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Biomedical subjects

V Fuster

Publications and source records attributed to V Fuster.

At least 109 records · Page 6Linked to original sources
PubMed1999

Tissue characteristics of restenosis after percutaneous transluminal coronary angioplasty in diabetic patients.

OBJECTIVES: The purposes of this study were to analyze coronary specimens from patients with diabetes mellitus (DM) and to compare them with specimens from patients without DM. BACKGROUND: Diabetes mellitus is associated with an increased incidence of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Increased hypercellular smooth muscle cell proliferation with exaggerated intimal hyperplasia formation may be responsible for this predisposition. METHODS: Eighteen coronary atherectomy specimens with restenosis after PTCA from patients with DM were compared with 18 coronary atherectomy specimens with restenosis after PTCA from patients without DM. Total and segmental areas were quantified on trichrome-stained tissue of hypercellular tissue, collagen-rich sclerotic tissue, atheroma and thrombus. Demographic and angiographic data were similar in both groups. RESULTS: The percentage of total plaque area composed of hypercellular tissue was lower in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (19 +/- 6% vs. 44 +/- 5%; p = 0.003). The percentage of collagen-rich sclerotic tissue area was larger in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (77 +/- 9% vs. 53 +/- 4%; p = 0.004). The percentages of atheroma and thrombus were similar in both groups. CONCLUSIONS: Intimal hypercellular tissue content is reduced in restenotic tissue from patients with DM. Collagen-rich sclerotic content is increased in restenotic lesions from patients with DM. These results suggest an accelerated fibrotic rather than a proliferative response in diabetic lesions from patients with restenosis after PTCA.

Aged↗
PubMed1999

50th anniversary historical article. Myocardial infarction and coronary care units.

The results of treatment of 250 patients with established acute myocardial infarction in a coronary care unit in a university hospital are described. The criteria for diagnosis have been carefully defined. In 62 percent of patients admitted with a tentative diagnosis of acute infarction, the initial impression was confirmed. Fifteen percent of patients admitted to the unit were classified as having possible infarction; in this group, the mortality rate was 3 percent. A classification of functional severity based on clinical evidence of heart failure or shock is presented. Morbidity and mortality in acute myocardial infarction are related to the functional severity of the illness. Although arrhythmia is common, the overriding importance of five life-threatening arrhythmias is emphasized. Mortality of patients in the coronary care unit was not improved in comparison to those treated under regular care until strong central direction of therapeutic programs, immediate treatment of arrhythmia in cardiac arrest, and delegation of some medical authority to trained nurses was accomplished. The change in concept of the purposes and practices of special coronary care from resuscitation to prevention of arrhythmia is emphasized. The mortality in myocardial infarction complicated by shock remains high. In the absence of shock, aggressive medical treatment in the coronary care unit reduced mortality from 26 to 7 percent. The implications of these data in the management of patients admitted to a hospital with a diagnosis of acute myocardial infarction are discussed.

Anniversaries and Special Events↗
PubMed1999

50th anniversary historical article. Acute coronary syndromes: the degree and morphology of coronary stenoses.

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.

Acute Disease↗
PubMed1999

Antithrombotic effect of FK506 vs cyclosporine in cardiac transplant recipients: potential implications in transplant arteriopathy.

BACKGROUND: An activated coagulation system has been implicated as a potential initiating or inciting factor in the development and progression of cardiac allograft vasculopathy (CAV). METHODS: By performing ex vivo perfusion studies of blood thrombogenicity under constant rheologic conditions and with a constant substrate, we sought to determine the relative effects on the coagulation system of FK506 vs cyclosporine in patients who have undergone cardiac transplantation. RESULTS-CONCLUSIONS: Compared with cyclosporine, FK506 significantly decreased the propensity to form thrombus; this suggests that FK506 may have a favorable impact on the development of CAV.

Blood Coagulation↗
PubMed1999

The diagnostic accuracy of ex vivo MRI for human atherosclerotic plaque characterization.

