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Biomedical subjects

V Fuster

Publications and source records attributed to V Fuster.

At least 397 records · Page 22Linked to original sources
PubMed1986

Pathogenesis and prevention of aortocoronary bypass graft occlusion.

Aortocoronary bypass graft occlusion starts intraoperatively, is progressive over time, and correlates with the return of ischaemic symptoms and left ventricular dysfunction during exercise. Based on an animal model and tests of in vivo platelet consumption and deposition, a prospective, randomized, double-blind trial was designed and carried out comparing dipyridamole (instituted two days before operation plus aspirin (added seven hours after operation) with a placebo in 407 patients. Vein-graft angiography was performed in 88% of patients early after operation. Within 4-6 months of operation, 4% of 488 distal anastomoses were occluded in the treated patients and 15% of 520 distal anastomoses were occluded in the placebo group. The proportion of patients with one or more distal anastomoses occluded was 10% of 176 patients in the treated group and 30% of 184 patients in the placebo group (p = 10(-6)). Unlike other less convincing studies that did not start therapy before operation and did not affect high risk subgroups, benefit in graft patency in this study persisted in each of over 50 subgroups of high and low risk. Perioperative bleeding was similar in the two groups. Late after operation (11-18 months, median 12 months), 11% of 478 vein-graft distal anastomoses were occluded in the treated group, and 25% of 486 were occluded in the placebo group. The proportion of patients with one or more distal anastomoses occluded was 22% of 171 patients in the treated and 47% of 172 patients in the placebo group (p = 10(-6)).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMed1986

Porcine von Willebrand disease: implications for the pathophysiology of atherosclerosis and thrombosis.

A role of von Willebrand factor-mediated platelet function in porcine atherogenesis is strongly suggested by these studies. This influence of platelet function is probably most important in experimental systems that involve long-term observation and low or moderately elevated levels of serum cholesterol. On the other hand, effects of platelet function on development of atherosclerosis in animals with extremely high serum cholesterol levels are difficult to demonstrate and may be of relatively less importance. These observations are consistent with the results of numbers of recent studies describing the relationship of vascular injury to intimal smooth muscle cell proliferation. There is considerable evidence that lipid-rich intimal lesions occur in hypercholesterolemic animals with no antecedent denudation of endothelium or platelet adherence. It is difficult to ascribe intimal proliferation to platelet effects in this setting. On the other hand, endothelial cells, smooth muscle cells, and monocytes, which are all known to be involved in the atherosclerotic process, can produce mitogenic and chemotactic proteins, including platelet-derived growth factor. Therefore, metabolic aberrations of various kinds, including those initiated by mechanical injury or hypercholesterolemia, may promote proliferation in the vascular wall and resultant lesion development. Data from studies of pigs with vWD suggest a contribution of platelets to this process, but the effects of this contribution are modulated by numbers of variables, most of which are yet to be identified. The control of these multiple variables will be necessary before a clear understanding of the magnitude of the platelet-mediated effects can be gained. This will require carefully defined conditions of hypercholesterolemia, special attention to the immunologic variables and study of properly selected vascular segments under known conditions of flow. This later element will be especially important in the study of vWF-mediated platelet function, since shear forces are a critical determinant of vWF function. Systems that model flow conditions in various segments of the aorta, carotid, and coronary arteries are presently under development for this purpose. Finally, studies examining the molecular basis of vWF-mediated and other platelet functions will probably guide the most productive use of these models. Platelet membrane glycoprotein (GP) receptor Ib and the complex GP IIb and IIIa have been shown in ex vivo studies to be binding sites for vWF molecules.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Intraoperative echocardiography for the evaluation of valvular regurgitation: experience in 263 patients.

