The effects of smoking on the treatment of angina has been studied in 10 patients. Each patient underwent 4 randomized 1-week treatments consisting of on and off smoking, and on and off propranolol (360 mg/day). At the end of each treatment a maximal exercise test was performed using 16 praecordial leads. Smoking was associated with a significantly higher heart rate, blood pressure, area and severity of ST-segment depression. This was not abolished by propranolol. Thus, smoking aggravates the simple haemodynamic variables used to assess myocardial oxygen requirements and the electrocardiographic signs of ischaemia; this is true even after treatment with propranolol.

Angina Pectoris↗
PubMed1981

The dose-response effects of nifedipine of ST-segment changes in exercise testing: preliminary studies.

This study examines the effects of increasing doses of nifedipine on exercise-induced ST-segment depression in patients with severe typical stable angina pectoris. 10 patients underwent four 1-week treatment periods in a single-blind clinical trial. These were nifedipine 0, 30, 60, and 90 mg in divided doses daily. At the end of each week a maximum exercise test was performed using 16 precordial electrocardiographic leads and the ST-segment changes measured immediately after exercise. In 4 patients nifedipine produced no effects on these electrocardiographic parameters; 4 patients improved and 2 deteriorated. Thus, a dose of nifedipine, effective in 1 patient, can have opposite effects in another.

Angina Pectoris↗
PubMed1981

Myocardial ischemia and angina pectoris: the clinical problem in patients.

The morbidity and mortality suffered by patients with coronary artery disease is probably caused by the development of myocardial ischemia. Angina pectoris occurs not only during stress but also at rest and at night. This suggests that myocardial ischemia may be caused by a variety of mechanisms. Ambulatory monitoring of ST segment changes was performed in 60 patients presenting with angina, positive ECG stress tests and coronary artery disease. 85% of ischemic ECG events were asymptomatic, 37% occurred with no increase in heart rate and 15% of episodes either lasted 20 minutes or more or fluctuated in severity. A controlled pilot study in ten patients showed that the combination of high dose propranolol and nifedipine produced a significant decrease in chest pain and episodes of ST depression. Radionuclide studies in 50 patients with angina and coronary artery disease have shown that stress (i.e., atrial pacing) produced different patterns of disturbed regional myocardial perfusion related to the patient's exercise capacity and eventually leading to a decrease in regional myocardial perfusion during the ischemic episode. St segment depression appeared only after the decrease in regional myocardial perfusion. These findings combined with past research suggest that patients with angina and coronary artery disease can suffer frequent asymptomatic disturbances of the regional myocardial perfusion. The frequency of these episodes and the time course for the recovery of the metabolic consequences mean that segments of ventricular myocardium may be constantly abnormal. The relative importance of changes in coronary tone and malfunction of platelets in the diseased coronary tree needs to be examined in clinical research. Pilot studies of antiplatelet agents have shown a significant beneficial effect on episodes of ischemia occurring at night and those occurring without any increase in heart rate. The techniques and observations in these patients with coronary artery disease all suggest that acute transient regional myocardial ischemia is caused by a variety of mechanisms. Further research using objective methods is required to discover the causes of ischemia and to rationalize treatment. f

Angina Pectoris↗
PubMed1980

The effects of propranolol on myocardial perfusion and metabolism during acute regional ischaemia.

The unique physical properties of the short-lived inert and freely diffusing isotope 81mkrypton allow a continuous observation to be made of regional myocardial perfusion. Eighteen dogs were anaesthetised and a reversible snare placed on the left anterior descending coronary artery (LAD). 81mKrypton was used to study regional myocardial perfusion, and myocardial metabolism was assessed using the epicardial ECG and release of creatine kinase activity (CK). Six dogs did not undergo LAD occlusion ("sham operated"); in six other dogs the LAD was occluded (controls), and another six dogs were given propranolol, 0.5 mg/kg, 20 min after LAD occlusion. All the parameters were measured before and for 5 h after LAD occlusion. When compared to controls, dogs treated with propranolol showed significant improvement (p less than 0.01) in regional myocardial perfusion; smaller loss of electrically active myocardium for any given degree of early ST-segment elevation; and a delay in the release of CK activity from a local coronary vein. These results suggest that propranolol exerts a beneficial effect following the development of acute myocardial infarction.

Animals↗
PubMed1980

Electrophysiological manifestations of non-penetrating cardiac trauma.

Electrophysiological disturbances were observed in four cases of non-penetrating cardiac trauma. Ventricular tachycardia occurred both as an early and late complication in three, responding to medical treatment in two; it was cured by cryoablation in the other case. The fourth patient developed an isolated conduction defect associated with anteroseptal myocardial infarction, the coronary arteries and left ventricular function being normal.

Adult↗
PubMed1980

Hypoplastic and fibrotic sinus node associated with intractable tachycardia in a neonate.

