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: ObjectivesThis study was designed to determine if non-aspirin non-steroidal anti-inflammatory drugs (NANSAIDs) are associated with lower odds of myocardial infarction (MI) and if NANSAIDs, particularly ibuprofen, interfere with aspirin''s cardioprotective effect.: BackgroundThe NANSAIDs may reduce the risk of MI but may also interfere with aspirin''s cardioprotective effect.: MethodsA case-control study was conducted, with cases of first, nonfatal MI identified prospectively and controls identified randomly from the community.: ResultsThe use of NANSAIDs was associated with a significant reduction in MI among those not using aspirin (adjusted odds ratio [OR] 0.53; 95% confidence interval [CI]: 0.42 to 0.67). This was true for both ibuprofen (adjusted OR 0.52; 95% CI: 0.39 to 0.69) and naproxen (adjusted OR 0.48; 95% CI: 0.28 to 0.82). Although aspirin itself was associated with decreased odds of MI in those not also using NANSAIDs (adjusted OR relative to no aspirin use 0.79; 95% CI: 0.63 to 0.98), it was not associated with decreased odds of MI among those who were using NANSAIDs (OR 1.28; 95% CI: 0.85 to 1.94; p value for interaction = 0.026). The association of aspirin and reduced odds of MI diminished with increasing frequency of NANSAID use (test for interaction p = 0.006), particularly for ibuprofen (p = 0.018). Among frequent (4 times/week) NANSAID users, the OR for aspirin versus no aspirin was 2.04 (95% CI: 1.06 to 3.94). Users of prophylactic aspirin plus frequent ibuprofen had an OR relative to aspirin-only users of 2.03 (95% CI: 0.60 to 6.84).: ConclusionsIn the absence of aspirin use, NANSAIDs are associated with reduced odds of MI. In those using aspirin, NANSAIDs do not provide additional protection. Additional study is needed to determine the clinical impact of using NANSAIDs along with aspirin for cardioprotection. [Copyright &y& Elsevier]

Patients with heart failure (HF) and their families experience stress and suffering from a variety of sources over the course of the HF experience. Palliative care is an interdisciplinary service and an overall approach to care that improves quality of life and alleviates suffering for those living with serious illness, regardless of prognosis. In this review, we synthesize the evidence from randomized clinical trials of palliative care interventions in HF. While the evidence base for palliative care in HF is promising, it is still in its infancy and requires additional high-quality, methodologically sound studies to clearly elucidate the role of palliative care for patients and families living with the burdens of HF. Yet, an increase in attention to primary palliative care (e.g., basic physical and emotional symptom management, advance care planning), provided by primary care and cardiology clinicians, may be a vehicle to address unmet palliative needs earlier and throughout the illness course. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to investigate whether a surrogate for renal neurohormonal activation, blood urea nitrogen (BUN), could identify patients destined to experience adverse outcomes associated with the use of high-dose loop diuretics (HDLD). Background: Loop diuretics are commonly used to control congestive symptoms in heart failure; however, these agents cause neurohormonal activation and have been associated with worsened survival. Methods: Subjects in the BEST (Beta-Blocker Evaluation of Survival Trial) receiving loop diuretics at baseline were analyzed (N = 2,456). The primary outcome was the interaction between BUN- and HDLD-associated mortality. Results: In the overall cohort, HDLD use (≥160 mg/day) was associated with increased mortality (hazard ratio [HR]: 1.56; 95% confidence interval [CI]: 1.35 to 1.80). However, after extensively controlling for baseline characteristics, this association did not persist (HR: 1.06; 95% CI: 0.89 to 1.25). In subjects with BUN levels above the median (21.0 mg/dl), both the unadjusted (HR: 1.59; 95% CI: 1.34 to 1.88) and adjusted (HR: 1.29; 95% CI: 1.07 to 1.60) risk of death was higher in the HDLD group. In patients with BUN levels below the median, there was no associated risk with HDLD (HR: 0.99; 95% CI: 0.75 to 1.34) and after controlling for baseline characteristics, the HDLD group had significantly improved survival (HR: 0.71; 95% CI: 0.49 to 0.96) (p interaction = 0.018). Conclusions: The risk associated with HDLD use is strongly dependent on BUN concentrations with reduced survival in patients with an elevated BUN level and improved survival in patients with a normal BUN level. These data suggest a role for neurohormonal activation in loop diuretic–associated mortality. [Copyright &y& Elsevier]

