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Biomedical subjects

D R Ricci

Publications and source records attributed to D R Ricci.

34 records · Page 2Linked to original sources
PubMed1980

Coronary hemodynamic effects of ergonovine maleate in human subjects.

The coronary hemodynamic effects of ergonovine maleate were examined in 15 patients with a chest pain syndrome not thought to be variant angina. Ergonovine was given intravenously in sequential doses of 0.05, 0.1 and 0.25 mg while measurements were made of systemic hemodynamic variables, coronary sinus blood flow and coronary arteriovenous oxygen difference at intervals during the protocol. Coronary arterial diameters were measured from the 35 mm cineangiogram. Despite an increase in myocardial metabolic demand, as estimated with the heart-rate-blood pressure product, there was no apparent increase in coronary vascular resistance. In addition, there was a significant widening of the coronary arteriovenous oxygen difference in five of the seven patients in whom it could be measured. However, neither chest pain nor ischemic electrocardiographic changes were evoked. Although ergonovine also produced a diminution in epicardial coronary arterial diameters, this effect was not sufficient to explain the absence of appropriate coronary vasodilation. These results suggest that ergonovine may limit the normal vasodilatory response of the arteriolar bed to increases in myocardial metabolic demand.

Adult↗
PubMed1979

Profiles of radionuclide left ventricular ejection fraction changes induced by supine bicycle exercise in normals and patients with coronary heart disease.

This paper presents the profiles of left ventricular ejection fraction (EF) during and following supine bicycle exercise in normal subjects and in patients with coronary heart disease, as well as the relationship of the described patterns to clinical parameters. Twenty normal men and 40 patients with coronary artery disease were studied using gated equilibrium radionuclide angiography (EQ-EF). In the normals, during exercise, EF increased by a mean of 25% of the resting value, with an increase of no less than 11%. The exercise-limiting symptom in patients with coronary artery disease was angina pectoris in 20 and fatique in the other 20 patients. In the angina patients, there was a mean decrease in EF of 20%, and in the other coronary artery disease patients ejection fraction change little. Only two patients with coronary artery disease increased from a normal resting value to peak exercise by more than 11%, and they had isolated right coronary lesions. An "overshoot" elevation of ejection fraction above resting levels was demonstrated following termination of exercise in most patients. The patients with a significant fall in exercise ejection fraction more frequently had abnormal exercise-induced ECG changes as well as abnormal left ventriculograms and more severe coronary artery disease at cardiac catheterization than the patients with little change in ejection fraction. We conclude that 1) normals could be separated from most patients with significant coronary artery disease in this study population; 2) ejection fraction must be measured at maximal exercise for it to have diagnostic value, since there could be normal rise before and after peak exercise and an abnormal response missed; and 3) the ejection fraction response to exercise reflects the severity of the underlying coronary artery disease. The described patterns of exercise-induced changes in left ventricular ejection fraction are important to consider when using this new technique to diagnose and evaluate patients with coronary artery disease.

Adult↗
PubMed1979

Altered adrenergic activity in coronary arterial spasm: insight into mechanism based on study of coronary hemodynamics and the electrocardiogram.

To elucidate the pathophysiologic mechanism of coronary arterial spasm, the hypothesis was examined that underlying alterations in sympathetic activity may account for this syndrome in some patients. Observations were directed to alterations in coronary arterial hemodynamics and the electrocardiogram. Spasm of the left anterior descending coronary artery produced a mean increase in coronary vascular resistance of 107 percent (P less than 0.05) in four patients in whom coronary sinus blood flow was measured with the thermodilution technique. The alpha adrenergic blocking agent phentolamine, given intravenously, acutely reversed coronary spasm and its clinical manifestations in eight patients and reduced coronary resistance. In four patients, administration of the long-acting oral alpha blocking agent phenoxybenzamine (20 to 80 mg/day) caused disappearance of symptoms during a follow-up period of 3 to 12 months. Transient prolongation of the corrected Q-T interval preceded spontaneous or ergonovine maleate-provoked coronary spasm in 11 patients with variant angina pectoris, whereas no significant change in the Q-T interval followed ergonovine administration in 27 control patients with atypical chest pain who did not have coronary spasm. T wave inversions in the resting electrocardiogram were normalized by isoproterenol infusion in one patient and by long-term phenoxybenzamine treatment in four patients with variant angina pectoris. These Q-T and T wave changes are analogous to those described with unilateral or asymmetric stellate ganglion stimulation in animals. These observations suggest that alterations in the sympathetic nervous system that are consistent with asymmetric stellate ganglion activity and transient alpha adrenergic receptor stimulation can presage the development of coronary arterial spasm in some patients with variant angina pectoris.

Adult↗
PubMed1979

The effects of ergonovine maleate on coronary arterial size.

Changes in coronary arterial size due to ergonovine maleate are described and quantitated in 90 patients--18 with typical angina pectoris, 56 with atypical chest pain, nine with variant angina pectoris, and seven heart transplant (allograft) recipients. We observed two angiographic changes in the diameter of coronary arteries: 1) spasm, which was characterized by occlusion or marked (greater than 85%) focal or diffuse vessel narrowing, or 2) relatively mild and diffuse vessel narrowing, which was interpreted as the normal pharmacologic response to the drug. Serial bolus injections of 0.05 mg, 0.10 mg and 0.25 mg of ergonovine maleate produced diffuse narrowing of the diameter of coronary arteries of 10 +/- 1.5%, 16 +/- 1.4% and 20 +/- 1.3% (mean +/- SEM), respectively, in the 72 patients with anginal syndromes who did not develop coronary spasm. The degree of coronary arterial narrowing was the same in heart transplant recipients and in patients with normally innervated hearts who did not develop coronary spasm. We believe the normal pharmacologic response to ergonovine maleate was due to a direct vasoconstrictor action of the drug; this action was independent of neural control extrinsic to the heart.