A case of fetal and neonatal persistent atrial tachycardia is described in a child with complete transposition of the great arteries. At autopsy, serial sections of the conducting tissue showed that the sinus node was hypoplastic and markedly fibrotic. The sinus node consisted of a small area of cells clustered around the nodal artery. Although the underlying mechanism of neonatal persistent tachycardia is unclear, it is possible that the hypoplasia and fibrosis of the sinus node was the substrate in the present case. This mechanism should be considered in any newborn infant in whom sinus rhythm cannot be established.

Ductus Arteriosus, Patent↗
PubMed1980

Plasma lysosomal enzyme activity in acute myocardial infarction and the effects of drugs.

The activity of N-acetyl-beta-glucosaminidase (NAG) was found to be increased in serial plasma samples from patients with acute myocardial infarction (AMI). Maximum activity occurred 18 hr after the onset of chest pain, and a further peak of activity was found at 72 hr. Four isozymes of NAG were resolved from samples of human myocardium. All four isozymes were present in plasma from patients with AMI but not in normal plasma. beta-Glucuronidase, which is also present in myocardium, had increased activity in plasma at 18 hr but not at 72 hr in patients with AMI. Lysozyme, a lysosomal enzyme in white blood cells, had increased activity in plasma at 72 hr. There was a linear relationship (r = 0.98) between peak levels of NAG at 18 hr and the peak activity of the MB-isozyme of creatine kinase (CK-MB). Three groups of 10 patients were treated with drugs known to stabilize lysosomes during experimental myocardial anoxia. The first group received 25 mg/kg methylprednisolone sodium succinate i.v. within 4 hr of the onset of chest pain. The second group received propranolol, 5-mg, i.v. within 4 hr of the onset of chest pain. The second group received propranolol, 5-mg, i.v. within 4 hr of the onset of chest pain, and the third group comprised patients who developed AMI while on propranolol therapy and were maintained on this drug after admission to the hospital. All three groups showed an alteration in the pattern of lysosomal and cytosolic enzyme activity and a relative reduction in NAG activity compared to CK-MB.

Acetylglucosaminidase↗
PubMed1979

Indication and clinical significance of exercise surface mapping.

A technique of recording electrocardiographic maps after exercise is described. This technique allows a measurement to be made of the area of ST segment changes that are projected onto the front of the chest after exercise. A comparison of the sensitivity and specificity of this technique with the orthogonal lead system and a single chest lead showed that praecordial exercise mapping was significantly superior to the other two lead systems in the diagnosis of ischaemic heart disease and may help in identifying patients with extensive disease. In addition information obtained from praecordial exercise mapping can be used to increase the data that are obtained from Holter monitoring of ST segments. The place of the technique in the management of medical and surgical treatment remains to be evaluated.

Coronary Disease↗
PubMed1979

Relation between the precordial projection of S-T segment changes after exercise and coronary angiographic findings.

The recent introduction of electrocardiographic mapping permits measurement of the precordial area and severity of exercise-induced S-T segment changes. This study was designed to compare this technique with a modified 12 lead electrocardiogram in defining the degree and site of coronary artery disease. One hundred patients, who later had diagnostic coronary arteriography, underwent an exercise test using both 16 point precordial mapping and a modified 12 lead electrocardiogram. The sensitivity of electrocardiographic mapping (96 percent) for the diagnosis of coronary artery disease was significantly greater than that of the modified 12 lead electrocardiogram (80 percent). However, the specificity of the two lead systems was similar. Typical precordial projections of S-T segment change were found when the left main stem or proximal left anterior descending coronary artery were narrowed or when there was isolated disease of the left anterior descending or right coronary artery. Widespread precordial changes were found in patients with three vessel disease. Although there was no significant difference in the sensitivity (66 percent) and specificity (100 percent) of electrocardiographic mapping and of the 12 lead system in identifying three vessel disease, there was a significant difference in sensitivity (electrocardiographic mapping 74 percent, 12 lead system 42 percent) in identifying isolated single vessel disease. In addition, information regarding the presence of left main stem or proximal left anterior descending coronary arterial narrowing was obtained only with electrocardiographic mapping. The superiority of electrocardiographic mapping over the modified 12 lead electrocardiogram has been shown, and clinical application of this technique should be useful in the management of patients presenting with chest pain.

Adult↗
PubMed1979

Projection of electrocardiographic signs in praecordial maps after exercise in patients with ischaemic heart disease.

