Search PubMed⌕ Search

Biomedical subjects

D C Harrison

Publications and source records attributed to D C Harrison.

At least 145 records · Page 8Linked to original sources
PubMed1979

Research related to noninvasive instrumentation.

In the past three decades, techniques that permit noninvasive quantitation of the function of the heart have been developed. Exercise electrocardiography has been widely used to determine the presence or absence of ischemic heart disease. Echocardiography permits detection of valvular, congenital and arteriosclerotic disease and quantitation of its severity. Selective use of isotopes allows nuclear angiogarphy, myocardial perfusion studies and detection of damage to cellular myocardium. New techniques such as computerized axial tomography, magnetometry, focused pulsed Doppler, and wider application of computer-enhanced image processing are important future directions for noninvasive monitoring.

Cardiovascular Diseases↗
PubMed1978

Electrophysiologic findings in patients with idiopathic hypertrophic subaortic stenosis.

Thirteen patients with catheterization-proved idiopathic hypertrophic subaortic stenosis underwent intracardiac electrophysiologic study. There was a large incidence of arrhythmias and a strikingly large incidence of conduction system abnormalities among these patients. The P-A and A-H intervals were normal in all patients. Atrial pacing resulted in Mobitz type 1 block proximal to the His bundle at an abnormal rate (less than 140/min) in 2 of 12 patients (17 percent). H-V intervals were prolonged (greater than 50 msec) in 10 of 12 patients (83 percent) and were greater than 60 msec in 7 patients (58 percent). The atrial effective refractory period was prolonged in 3 of 12 patients and was markedly prolonged in 1 of them. Effective refractory period of the atrioventricular (A-V) node, determined in five patients, was prolonged in three. Dual responses of the A-V node to atrial extrastimuli were found in seven patients. Dual A-V nodal repsonses were evoked with propranolol in three patients and persisted in the other four patients with dual responses despite propranolol administration.

Adult↗
PubMed1978

Dose-dependent acebutolol disposition after oral administration.

The relationship between dose and area under the blood concentration-time curve has been studied in 6 healthy subjects following both oral and intravenous doses of acebutolol. There is a more than proportional increase in area with increasing oral doses, and the area over a dosing interval following multiple oral doses is greater than the total area after a single dose of the same size. The role of an acetyl metabolite in producing these effects is discussed, as is the relevance of these observations to the clinical use of acebutolol.

Acebutolol↗
PubMed1978

Combined nitroprusside-dopamine therapy in severe chronic congestive heart failure. Dose-related hemodynamic advantages over single drug infusions.

To assess the circulatory effects of afterload reduction and inotropism individually and in combination as rational therapy for refractory heart failure, nitroprusside and dopamine were administered to 13 patients with severe cardiac decompensation. Dopamine at average doses of 3 and 7 microgram/kg per min produced increases in cardiac output and reductions in peripheral resistance. At doses of 15 microgram/kg per min, dopamine increased heart rate, peripheral arterial pressure and side effects. Nitroprusside alone decreased left-sided filling pressures and increased cardiac output. When the agents were administered together, the increases in cardiac output were significantly greater than with either agent alone and there was physiologic improvement in overall circulatory function. The relations among changes in afterload (systemic impedence), preload (filling pressures) and cardiac index help to explain the salutary effects of combined therapy in patients with refractory heart failure.

Adolescent↗
PubMed1978

Early anthracycline cardiotoxicity.

Eight patients in whom cardiac dysfunction developed within four weeks of receiving their first or second course of daunorubicin or doxorubicin are described. Four patients presented with pericarditis; three of these four had evidence of myocardial dysfunction. Histopathologic analysis of these patients was consistent with an acute myocyte damage and secondary inflammatory process. An additional group of four patients presented with symptoms and signs of heart failure. These patients were either elderly or had evidence of previous cardiac disease. One of these patients suffered a myocardial infarction 24 hours after receiving 60 mg/m2 of daunorubicin; earlier doses in the same course had been associated with evidence of myocardial ischemia. We conclude that anthracycline antibiotics may manifest clinically significant cardiotoxicity at total cumulative doses much less than have been associated with chronic cardiomyopathy.

