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Biomedical subjects

S M Cobbe

Publications and source records attributed to S M Cobbe.

11 recordsLinked to original sources
PubMed1992

Effects of the class III antiarrhythmic drug dofetilide on ventricular monophasic action potential duration and QT interval dispersion in stable angina pectoris.

The effects of intravenous dofetilide on ventricular monophasic action potential duration and effective refractory period at the right ventricular apex and outflow tract were studied in 18 patients (aged 37 to 70 years) with ischemic heart disease. Six patients received low-dose dofetilide as a 3 micrograms/kg loading dose over 15 minutes and a 1.5 micrograms/kg maintenance dose over 45 minutes; 6 received high-dose dofetilide 6 + 3 micrograms/kg and 6 placebo. During atrial pacing at a cycle length of 800 ms high-dose dofetilide prolonged right ventricular apex monophasic action potential duration by 45 ms (16%) and the effective refractory period by 40 ms (16%). At the right ventricular outflow tract, monophasic action potential duration was prolonged by 45 ms (15%) and effective refractory period by 55 ms (21%). During atrial pacing at a cycle length of 500 ms high-dose dofetilide prolonged the right ventricular apex monophasic action potential duration by 40 ms (18%) and the effective refractory period by 43 ms (21%). The right ventricular outflow tract monophasic action potential duration was prolonged by 33 ms (14%) and effective refractory period by 45 ms (21%). Dofetilide produced no increase in the dispersion of repolarization between the 2 sites. During the maintenance infusion QTc prolongation by high-dose dofetilide averaged 43 ms (10%) with no increase of interlead QT dispersion. The effects of dofetilide on QT interval and effective refractory period are shown to be due to a direct effect on action potential duration with no effect on dispersion. No rate dependence of monophasic action potential prolongation was detected at these cycle lengths.

Action Potentials↗
PubMed1992

Beta endorphin release in patients after spontaneous and provoked acute myocardial ischaemia.

BACKGROUND: In animal models of circulatory shock and heart failure concentrations of the endogenous opioid peptide beta endorphin are raised and opioid receptor blockade improves haemodynamic variables and survival. This study was performed to identify whether acute myocardial ischaemia provokes the release of beta endorphin in humans. METHODS: Observational study in a university cardiology centre. Serial measurements of beta endorphin made by specific radioimmunoassay were correlated with other clinical and neuroendocrine variables that were measured prospectively. Fifty five patients with acute myocardial ischaemia and 26 patients undergoing elective coronary angioplasty of the left anterior descending coronary artery were studied. RESULTS: beta endorphin concentrations were raised above the upper limit of normal in 31/42 (74%) patients with confirmed myocardial infarction, 3/13 (23%) patients with unstable angina, and 10/24 (42%) patients after coronary angioplasty. There was no evidence of myocardial release of beta endorphin. There were significant positive correlations between beta endorphin and the concentrations of adrenocorticotrophic hormone, cortisol, and arginine vasopressin. In patients with acute myocardial ischaemia there was a significant positive correlation between the peak concentrations of creatine kinase and beta endorphin but no correlation with visual analogue scores of the intensity of chest pain. The highest beta endorphin concentrations were seen in patients whose clinical course was complicated by the development of heart failure. CONCLUSIONS: beta endorphin release is a component of the neuroendocrine activation associated with myocardial ischaemia/infarction.

Acute Disease↗
PubMed1992

Symptomatic and silent myocardial ischaemia in hypertensive patients with left ventricular hypertrophy.

OBJECTIVE: To assess the prevalence of symptomatic and silent myocardial ischaemia in patients with hypertensive left ventricular hypertrophy. DESIGN: Cross sectional study. SETTING: University department of medical cardiology. PATIENTS: 90 patients (68 men and 22 women; mean age 57 (range 25 to 79)) with left ventricular hypertrophy due to essential hypertension. INTERVENTIONS: 48 hour ambulatory ST segment monitoring (all patients), exercise electrocardiography (n = 79), stress thallium scintigraphy (n = 80), coronary arteriography (n = 35). RESULTS: 43 patients had at least one episode of ST segment depression on ambulatory electrocardiographic monitoring. The median number of episodes was 16 (range 1 to 84) with a median duration of 8.6 (range 2 to 17) min. Over 90% of these episodes were clinically silent. 26 patients had positive exercise electrocardiography and 48 patients had reversible thallium perfusion defects despite chest pain during exercise in only five patients. 18 of the 35 patients who had coronary arteriography had important coronary artery disease. Seven of these patients gave no history of chest pain. CONCLUSIONS: Symptomatic and silent myocardial ischaemia are common in hypertensive patients with left ventricular hypertrophy, even in the absence of epicardial coronary artery disease.

