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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Despite substantial basic and clinical efforts to address the problem of restenosis after percutaneous coronary intervention, effective preventive therapies have not yet been developed. Nevertheless, the accumulated information has provided much insight into the process of restenosis in addition to allowing standards to be developed for adequate clinical trials. The pathophysiology of restenosis increasingly appears to be distinct from that of primary atherosclerosis. Restenosis involves elastic recoil, incorporation of thrombus into the lesion and fibrocellular proliferation in varying degrees in different patients. Lack of an animal model that satisfactorily mimics restenosis is a major impediment to further understanding of the process. Clinical studies are hampered by difficulties in finding a single unifying definition of restenosis and by variable methods of reporting follow-up. Reporting of clinical outcomes of all patients in angiographic substudies would allow a more satisfactory interpretation of the results of clinical trials. Current noninvasive test results are not accurate enough to substitute for angiographic and clinical outcome data in intervention trials. In the majority of observational studies, only diabetes and unstable angina have emerged as consistently associated with restenosis; whereas most of the standard risk factors for atherosclerosis have a less consistent relation. Disappointingly, the new atherectomy and laser technologies have not affected restenosis rates. The one possible exception is coronary stenting, as a result of the larger luminal diameter achieved by the placement of the stent. In conclusion, although substantial continued effort is necessary to explore the basic aspects of cellular proliferation and mechanical alteration of atherosclerotic vessels, attention to the principles of clinical trials and observation are required to detect the impact of risk factors and interventions on the multifactorial problem of restenosis. Adequate sample sizes, collection of clinical and angiographic outcomes and factorial study designs hold promise for unraveling this important limitation of percutaneous intervention.
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PMID:Restenosis after coronary angioplasty: an overview. 201 78

Mode of death, frequency of a healed or an acute myocardial infarct, or both, number of major epicardial coronary arteries severely narrowed by atherosclerotic plaque, and heart weight were studied at necropsy in 889 patients 30 years of age or older with fatal atherosclerotic coronary artery disease. No patient had had a coronary bypass operation or coronary angioplasty. The 889 patients were classified into four major groups and each major group was classified into two subgroups: 1) acute myocardial infarct without (306 patients) or with (119 patients) a healed myocardial infarct; 2) sudden out of hospital death without (121 patients) or with (118 patients) a healed myocardial infarct; 3) chronic congestive heart failure with a healed myocardial infarct without (137 patients) or with (33 patients) a left ventricular aneurysm; and 4) sudden in-hospital death without (20 patients) or with (35 patients) unstable angina pectoris. The mean age of the 687 men (77%) was 60 +/- 11 years, and of the 202 women (23%), 68 +/- 13 years (p = 0.0001). Although men included 77% of all patients, they made up approximately 90% of the out of hospital (nonangina) sudden death group. The frequency of systemic hypertension and angina pectoris was similar in each of the four major groups. The frequency of diabetes mellitus was least in the sudden out of hospital death group and similar in the other three major groups. The mean heart weight and the percent of patients with a heart of increased weight were highest in the chronic congestive heart failure group; values were lower and similar in the other three major groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mode of death, frequency of healed and acute myocardial infarction, number of major epicardial coronary arteries severely narrowed by atherosclerotic plaque, and heart weight in fatal atherosclerotic coronary artery disease: analysis of 889 patients studied at necropsy. 213 74

This study analyzes data from New York State's new Cardiac Surgery Reporting System, which contains information about cardiac preoperative risk factors, postoperative complications, and hospital discharge. The purposes of the study were to determine the set of significant clinical risk factors and to identify cardiac surgical centers most likely to have serious quality-of-care problems. Significant risk factors for in-hospital death were age, gender, ejection fraction, previous myocardial infarction, number of open heart operations in previous admissions, diabetes requiring medication, dialysis dependence, disasters (acute structural defect, renal failure, cardiogenic shock, gunshot), unstable angina, intractable congestive heart failure, left main trunk narrowed more than 90%, and type of operation performed. Four of the 28 hospitals had significantly higher mortality rates than expected, given the risk factors of their patients. Subsequent site visits and medical record reviews confirmed that these facilities had high percentages of quality-of-care problems among cases resulting in mortality.
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PMID:Adult open heart surgery in New York State. An analysis of risk factors and hospital mortality rates. 201 24