Because of the limited orifice size and potential complications associated with prosthetic valves, native valve repair and reconstruction is an attractive surgical alternative. However, significant residual valvular regurgitation, which cannot be reliably detected intraoperatively by current methods, increases postoperative morbidity and mortality. Direct epicardial two-dimensional echocardiography with contrast injections can be applied intraoperatively to rapidly and accurately assess the presence and severity of valvular regurgitation in the baseline and postoperative state. Five milliliters of dextrose or saline are injected into the appropriate cardiac chamber, generating echogenic microbubbles (contrast) that normally exit in an antegrade direction, but reflux retrograde in the presence of valvular regurgitation. In a total of 263 patients who underwent intraoperative contrast echocardiography, 177 mitral, aortic, and tricuspid valves were adequately assessed by preoperative catheterization and results were compared with those of intraoperative contrast echocardiography. The sensitivity and specificity of the intraoperative detection of valvular regurgitation by echocardiography were 0.97 and 0.98, respectively, for all valves, 1.00 and 0.90 for mitral valves, and 0.91 and 1.00 for aortic valves. Moreover, intraoperative contrast echocardiography can also provide quantification of valvular regurgitation. In 120 mitral valves evaluated, the correlation between the degree of regurgitation determined by preoperative ventriculography and by intraoperative contrast echocardiography (both on a scale of 0 to 4+) was 0.93. Importantly, 11 patients who had mitral surgery (eight after mitral valve repair, and three after valve replacement) were identified as having significant postprocedure mitral regurgitation by intraoperative contrast echocardiography only, not by other methods. Additionally, nine patients were found to have significant tricuspid regurgitation by intraoperative contrast echocardiography after mitral surgery and underwent successful tricuspid annuloplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗
PubMed1985

Response of the right ventricle to exercise in isolated mitral stenosis.

Eight patients in sinus rhythm, with varying degrees of isolated mitral stenosis (mitral valve area 0.6 to 1.3 cm2 and total pulmonary vascular resistance 5.0 to 17.5 U-m2), underwent supine rest and symptom-limited exercise radionuclide ventriculography to determine right ventricular (RV) and left ventricular ejection fraction (EF). Cardiac catheterization with hemodynamic measurements at rest and at peak exercise was performed within 24 hours of radionuclide ventriculography. Four of the 8 patients underwent corrective mitral surgery resulting in normal mean pulmonary artery pressures and total pulmonary vascular resistance at rest. These 4 patients had repeat radionuclide ventriculography at rest and during exercise 1 to 2 months after surgery. Preoperatively, all 8 patients had an abnormal exercise RVEF response (mean change +/- standard deviation [SD], -5.0 +/- 4.5%), coincident with an increase in mean pulmonary artery pressure during exercise (mean change, 15 +/- 5.0 mm Hg). The change in RVEF from rest to exercise, corrected for duration of exercise, correlated with peak exercise mean pulmonary artery pressure (r = -0.71, p = 0.05), as well as total pulmonary vascular resistance at rest (r = -0.82, p = 0.02). Postoperatively, all 4 patients who underwent surgical correction showed a normal RVEF response during exercise (mean change +/- SD, +6.8 +/- 4.0%). Thus, in patients with acquired mitral stenosis and no coronary artery disease (1) loading conditions and not contractility are prime determinants of RV exercise response, and (2) an exercise-induced decrease in RVEF may be a sensitive marker for increased total pulmonary vascular resistance and pulmonary hypertension.

Adult↗
PubMed1985

Isolated aortic stenosis with severe pulmonary hypertension.

Severe pulmonary hypertension is rare in patients with aortic stenosis. When present, it usually implies either associated mitral valve disease, poor left ventricular function, or pulmonary disease. In this case report, severe pulmonary hypertension was present in a patient with isolated aortic stenosis and normal left ventricular systolic function. Pulmonary hypertension was probably related to left ventricular diastolic dysfunction. Following successful aortic valve replacement, pulmonary pressures declined but symptoms of shortness of breath persisted and the patient still required daily diuretics.

Aged↗
PubMed1985

Total correction of tetralogy of Fallot at age 40 years and older: long-term follow-up.

