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Objectives. The present study examined the association of estrogen (E2) and the inflammatory response of endothelium in coronary artery disease (CAD) by measuring circulating cellular adhesion molecules (cCAMs) in subjects with atherosclerosis.Background. Atherosclerotic plaque demonstrates features similar to inflammation. Endothelial cell activation by inflammatory cytokines induces expression of cellular adhesion molecules (CAMs), thereby perhaps augmenting leukocyte adhesion and recruitment and subsequent development of atherosclerosis. The incidence of CAD is lower in women; this may be due to the cardioprotective effects of E2.Methods. Consecutive eligible subjects with CAD admitted for cardiac catheterization were studied. The groups evaluated were men, postmenopausal women receiving E2replacement therapy (ERT), postmenopausal women not receiving ERT and premenopausal women. Control groups included men and women without CAD. Preprocedural blood samples were drawn from all groups. Measurements of cCAMs, E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 were performed by enzyme-linked immunoabsorbant assay. E2levels were assessed by radioimmunoassay.Results. We observed a statistically significant increase in all cCAMs in men with CAD and postmenopausal women with CAD not receiving ERT compared with postmenopausal women with CAD receiving ERT. Premenopausal women with CAD and postmenopausal women with CAD receiving ERT had a significant increase in VCAM-1 alone compared with the female control group.Conclusions. A possible mechanism by which E2exerts one of its cardioprotective effects is by limiting the inflammatory response to injury by modulating the expression of CAMs from the endothelium.

There are now extensive data suggesting that the progression of atherosclerosis can be altered by cholesterol-lowering therapy. The changes in stenosis severity, measured angiographically, are small relative to the clinical benefit noted. Other factors, in addition to changes in stenosis severity, are probably operative. Effects of cholesterol-lowering on endothelial function, perhaps mediated by reductions in PAI-1 levels, may be one of these mechanisms. This uncontrolled study requires further investigation to elucidate the independent relation between lovastatin, PAI-1, and fibrinogen.

Clinical and anatomic determinants of primary success of percutaneous transluminal coronary angioplasty were retrospectively evaluated in 299 pa tients. Successful angioplasty (residual stenosis

Left ventricular diastolic properties are important markers of pump function and are frequently abnormal when myocardial insults alter tissue structure. Alterations can be limited to the early diastolic phase (early active relaxation) or to late diastolic filling (late ventricular compliance), but more often involve regulation of both phases of diastole. In asymptomatic patients with arterial hypertension, left ventricular relaxation is often prolonged, independently, at least in part, of cardiac loading conditions and left ventricular geometry, but this abnormality is associated with early signs of systolic dysfunction. Uncontrolled hypertension, diabetes, and obesity are most often associated with ischemic heart disease and impaired diastolic function. Reducing blood pressure with antihypertension therapy will reduce myocardial afterload, regress LVH, and improve systolic and diastolic function. In patients with symptoms of CHF with a normal ejection fraction, however, changes in therapy may be indicated. Greater emphasis should be placed on using medications that decrease myocardial load, but also reduce the effects of neurohormonal activation.

To determine the success rate and the safety of percutaneous transluminal coronary angioplasty in patients with unstable angina pectoris (group 1) versus stable angina (group 2), we studied 299 consecutive patients who underwent coronary angioplasty of 373 consecutive lesions. Of these patients, 149 had unstable angina pectoris and dilation of 188 arteries. The success rate was high and similar in both groups (95 and 93%, respectively). The groups did not differ in regard to the lesion characteristics, vessels and number of sites dilated except for an increase in the presence of thrombus in the unstable angina group (p0.03). Although there was a higher incidence of coronary thrombus and more acute myocardial infarction in group 1, the major complication rate did not differ from that of group 2 and was low in both of them (3 and 2%, respectively). No deaths occurred. Six patients (3 in each group) needed urgent coronary artery bypass grafting while 3 additional patients developed acute Q-wave myocardial infarction (all of them in group 1). Thus, percutaneous transluminal coronary angioplasty is a safe and successful procedure in patients with unstable angina as well as in patients with stable angina pectoris.

