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Biomedical subjects

T L Wenger

Publications and source records attributed to T L Wenger.

32 records · Page 2Linked to original sources
PubMed1983

Sinus node dysfunction.

The syndrome of sinus node dysfunction has become increasingly recognized as a cause of symptoms and morbidity, particularly in the elderly population. This syndrome does not represent a homogeneous disease entity. Increased investigation has shown that many pathologic conditions and pathophysiologic mechanism may lead to one of the several clinical and electrocardiographic manifestations of the sick sinus syndrome. Attempts to improve diagnostic accuracy, identify underlying mechanisms and to predict the outcome of therapy have led to the development of various diagnostic tests. However, at present these have proven of limited clinical value and the mainstay of diagnosis remains ECG monitoring. Treatment is directed at the control of symptoms with pacemaker therapy for bradyarrhythmias and combined pacemaker and antiarrhythmic drug therapy for the bradycardiatachycardia syndrome.

Anti-Arrhythmia Agents↗
PubMed1982

Effect of myocardium at risk on outcome after coronary artery occlusion and release.

The relationship between the probability of sustaining ventricular fibrillation during occlusion or release of a canine coronary artery and the amount of myocardium made ischemic has never been carefully assessed. We occluded the left anterior descending coronary artery above or below the septal artery for 20 min and then released the ligation. The amount of left ventricle perfused by the ligated vessel was determined by injection of different color monastral dyes above and below the ligation. Despite careful ligature placement immediately proximal or distal to the septal artery, there was wide variation in the amount of left ventricle perfused by the ligated vessel, or myocardium "at risk." Myocardium at risk ranged between 24 and 51 g for ligations placed above the septal artery and 14 and 27 g for ligations placed below the septal artery. Ventricular fibrillation during occlusion and after release correlated significantly with the amount of myocardium at risk. This relationship was well described using the logistic risk regression model. The model predicts uniformly low and uniformly high probability of ventricular fibrillation with small and large amounts of myocardium at risk, respectively, and a direct correlation for midrange values of myocardium at risk. This relationship can account for a substantial portion of non-drug related variability in outcome of antiarrhythmic trials using the canine coronary occlusion or release model.

Animals↗
PubMed1980

Hypersensitive carotid sinus syndrome manifested as cough syncope.

We describe a patient with cough syncope who was found to have carotid sinus hypersensitivity with mixed cardioinhibitory and vasodepressor responses. Symptoms were ameliorated by denervation of the more hypersensitive carotid sinus. Spontaneous atypical Wenckebach cycles in this patient were caused by the combined hypersensitive cardioinhibitory and vasodepressor responses. This report stresses the importance of checking blood pressure as well as heart rate in all patients in whom carotid sinus syndrome is suspected.

Blood Pressure↗
PubMed1978

Risk stratification after acute myocardial infarction.

One hundred patients admitted to the hospital with acute myocardial infarction who lived 10 days and agreed to enroll were studied. Data from the history, hospital course and a 24 hour Holter electrocardiographic recording were related to cardiac mortality in the 6 months after enrollment. Fifteen cardiac deaths occurred during this period; 12 of these were sudden. The univariates with the strongest association with mortality were (in descending order): blood urea nitrogen level, serum creatinine level, serum uric acid level, enlarged heart 2 weeks after infarction, ventricular tachycardia 2 weeks after infarction, peak creatine kinase level and left ventricular failure in the coronary care unit. The odds of dying if one of these factors was present rather than absent ranged from 3.6 to 11.5. Groups with two or these univariates had up to 20 times the odds of dying in 6 months. A period of greately enhanced risk for cardiac death persists for about 6 months after acute myocardial infarction. Relatively simple clinical variables can identify the groups at highest and lowest risk. This information is useful for designing management strategies.

Acute Disease↗
PubMedDate not supplied

Myocardial procainamide concentration in canine atria and ventricles.

The aim of this investigation was to examine the distribution of procainamide in the canine heart. Eight anesthetized open-chest dogs received intravenous infusions of 14C-labeled procainamide at 40 micrograms/kg/min for 4 hr. Just prior to the end of the infusion period, 51Cr-labeled microspheres were injected into the left atrium to measure regional myocardial blood flow. The heart was then excised and dissected into regional myocardial sections from each cardiac chamber. Samples from each section were combusted, and the liberated 14CO2 was trapped and counted to determine regional myocardial procainamide concentration. The remainder of each section was analyzed for 51Cr to determine regional myocardial blood flow. Plasma procainamide concentration (mean +/- SE) at the termination of the infusion was 2.68 +/- 0.14 micrograms/ml. Left ventricular procainamide concentration was 6.09 +/- 0.46 micrograms/g. The right ventricular drug concentration was 94% (NS), the left atrial concentration was 85% (p less than 0.005), and the right atrial concentration was 79% (p less than 0.005) of the left ventricular concentration. Within the myocardium of each cardiac chamber there was no correlation between drug concentration and blood flow. We conclude that these concentration differences are insufficient to explain differences in procainamide efficacy between ventricular and atrial arrhythmias.

Animals↗