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At least 955 records · Page 53Linked to original sources
PubMed1981

Effect of exercise training on plasma high-density lipoprotein cholesterol in coronary disease patients.

The effects of chronic exercise training on plasma high-density lipoprotein cholesterol (HDL-C) were studied in 18 male coronary patients. Exercise consisted of aerobic activities utilizing approximately 70% of maximal oxygen uptake (VO2 max) for 20 to 40 minutes, three times weekly for 3 months. Significant increased in VO2 max, HDL-C, HDL-C/total cholesterol, and a decrease in percent body fat were documented after training. No significant changes were found in total cholesterol, triglyceride, body weight, or low-density lipoprotein cholesterol. Vigorous physical training can contribute to increased in HDL-C in patients with coronary disease without changes in total cholesterol or body weight.

Adult↗
PubMed1994

[Activity of leukocyte elastase in coronary disease diagnosed by coronarography].

OBJECTIVE: To evaluate the clinical usefulness of leukocyte elastase concentration for diagnosis of coronary artery disease. BACKGROUND: Recent research has shown the important role elastase, a proteolytic enzyme released by neutrophils, in the pathogenesis of coronary atherosclerotic disease. METHODS: 95 patients underwent coronary angiography during investigation of chest pain and/or heart valve disease; 38 had normal coronary arteriograms (Group I) and 57 had coronary lesions (Group II). The patients were characterized as regards presence or absence of stable or unstable angina, family history of coronary artery disease, smoking, diabetes mellitus, hypertension, leukocyte counts, plasma lipid and elastase concentrations. Among Group II patients, those with simple atheromatous plaques were distinguished from those with complex plaques. RESULTS: Elastase concentrations were greater in the Group II than in the Group I (41 +/- 21 vs 27 +/- 14 micrograms/L) (p < 0.001), and greater among complex plaque patients than among simple plaque patients (53 +/- 27 vs 33 +/- 12 micrograms/L) (p < 0.001). Logistic regression analysis showed than elastase concentration, angina, age and sex had independent value for prediction of coronary artery disease and that the risk increased by 7% for every 1 microgram/L increase in elastase concentration. Among Group II patients, the risk of complex plaque was greatest for those with unstable angina and high elastase concentration, increasing by 6% for every 1 microgram/L increase in elastase concentration. CONCLUSIONS: Peripheral blood leukocyte elastase concentration is a sensitive diagnostic marker of coronary artery disease. High values suggest the presence of complex atheromatous plaques.

Aged↗
PubMed1985

Haemodynamic effects of molsidomine in patients with severe chronic coronary disease.

The haemodynamic effects of a single dose of intravenous molsidomine were assessed in 12 patients with severe coronary disease. The investigation was carried out at rest during angina induced by pacing and after molsidomine during pacing at the rate at which angina had been produced. During angina, left ventricular systolic and end-diastolic pressure rose, left ventricular stroke work fell and coronary flow and myocardial oxygen consumption increased by 58.3% above the control levels. After the administration of molsidomine, atrial stimulation was not followed by angina and there were no significant changes in systolic blood pressure. Left ventricular end-diastolic pressure fell sharply and coronary flow and myocardial oxygen consumption were only 38% and 33% higher, respectively, than the control levels. The beneficial effects of molsidomine in ischaemic heart disease, therefore, are the result of peripheral vasodilation which, by reducing the preload and afterload, lowers the oxygen requirements of the myocardium and thus increase the threshold for angina. A direct action on the coronary network can not be excluded but if such an action does exist it must be very small in the light of the marked systemic effect.

Adult↗
PubMed2000

Low molecular weight heparins and coronary artery disease.

Coronary artery disease encompasses a wide spectrum of conditions including silent ischemia, exertional angina, unstable angina, and myocardial infarction. Acute coronary syndromes (unstable angina and myocardial infarction) are caused by the rupture of an atherosclerotic plaque, platelet activation, and fibrin deposition resulting in thrombosis. Aspirin and unfractionated heparin (UFH) have traditionally been the treatment of choice in patients with acute coronary syndromes; however, low molecular weight heparins (LMWHs) offer potential advantages over UFH. Available evidence indicates that LMWH is superior to UFH in reducing ischemic events or death in the acute phase of unstable angina or non-Q-wave myocardial infarction. Long-term therapy with lower doses of LMWH may not offer any advantage to aspirin in the prevention of coronary events or death. Major bleeding complications are similar for LMWH and UFH although minor bleeding complications are more common with LMWH, primarily due to injection-site hematomas. Finally, use of LMWH appears to be cost- effective compared with UFH. The available evidence supports improved clinical outcomes, favorable safety profile, and cost savings associated with LMWH use in the management of unstable angina and non-Q-wave myocardial infarction and should be favored over UFH.