Adult↗
PubMed1978

Continuous monitoring of mixed venous oxygen tension (PvO2) in cardiorespiratory disorders.

The development of a miniature polarographic electrode mounted in the tip of a double-lumen plastic catheter has made possible continuous in-vivo monitoring of oxygen tension. Inexpensive catheters of this type have already proved of value as a means of continuously monitoring arterial oxygen tension in the newborn. In 25 patients with acute respiratory failure we found that these catheters could be safely and easily flow-guided into the pulmonary artery. In this way continuous recordings of mixed venous oxygen tension (PvO2) could be made for a period of several days. In our experience a sustained fall of PvO2 below 40 mm Hg proved to be a reliable indicator of respiratory or cardiac deterioration not always obvious by observation. In the patients described, falls of this order were seen after reductions in inspired oxygen concentration, in acute respiratory failure, in accidental underventilation, and in hypovolaemia and cardiac arrythmias. In some very ill patients routine nursing care involving movement of the patient caused pronounced falls of PvO2. Although electrode drift was an occasional problem, this could be checked by intermittent blood-sampling and recalibration if necessary.

Aged↗
PubMed1978

Acute effects of diuretics on potassium exchange, mechanical function and the action potential in rabbit myocardium.

1. We have studied the acute effects of frusemide, triamterene and amiloride on potassium exchange, the action potential and mechanical function of isolated rabbit myocardium. 2. Potassium exchange in the myocardium was unaltered by these diuretics. 3. Frusemide and amiloride did not affect the action potential of rabbit papillary muscles. Triamterene caused a transient shortening of the action potential. 4. Frusemide and triamterene did not alter myocardial mechanical function in rabbit papillary muscles or the interventricular septum. Amiloride caused a reduction of about 5% in developed tension in two out of three papillary muscles.

Action Potentials↗
PubMedDate not supplied

Efficacy of out of hospital defibrillation by ambulance technicians using automated external defibrillators. The Heartstart Scotland Project.

During the Heartstart Scotland project all 407 ambulances in Scotland were equipped with automated external defibrillators (AEDs). All cases of chest pain or collapse aged over 10 years were monitored and multiple 3-s rhythm strips recorded in a solid state memory module. A shockable rhythm was defined as an organised rhythm of > or = 180 beats/min or a disorganised rhythm of > or = 100 beats/min and amplitude > 0.1 mV. We analysed all the stored rhythm strips in two patient populations to determine the ability of the AED and ambulance crews to detect a shockable rhythm and to initiate appropriate defibrillation. The first population comprised 493 patients, all of whom had received shocks. A total of 4741 rhythm strips were analysed, of which 1461 were true positives, 33 false positives, 3161 true negatives and 86 false negatives. Overall sensitivity of the AED was 94.4% and specificity 99.0%. The second population comprised a random sample of 200 shocked and 200 non-shocked arrests. The combined group contained 4154 rhythm strips of which 562 were true positives, 12 false positives, 3460 true negatives and 120 false negatives. Overall sensitivity of the system (AED+crew) was 82.4% and specificity 99.7%. However, only 66 of the 120 false negatives were attributable to the AED giving a sensitivity of 90.3% for the AED. The sensitivity of the AED is dependent on the prevalence of shockable rhythms, but will be within the range 90.3-94.4% for most emergency medical services. We conclude that early management of potentially lethal arrhythmias by ambulance technicians using AEDs is practical with acceptable sensitivity and specificity.

Ambulances↗
PubMedDate not supplied

Approaches to experimental arrhythmias in heart failure.

Sudden cardiac death accounts for at least 50% of the mortality of patients with heart failure. Available clinical evidence suggests that lethal ventricular arrhythmias are responsible for the vast majority of cases of sudden death in heart failure. However, despite extensive clinical investigation over the last decade, there has been relatively little experimental study of the mechanisms underlying the development of lethal ventricular arrhythmias in heart failure. In addition to the original process leading to myocardium alterations, the role of other arrhythmogenic mechanisms such as ventricular overload and neuro endocrine activation remains to be elucidated. In ventricular hypertrophy both reentry and triggered activity may induce arrhythmias. Some studies on experimental models of heart failure did not provide consistent results concerning electrophysiological modifications and their relations with arrhythmias. Few studies in man in vivo are in favor of prolongation as well as increased dispersion of repolarisation in patients undergoing heart transplantation for idiopathic dilated cardio-myopathy. Further studies will need to be undertaken to clarify mechanisms underlying arrhythmias in heart failure.

Animals↗