Unreliability of exercise-induced R wave changes as indexes of coronary artery disease

To investigate the diagnostic value of exercise-related QRS amplitude changes, the responses of 40 young normal subjects and 28 patients with chest pain and no significant coronary arterial obstruction were compared with those of 73 patients with coronary arterial narrowing of various degrees of severity. All underwent submaximal, multiple lead multistaged treadmill exercise testing. The combined normal group showed an average decrease in R wave amplitude between rest and exercise of 1.1 ± 2.8 mm (mean ± standard deviation) in lead V₅; those with coronary artery disease had an increase of 0.6 ± 3.4 mm (P = 0.001). Similar but less pronounced differences were observed in lead II (a decrease of 1.9 ± 2.3 mm in normal subjects versus a decrease of 0.5 ± 3.1 mm in those with coronary disease, P = 0.01). When derived R wave criteria were used, the test sensitivity averaged 52 percent and the specificity 63 percent; these values were inferior to the sensitivity of 88 percent and specificity of 72 percent of S-T segment criteria in the same group of patients. No significant relation was found between the extent of coronary artery disease and R wave changes, and an analysis of multiple variables suggested possible correlations with factors not directly related to ischemia. It is concluded that exercise-induced QRS amplitude changes are unreliable predictors of the presence, absence or severity of coronary artery disease.     

Cushing's syndrome due to adrenal adenoma with persistent diurnal cortisol secretory rhythm.

A 41-yr-old female with presumed Cushing's syndrome was found to have a diurnal cortisol rhythm characterized by low values of 8:00 a.m. and consistently high values at 4:00 p.m. and midnight. Hourly sampling of plasma cortisol over 24 hr confirmed this rhythm, as did measurement of urinary free cortisols in samples collected every 6 hr over 24 hr. Hypercortisolemia was not suppressed by 2 mg of dexamethasone given every 6 hr for 24 hr. The adrenal tissue was responsive to ACTH. Iodocholesterol scanning revealed unilateral activity, and the patient's syndrome was cured by resection of an adrenal adenoma. In this patient a diurnal cortisol secretory pattern was present due to the secretory activity of the adenoma. The cause of the abnormal but persistent diurnal pattern is unknown.     

Effects of exogenous insulin, glucagon, and somatostatin on islet hormone secretion in the perfused chicken pancreas

The effects of exogenous insulin were examined in the isolated perfused chicken pancreas with the duodenum excluded. At low background glucose (50 mg/dl), exogenous insulin infused at a concentration of 20,000 microU/ml elicited clear stimulation of somatostatin secretion while simultaneously inhibiting glucagon release. When the background glucose concentration was elevated to 750 mg/dl, exogenous insulin, had no effect on either somatostatin or glucagon release. When graded doses of exogenous insulin were infused into the chicken pancreas at low background glucose, low concentrations (200 microU/ml) had little effect on somatostatin or glucagon release, but higher concentrations (2000 and 20,000 microU/ml) had clear effects on both somatostatin and glucagon secretion. Glucagon infused at 100 ng/ml stimulated both insulin and somatostatin release. When somatostatin was infused at 25 ng/ml, clear inhibition of glucagon was seen with insulin inhibited to a lesser extent. This study supports the notion of a negative feedback relation between B and D-cells of the pancreatic islets and suggests a paracrine mediation.     

Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man

Of 42 patients with supraventricular tachycardia related to dual atrioventricular (A-V) nodal pathway conduction, 8 had sustained tachycardia induced during programmed ventricular stimulation. The characteristics of the tachycardia in three patients suggested that the A-V nodal reentrant tachycardia used a slow pathway for anterograde conduction and a fast pathway for retrograde conduction (slow-fast form). In these patients, the retrograde effective refractory period was longer in the slow than in the fast pathway. Ventriculoatrial (V-A) conduction curves (V₁-V₂, A₁-A₂) were smooth. Ventricular premature beats, being conducted retrograde over the fast pathway, could activate the slow pathway in an anterograde direction, initiating the slow-fast form of A-V nodal reentrant tachycardia. In the remaining five patients, the tachycardia used a fast pathway for anterograde conduction and a slow pathway for retrograde conduction (fast-slow form). In these patients, the retrograde effective refractory period was longer in the fast than in the slow pathway. V-A conduction curves (V₁-V₂, A₁-A₂) could be either smooth or discontinuous if there was a sudden increase in V-A conduction time. Ventricular premature beats, conducted retrograde over the slow pathway, could activate the fast pathway in an anterograde direction, establishing a tachycardia circuit in reverse of the slow-fast form. In both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction.The fast-slow form of A-V nodal reentrant tachycardia, similar to the slow-fast form, could also be induced during atrial premature stimulation in two patients. In this situation, the slow pathway having an anterograde effective refractory period longer, than that of the fast pathway was a requisite condition; anterograde A-V nodal conduction curves (A₁-A₂, H₁-H₂) were smooth. Atrial premature beats, conducted anterograde over the fast pathway, could activate the slow pathway in a retrograde direction resulting In an atrial echo or sustained fast-slow form of A-V nodal reentrant tachycardia.     