Adult↗
PubMed1978

Electrophysiological effects of edrophonium in the innervated and the transplanted denervated human heart.

In order to determine the mechanism of action of edrophonium on the cardiac conduction system, we used His bundle recording and pacing techniques to examine the electrophysiological effect of edrophonium in 6 patients undergoing diagnostic evaluation for coronary artery disease and in 9 cardiac transplant recipients who were free of acute graft rejection. After control measures were made of sinus cycle length, conduction intervals, and conduction system refractory periods, edrophonium was administered by constant intravenous infusion, and all electrophysiological measurements were repeated. In the normally innervated patients, edrophonium significantly increased sinus cycle length from 778 +/- 21 ms to 883 +/- 36 ms (P less than 0.01), AH interval from 88 +/- 11 ms to 100 +/- 12 ms (P less than 0.01), and AV nodal functional refractory period from 351 +/- 44 ms to 391 +/- 36 ms (P less than 0.05). In the patients with transplanted hearts, edrophonium had no electrophysiological effect other than increasing the cycle length of the remnant recipient atrium from 722 +/- 21 ms to 798 +/- 31 ms (P less than 0.01). We conclude that the electrophysiological effects of edrophonium in man are mediated primarily through autonomic innervation of the heart.

Autonomic Nervous System↗
PubMed1978

Reduction of coronary blood flow during coronary artery spasm occurring spontaneously and after provocation by ergonovine maleate.

A 50-year-old man suffering from recurrent chest pain accompanied by transient ST-segment elevation developed spasm of the left anterior descending coronary artery after receiving ergonovine maleate. During spontaneous chest pain, thermodilution coronary sinus blood flow fell from 96 ml/min to 46 ml/min, while the coronary sinsu arteriovenous oxygen difference widened from 9.82 volumes percent to 11.3 volumes percent. During spontaneous relief of pain, coincident with resolution of the ST-segment changes, coronary sinus blood flow gradually rose to 135 ml/min, while coronary sinus arteriovenous oxygen difference narrowed to 6.82 volumes percent. Similar aterations in coronoary sinus blood flow accompanied chest pain provoked by ergonovine maleate. A thallium-201 scan confirmed a perfusion defect in the distribution the left anterior descending coronary artery. Thus, coronary artery spasm can produce a marked deficity in coronary blood flow that is associated with increased myocardial oxygen extraction; release of spasm creates a hyperemic response.

Coronary Angiography↗
PubMed1978

Clinical electrophysiologic effects of tocainide.

The electrophysiologic properties of tocainide were evaluated by electrophysiologic studies in 11 patients before, during and after a constant intravenous infusion of the drug for 15 minutes. Peak plasma tocainide concentrations averaged 11.0 +/- 1.7 microgram/ml (SEM), range 3.7 to 22.7. AH, HV, QRS, QTc and RR intervals were measured every 5 minutes during sinus and atrial-paced rhythms and showed small changes which were not statistically significant for HV and QRS. Mild shortening of RR was significant (P less than 0.05) at 15 minutes only. AH tended to increase slightly for spontaneous (but not paced) rhythm, becoming significant at 15 minutes only (P less than 0.05). QTc decreased slightly, a change which was significant (P less than 0.05) for paced but not spontaneous rhythm. A progressive rise in mean arterial pressure occurred during infusion and persisted through 30 minutes (P less than 0.001). Comparison of electrophysiologic studies at 0 and 30 minutes showed decreased in mean effective refractory periods of atrium, A-V node, and right ventricle by 17, 22, and 23 msec, respectively (P less than 0.05, 0.01, 0.01). Functional refractory period of the A-V node showed an average decrease which was not significant. Sinus node recovery time and Wenckebach cycle length were unchanged. The drug was well tolerated in all 11 patients. Hypotension in a twelfth patient may or may not have been drug related. These results obtained at therapeutic plasma concentrations suggest qualitative similarities between the conduction system effects of tocainide and those published for lidocaine.

Aged↗
PubMed1978

The hemodynamic effects of intravenous tocainide in patients with heart disease.