Praecordial surface maps of the electrocardiogram were recorded before and after exercise using 16 electrodes covering the left hemithorax. The ST segment and R and S wave changes were measured in the praecordial maps from 20 individuals with no detectable cardiovascular disease. These showed no significant alteration in ST segments of R/S. In contrast in 40 patients with angiocardiographically proven coronary artery disease it was possible clearly to outline the distribution, severity, and time course of praecordial areas of ST segment depression (36 patients) and ST segment elevation (10 patients). In addition these praecordial areas of ST segment changes were accompanied by a regional and significant fall in the R/S. The praecordial electrocardiogram with exercise complements the anatomical information obtained from the coronary arteriogram by clearly outlining electrocardiographic projections of regional myocardial ischaemia or cell death.

Adult↗
PubMed1979

Precordial mapping of ST-segment elevation and Q waves following anterior myocardial infarction. The effects of established beta-blocking drugs.

The electrocardiographic (ECG) signs of ST-segment elevation and the development of Q was using 72-lead precordial surface mapping, and the release of creatine kinase (CK) activity has been studied in 47 patients with uncomplicated anterior myocardial infarction. These findings were compared with a further nine patients who had acute myocardial infarction but were receiving long-term beta-blocking drugs. It was found that ST-segment elevation and Q waves had rapidly changing and different natural histories and that beta-blocking drugs altered the natural history of ST-segment changes but had no effect on the pattern and time course for the loss of electrically active myocardium. There was a close relationship between the precordial area of ST-segment elevation at 2--3 h and the final development of Q waves in the patients with uncomplicated anterior myocardial infarction. No similar relationship could be found in those on beta-blocking drugs. The pattern of changes in plasma CK and its MB isoenzymes activity were similar for both groups. The relationship between early ST-segment elevation and the final area of Q waves may prove useful in clinical practice. This may not apply where beta-blocking drugs are commenced before the initial recording of ST-segment elevation.

Acute Disease↗
PubMed1979

An experimental model for angina pectoris using krypton-81m. The dynamic balance between myocardial perfusion and metabolism.

16 anesthetized and open chest dogs were studied. Regional myocardial perfusion was assessed using a constant infusion of krypton-81m (half-life 13 sec) into the aortic sinuses and a gamma camera linked to a digital computer. The epicardial electrocardiogram was recorded and the plasma activity of creatine kinase was measured in serial blood samples from the aorta and a local coronary vein draining the area of myocardium supplied by the left anterior descending coronary artery (LAD). These parameters were observed throughout the whole period of a 5-h experiment. Two reversible snares were positioned on the middle portion of this artery. A critical narrowing of this vessel was produced and a peripheral venous infusion of isoproterenol (causing a 5--10% increase in heart rate and a 10--15% fall in blood pressure) was used to increase myocardial oxygen demand. During infusion there was both a relative and absolute fall in regional myocardial perfusion together with evidence of myocardial ischemia in the epicardial electrocardiogram. Provided the infusion was discontinued within 30 min (8 dogs) myocardial perfusion and the epicardial electrocardiogram returned to normal during a 5-h recovery period. In addition there was no efflux of creatine kinase activity from the ischemic area. When infusion was continued for 1 h (4 dogs) permanent alterations in myocardial perfusion and the epicardial electrocardiogram occurred and there was increased creatine kinase activity released from the area of myocardium by the narrowed vessel. Infusion for 40 min in 4 dogs produced permanent alterations in the parameters measured in 2 and complete recovery in the remaining 2. A further 4 dogs were studied in the same way but without a snare on the coronary artery. Isoproterenol given for 1 h produced no effects on any of the parameters either during or after infusion.

Angina Pectoris↗
PubMed1978

The effect of established beta-adrenoreceptor-blocking therapy on the release of cytosolic and lysosomal enzymes after acute myocardial infarction in man.

1. Serial venous blood samples were obtained from 45 patients with acute myocardial infarction. Ten of these patients were receiving beta-adreno-receptor-blocking drugs at the time of onset of chest pain and continued on these drugs during their stay in the coronary care unit. The activities of creatine kinase and its MB-isoenzyme (CK-MB) were assayed in the plasma. A lysosomal enzyme, beta-N-acetylglucosaminidase, was also assayed. 2. In the 35 untreated patients it was found that creatine kinase activity was maximal at a mean time of 21.3 +/- 1.3 h after the onset of chest pain, whereas in the patients receiving beta-adrenoreceptor-blocking drugs peak activity of the enzyme occurred at 24.4 +/- 0.7 h. 3. Peak CK-MB acitivity was also delayed from 18.1 +/- 1.6 h in the control group to 22.4 +/- 1.2 h in the treated patients. 4. The lysosomal enzyme showed a similar pattern of changes to that of CK-MB. Maximum activity in plasma occurred at 18.0 +/- 1.0 h after the onset of chest pain in the control group of patients. In the treated patients peak lysosomal enzyme activity was not found until 24.2 +/- 1.2 h. 5. These alterations in the time-course of plasma enzyme changes after acute myocardial infarction are consistent with the suggestion that beta-receptor antagonists may delay tissue damage during myocardial ischaemia.

Acetylglucosaminidase↗