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Biomedical subjects

R P Croke

Publications and source records attributed to R P Croke.

16 recordsLinked to original sources
PubMed1981

Progression of coronary artery disease in medically and surgically treated patients 5 years after randomization.

Repeat angiography was performed at 63 +/- 9 months in 26 medically treated patients and at 66 +/- 10 months in 32 surgically treated patients with chronic angina. The native coronary arteries were divided into three major trunk vessels and 15 angiographic segments. Progression of disease was defined as the appearance of new (greater than 50%) obstruction or significant worsening of existing lesions in a segment or vessel. The incidence of progression was similar in medical and surgical patients, comparing individual segments (69 of 312 [22%] and 91 of [23%], respectively) or vessels (49 of 78 [63%] and 60 of 96 [63%], respectively). In both medical and surgical patients, segments initially free of disease showed a 14% incidence of developing new lesions, compared with the 37% progression in segments initially diseased (p less than 0.001). In the surgical patients, progression occurred in 48 of 219 (22%) nongrafted and 43 of 177 (24%) grafted segments (NS). When analyzed by major trunk vessel, progression occurred in 40 of 57 grafted arteries (70%) and 20 of 39 nongrafted arteries (51%) (NS). The incidence of new total occlusions was similar in medical and surgical patients (6% and 8%, respectively); new total occlusions occurred predominantly in diseases segments (15% and 22%, respectively). In patients with stable angina pectoris who have medical or surgical treatment assigned by randomization, progression of coronary disease at 5 years is not influenced by which mode of therapy was received. Vessels initially free of disease are at relatively low risk for development of disease within 5 years. In surgical patients, grafted and nongrafted vessels show similar rates of progression.

Angiography↗
PubMed1979

Echocardiographic aortic ejection area as a reflection of left ventricular stroke volume.

Systolic cusp separation of normal aortic valves has been shown by echocardiography and by angiography to be related to left ventricular stroke volume. In this study, stroke volume was compared with echocardiographic area between the aortic cusps in systole (aortic ejection area). An excellent correlation was observed (r = 0.93) over a wide range of stroke volumes, even in the presence of mitral regurgitation. Stroke volume appears to correlate more closely with aortic ejection area than with angiographic or echocardiographic measurements of peak systolic cusp separation.

Aortic Valve↗
PubMed1979

Lack of ouabain effect on pacing-induced myocardial ischemia in patients with coronary artery disease.

Sixteen patients with significant two and three vessel coronary artery disease but without clinical congestive heart failure were studied during rapid atrial pacing before and after infusion of 0.015 mg/kg of ouabain. Seven patients with a decreased (less than 50 percent) ejection fraction and nine patients with a normal ejection fraction had a significant (P less than 0.05) increase in resting arterial systolic pressure after the administration of ouabain. However, resting values for coronary sinus flow, coronary vascular resistance, myocardial oxygen consumption and myocardial lactate extraction did not change significantly in either group. During pacing, patients with a decreased ejection fraction demonstrated more ischemia than patients with a normal ejection fraction; however, the administration of ouabain did not significantly alter pacing-related changes in coronary sinus flow, myocardial oxygen consumption, myocardial lactate extraction, ischemic electrocardiographic changes or onset of chest pain in either group. The administration of ouabain has a negligible effect on coronary hemodynamics, myocardial metabolism or clinical signs of ischemia in patients with coronary artery disease with normal or abnormal left ventricular function.

Adult↗
PubMed1979

Improved survival after surgical therapy for chronic angina pectoris: one hospital's experience in a randomized trial.