Whether total surgical correction of tetralogy of Fallot in adults aged 40 years old or older has acceptable operative risk and gratifying long-term results is unknown. The Mayo Clinic experience (June 1960 to May 1982) with 30 patients 40 to 60 years old (mean 47) who had total surgical correction of tetralogy of Fallot was reviewed. Preoperatively, 4 patients (13%) were in functional class I, 9 (30%) in class II and 17 (57%) in classes III and IV. Eight patients (27%) had had preoperative complications: five had a cerebrovascular accident and three had infective endocarditis. Only 11 patients (37%) had had palliative surgery 16 to 34 years (mean 22) before total surgical correction. Total surgical correction was successful in all patients. Right ventricular to left ventricular (RV/LV) pressure ratio of 0.65 or less was achieved in 28 (93%) of the 30 patients. One patient died of ventricular fibrillation (RV/LV ratio = 0.8) 2 days postoperatively, one had complete heart block and one had a cerebrovascular accident 7 days after operation. At follow-up of 5 to 266 months (mean 110), there were seven late deaths: two sudden at 5 and 21 years, respectively, after operation, one from myocardial infarction at 11 years, one from cerebrovascular accident at 11 years, one from congestive heart failure (RV/LV ratio = 1.0) at 8 years and two from noncardiac causes. Of the 22 patients who survived, 16 are in class I, 5 are in class II and 1 is in class III.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Systemic embolism in chronic left ventricular aneurysm: incidence and the role of anticoagulation.

The incidence and prevention of systemic embolism in patients with chronic left ventricular aneurysm have been controversial. This retrospective study investigated the incidence of clinically evident embolic events and the effect of oral anticoagulation in patients with unequivocal angiographically defined left ventricular aneurysm. Between 1971 and 1979, 76 patients met the ventriculographic criteria and received initial medical management. The median interval from myocardial infarction to ventriculography was 11 months (range 1 month to 16 years) and subsequent median follow-up time was 5 years. Twenty patients receiving anticoagulant therapy were followed up for a total of 40 patient-years and 69 patients not on anticoagulant therapy were followed up for a total of 288 patient-years; 13 patients were included in both subsets. Twenty-eight patients died during follow-up and the 3 and 5 year survival rates were 75 and 61%, respectively. Only one patient not receiving anticoagulant therapy had a clinical embolic event, resulting in an incidence of 0.35 per 100 patient-years. Therefore, in the absence of other predisposing conditions, the extremely low incidence of systemic emboli in these patients with chronic (first documented at least 1 month after myocardial infarction) left ventricular aneurysm does not justify the use of long-term oral anticoagulant therapy.

Adult↗
PubMed1985

Coronary angiographic morphology in myocardial infarction: a link between the pathogenesis of unstable angina and myocardial infarction.

It has previously been shown that analysis of coronary morphology can separate unstable from stable angina. An eccentric stenosis with a narrow neck or irregular borders, or both, is very common in patients who present with acute unstable angina, whereas it is rare in patients with stable angina. To extend these observations to myocardial infarction, the coronary morphology of 41 patients with acute or recent infarction and nontotally occluded infarct vessels was studied. For all patients, 27 (66%) of 41 infarct vessels contained this eccentric narrowing, whereas only 2 (11%) of 18 noninfarct vessels with narrowing of 50 to less than 100% had this lesion (p less than 0.001). In addition, a separate group of patients with acute myocardial infarction who underwent intracoronary streptokinase infusion were also analyzed in similar fashion. Fourteen (61%) of 23 infarct vessels contained this lesion after streptokinase infusion compared with 1 (9%) of 11 noninfarct vessels with narrowing of 50 to less than 100% (p less than 0.01). Therefore, an eccentric coronary stenosis with a narrow neck or irregular borders, or both, is the most common morphologic feature on angiography in both acute and recent infarction as well as unstable angina. This lesion probably represents either a disrupted atherosclerotic plaque or a partially occlusive or lysed thrombus, or both. The predominance of this morphology in both unstable angina and acute infarction suggests a possible link between these two conditions. Unstable angina and myocardial infarction may form a continuous spectrum with the clinical outcome dependent on the subsequent change in coronary supply relative to myocardial demand.

