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Biomedical subjects

D C Harrison

Publications and source records attributed to D C Harrison.

At least 181 records · Page 10Linked to original sources
PubMed1977

Surgical management of life-threatening ventricular arrhythmias in patients with coronary artery disease.

Twenty-one patients with coronary artery disease and severe, symptomatic ventricular arrhythmias underwent cardiac surgery after failure of medical managememt. All had coronary artery disease and either localized areas of severe hypokinesis (three patients), or ventricular aneurysms (18 patients) documented angiographically prior to surgery. Operation within one month after acute infarction resulted in an 80% in-hospital mortality, whereas operation more than one month postinfarction showed a 20% mortality. Operative treatment that included myocardial resection had a significantly lower mortality (P less than 0.05) than that which did not. With an average of 36.5 months of follow-up, 13 of the 21 patients were long-term survivors, despite the persistence of ventricular arrhythmias. Surgical treatment which includes myocardial resection and occurs more than one month after infarction should be considered in patients with symptomatic ventricular arrhythmias and severe, well-localized left ventricular wall motion abnormalities.

Adult↗
PubMed1977

The electrophysiologic effects of quinidine in the transplanted human heart.

Using His bundle recording techniques, we examined direct and autonomically mediated conduction system effects of quinidine in five cardiac transplant recipients who have anatomically denervated hearts. We made control conduction interval and refractory period measurements, and then infused 10 mg/kg quinidine gluconate over a 20-min period. At 30 min, we determined the electrophysiologic changes induced by quinidine. Quinidine significantly increased the atrial-His (AH) interval (from 97+/-9 [SEM] to 108+/-7 ms, P less than 0.001), the His-ventricular (HV) inteval (from 43.9 +/- 1 to 52.8 +/- 3 ms, P less than 0.01), the donor heart sinus cycle length (from 599 +/- 38 to 630 +/- 56 ms, P less than 0.08), and the atrial effective refractory period (from 214 +/- 14 to 241 +/- 11 ms, P less than 0.01). Quinidine significantly decreased the innervated, remnant atrial sinus cycle length (from 847 +/- 104 to 660 +/- 96 ms, P less than 0.01) and the blood pressure. The mean plasma concentration of quinidine at the time that electrophysiologic measurements were repeated was 4.37 +/- 0.449 micrograms/ml. We conclude that quinidine's predominant sinus nodal and atrioventricular nodal effects in man are autonomically mediated and opposite to its direct actions upon these structures. On the other hand, quinidine's prevailing effect on atrial refractoriness and His-Purkinje conduction in man is direct.

Blood Pressure↗
PubMed1976

Afterload reduction in the management of postinfarction ventricular septal defect.

The primary goal in the medical management of ventricular septal defect complicating myocardial infarction is to support cardiac function and control symptoms, if possible, for a period of 4 to 6 weeks. If the patient survives this period, surgical correction of the defect is technically easier and safer. In many cases, However, cardiac function is severly compromised, intractable biventricular failure develops,early operation is necessary and the likelihood of successful repair is diminished.

Female↗
PubMed1976

The effect of cycle length on cardiac refractory periods in the denervated human heart.

We have previously demonstrated that the transplanted human heart is functionally denervated. With the use of the extra stimulus technique during His bundle electrocardiography, refractory periods of the arterioventricular (A-V) conduction system were determined at several heart rates after pacing-induced changes in cycle length in eight patients who had previously undergone cardiac transplantation. Shortening of the cycle length was accompanied by a decrease in both the effective and functional refractory periods of the atrium. No consistent change in A-V nodal effective refractory period or functional refractory period could be demonstrated. Because A-V conduction was limited at shorter cycle lengths by the functional refractory periods of the atrium and A-V node, bundle branch refractory periods could be determined in three patients only at the longest cycle length studied. In four of the eight patients, atrial arrhythmias were produced at short cycle lengths with the introduction of early atrial extra stimuli. This may be due to a lack of vagal innervation of the atrium. These results contribute to our understanding of atrial arrhythmias.

Adult↗
PubMed1976

Circulatory response to vasodilator therapy in congestive cardiomyopathy.