Between 1972 and 1974, 121 patients with chronic stable angina pectoris and operative coronary artery disease, excluding significant left main coronary obstruction, were randomized to either medical therapy (60 patients) or surgical therapy (61 patients) as part of a larger Veterans Administration Cooperative Study of Surgery for Coronary Arterial Occlusive Disease. At the time of randomization, medical and surgical groups were similar with regard to clinical and hemodynamic features as well as degree of left ventricular impairment and extent of coronary disease. Follow-up to June 1, 1978, reveals significantly improved survival in surgical patients from 3 through 6 years after randomization. Sixteen cross-over patients (13 medical to surgery, and 3 surgical without surgery) do not appear to influence results. Results of this randomized study from a single hospital differ from the preliminary results of the larger cooperative study, primarily because of a higher mortality in the medical group. The medical mortality in our group is in keeping with other reports of the natural history of patients with angina pectoris, and we propose that the population of patients we randomized closely simulates the usual type of patient with chronic angina being considered for surgical treatment. Our good surgical results thus contrast significantly with the survival of medically treated patients, and this separates our study from the body of the Veterans Administration Cooperative Study.

Angina Pectoris↗
PubMed1978

Effects of pharmacologically-induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction.

Twenty patients with fixed coronary artery obstruction were studied during rapid atrial pacing and methoxamine infusion. During pacing to heart rates of 142 +/- 4 (mean +/- SEM) beats per minute coronary sinus flow increased from 108 +/- 8 to 187 +/- 15 cc/min and myocardial oxygen consumption increased by + 80 +/- 11%. During methoxamine infusion that raised arterial systolic pressure to 196 +/- 5 mm Hg, similar increases in coronary sinus flow (to 179 +/- 13 cc/min) and myocardial oxygen consumption (+ 77 +/- 12%) occurred. Chest pain and ischemic ST segment changes developed in 17 and 14 patients respectively during atrial pacing, an incidence significantly greater (P less than 0.05) than during infusion of methoxamine (6 and 3 patients). Myocardial lactate extraction which averaged 26 +/- 4% during control was decreased to 10 +/- 8% during pacing and to 24 +/- 7% during methoxamine; the difference between decreases was not significant. The data show that at similar increases in myocardial oxygen consumption stress of increased heart rate results in more myocardial ischemia than stress of increased afterload.

Blood Flow Velocity↗
PubMed1978

Hemodynamic effects of intravenous phentolamine in low output cardiac failu;e. Dose-response relationships.

Nineteen patients with chronic low output cardiac failure were studied before, during and after infusion of phentolamine in doses of 10, 20, 30 and 40 microgram/kg/min. Significant reduction of left- and right-sided pressures and increases in cardiac index and heart rate (HR) were present within 15 minutes of starting phentolamine at the 10 microgram/kg/min dose. Minimal additional effect was observed at 30 minutes. Increased dose from 10 to 20 mu/kg/min resulted in small but significant (P less than 0.05) additional reduction in pressures and increases in HR. No additional significant changes occurred at doses of 30 or 40 microgram/kg/min. Significant hemodynamic changes persisted for at least an hour (53 +/- 3 min) after the phentolamine infusion was discontinued. Near maximal ;emodynamic effects occur within 15 minutes of starting phentolamine infusion and can be achieved at doses of 10 to 20 microgram/kg/min. Increased HR during phentolamine infusion may limit its usefulness in patients with ischemic heart disease.

Cardiac Output↗
PubMed1978

The role of myocardial ischemia in pacing-induced elevation of arterial pressure.

One hundred sixteen patients with suspected or proven coronary arterial disease underwent rapid atrial pacing until the occurrence of pain in the chest or a heart rate of at least 160 beats per minute. Significant elevation of arterial systolic pressure of 25 percent or more above control was observed in 17 patients. Each of these patients had significant coronary arterial disease shown by coronary arteriographic studies. During rapid atrial pacing, each of these 17 patients had pain in the chest and ST-segment changes suggesting ischemia, and 15 had abnormal (less than 10 percent) extraction of myocardial lactate. In the 99 patients who did not have increased arterial systolic pressure during rapid atrial pacing, the frequencies of coronary arterial disease, ischemic ST-segment changes, and abnormal extraction of lactate during rapid atrial pacing were significantly (P less than 0.05) less. Increased arterial systolic pressure during rapid atrial pacing appears to be highly indicative of coronary arterial disease and myocardial ischemia. We suggest that myocardial ischemia may, under certain circumstances, be responsible for short-term increases in arterial pressure.