Effect of glucagon on cardiac conduction in man

His bundle electrograms were obtained in 26 patients before and after intravenous administration of glucagon (50 μg/kg). The group consisted of 4 patients with normal conduction and 22 patients with conduction disease. The P-A interval, measured in all patients, was 35 ± 1.4 msec (mean ± standard error of the mean) before and 30 ± 1.5 msec after infusion of glucagon (P < 0.001). The mean A-H interval during sinus rhythm in all patients and during pacing at 100/min in 21 patients was, respectively, 97 ± 6.0 msec and 114 ± 6.4 msec before, and 96 ± 6.0 msec and 114 ± 6.6 msec after infusion of glucagon (not significant). The mean H-V interval in 25 patients was 48 ± 2.6 msec before and 49 ± 2.0 msec after infusion of glucagon (not significant). The mean sinus rate and sinus recovery times were, respectively, 73 ± 3.0 beats/min and 1,025 ± 42.0 msec before and 81 ± 3.0 beats/min and 919 ± 27.0 msec after infusion of glucagon (P < 0.001 and < 0.01). Functional and effective refractory periods were measured (In milliseconds) with use of the atrial extrastimulus technique. The mean atrial functional and effective refractory periods (21 patients) were, respectively, 273 ± 11.6 and 252 ± 12.0 before and 256 ± 10.0 and 238 ± 9.6 after infusion of glucagon (P < 0.001 and < 0.01). Mean atrloventricular (A-V) nodal functional refractory period (22 patients) and effective refractory period (15 patients) were 465 ± 22.0 and 404 ± 33.0 before and 457 ± 23.0 and 395 ± 32.0 after the infusion (not significant). The mean effective refractory period of the His-Purkinje system (2 patients) was 440 ± 45.0 before and 425 ± 55.0 after infusion of glucagon (not significant).In summary, glucagon increased sinus nodal automaticity, as manifested by an increase in sinus rate and decrease of sinus nodal recovery time, and improved intraatrial conduction as manifested by a reduction of the P-A interval and atrial functional and effective refractory periods. Glucagon had no effect on A-V nodal or intraventricular conduction.     

Atrial pacing during selective aortocoronary saphenous vein bypass angiography

Selective aortocoronary bypass graft angiography was performed in 30 postoperative subjects. Thirty-one of 39 patent graft injections resulted in cardiac arrhythmias including sinus bradycardia, premature ventricular depolarizations, sinoatrial arrest and atrioventricular (A-V) block. In contrast, only 2 of 39 graft angiograms performed during right atrial pacing produced arrhythmias. We conclude the following: (1) Routine prophylactic right atrial pacing is a valuable method for preventing certain cardiac arrhythmias during aortocoronary graft opacification; and (2) the potential for rapid institution of right ventricular pacing provides safety in the event that angiographically induced A-V block occurs.     

Prevention of atherosclerosis

Primary prevention instituted early in life offers the most promising opportunity to affect morbidity and mortality of atherosclerosis. This conclusion is inevitable because of the sudden catastrophic nature of the first event in many patients and the demonstration of advanced pathologic changes in those who are symptomatic. There is little evidence that advanced lesions regress.A prerequisite to the achievement of the goal of primary prevention is the training of “preventive cardiologists” dedicated to accumulating new data and utilizing information now available for the design and implementation of such programs in the young. A scientific approach to primary prevention requires documentation of the basic mechanism of the cause and progression of plaque formation. This information is not presently available. However, it is now possible to identify children at high risk of premature development of complication of the disease utilizing known risk factors and their tendency to familial aggregation. A plan for identification and management of such children is outlined. As new data become available one can anticipate changes in methods of detection and management with a view toward improving results in primary prevention.