Recent evidence indicates that the type of atherosclerotic plaque, rather than the degree of obstruction to flow, is an important determinant of the risk of cardiovascular complications. In previous work, the feasibility of using MRI for the characterization of plaque components was shown. This study extends the previous work to all the plaque components and shows the accuracy of this method. Twenty-two human carotid endarterectomy specimens underwent ex vivo MRI and histopathological examination. Sixty-six cross sections were matched between MRI and histopathology. In each cross section, the presence or absence of plaque components were prospectively identified on the MRI images. The overall sensitivity and specificity for each tissue component were very high. Calcification and fibrocellular tissue were readily identified. Lipid core was also identifiable. However, thrombus was the plaque component for which MRI had the lowest sensitivity. A semiautomated algorithm was created to identify all major atherosclerotic plaque components. MRI can characterize carotid artery plaques with a high level of sensitivity and specificity. Application of these results in the clinical setting may be feasible in the near future.

Algorithms↗
PubMed1999

Antibiotics for myocardial infarction? A possible role of infection in atherogenesis and acute coronary syndromes.

The role of inflammatory mechanisms in the initiation, progression and clinical expression of atherosclerosis is increasingly appreciated. With this awareness, the possibility that acute or chronic infection may initiate or modulate these processes in an active area of investigation. Infectious organisms may influence the atherosclerotic process through direct local effects on the coronary endothelium, on vascular smooth muscle cells and on macrophages in the atherosclerotic lesion. Infection may also exert systemic effects by inducing the elaboration of cytokines, the creation of a hypercoagulable state and by activating monocytes, causing possible transmission of infectious material to atherosclerotic lesions. Macrophages may then elaborate multiple mediators which destabilise plaque, promoting rupture and progression. Seroepidemiological data have identified associations between clinically active atherosclerosis and evidence of infection with Helicobacter pylori, Chlamydia pneumoniae and some herpesviridae. In addition, pathological examinations have demonstrated the presence of infectious organisms in coronary artery plaques. Cytomegalovirus, for example, has been identified pathologically to be associated with transplant vasculopathy and with an increased risk of restenosis following coronary intervention. Finally, recent pilot trials have demonstrated that macrolide antibacterial treatment directed against C. pneumoniae reduces the risk of recurrent coronary events. Infectious organisms may therefore influence atherogenesis through multiple pathways, and pathological and seroepidemiological investigations provide evidence of this association. Future large-scale clinical trials are needed to further evaluate the evidence of causality and the efficacy of antibacterial therapy for coronary artery disease.

Acute Disease↗
PubMed1999

The role of platelet glycoprotein IIb/IIIa antagonists in percutaneous coronary revascularization procedures.

Platelet activation occupies a central role in arterial thrombosis after vascular injury, and the platelet glycoprotein GPIIb/IIIa integrin mediates the final common pathway for platelet aggregation. Agents of the recently developed pharmacologic class of inhibitors of the platelet GPIIb/IIIa receptor have been shown to decrease ischemic complications after coronary revascularization procedures. However, several issues need to be determined with respect to their specific indications, dosage, and combination with other antithrombotic therapies. Intracoronary thrombus formation during percutaneous coronary interventions (PCI) is the main pathogenic mechanism of the acute complications of PCI, but has also been implicated in the pathogenesis of their long-term results. In order to target intracoronary thrombosis, all PCIs have been performed during intense short-term anticoagulation with combination of unfractionated heparin plus aspirin. Compelling data on the central role of platelets in arterial thrombosis have made apparent the need for more potent antiplatelet agents for the treatment of patients undergoing PCI.

Angioplasty, Balloon, Coronary↗
PubMed1999

Higher rates of coronary angiography and revascularization following myocardial infarction may be associated with greater survival in the United States than in Canada. The CARS Investigators (Coumadin/Aspirin Reinfarction Study).