Adult↗
PubMed1977

Effect of reflex stimuli on vascular resistance and glycerol release in in vivo dog subcutaneous adipose tissue.

Although direct autonomic nerve stimulation and infusion of catecholamine has been shown to result in substantial amounts of lipolysis in dog subcutaneous adipose tissue, there is no evidence to indicate that reflex autonomic stimulation will result in qualitatively and quantitatively similar changes. The present studies were performed to evaluate the effects of reflex autonomic stimulation on vascular resistance and glycerol release in isolated, innervated and blood-perfused subcutaneous fat pad. Autonomic nerve stimulation at physiological frequencies was performed and resulted in release of glycerol that was compatible with previously reported data. Reflex stimulation by moderate and severe hypoxemia did not result in a significant glycerol release, but a maximal reflex stimulus (ventricular fibrillation) did. Since the majority of these reflex stimuli resulted in large change in vascular resistance, it would appear that reflex hemodynamic changes can occur in these preparations without concomitant changes in glycerol release. Alpha blockade of the vasoconstriction resulted in the appearance of rising glycerol output suggesting that vasoconstriction prevents lipolysis.

Adipose Tissue↗
PubMed1977

Reversal of advanced left ventricular dysfunction following aortic valve replacement for aortic stenosis.

A series of 12 consecutive patients who underwent aortic valve replacement (AVR) for aortic stenosis complicated by severe left ventricular dysfunction was reviewed. Ventricular dysfunction was reflected by pulmonary congestion, edema, renal and hepatic dysfunction, and by severely depressed ejection fractions (mean, 13%; range equal to 0-20%). Aortic valve replacement was accompanied by mitral commissurotomy in 1 patient and aortocoronary bypass in 5. Three of 5 patients with greater than 50% coronary obstruction died without reversal of heart failure, and 1 of the 5 died after a stroke. The 1 survivor of this group has done well. All 7 patients with minimal or no coronary disease survived operation and are now in New York Heart Association Class I or II. Postoperative catheterization (2 to 12 months) in 6 patients showed improved cardiac index and filling pressures. Left ventricular diastolic volume fell from 159 to 82 ml/m2, and ejection fraction rose from 13 to 45%. We conclude that left ventricular dysfunction owing to aortic stenosis alone is reversible and that AVR results in great clinical improvement. When coronary disease is present, survival may be accompanied by great improvement but the operative mortality is much higher.

Aged↗
PubMed1977

Comparative responses to dobutamine and nitroprusside in patients with chronic low output cardiac failure.

The acute hemodynamic effects of dobutamine and nitroprusside were compared in 19 patients with low output cardiac failure. At dosage levels yielding similar increases in cardiac index (12 patients), nitroprusside resulted in significantly lower arterial systolic and wedge pressures and did not increase heart rate suggesting advantages over dobutamine when reduction in myocardial oxygen requirement or pulmonary congestion is a major goal. Systemic arterial mean and diastolic pressures were minimally changed with dobutamine, but fell significantly with nitroprusside suggesting advantages of dobutamine over nitroprusside in patients where hypotension could limit coronary blood flow or perfusion of other vital organs. Reduction in pulmonary arteriolar resistance occurred only with nitroprusside. Arterial hypoxemia developed in three patients during nitroprusside infusion suggesting the possibility of increased right-to-left intrapulmonary shunting resulting from a direct vasodilating effect of nitroprusside on pulmonary arteriole smooth muscle. Although both inotropic and vasodilator drugs can result in hemodynamic improvement when administered to patients with chronic low output cardiac failure, significant differences of potential clinical importance exist between these two modes of therapy.

Adult↗