Angina Pectoris↗
PubMed1985

Angiographic morphology and the pathogenesis of unstable angina pectoris.

In 110 patients with either stable or unstable angina, the morphology of coronary artery lesions was qualitatively assessed at angiography. Each obstruction reducing the luminal diameter of the vessel by 50% or greater was categorized into one of the following morphologic groups: concentric (symmetric narrowing); type I eccentric (asymmetric narrowing with smooth borders and a broad neck); type II eccentric (asymmetric with a narrow neck or irregular borders, or both); and multiple irregular coronary narrowings in series. For the entire group, type II eccentric lesions were significantly more frequent in the 63 patients with unstable angina (p less than 0.001), whereas concentric and type I eccentric lesions were seen more frequently in the 47 patients with stable angina (p less than 0.05). Type II eccentric lesions were also present in 29 of 41 arteries in patients with unstable angina compared with 4 of 25 arteries in those with stable angina (p less than 0.0001) in whom an "angina-producing" artery could be identified. Therefore, type II eccentric lesions are frequent in patients with unstable angina and probably represent ruptured atherosclerotic plaques or partially occlusive thrombi, or both. A temporary decrease in coronary perfusion secondary to these plaques with or without superimposed transient platelet thrombi or altered vasomotor tone may be responsible for chest pain in some of these patients with unstable angina.

Angina Pectoris↗
PubMed1985

Left ventricular function after myocardial infarction: clinical and angiographic correlations.

There is a paucity of information correlating the angiographic findings immediately after myocardial infarction with the clinical status before infarction. Therefore, the coronary anatomy, collateral circulation and quantitative left ventricular function were studied in 39 patients who underwent angiography within 3 weeks of a first transmural myocardial infarction. In all patients, the vessel supplying the infarct was totally occluded at the time of angiography. Patients without angina before infarction (Group I) had fewer coronary obstructions than did patients with a long history of angina before infarction (Group II) (1.5 +/- 0.5 versus 2.5 +/- 0.5, respectively, p less than 0.001) but worse overall and regional left ventricular function. These paradoxical differences between Groups I and II were evident in patients with anterior as well as inferior infarction. Patients in Group I had significantly lower collateral scores than did patients in Group II (0.6 +/- 0.8 versus 1.9 +/- 0.9, respectively, p less than 0.0001) and 13 of 22 patients in Group I had no collateral vessels compared with only 1 of 17 in Group II (p less than 0.001). Partial preservation of anterior wall function in Group II patients with anterior infarction was related both to the presence of collateral vessels and to the more distal obstruction of the left anterior descending coronary artery in these patients as compared with patients with anterior infarction in Group I. In contrast, in patients with inferior wall infarction, no relation could be found between the presence of collateral vessels and regional left ventricular function, although only two patients in this series with inferior infarction did not have collateral vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1985

Role of platelets and thrombosis in coronary atherosclerotic disease and sudden death.

During the last decade, significant advances have been made in the understanding of the pathogenesis of coronary atherosclerotic disease. Two facts are important: 1) the early and some of the advanced coronary atherosclerotic lesions progress very slowly, probably by means of a complex stepwise biologic process with one of the steps being an interaction between platelets and the arterial wall; the process can be favored by the so-called risk factors of atherosclerotic disease, and 2) some of the advanced coronary atherosclerotic lesions progress very rapidly, probably by means of complicating anatomic events, one of which is related to a thrombogenic process. From a clinical point of view, technologic improvements, such as serial coronary arteriography, reperfusion during the acute coronary artery syndromes, postmortem coronary arteriography, and methods for serial histopathologic and histochemical studies, have brought to light the clinical importance of the processes of plaque rupture, dissecting hemorrhage and, most important, thrombosis. These complicated processes appear to be of paramount importance in the pathogenesis of some of the acute coronary syndromes including unstable angina, myocardial infarction and sudden coronary death. Antithrombotic and platelet inhibitor therapy is under investigation and appears promising in some of these patient subsets.

Angina, Unstable↗
PubMed1985

Platelet-inhibitor therapy in cardiovascular disease. Effective defense against thromboembolism.