Objectives: The aim of this study was to compare the accuracy of genetic tables and formal pharmacogenetic algorithms for warfarin dosing. Background: Pharmacogenetic algorithms based on regression equations can predict warfarin dose, but they require detailed mathematical calculations. A simpler alternative, recently added to the warfarin label by the U.S. Food and Drug Administration, is to use genotype-stratified tables to estimate warfarin dose. This table may potentially increase the use of pharmacogenetic warfarin dosing in clinical practice; however, its accuracy has not been quantified. Methods: A retrospective cohort study of 1,378 patients from 3 anticoagulation centers was conducted. Inclusion criteria were stable therapeutic warfarin dose and complete genetic and clinical data. Five dose prediction methods were compared: 2 methods using only clinical information (empiric 5 mg/day dosing and a formal clinical algorithm), 2 genetic tables (the new warfarin label table and a table based on mean dose stratified by genotype), and 1 formal pharmacogenetic algorithm, using both clinical and genetic information. For each method, the proportion of patients whose predicted doses were within 20% of their actual therapeutic doses was determined. Dosing methods were compared using McNemar''s chi-square test. Results: Warfarin dose prediction was significantly more accurate (all p < 0.001) with the pharmacogenetic algorithm (52%) than with all other methods: empiric dosing (37%; odds ratio [OR]: 2.2), clinical algorithm (39%; OR: 2.2), warfarin label (43%; OR: 1.8), and genotype mean dose table (44%; OR: 1.9). Conclusions: Although genetic tables predicted warfarin dose better than empiric dosing, formal pharmacogenetic algorithms were the most accurate. [Copyright &y& Elsevier]

Objectives: We endeavored to determine under what conditions a strategy of upstream use of small molecule platelet glycoprotein (GP) IIb/IIIa inhibitors for all acute coronary syndromes (ACS) patients is cost effective compared to that of selective use of abciximab in only those patients requiring percutaneous coronary intervention (PCI). Background: Small molecule GP IIb/IIIa inhibitors have shown benefit in ACS, but abciximab, the more expensive GP IIb/IIIa inhibitor, may be more effective during PCI. However, abciximab does not have proven efficacy in medical management. No prior study has attempted to balance these competing benefits. Methods: A decision analysis was performed to examine two strategies: 1) treat all ACS patients upstream with a small molecule GP IIb/IIIa inhibitor and continue through medical management and PCI, if performed; or 2) wait, and selectively use abciximab only in patients who ultimately undergo PCI. Applicable randomized controlled trial data were used for the principal analysis. Results: The strategy of upstream use of a small molecule GP IIb/IIIa inhibitor was superior to selective use, and economically acceptable, with a cost-effectiveness ratio of $18,000 per year of life gained. The superiority of the upstream use strategy persisted over the majority of sensitivity analyses. When stratified by risk according to Thrombolysis in Myocardial Infarction risk score, a strategy of upstream use was only cost effective in those patients with moderate or high risk. Conclusions: Upstream use of small molecule GP IIb/IIIa inhibition in ACS patients with moderate or high risk for cardiovascular events is a cost-effective approach that should be considered in this subset of patients. [Copyright &y& Elsevier]

: ObjectivesWe sought to determine whether the stringent stress test criteria for crossover to cardiac catheterization in the conservative arm of the Fast Revascularization During Instability in Coronary Artery Disease (FRISC-II) trial subjected this strategy to a disadvantage by failing to identify patients with surgical coronary artery disease (CAD).: BackgroundIn FRISC-II, an invasive strategy provided superior outcomes compared with a conservative strategy for patients with acute coronary syndromes. However, compared with the stress test criteria for crossover to catheterization in the Veterans Affairs Non–Q-Wave Infarction Strategies in Hospital (VANQWISH) trial, the FRISC-II criteria were more restrictive and did not use nuclear imaging or pharmacologic stress testing.: MethodsWe analyzed the conservative arm of VANQWISH to identify the prevalence of surgical CAD in those patients who met the VANQWISH, but not FRISC-II, criteria for catheterization.: ResultsOf 385 VANQWISH patients, 90 (23%) met the FRISC-II criteria for catheterization. Another 98 patients (25%) met only VANQWISH stress test criteria (60 patients by exercise and 38 by pharmacologic nuclear stress testing). Among subjects who underwent predischarge angiography, those meeting only VANQWISH stress test criteria had a high prevalence of surgical CAD (51%), comparable to patients who met FRISC-II criteria (54%, p = 0.805).: ConclusionsThe overly stringent risk stratification protocol for conservative-arm patients in FRISC-II could have failed to identify almost as many patients with surgical CAD as it identified. A lower threshold for catheterization in the FRISC-II conservative patients might have improved their outcomes and therefore diminished the putative benefit of an invasive strategy. [Copyright &y& Elsevier]