Pulmonary blood volume ratio response to exercise; a noninvasive determination of exercise-induced changes in pulmonary capillary wedge pressure.
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Biomedical subjects
Publications and source records attributed to P C Block.
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To determine if there is release of endothelial cells or plaque contents after percutaneous transluminal angioplasty, effluent from atherosclerotic segments of the aorta and iliac arteries of rabbits were collected before and after angioplasty. No endothelial cells or cholesterol plates were identified in the preangioplasty effluents. Only a few single endothelial cells and cholesterol crystals were found in effluents after angioplasty. We conclude that embolization of endothelial fragments and cholesterol plates occurs during angioplasty, but only to a minor degree, and is probably not clinically important.
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Heart failure (CHF) appearing late after aortic (AV) or mitral valve (MV) replacement (R) may be due to mechanical factors such as prosthetic or native dysfunction, or due to myocardial disease. We studied 41 patients who developed CHF late (6 weeks to 11 years) after AVR or MVR with gated blood pool scan (RNV) to analyze the spectrum of ejection fraction (EF) and its clinical correlates. Of the 17 patients who developed CHF after AVR, 10 had RNV EF greater than 0.5 (all of whom had severe valve or prosthetic dysfunction as the primary cause of CHF) and seven had EF less than 0.5 (five with severe myocardial disease and two with prosthetic dysfunction). Of the 24 with CHF after MVR, 13 had RNV EF greater than 0.5. In contrast to post-AVR patients, only 8 of the 13 patients had mechanical causes of CHF (seven prosthetic dysfunction and one constrictive pericarditis). Of the 11 patients after MVR with EF less than 0.5, nine had severe myocardial disease and two had prosthetic dysfunction. Thus (1) reduced EF in patients and CHF-after AVR or MVR suggests myocardial disease as the basis for CHF, and (2) normal EF implies a mechanical cause of CHF after AVR but may be associated with either myocardial or mechanical factors after MVR.
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A cohort of 189 men was followed up for 1 year after performance of coronary angiography and determination of risk factors to ascertain which risk factors or clinical and laboratory findings could aid in predicting the patients who would have a substantial cardiac morbid event. Data on clinical signs and symptoms, psychosocial assessments, angiographic findings and presence of standard risk factors for coronary artery disease were collected in each case. Twenty-five percent of the men experienced a substantial cardiac morbid event (hospitalization, myocardial infarction, resuscitation or death). With or without inclusion of the patients who underwent surgery, discriminant analysis equations were successful in predicting morbidity on the basis of risk factor data. For the whole sample such analysis was significant at p < 0.00005 and accurately predicting the fate of 78 percent of the subjects. With exclusion of the surgically treated patients, the discriminant analysis accurately predicted future morbidity 83 percent of the time (p < 0.0001). The following risk factors for increased morbidity were common to both analyses: severity of angina, history of myocardial infarction, family history of heart disease, fatigue and absence of type A behavior.
Twelve autopsy human hearts were submitted to coronary angiography and coronary arterial balloon angioplasty. The effect of angioplasty was determined by follow-up coronary angiography as well as gross and microscopy inspection of the coronary arteries dilated. Fifty-four dilations were performed in 24 coronary arteries. Angiographically 50 of the 54 dilations resulted in a mean (+/- standard deviation) increase in luminal diameter ranging from 1.9 +/- 0.9 to 2.7 +/- 0.8 mm. Failure to increase luminal size was usually related to a predilation coronary diameter greater than that of the inflated angioplasty balloon. Dilation resulted in mural disruption with intimal or medial tears, or both, in 65 percent of arteries dilated. Disruption was more frequent in arteries with atherosclerosis and calcification. The mechanism of luminal enlargement in coronary angioplasty may be focal damage to the arterial wall with intimal or medial splitting as opposed to plaque compression as initially suggested.
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Stress thallium-201 myocardial imaging was used in two angina-free patients with severe congestive heart failure to identify clinically silent areas of ischemic myocardium and to distinguish between scar and reversibly ischemic myocardium as a cause for akinesia of left ventricular wall segments. Subsequent myocardial revascularization in these patients led to considerable improvement in their clinical state and findings in postoperative nuclear scans. Thus, stress myocardial imaging may be useful in selecting patients with severe left ventricular failure but no angina pectoris for myocardial revascularization.
