Biomedical subjects

H F Weil

Publications and source records attributed to H F Weil.

4 recordsLinked to original sources

PubMed2000

Race-related differences among patients with left ventricular dysfunction: observations from a biracial angiographic cohort. Harlem-Bassett LP(A) Investigators.

BACKGROUND: This study was designed to describe race-related differences in left ventricular function among a consecutive series of patients undergoing cardiac catheterization and to identify racial differences in coexistent medical and social conditions that are associated with the development of heart failure (HF). METHODS AND RESULTS: This was a prospective cohort study conducted at 2 university-affiliated teaching hospitals. We used the database of the Harlem-Bassett Lp(a) Study. We included all black (N = 143) or white (N = 313) patients from the main study database for whom complete survey, laboratory, coronary angiographic, and ventriculographic data were available. "Left ventricular dysfunction" was arbitrarily defined as an ejection fraction < or =0.40 or prior pharmacologic treatment for HF. We found that blacks were younger, had a higher proportion of women, and had fewer years of formal education than their white counterparts. Coronary artery disease was less common among blacks, although this group had a higher prevalence of hypertension, diabetes, cigarette smoking, illicit drug use, and alcohol consumption. Black patients had a higher prevalence of previous treatment for HF, larger left ventricular volumes, and lower ejection fractions than white patients. Blacks with left ventricular dysfunction were more likely to have had a previous myocardial infarction or a history of hypertension compared with those without left ventricular dysfunction. CONCLUSIONS: Regarding left ventricular dysfunction and HF, we conclude that blacks seem to have a much higher burden of disease than whites. Our observations support prior evidence that hypertension is linked to race-related differences in the epidemiology of HF. The interaction between race and access to quality care for HF remains an important area for future investigation.

Adult↗

PubMed2000

High levels of Lp(a) with a small apo(a) isoform are associated with coronary artery disease in African American and white men.

Elevated levels of lipoprotein(a) [Lp(a)] and the presence of small isoforms of apolipoprotein(a) [apo(a)] have been associated with coronary artery disease (CAD) in whites but not in African Americans. Because of marked race/ethnicity differences in the distribution of Lp(a) levels across apo(a) sizes, we tested the hypothesis that apo(a) isoform size determines the association between Lp(a) and CAD. We related Lp(a) levels, apo(a) isoforms, and the levels of Lp(a) associated with different apo(a) isoforms to the presence of CAD (>/=50% stenosis) in 576 white and African American men and women. Only in white men were Lp(a) levels significantly higher among patients with CAD than in those without CAD (28.4 versus 16.5 mg/dL, respectively; P:=0.004), and only in this group was the presence of small apo(a) isoforms (<22 kringle 4 repeats) associated with CAD (P:=0.043). Elevated Lp(a) levels (>/=30 mg/dL) were found in 26% of whites and 68% of African Americans, and of those, 80% of whites but only 26% of African Americans had a small apo(a) isoform. Elevated Lp(a) levels with small apo(a) isoforms were significantly associated with CAD (P:<0.01) in African American and white men but not in women. This association remained significant after adjusting for age, diabetes mellitus, smoking, hypertension, HDL cholesterol, LDL cholesterol, and triglycerides. We conclude that elevated levels of Lp(a) with small apo(a) isoforms independently predict risk for CAD in African American and white men. Our study, by determining the predictive power of Lp(a) levels combined with apo(a) isoform size, provides an explanation for the apparent lack of association of either measure alone with CAD in African Americans. Furthermore, our results suggest that small apo(a) size confers atherogenicity to Lp(a).

Black or African American↗

PubMed1999

Cardiology or primary care for heart failure in the community setting: process of care and clinical outcomes.

STUDY OBJECTIVES: Severity of illness, treatment choices, and clinical outcomes may vary with physician training. This study was performed to determine whether such differences exist among patients with congestive heart failure (CHF) treated by cardiologists and by noncardiologists in the community hospital setting. DESIGN: Prospective cohort study. SETTING: Ten acute-care community hospitals. PATIENTS, MEASUREMENTS, AND RESULTS: Two thousand four hundred fifty-four patients with CHF were identified and followed up for 6 months after hospital discharge. Patients who were not treated by a cardiologist (group I; n = 977) were compared with patients whose attending physician was a cardiologist (group II; n = 419) and patients who received consultative care from a cardiologist (group III; n = 1,058). When compared with group I patients, group II patients were more likely to receive the recommended diagnostic tests and treatment strategies, although some of these differences could be explained by variations in the case mix. Group II patients had higher hospital charges, but lower CHF readmission rates and better postdischarge quality-of-life measures. No differences in adjusted mortality rates were observed. CONCLUSIONS: In the community-hospital setting, the clinical practices of cardiologists are more compatible with published treatment guidelines than the clinical practices of other physicians. The benefits of cardiology specialty care include lower CHF readmission rates and better postdischarge quality-of-life measures, rather than lower mortality rates, fewer hospital charges, or shorter length of stay.

Aged↗

PubMed1997

Epidemiology of thrombotic-hemostatic factors and their associations with cardiovascular disease.

Abundant evidence proves that thrombosis is involved in the acute presentation of coronary, cerebrovascular, and peripheral vascular diseases. However, the role of thrombotic factors in the development of the atherosclerotic lesions themselves has been more difficult to prove. This difficulty has been due, at least in part, to several methodologic issues in the study of hemostatic factors and cardiovascular disease (CVD). These include the possibility that associations between CVD and hemostatic factors may not be causal but rather due to confounding by other factors, acting as part of an extended causal pathway or requiring interaction with other risk factors or atherosclerotic disease, or may result from disease rather than causing the disease. In addition, several challenges remain in the measurement of hemostatic factors. Nonetheless, a growing number of studies have examined the association of CVD with coagulation factors (fibrinogen, factor VII, factor VIII, and platelet aggregability) and fibrinolytic factors [tissue plasminogen activator, plasminogen activator inhibitor 1, lipoprotein(a), and plasminogen or global fibrinolytic activity]. Of these, only for fibrinogen is there significant, strong, and consistent evidence of a causal association. Given the preliminary nature of these associations, any association between dietary factors and hemostatic factors other than fibrinogen is difficult to invoke as evidence for a deleterious effect of diet on CVD risk via thrombogenic mechanisms.

Blood Coagulation↗