Spectrum of calcific aortic valve disease: pathogenesis, disease progression, and treatment strategies.
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Publications and source records attributed to Rosario V Freeman.
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Aortic stenosis is the most commonly encountered valvular disease in the elderly, with approximately 2-3% of individuals over 65 years of age afflicted. The most common cause of acquired aortic stenosis is calcific degeneration, characterized by a slowly progressive, asymptomatic period which can last decades. Once symptomatic, the clinical manifestation of aortic stenosis is from functional obstruction of left ventricular outflow and the additional hemodynamic effects on the left ventricle and vasculature. With advances in echocardiography, individuals with aortic stenosis are increasingly diagnosed in the asymptomatic latent period. However, echocardiographic measures alone cannot identify clinically significant outflow obstruction as there is considerable overlap in hemodynamic severity between symptomatic and asymptomatic individuals. Current clinical guidelines predicate the timing of surgical valve replacement on the presence or absence of symptoms. Management for symptomatic, significant stenosis is surgical valve replacement as there are no current medical therapies reliably proven to decrease aortic stenosis severity or improve long-term outcomes. However, recent retrospective studies have demonstrated an association between atherosclerotic disease risk factors, such as hyperlipidemia and aortic stenosis. Given these findings, there are now advocates for prospective primary prevention trials for aortic stenosis in patients with mild or moderate valvular disease. The following paper will discuss etiology, diagnostic evaluation and therapeutic options of acquired aortic stenosis. This review will discuss etiology, diagnostic evaluation, and therapeutic options of acquired aortic stenosis.
OBJECTIVES: The purpose of this study was to examine the in-hospital outcome and influence of glycoprotein (GP) IIb/IIIa antagonists on patients with acute coronary syndromes (ACS) across a range of renal function. BACKGROUND: Recent studies demonstrate increasing cardiovascular risk with progressive renal dysfunction. Previous studies investigating GP IIb/IIIa antagonist use have excluded patients with renal dysfunction. METHODS: Patients presenting with ACS between January 1999 and May 2000 were identified, and data on demographics, in-hospital management, and clinical events were collected using standardized definitions. Patients were stratified according to renal function assessed by calculated creatinine clearance (CrCl) at presentation. Primary outcome measures included in-hospital mortality and major bleeding events. RESULTS: Renal insufficiency was present in 312 of 889 patients. There were 40 in-hospital deaths. In non-dialysis-dependent patients, as CrCl worsened, there was a decline in utilization of routine diagnostics and therapeutics, an increase in in-hospital mortality (p = 0.002), and an increase in major bleeding (p = 0.03). Although the use of GP IIb/IIIa antagonists was associated with an increase in major bleeding (p < 0.001), there was a protective effect on in-hospital mortality (p = 0.04) after controlling for CrCl. CONCLUSIONS: Renal dysfunction is present in a substantial proportion of patients with ACS and is associated with increased in-hospital death. Although GP IIb/IIIa antagonist use in patients with ACS and renal insufficiency resulted in increased bleeding events, its administration was associated with a decreased risk of in-hospital mortality. These preliminary findings need to be confirmed in future randomized clinical trials.
This study was undertaken to determine the incidence, risk factors, and in-hospital outcome of nephropathy requiring dialysis (NRD) after percutaneous coronary intervention (PCI), and to evaluate the role of a weight- and creatinine-adjusted maximum radiographic contrast dose (MRCD) on NRD. Data were obtained from a registry of 16,592 PCIs. The data were divided into development and test sets. Univariate predictors were identified and a multivariate logistic regression model was developed. The MRCD was calculated for each patient as: MRCD = 5 ml x body weight (kilograms)/serum creatinine (milligrams per deciliter). Predictive accuracy was assessed by receiver-operating characteristic curve analysis. In the development set, 41 patients (0.44%) developed NRD with a subsequent in-hospital mortality rate of 39.0%. NRD increased with worsening baseline renal dysfunction. Other risk factors included peripheral vascular disease, diabetes mellitus, congestive heart failure, and cardiogenic shock. There was a direct relation between the number of risk factors and NRD. After adjustment for baseline risk factors, MRCD was the strongest independent predictor of NRD (adjusted odds ratio 6.2, 95% confidence interval 3.0 to 12.8). NRD and in-hospital mortality were both significantly higher in patients who exceeded the MRCD compared with patients who did not (p <0.001). In conclusion, NRD following PCI is a rare complication with a poor prognosis. Baseline clinical characteristics identify patients at greatest risk for NRD. Optimization of procedural variables such as timing of the intervention relative to the diagnostic catheterization, staging coronary procedures, or dosing within the MRCD may help reduce the risk of this complication in high-risk patients. A risk prediction tool for NRD with guidelines for prevention is presented.
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