Percutaneous coronary transluminal angioplasty is currently being proposed as a possible treatment for some patients with significant coronary arterial lesions. In this study scanning electron microscopy was used to assess the morphologic changes caused by the angioplasty balloon catheter in normal canine coronary arteries. Balloon inflation uniformly caused endothelial denudation with virtually immediate dense platelet adhesion to the subendothelial matrix. This platelet adhesion was unaffected by pretreatment with aspirin (35 mg/kg body weight) or heparin (2,000 units). However, intravenous administration of low molecular weight dextran almost completely prevented platelet adhesion to the exposed subendothelial connective tissues. It is concluded that even in normal canine coronary arteries (1) loss of endothelium is seen after transluminal angioplasty; (2) this endothelial damage stimulates platelet adhesion and thrombus formation; and (3) the immediate layering of platelets can be prevented by administration of low molecular weight dextran.
Using angiographic evidence of coronary artery disease, we have examined whether certain populations were particularly susceptible for risk engendered by Type A personality. Two hundred three men were studied with the Jenkins Activity Surveys; 103 of them were also studied with the Rosenman semistructured interview. The extent of vessel disease was found unrelated to Type A in each of the three ethnic groups studied--Irish Catholic, Italian Catholic, and white Anglo-Saxon Protestant. Likewise, no relationship between Type A and vessel disease was discerned in high depressed, low depressed, high stressed, or low stressed individuals. Finally, we examined whether cardiac symptomatology could affect any relationship found between Type A personality and vessel disease. No significant relationship was discerned in patients who had experienced or had not experienced a myocardial infarction or in patients with mild, moderate, or severe exertional angina.
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The morphologic consequences of transluminal angioplasty of stenotic atherosclerotic coronary arteries are unknown. This study describes the production of aortoiliac atherosclerosis in rabbits and reports the morphologic changes after transluminal angioplasty of stenotic arterial lesions. Atherosclerotic lesions were evaluated angiographically before and after transluminal angioplasty and were studied histologically and by electron microscopy after angioplasty. Moderatley stenotic aortic segments showed denudation of endothelial cells and deposition of a carpet of platelets enmeshed in fibrin. Medial and intimal compression were not seen. Intimal plaque disruption and splitting of atheromatous plaques were observed in more stenotic vessels where dilatation during angioplasty is relatively greater. Transluminal angioplasty, therefore, acutely causes desquamation of endothelial cells and superficial plaque elements, splitting of atheroma and subsequent deposition of platelets and fibrin in the area of angioplasty. This experimental model may be useful to evaluate the morphologic changes after angioplasty and might be used in further studies to determine the long-term pathophysiologic changes after transluminal angioplasty.
To elucidate the pathophysiologic mechanisms of transluminal angioplasty, normal coronary arteries in dogs, atherosclerotic human coronary arteries, and atherosclerotic vessels in rabbits were studied after angioplasty. Normal canine coronary arteries showed desquamation of endothelium, exposure of subendothelial connective tissue elements, and deposition of a carpet of platelets, fibrin, and occasional red blood cells. Administration of low molecular weight dextran before angioplasty decreased platelet deposition. Atherosclerotic human coronary arteries studied postmortem showed enlargement of lumen size after angioplasty due to splitting and disruption of the plaque and the underlying media. Endothelial desquamation and splitting of the plaque were also seen in atherosclerotic vessels in rabbits after angioplasty. The amount of splitting seems to depend on the relative size of the stenotic vessel and the inflated angioplasty balloon. Animals studied sequentially showed retraction of the separated intimal plaque elements and further lumen enlargement after 1-2 weeks. Two mechanisms of successful angioplasty are suggested by these studies: (1) desquamation of superficial plaque elements and (2) splitting of the plaque with retraction of intimal flaps as healing occurs. These mechanisms have important implications for the treatment of patients undergoing percutaneous transluminal angioplasty.