Sudden fissuring of an atherosclerotic plaque has been suggested as the primary trigger of transient spontaneous ischemia in both the coronary and cerebral circulation. Measurements of urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2, as well as results of Aspirin trials, have suggested that episodic platelet activation at the site of this acute vascular lesion is mediated, at least partly, by enhanced thromboxane (TX) A2 biosynthesis. Thus, episodic increases in metabolite excretion have been detected in unstable angina. Aspirin (75-325 mg/day) prevents about one third of all fatal and nonfatal thrombotic events in this setting. That a similar "dynamic" thrombotic process occurs during the early phase of acute myocardial infarction is suggested by thromboxane metabolite measurements and by the results of the ISIS-2 trial showing a similar impact of short-term Aspirin therapy to that seen in unstable angina. Percutaneous transluminal coronary angioplasty is associated with transiently enhanced TXA2 biosynthesis and Aspirin-suppressable periprocedural thrombotic complications. On the other hand, both non-insulin-dependent diabetes mellitus and type IIa hypercholesterolemia are associated with a relatively reproducible and persisting abnormality of TXA2-dependent platelet function. This association is likely to reflect a systemic rather than localized stimulus to platelet activation and a continuous rather than episodic alteration. Low-dose (50 mg/day) Aspirin can largely suppress thromboxane metabolite excretion in both diseases. Thus, low-dose Aspirin and/or selective prostaglandin H2/TXA2-receptor antagonists may be important tools to test the hypothesis that TXA2-dependent platelet activation represents an important transducer of the enhanced thrombotic risk associated with these metabolic abnormalities.
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PMID:Thromboxane biosynthesis in cardiovascular diseases. 226 Jan 37

In a consecutive series of 4,697 patients undergoing coronary artery bypass surgery, these risk factors were found to be significant for increased postoperative mortality: age greater than 70, female sex, unstable angina, prior myocardial infarction, hypertension, diabetes mellitus, and ejection fraction less than .40. A comparison by year (1980-1988) revealed a steadily increasing incidence of these risk factors. Future analysis of coronary artery bypass mortality should include risk-factor stratification.
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PMID:Coronary artery bypass surgery: emerging trends in mortality. 232 52

To assess the possible progression of coronary artery disease after percutaneous transluminal coronary angioplasty (PTCA) and its relation to risk factors and restenosis, 124 patients who underwent a first successful PTCA were studied. All had routine follow-up angiography 5 to 8 months after PTCA. Restenosis was defined as a 30% decrease in diameter stenosis or a return to greater than 50% stenosis, and progression (in any nondilated site) as a 20% decrease in diameter stenosis, assessed by a video-densitometric computer-assisted technique. Univariate and multivariate analysis with respect to progression was carried out for age, sex, initial unstable angina, previous myocardial infarction, diabetes mellitus, hypertension, hypercholesterolemia (greater than or equal to 6.2 mmol), smoking habits, Jenkins' score, dilated artery and restenosis. Forty-one patients (33%) had restenosis, and 23 (19%) had evidence of progression; 20 (87%) of these latter patients had restenosis and 3 (13%) did not. Univariate correlates of progression were: previous myocardial infarction (p less than 0.05), higher Jenkins' score (p less than 0.0003) and restenosis (p less than 0.0001). Restenosis was the only multivariate correlate (p less than 0.00003). Progression at routine angiography after PTCA is not rare, and appears to be related to both the initial extent of coronary artery disease and restenosis.
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PMID:Risk factors for progression of atherosclerosis six months after balloon angioplasty of coronary stenosis. 232 59

Neutrophils, a source of proteolytic enzymes and oxygen free radicals, have been shown to participate in animal models of myocardial ischemic injury. To characterize neutrophil activation in human ischemic heart disease, a specific neutrophil elastase-derived fibrinopeptide in plasma was measured in 25 patients with stable angina pectoris, 29 patients with unstable angina pectoris, 17 patients with acute myocardial infarction and 22 control subjects. Mean plasma levels (+/- standard error) of a neutrophil elastase-derived fibrinopeptide (B beta 30-43) measured by a specific radioimmunoassay were fivefold higher in patients with acute myocardial infarction (877 +/- 337 pmol/liter, p less than 0.02) and 13-fold higher in patients with unstable angina (2,277 +/- 613 pmol/liter, p less than 0.006) as compared with control subjects (172 +/- 74 pmol/liter). Mean plasma levels of peptide B beta 30-43 in patients with stable angina (676 +/- 334 pmol/liter), although higher than in control subjects, were not significantly increased (p = 0.64). Total leukocyte counts were 11.0 +/- 0.6 x 10(6)/ml in those with acute myocardial infarction, 9.2 +/- 0.7 x 10(6)/ml in those with unstable angina, 7.1 +/- 0.3 x 10(6)/ml in those with stable angina and 7.7 +/- 0.4 x 10(6)/ml in control subjects. Although total leukocyte counts in patients with unstable angina pectoris and acute myocardial infarction were higher (p less than 0.01) than in patients with stable angina or in control subjects, elevations in peptide B beta 30-43 levels were independent of the differences in both leukocyte count and absolute neutrophil count as well as in history of smoking, hypertension, diabetes mellitus or treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased neutrophil elastase release in unstable angina pectoris and acute myocardial infarction. 234 35