Vasodilator therapy has been shown to have beneficial effects in heart failure. In order to evaluate the haemodynamic actions of vasodilator administration in primary congestive cardiomyopathy, sodium nitroprusside was infused intravenously at a rate of 15 to 100 mug/min to 12 patients. Mean arterial pressure fell 15 per cent from 86+/-3-0 to 72+/-2-4 mmHg (11-40 +/- -4 to 9-6 +/- 0-3 kPa), and there was a small but significant decrease in mean heart rate from 96 +/- 4-8 to 90 +/- 4-4 beats/min. These changes were accompanied by a significant decrease in mean pulmonary artery pressure from 40 +/- 2-2 to 26 +/- 2-8 mmHg (5-3 +/- 0-3 kPa to 3-5 +/- 0-4 kPa), mean pulmonary capillary wedge pressure from 25 +/ -2-2 to 16 +/- 2-1 mmHg (3-3 +/- 0-3 to 2-1 +/- 0-3 kPa), and left ventricular end-diastolic pressure from 27 +/- 1-8 to 17 +/- 1-5 mmHg (3-6 +/- 0-3 to 2-3 +/- 0-2 kPa). Cardiac index increased by an average of 48 per cent from 2-1 to 3-1 l/min per m2, and left ventricular stroke work index increased from 18-4 +/- 1-6 to 21-3 +/- 1-9 g m/m2. These results show that pronounced left ventricular dysfunction in patients with congestive cardiomyopathy is improved during vasodilator therapy.

Adult↗
PubMed1976

Autonomic nervous system and arrhythmias: studies in the transplanted denervated human heart.

The function of the cardiac autonomic nervous system (ANS) was evaluated by comparison of normal subjects with cardiac transplant recipients. By use of standard intracardiac His bundle recording techniques, the following conclusions regarding basic cardiac electrophysiology were drawn: (1) the sinus node functions normally at rest despite autonomic denervation; (2) the AV node does not show the expected decrease in functional refractory period with increased heart rate in the denervated state, and (3) the adrenergic receptor of the cardiac conduction system does not depend upon autonomic innervation to function normally. Electrophysiologic studies of digitalis demonstrated: (1) in therapeutic doses, the AV nodal blocking effect of digitalis is autonomically mediated; (2) sinus node slowing by digitalis also requires an intact autonomic innervation. Arrhythmia analysis in 47 transplant patients revealed an increased incidence of ventricular arrhythmias in autonomic cardiac denervation. In addition, sudden death in the ischemic denervated heart does occur, weakening the concept of a primary role of the cardiac ANS in this phenomenon.

Arrhythmias, Cardiac↗
PubMed1976

Normal myocardial contractile state in the presence of quinidine.

Since quinidine is one of the few agents available to treat and prevent ventricular arrhythmias in ambulatory patients, its hemodynamic effects have been reevaluated. When given in therapeutic doses to anesthetized mongrel dogs, quinidine significantly reduced heart rate, aortic pressure and flow, but it did not significantly change the first derivative of the left ventricular pressure curve (left ventricular dp/dt) in nine dogs. A subsequent group of dogs was studied after vagotomy and practolol administration to block cardiac reflexes. This group showed significant reductions in heart rate, aortic pressure and left ventricular dp/dt, with the latter returning to predrug control values when preload, afterload and heart rate were maintained constant. These studies suggest that quinidine does not directly affect myocardial contractility when given in therapeutic doses. Furthermore, the reduction in heart rate in these animals provides support for a direct depressant effect of quinidine on the sinus node. The adverse effects of quinidine on cardiac function previously reported may be due to the use of toxic doses or are secondary to quinidine peripheral circulatory effects, rather than due to a direct reduction in cardiac contractile state.

Animals↗
PubMed1976

Evaluation of left ventricular function in patients with aortic regurgitation using afterload stress.