Platelet deposition can occur in areas of vascular damage and on prosthetic materials such as heart valves or grafts; mural thrombus formation, with eventual organization, progression to fatal occlusion, thrombolysis, or arterial embolization can follow. Use of antiplatelet drugs in patients undergoing certain cardiovascular surgical procedures or having rapid progression of atherosclerosis may reduce the thromboembolic risk.

Angioplasty, Balloon↗
PubMed1985

Intracardiac thrombi and systemic thromboembolism: detection, incidence, and treatment.

The detection of thrombus in the left atrium is discussed in this chapter, along with the problem of arterial thromboembolism in patients with valvular heart disease and prosthetic heart valves. The detection and occurrence of thrombus within the left ventricle are considered, as is the frequency of thromboembolism in acute myocardial infarction, left ventricular aneurysm, and cardiomyopathy. Treatment recommendations are given for each of these medical problems.

Anticoagulants↗
PubMed1985

Balloon angioplasty. Natural history of the pathophysiological response to injury in a pig model.

The restenosis or occlusion that frequently follows balloon angioplasty is poorly understood. Thus, the pathophysiological response to angioplasty of the common carotid artery in 38 heparinized normal pigs was investigated by quantification of the 111In-labeled platelet deposition and histological and electron microscopic examination from 1 hour to 60 days after angioplasty. At 1 hour, the following findings were noted: complete endothelial denudation in all arteries, marked platelet deposition (44.7 +/- 20.7 X 10(6)/cm2), mural thrombus in seven of 10 pigs, and a medial tear extending through the internal elastic lamina in nine of 18 arteries. All nine arteries with tears had associated mural thrombus and severe platelet deposition (76 X 10(6)/cm2); in contrast, the nine arteries without a tear had no mural thrombus and much lower platelet deposition (6 X 10(6)/cm2). Necrosis of medial smooth muscle cells was evident at 24 hours. Platelet deposition remained high at 24 hours (40.5 +/- 20.6 X 10(6)/cm2), but was markedly reduced at 4 days (4.4 +/- 1.5 X 10(6)/cm2), coincident with partial regrowth of endothelium or periluminal lining cells. No significant platelet deposition was noted at 7 days, when the endothelial cell type of regrowth was largely complete. Intimal proliferation of smooth muscle cells was mild and patchy at 7 days, significantly greater and more uniform at 14 days, and unchanged at 30 and 60 days after angioplasty. Complete thrombotic occlusion occurred in four (11%) of the 38 pigs. A significant stenosis present at 30 days after angioplasty was shown by histological examination to be due to organization of mural thrombus.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon↗
PubMed1985

Natural history of idiopathic dilated cardiomyopathy. Implications for future therapy.

Idiopathic dilated cardiomyopathy can present in a number of different ways, with the majority of patients having heart failure. Natural history studies show a poor prognosis for most patients with this disease. However, a substantial number may stabilize or even improve, and have a survival curve similar to patients without the disease. Patients can be stratified for relative risk of mortality by age, cardiomegaly on chest roentgenograph, ventricular function, and quantitative assessment of ventricular arrhythmias. Therapy can be divided into three categories: alteration of factors associated or contributors to ventricular dysfunction, supportive therapy, and investigational therapy. The efficacy of therapy should be judged by its effect on functional capacity and survivorship. The first category includes controlling hypertension and abstaining from alcohol. This often leads to improved functional status, and may improve survival. The second category includes anticoagulant therapy and, most importantly, medications for heart failure (digoxin, diuretics, vasodilators, nonglycoside inotropes, etc.). These agents may improve functional status, but in general have had little impact on survival. Investigational medical therapy for future use depends upon identification of factors involved in the genesis of the disease and the pathophysiologic mechanisms responsible for morbidity and mortality. The inflammatory component in the genesis and/or maintenance of cardiomyopathy, the importance of frequent ventricular arrhythmias in prognosis and the influence of endogenous vasoconstrictors on heart failure and arrhythmias, have been mentioned as such areas of interest.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