Acute coronary syndrome (ACS) is a continuum of disease that includes non-ST-segment elevation ACS and ST-segment elevation myocardial infarction. The purpose of this article is to define the developing role of ticagrelor in ACS and compare it to currently available P2Y₁₂ receptor inhibitors. While clopidogrel remains the "workhorse" P2Y₁₂ receptor inhibitor for many patients with ACS and prasugrel has an established role in select situations, clinicians must now assimilate the evolving role of ticagrelor. Although ticagrelor offers important advances in the management of ACS (eg, reversibility), there are also notable clinical considerations (eg, unique adverse effects such as dyspnea). Based on the current evidence, we propose an algorithm to aid clinicians in the selection of a P2Y₁₂ receptor inhibitor for patients with ACS in various clinical situations.
Background: Vitamin D deficiency has been associated with cardiovascular mortality and sudden cardiac death in heart failure patients. Vitamin D may influence parathyroid hormone, the renin-angiotensin axis, natriuretic peptide gene expression, cardiac contractility, and cardiopulmonary function. Heart Failure (HF) studies using vitamin D to date have typically not used adequate repletion doses. Objectives: The primary objectives of this research were to determine if vitamin D repletion over a six month period in New York Heart Association (NYHA) Class II-III HF patients would result in a change in neurohormonal markers, cardiopulmonary exercise parameters, circulating 25- hydroxyvitamin D, and quality of life. Methods: A randomized, double-blinded, placebo-controlled trial assessing adjunctive Vitamin D3 supplementation in the treatment of NYHA Class II-III HF patients was conducted. Patients received 10,000 International Units (IU) per day of vitamin D3 or placebo for 6 months. Inclusion Criteria: 1) 25-hydroxyvitamin D level ≤32 ng/ml 2) stable medical regimen for 3 months. Exclusion Criteria: 1) any clinically unstable medical disorder 2) supplementation of vitamin D3 or D2 of greater than or equal to 2,000 IU/day. Study endpoints were: 1) B-type Natriuretic Peptide (BNP), 2) cardiopulmonary exercise parameters using Shape HF, 3) 25-hydroxyvitamin D, 4) intact parathyroid hormone (PTH), and 5) quality of life with the Kansas City Cardiomyopathy Questionnaire (KCCQ). Statistical analysis included independent samples t-test and multivariate regression. Results: A total of 34 patients completed the study. When adjusted for baseline 25-hydroxyvitamin D, the difference between groups for BNP was significant ([[Unable to Display Character: ∆]]540 ±1928 pg/ml placebo vs [[Unable to Display Character: ∆]] 35 pg/ml ±1054 pg/ml treatment p=0.009). 25-hydroxyvitamin D was [[Unable to Display Character: ∆]]48.9 ±32 ng/ml treatment vs [[Unable to Display Character: ∆]]3.6 ± 9.4 ng/ml placebo, p<0.001 (mean 68 ng/ml treatment vs 23 ng/ml placebo). No toxicity was observed with treatment. PTH and exercise chronotropic response index trended towards improvement in the treatment group vs placebo group, respectively (([[Unable to Display Character: ∆]]-20 ±20 pg/ml vs [[Unable to Display Character: ∆]]7 ±54pg/ml (p=0.06)) and ([[Unable to Display Character: ∆]]0.13±0.26 versus [[Unable to Display Character: ∆]]-0.03 ± 0.23, p=0.12)). KCCQ quality of life total symptom ([[Unable to Display Character: ∆]]16 ±16 treatment vs [[Unable to Display Character: ∆]]-12 ±15 placebo, p< 0.001) and individual scores significantly improved from baseline in the treatment group. Conclusions: Preliminary results show that vitamin D3 treatment of 10,000 IU/day in heart failure patients is safe, results in adequate circulating 25-hydroxyvitamin D levels, and achieves improvement in surrogate endpoint markers of HF outcomes.
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