BACKGROUND: Significant differences are known to exist between the United States and Canada with respect to coronary catheterization and intervention. In a post hoc analysis, it was hypothesized that these differences may have the greatest impact on outcome in patients at risk for recurrent events such as those following myocardial infarction (MI). PATIENTS AND METHODS: The hypothesis was tested in a nonrandomized comparison of the catheterization and revascularization patterns for patients following acute MI in 7029 patients in the United States and 1774 patients in Canada who participated in the Coumadin/Aspirin Reinfarction Study (CARS). CARS tested the effectiveness of low dose warfarin in combination with acetylsalicylic acid (ASA) versus ASA alone in reducing cardiovascular morbidity and mortality. RESULTS: Before study enrollment (median day 7 to 8), 84.5% of the American patients underwent coronary angiography compared with only 7.7% in Canada (P<0.01). CARS patients in the United States underwent significantly more frequent angioplasty during their hospital admission before study enrollment than their Canadian counterparts (55.8% versus 3.0%, respectively, P<0.01), and there was a more frequent use of intravenous heparin among American CARS patients (96% versus 88%, respectively, P<0.01) but less frequent administration of thrombolytic therapy (44% versus 49%, respectively, P<0.01). For follow-up of up to 32 months, American CARS patients had significantly fewer primary events (cardiovascular deaths, nonfatal MI, nonfatal ischemic stroke) than Canadian patients. Cumulative estimate of a primary end point comparing American with Canadian patients was, respectively, 2.0% versus 3.1% at one month, 8.0% versus 11.3% at one year and 11.6% versus 15.0% at two years. Thus, time to the primary event was significantly longer in American patients (P=0.0001). All-cause mortality estimates at 12 months were 2.2% and 4.0%, respectively, for the American and Canadian CARS subgroups. When management for the index MI (ie, angiography and angioplasty) is included in the model, the risk of death for Canadian versus American subgroups of CARS is not statistically different (0.9, 95% CI 0.6 to 1.2, P=0.40). CONCLUSION: Among study participants, American patients experienced a better outcome than Canadian patients, which may be attributable to more aggressive management based on early coronary angiography and angioplasty. However, angioplasty before study enrollment in American patients may have resulted in enrollment of lower risk patients. This selection bias limits the scope of the comparison.

Aged↗
PubMed1999

Understanding the coronary disease process and the potential for prevention: a summary.

This presentation describes the atherothrombotic processes leading to acute coronary syndromes based on the recent studies of vascular biology. It outlines the mechanism of action and the evolving impact of lipid-lowering therapy in stabilization and secondary prevention of such processes. The present understanding of the pathogenesis of each phase of progression and of the various lesions preceding myocardial infarction emphasizes the physical, structural, cellular, and chemical properties of "vulnerable or unstable plaques" prone to disruption.

Coronary Artery Disease↗
PubMed1999

Determinants of protogenetic interval in a west Mediterranean rural population: La Alpujarra (southeast Spain).

This paper analyzes the protogenetic interval determinants and the influence on family size. The data came from La Alpujarra (Southeast Spain), consisting on a sample of 847 families marrying through-out the first half of the present century. The marital fertility includes 85% deliveries, 5% premarital births and the remaining 10% premarital conceptions. The protogenetic interval was clearly associated with the reproductive success since family size was nearly one child greater for short intervals (= < 16 months). The protogenetic interval largely depends on the occurrence of miscarriages preceding the first liveborn delivery as well as on maternal age. Consanguineous couples show slightly shorter intervals. A temporal decrease of protogenetic intervals was observed.

Birth Intervals↗
PubMed1998

Noninvasive In vivo high-resolution magnetic resonance imaging of atherosclerotic lesions in genetically engineered mice.

BACKGROUND: The pathogenesis of atherosclerosis is currently being investigated in genetically engineered small animals. Methods to follow the time course of the developing pathology and/or the responses to therapy in vivo are limited. METHODS AND RESULTS: To address this problem, we developed a noninvasive MR microscopy technique to study in vivo atherosclerotic lesions (without a priori knowledge of the lesion location or lesion type) in live apolipoprotein E knockout (apoE-KO) mice. The spatial resolution was 0.0012 to 0.005 mm3. The lumen and wall of the abdominal aorta and iliac arteries were identified on all images in apoE-KO (n=8) and wild-type (n=5) mice on chow diet. Images obtained with MR were compared with corresponding cross-sectional histopathology (n=58). MR accurately determined wall area in comparison to histopathology (slope=1.0, r=0.86). In addition, atherosclerotic lesions were characterized in terms of lesion shape and type. Lesion type was graded by MR according to morphological appearance/severity and by histopathology according to the AHA classification. There was excellent agreement between MR and histopathology in grading of lesion shape and type (slope=0.97, r=0.91 for lesion shape; slope=0. 64, r=0.90 for lesion type). CONCLUSIONS: The combination of high-resolution MR microscopy and genetically engineered animals is a powerful tool to investigate serially and noninvasively the progression and regression of atherosclerotic lesions in an intact animal model and should greatly enhance basic studies of atherosclerotic disease.