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) probably results from pathophysiological mechanisms that are initiated during PTCA. Platelet deposition or exposed subendothelial connective tissue initiates complex blood element and vessel wall interactions that are not completely understood and leads to a proliferative response at the site of injury. The incidence of restenosis is also related to clinical, anatomic, and procedural variables. An increased frequency of restenosis is seen in patients who have recent onset of angina, unstable angina, or vasospastic angina, and in those who have diabetes. Stenoses in the proximal left anterior descending coronary artery, the ostium of the right coronary artery, and the proximal portion of a bypass vein graft have higher rates of restenosis than lesions at other sites. Restenosis can be predicted by an incomplete PTCA, which is identified by a high residual pressure gradient across the stenosis. Mechanical and pharmacological methods of preventing restenosis are under investigation. Intravascular stenting with expandable metal sleeves and laser angioplasty have shown encouraging results. Longer balloon inflation time can help prevent early elastic recoil. Platelet inhibitors (e.g., aspirin, dipyridamole, and sulfinpyrazone) do not appear to have an effect on restenosis. Agents, however, that interfere with platelet deposition at the PTCA site and that modify the effect of platelet-derived growth factor and medial cell proliferation show promise for control of restenosis.
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PMID:Restenosis after percutaneous transluminal coronary angioplasty--anatomic and pathophysiological mechanisms. Strategies for prevention. 240 72

The paper deals with the rheological properties of the blood of 38 male patients affected by ischaemic heart diseases (age: 40-75 years) and 19 healthy test persons of comparable age. The following haemorheological properties were measured. 1. Relative plasma viscosity 2. Erythrocyte aggregation 3. Erythrocyte deformability 4. Thrombocyte aggregation and 5. Whole blood viscosity. For the purpose of representing and assessing the results of measurement obtained a division was made into different groups according to the appearances of ischaemic heart disease (chronic ischaemic heart disease, unstable angina pectoris, acute heart infarct) and risk factors (smoking, diabetes mellitus, blood high pressure and hyperlipidaemia). The methods 1-3 proved to be especially suitable for representing gradual differences in the examined rheological parameters. The results obtained are discussed and evaluated.
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PMID:[Hemorheologic findings in patients with ischemic heart disease]. 248 31

Unstable angina pectoris is a broad, nonspecific diagnosis encompassing a wide variety of clinical syndromes. The intravenous administration of nitroglycerin preoperatively is indicative of a more acute clinical situation, and allows for selection and analysis of a more homogeneous patient population. We reviewed the results of coronary artery bypass grafting for unstable angina defined as angina necessitating intravenous administration of nitroglycerin preoperatively. There were 129 patients (83 men and 46 women) with a mean age of 63.2 years (range, 36 to 86 years). Complications included operative death in 6.2%, postoperative low cardiac output in 11%, and perioperative myocardial infarction in 9%. Twenty perioperative variables were analyzed to identify risk factors for these end points. For operative death, age (p less than 0.05), cross-clamp time (p less than 0.05), and cardiopulmonary bypass time (p less than 0.001) were significant in the univariate analysis, but only age (p less than 0.05, F = 4.6) was an independent predictor using multivariate analysis (stepwise linear regression). For low cardiac output, univariate analysis demonstrated that cross-clamp time (p less than 0.01), preoperative use of an intraaortic balloon for angina (p less than 0.05), left ventricular score (p less than 0.05), number of diseased coronary vessels (p less than 0.05), and cardiopulmonary bypass time (p less than 0.001) were significant variables. However, only use of an intraaortic balloon for angina (p less than 0.0001, F = 14.3) and left ventricular score (p less than 0.005, F = 11.1) were significant independent predictors in the multivariate model. For perioperative myocardial infarction, only diabetes requiring insulin (p less than 0.005) was a significant predictor.
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PMID:Coronary artery bypass grafting for unstable angina pectoris: risk analysis. 249 72


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