In order to evaluate its hemodynamic actions, tocainide, a new orally effective antiarrhythmic drug, was given intravenously over a 15 minute period to 12 patients with compensated left ventricular dysfunction. Doses were 0.5 (4 patients) or 0.75 (8 patients) mg/kg/min. Hemodynamics and drug plasma concentrations were measured at the end and 15 minutes after the end of the infusion. Tocainide infusion produced small but statistically significant increases in the pulmonary and systemic vascular resistance, aortic and pulmonary arterial pressure, and left and right ventricular end-diastolic pressure. There was no significant change in left ventricular dp/dt, heart rate, or cardiac index. In patients with compensated left ventricular dysfunction, tocainide produces a small rise in vascular resistance and arterial pressure. Overall cardiac function is maintained with a small increase in left ventricular end-diastolic pressure.

Adult↗
PubMed1978

Long-term tocainide therapy for ventricular arrhythmias.

Long-term tocainide therapy has been evaluated in 17 patients with ventricular arrhythmias. Ventricular tachycardia and/or fibrillation was recurrent and sustained in nine patients, and symptomatic but unsustained in three others. Five patients had frequent but only mildly symptomatic ventricular irritability. In all patients, arrhythmias could not be managed with quinidine, procainamide or propranolol. Tocainide doses ranged from 300 to 700 mg every 8 hours (mean steady-state plasma concentrations ranged from 5.75 to 12.18 microgram/ml). Tocainide therapy was unsuccessful in eight patients; three died during therapy and five had no antiarrhythmic response. The data suggest that evaluation of long-term drug efficacy, using the criterion of reduction of asymptomatic arrhythmias, is best documented by multiple sequential ambulatory electrocardiographic recordings, both on and off the drug. Tocainide controlled arrhythmias in nine patients (53%), with criteria of success being continued reduction of ectopic beats and/or control of symptomatic recurrences. Seven patients remain on therapy. Side effects generally have been minor and well-tolerated.

Adult↗
PubMed1978

Depressant effect of digoxin on atrioventricular conduction in man.

We examined the effect of chronically administered digoxin on atrioventricular (A-V) conduction in nine cardiac transplant recipients. We assessed A-V conduction by measuring the duration from the pacing stimulus to the onset of the QRS complex (S'R interval) and by determining the occurrence of Wenckebach periodicity during rapid atrial pacing. We made measurements during a control period and during a period of digoxin administration of up to 37 days. During the digoxin period, the cycle length at which Wenckebach block occurred was prolonged by 14% of the control value and the S'R interval was significantly prolonged at paced rates of 110 beats per minute and faster. After digoxin was discontinued, the Wenckebach periodicity and S'R interval returned to control values. Atropine and propranolol did not alter digoxin's effect on A-V conduction. We conclude that digoxin exerts a direct (or non-neurally mediated) depressant effect upon A-V conduction in man, although the stress of tachycardia is necessary to demonstrate the effect.

Atrioventricular Node↗
PubMed1978

Effects of alpha adrenergic blockade upon coronary hemodynamics.

The effect of alpha adrenergic block-ade on coronary blood flow regulation at rest was studied in 11 normally innervated patients and 8 cardiac allograft recipients by measuring arterial pressure and coronary sinus blood flow by thermodilution before and after alpha adrenergic blockade with phentolamine. Coronary vascular resistance was calculated by using coronary sinus blood flow and mean arterial pressure, and metabolic demand was estimated by the product of systolic arterial pressure and heart rate. In addition, the coronary sinus blood flow response to tachycardia was examined in 9 innervated patients and 12 denervated patients, with measurements repeated after phentolamine in 8 of the 9 innvervated patients and 6 of the 12 denervated patients. There was a 7.3+/-4.4% increase in coronary sinus blood flow in the innervated patients in response to alpha blockade, whereas the transplanted patients had an 8.2+/-1.8% fall in coronary sinus blood flow, despite equivalent changes in rate pressure product. The innervated patients also demonstrated a significantly greater increase in coronary sinus blood flow than did the transplanted patients during the first 5 s of an abrupt increase in heart rate (26+/-4 vs. 8+/-2.5 ml/min, P <0.001). This early response was blunted after alpha adrenergic blockade. We conclude that there is basal alpha adrenergic tone present on the coronary vasculature in man that is withdrawn by a sudden increase in heart rate.

Adolescent↗