Animals↗
PubMed1998

Hirudin reduces tissue factor expression in neointima after balloon injury in rabbit femoral and porcine coronary arteries.

BACKGROUND: Tissue factor (TF) is a transmembrane glycoprotein that, after binding to factor VII/VIIa, initiates the extrinsic coagulation pathway, resulting in thrombin generation and its sequelae. Thrombin has been shown to induce TF mRNA in endothelium, monocytes, and smooth muscle cells, further perpetuating the thrombogenic cycle. This study was designed to determine the effect of specific inhibition of thrombin by recombinant hirudin (r-hirudin) on TF distribution after balloon angioplasty in the cholesterol-fed rabbit femoral artery and porcine coronary artery models. METHODS AND RESULTS: Thirty-five femoral arteries from 32 cholesterol-fed New Zealand White rabbits and 84 coronary arteries from 55 Yorkshire-Albino swine were studied by use of a recently developed in situ method of TF localization based on digoxigenin labeling of recombinant factor VIIa (Dig-VIIa), with correlative studies of TF immunoreactivity by use of anti-rabbit (AP-1) or anti-human (sTF) antibodies. At sites of balloon angioplasty in rabbit femoral or pig coronary arteries (double or single injury), TF-antibody and Dig-VIIa staining were noted in association with endothelial cells, smooth muscle cells, and foam cells and within the fibrous tissue matrix primarily of the adventitia and neointima. Staining was significantly greater after balloon angioplasty than in vessels that had not undergone angioplasty but was similar after single and double balloon injury. Animals treated with r-hirudin (rabbits, 1 mg/kg bolus plus 2-hour infusion; pigs, 1 mg/kg bolus plus 0.7 mg x kg(-1) x d(-1) infusion for 14 days with implantable pump) had diminished TF-antibody and Dig-VIIa staining 28 days after balloon angioplasty compared with controls (bolus heparin only). This effect was more prominent on the neointima and was more striking in the porcine than the rabbit model. CONCLUSIONS: TF expression, persistent 1 month after balloon angioplasty in rabbit femoral arteries and porcine coronary arteries, is attenuated by specific thrombin inhibition with hirudin. These results suggest that thrombin inhibition, in addition to its effect on acute thrombus formation and its effect on luminal narrowing by plaque in experimental animals, may result in a prolonged reduction in thrombogenicity of the restenotic plaque through this effect on TF expression.

Angioplasty, Balloon↗
PubMed1998

Effects of practice setting on quality of lipid-lowering management in patients with coronary artery disease.

We undertook a study to determine whether there were differences in the quality of lipid management in patients with coronary artery disease (CAD) in 2 different practice settings (which represent different socioeconomic classes), and to determine the level of compliance with the National Cholesterol Education Program guidelines by academic physicians in managing patients with CAD. A retrospective cross-sectional study was performed using a systematic chart review of 270 medical records (131 from the cardiology clinic, 139 from the cardiology private practice) of patients with known CAD at an academic tertiary care center in New York City. The total proportion of patients with CAD having a lipid profile ordered in the clinic and private suite was 43%. Of these people, 22% had a low-density lipoprotein cholesterol (LDL) < or = 100 mg/dl and 54% had an LDL < or = 130 mg/dl (10% and 23% of the total population, respectively). The total proportion of patients taking lipid-lowering medications was 29%. When comparing the quality of treatment between the 2 settings, there were no statistically significant differences in the percentages of patients who had lipid profiles measured (40% clinic vs 47% private suite, p >0.10), in the percentage of patients with LDL < or = 130 mg/dl (50% clinic vs 57% private suite, p >0.10) or in the weighted percentage of patients taking lipid-lowering medications (29% clinic vs 48% private suite, p = 0.099). The performances of individual physicians, however, varied widely. The percentages of patients with lipid profiles measured by individual physicians ranged from 0% to 83%, while the percentages of patients on drug treatment by a physician ranged between 10% and 88%. These findings indicate that socioeconomic differences, represented by different practice settings, do not account for differences in the screening for, control of, or use of medications in managing hyperlipidemia. Rather, individual physicians are accountable for differences in lipid management.

Age Factors↗