LEARNING OUTCOME: To define medical nutrition therapy practice guidelines for individuals taking lovastatin for hyperlipidemia. When medical nutrition therapy fails to adequately control blood cholesterol levels and drug therapy is initiated, maintenance of a heart healthy diet is often perceived to be of little importance. In order to develop practice guidelines, more information is needed regarding the impact of dietary intake on low density lipoprotein (LDL) in those who do require hypolipemic agents. Data was analyzed from 78 subjects (baseline mean LDL=213mg/dl) who participated in a clinical trial to assess the efficacy of the Step One diet and lovastatin in reducing LDL-cholesterol. This subset of subjects failed to achieve their LDL goal of ≤ 160mg/dl or ≤130mg/dl (based upon low or high risk for coronary heart disease, respectively) after receiving nutrition counseling on the Step One by a registered dietitian. They were started on 20mg lovastatin and returned every 6 weeks, for a total of 48 weeks, to obtain a fasting lipid profile and dosage adjustment to attain LDL goals. At each visit, 2-day food records were completed and analyzed using Dine software. A multiple logistic regression model was used to control for the average weekly dosage of lovastatin and nutrient intake was determined by averaging the values obtained from food record analysis during the medication phase. The results indicated that saturated fat in synergy with total fat intake was predictive of the subject's success in meeting their LDL goal. As the intake of saturated fat decreased (p=0.02) and was replaced with unsaturated sources (p=0.01), the subjects were more likely to meet their LDL goal. Thus, dietary compliance to a low saturated fat diet, with emphasis on unsaturated fats, is recommended for individuals prescribed this medication. In typical practice settings, nutrition intervention by a registered dietitian is beneficial, even if patients cannot attain LDL goals with diet alone. An unrestricted diet may necessitate a higher dosage of lovastatin which increases the risk of potentially serious side effects and has significant economic impact.

To impact on the development of clinical congestive heart failure as a complication of doxorubicin therapy, left ventricular ejection fraction was monitored with serial resting radionuclide angiocardiography in 1,487 patients with cancer over a seven-year period in both university and community hospital environments. A high-risk subset of 282 patients was selected for retrospective analysis of their clinical outcome. High-risk patients were identified by one or two of the following three criteria: decline of 10 percent or more in absolute left ventricular ejection fraction from a normal baseline to 50 percent or less; high cumulative dose of doxorubicin (more than 450 mg/m2); abnormal baseline left ventricular ejection fraction (less than 50 percent). Clinical congestive heart failure occurred in 46 (16 percent) during the treatment period, and in an additional three patients (1.3 percent) at last follow-up examination 11.8 +/- 14.2 months following discontinuation of doxorubicin. Total cumulative dosages of doxorubicin that precipitated congestive heart failure (75 to 1,095 mg/m2) and those that did not (30 to 880 mg/m2) varied widely. Decline of 10 percent or more in absolute left ventricular ejection fraction to a value of 50 percent or less preceded administration of the final dose of doxorubicin that precipitated clinical congestive heart failure in the majority of patients in whom congestive heart failure developed. Clinical congestive heart failure improved in 87 percent given routine therapy with digitalis, diuretics, and/or vasodilators. Criteria for monitoring left ventricular ejection fraction and discontinuing doxorubicin were formulated. The occurrence of clinical congestive heart failure was compared in those patients whose management was concordant with proposed criteria (Group A) and in those whose management was not (Group B). Group A had a lower incidence of congestive heart failure compared with Group B (2.9 percent versus 20.8 percent, p less than 0.001) and had only mild congestive heart failure that resolved with treatment (n = 2) and no deaths due to congestive heart failure. Multivariate analysis with proportional-hazards regression (Cox's model) demonstrated a fourfold reduction in the incidence of congestive heart failure independent of other clinical predictor variables in those patients whose management was concordant with proposed guideline criteria. The incidence, persistence, late development, predictability, and reversibility of clinical congestive heart failure were comparable in university and community hospital settings.(ABSTRACT TRUNCATED AT 400 WORDS)

Maternal cardiovascular complications have been attributed to the dramatic hemodynamic changes associated with labor and delivery in patients with Takayasu's arteritis. The role of central hemodynamic monitoring in the management of a pregnant patient with severe Takayasu's arteritis is discussed.