Left ventricular function was assessed in 14 patients with chronic aortic regurgitation by afterload elevation with angiotensin. Seven of 14 patients maintained their resting ejection fraction with angiotensin (group A), while the remaining seven experienced a decline of greater than 0.10 in ejection fraction (group B). Six of seven group A patients showed an appropriate rise in left ventricular stroke work index in response to the angiotensin-induced rise in left ventricular end-diastolic pressure. In contrast, six of seven group B patients showed abnormal, flat, or declining stroke work indices. Included in the seven group B patients were two patients with left ventricular dysfunction secondary to coronary artery disease. The five other group B patients, who did not have coronary diseases, exhibited similar stress-induced ventricular dysfunction, despite the absence of any significant resting hemodynamic differences from patients in group A. These five stress-induced dysfunction patients were distinctive from patients who maintained their ejection fraction level in that the former all had regurgitant fractions of greater than 0.50, whereasl all gruop A patients had regurgitant fractions of less than 0.50. Similarly, these five stress-induced dysfunction patients had significantly larger left ventricular end-diastolic volumes than did the group A patients. These data suggest that patients with pronounced aortic regurgitation measured in terms of regurgitant fraction greater than 0.50 and left ventricular end-diastolic volume of greater than 160 cm3/m2 exhibit impaired ventricular function if appropriately stressed. As most of the patients with stress-induced dysfunction had a normal ejection fraction at rest, it may be that stress-induced dysfunction represents a stage before overt resting dysfunction and cardiac failure.

Adult↗
PubMed1976

Echocardiographic evaluation of the stent mounted aortic bioprosthetic valve in the mitral position. In vitro and in vivo studies.

Echocardiograms were performed on 20 clinically stable patients following mitral valve replacement with glutaraldehyde-preserved porcine aortic heterografts and three patients with antibiotic sterilized aortic homografts mounted in the mitral position. Such valves were evaluated in a test chamber at varied flow rates resulting in improved understanding of movements seen with the echocardiogram in vivo. The technique for recording the valvular stent and leaflets is described and a method for measuring several parameters is demonstrated. Initial diastolic slope averaged 2.4 +/- 0.5 cm/sec (range 1.9 to 3.3 cm/sec). Left ventricular outflow tract measured from the anterior portion of the stent to the interventricular septum averaged 1.5 +/- 0.5 cm at end-diastole and 1.3 +/- 0.6 cm at end-systole. Leaflet excursion averaged 1.5 +/- 0.3 cm (with a range from 1.0 to 2.1 cm). The ratio of internal to external stent diameters averaged 0.66 +/- 0.05 (with a range from 0.56 to 0.74).

Animals↗
PubMed1976

Clinical efficacy and pharmacokinetics of a new orally effective antiarrhythmic, tocainide.

Tocainide, a new oral antiarrhythmic agent, was studied in man in a short-term protocol designed to evaluate the efficacy, kinetics, and toxicity of this compound. Premature ventricular contractions (PVCs) were suppressed by less than 70% in 11 of 15 patients compared with pre-drug placebo controls. For these 11 responders, there was an average PVC reduction of 91% +/- 10 (range 70 to 100%) at tocainide doses not associated with side effects. Mild transient central nervous system toxicity was observed in some patients near the time of peak concentrations during the highest dose administered. The drug was found to have linear kinetics over the dose range studied and a plasma half-life of 13.5 +/- 2 hours. Plasma concentration-response curves indicate antiarrhythmic activity over all plasma concentrations, with 70% PVC reduction above 6.0 mug/ml. This study suggests that tocainide is a safe and effective antiarrhythmic agent during short-term administration and is worthy of further clinical trials.

Administration, Oral↗
PubMed1976

Pulmonary hypertension in patients using oral contraceptives. A report of six cases.

Six young women who had taken progestational agents for a period of time ranging from six months to five years developed symptoms and signs of pulmonary hypertension. Cardiac catheterization confirmed the presence of severe pulmonary hypertension without evidence of other cardiac or pulmonary abnormalities to explain this phenomenon. Three of the patients had potential predispositions to pulmonary hypertension, including a corrected patent ductus arteriosus with mild pulmonary hypertension in one, collagen vascular disease in a second, and family history of pulmonary hypertension in a third. Three patients had no known predisposing factors. Although the relationship between oral contraceptives and severe pulmonary hypertension is problematic, there have been isolated reports of cases of pulmonary hypertension secondary to oral contraceptive usage. These cases and the possible pathophysiologic mechanisms responsible are discussed.

Adult↗