Adult↗
PubMed1979

Role of tachycardia as an inotropic stimulus in man.

We examined the inotropic effect of tachycardia in nine postsurgical aortocoronary bypass graft patients (with intact cardiac innervation) and nine cardiac allograft recipients (with denervated hearts). The changes in stroke volume (SV) and velocity of circumferential fiber shortening (VCF) which accompany sudden increases and decreases in atrial pacing frequency were determined by computer-aided fluoroscopic analysis of the motion of surgically implanted midwall myocardial markers. Because the first beat after a change in rate retains the frequency characteristics of the preceding rate, we compared the first posttachycardia beat with control beats and late tachycardia beats with the first tachycardia beat; afterload and preload for each pair of beats were similar. For an increase in heart rate of 50 beats/min, SV and VCF rose 79 and 64% from the first tachycardia beat to late tachycardia beats, and SV and VCF rose 8 and 35% from control beats to the first posttachycardia beat in the innervated group. Responses in the denervated group were not significantly different from those in the innervated group. The degree of the inotropic response was positively correlated with the magnitude of the increase in heart rate (r = 0.91). The decay in augmented contractility after decreasing the rate back to control levels fits an exponential relationship with a mean t((1/2)) of 1.7 s. Thus, in conscious man, increases in heart rate represent a positive inotropic stimulus, independent of other factors influencing ventricular performance and unaffected by neural innervation, and should be considered when changes in cardiac function are interpreted during serial studies or after drug administration.

Adolescent↗
PubMed1979

Validity of left-ventricular ejection fractions measured at rest and peak exercise by equilibrium radionuclide angiography using short acquisition times.

To validate ejection fraction (EF) calculations from 5 and 2 minutes of multiple-gated equilibrium radionuclide angiographic data and to establish its utility during alterations in cardiac performance, we studied 38 patients with chest pain suggestive of coronary artery disease. Twenty-four patients underwent contrast ventriculography (CV) as well as first-pass (FP) and equilibrium (EQ) radionuclide angiography at rest, and 14 additional patients had both radionuclide tests performed at rest as well as during peak supine bicycle exercise. The resting 5-min acquisition ejection fractions were compared between each method and the following correlations were generated: r = .92, n = 24 (CV-EQ), r = .92, n = 24 (CV-FP), and r = .95, n = 38 (FP-EQ). The variability of EQ-EF calculations between two independent observers was less than 2%; the mean absolute difference between two sequential 2-min acquisitions and the 5-min recordings was -.1 +/- 1.6%, and the reproducibility of sequential 2-min ejection fractions was excellent (r = .98). EQ and FP ejection fractions at symptom-limited exercise correlated well (r = .96, n = 14). We conclude that equilibrium radionuclide angiography is a valid method to measure EF both at rest as well as during peak exercise even when 2-min acquisition periods are used.

Adult↗
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

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↗
PubMed1977

Nonhypoxemic hazards of prolonged myoclonus.

Hyperkalemia, hyperthermia, and systemic hypotension developed in a patient with generalized myoclonus. These disorders reached life-threatening proportions but were rapidly and completely corrected after the patient was paralyzed with pharmacologic agents. Induced neuromuscular blockade may be indicated when the systemic effects of pathologically contracting muscle become life-threatening.

Acidosis↗
PubMed1977

Recurrent tachyarrhythmia associated with a bifocal demand pacemaker.

A recurrent tachyarrhythmia complicated the course of a patient with a permanent atrioventricular sequential (bifocal) demand pacemaker. Investigation by intracardiac electrocardiographic studies revealed that the arrhythmia was associated with normally functioning bifocal pacemaker, whose atrioventricular sequential interval approximated the patient's conduction time from atrium to ventricle. The mechanism of initiation and conversion of the arrhythmia was elucidated. Appreciation of this arrhythmia is necessary for appropriate clinical use of a bifocal demand pacemaker.

Bradycardia↗
PubMed1977

Effects of heart rate augmentation on left ventricular volumes and cardiac output of the transplanted human heart.

The response of the donor left ventricle to atrial pacing was measured in 11 patients 12 to 64 days after cardiac transplantation. At operation seven miniature tantalum coils were placed into the midwall of the donor left ventricle so as to outline the ventricle in a 30 degrees right anterior oblique projection. Computer aided fluoroscopic analysis of marker dynamics allowed calculation of end-diastolic and end-systolic volumes, stroke volume, cardiac output, and ventricular filling characteristics. Recipients were studied in a resting, unsedated state during a period of clinical stability that did not immediately follow or precede an episode of graft rejection. Augmentation of heart rate by an average of 40 beats per minute above sinus rate produced significant reductions in end-diastolic volume (-19%), end-systolic volume (-8%), stroke volume (-31%), and the duration of systole (-19%), and diastole (-40%). Cardiac output was invariant with rate. In all patients, end-diastolic volume reduction at augmented rates was brought about by abbreviated diastolic filling as initiation of contraction occurred at an earlier point on a common, incremental filling curve. Previous studies have shown that the normal inverse relationship between heart rate and stroke volume is not available to the transplanted heart in the immediate postoperative period. The present study shows that this intrinsic mechanism becomes available to the denervated heart in the subsequent recovery period after surgery.

Cardiac Output↗