Angina, Unstable↗
PubMed1999

[Coronary disease in patients with an abdominal aortic aneurysm].

The presence of coronary artery disease (CAD) evaluated with coronary angiography and eventual correction of CAD in abdominal aortic aneurysm (AAA) patients has been considered the main determinant of early and late outcome after AAA repair. This study reports our experience in CAD and AAA patients in terms of diagnosis and therapy of CAD. In a population of 126 patients (122 males, 4 females, mean age 67.5 years, range 37-81) who were candidates to elective repair for AAA with a diameter > or = 5 centimeters, we included coronary arteriography in 1) patients who were symptomatic for angina (15.9%); 2) patients with previous myocardial infarction (33.3%); 3) patients with previous coronary artery bypass (4%). We identified a group of 45 patients (35.7%) with significant CAD who had been treated before AAA surgery by coronary artery bypass grafting (CABG) in 37 cases or percutaneous coronary angioplasty (PTCA) in 8 cases. AAA repair was performed during the same hospital stay or at a later date. We did not report any morbidity and mortality related to cardiac or vascular procedures. We believe that among patients reporting cardiac symptoms (previous myocardial infarction, angina) the incidence of surgically-correctable CAD is not negligible (45/67, 67.2%). Therefore, invasive coronary study is strongly suggested in such cases to reveal and treat an eventual coronary artery stenosis prior to AAA repair. The absence of cardiac morbidity and mortality related to cardiac and vascular procedures supports this approach.

Adult↗
PubMed1995

Serum lipoprotein(a) concentrations are related to coronary disease progression without new myocardial infarction.

OBJECTIVE: To examine the association between serum lipoprotein(a) and angiographically assessed coronary artery disease progression without new myocardial infarction. PATIENTS AND DESIGN: 85 patients with coronary artery disease who underwent serial angiography with an interval of at least two years were studied. Progression of coronary artery disease was defined as an increase in diameter stenosis of 15% or more. Vessels on which angioplasty had been performed were excluded from the analysis. The patients were classified into two groups: a progression group without new myocardial infarction (n = 48) and non-progression group (n = 37). Risk factors including lipoprotein(a) were evaluated to see how they were related to progression without myocardial infarction. RESULTS: There were no differences between the two groups in the following factors: age, gender, the time interval between the angiographic studies, the distribution of the analysed coronary arteries, and history of well established coronary risk factors. Univariate analysis showed that serum lipoprotein(a) (P = 0.0002), cigarette smoking between the studies (P = 0.002), serum high density lipoprotein (P = 0.003), and serum low density lipoprotein (P = 0.01) were related to progression without myocardial infarction. Multivariate analysis selected two independent factors for progression without myocardial infarction: serum lipoprotein(a) (P = 0.003) and serum high density lipoprotein (P = 0.03). CONCLUSIONS: Serum lipoprotein(a) concentrations are closely related to the progression of coronary artery disease without new myocardial infarction. Lipoprotein(a) lowering treatment may be needed to prevent disease progression in patients with coronary artery disease and high serum lipoprotein(a).

Aged↗
PubMed2000

Treating ambulatory ischemia in coronary disease by manipulating the cell biology of atherosclerosis.

Obstructive coronary artery disease is the most common cause of morbidity and mortality in the developed world. Our understanding of the pathobiology of coronary atherosclerosis provides us with new opportunities to reduce myocardial ischemia by interventions that address these mechanisms directly. These interventions include lipid-lowering therapies that improve local coronary vasomotion, inflammation, and the procoagulant state. These interventions have also been shown to result in important reductions in clinical events, including angina pectoris, myocardial ischemia and infarction, and death. Ambulatory electrocardiography provides a versatile and quantifiable measure of regional myocardial ischemia. Reductions in ischemia, as quantified by this diagnostic modality, are associated with improved clinical outcomes that may reflect improvements in the cellular pathophysiology of coronary atherosclerosis. This review discusses new information regarding the interactions between low-density lipoprotein cholesterol, the cell biology of atherosclerosis, and the activity of ischemia in patients with coronary artery disease.

Anticholesteremic Agents↗