The hormonal derivative of vitamin D, 1,25-dihydroxyvitamin D (1,25[OH](2)D) or calcitriol, has been implicated in many physiologic processes beyond calcium and phosphorus homeostasis, and likely plays a role in several chronic disease states, in particular, cardiovascular disease. Experimental data suggest that 1,25(OH)(2)D affects cardiac muscle directly, controls parathyroid hormone secretion, regulates the renin-angiotensin-aldosterone system, and modulates the immune system. Because of these biologic effects, vitamin D deficiency has been associated with hypertension, several types of vascular diseases, and heart failure. We conducted a MEDLINE search of the English-language literature (1950-2008) to identify studies that examined these relationships; additional citations were obtained from the articles retrieved from the literature search. Treatment with vitamin D lowered blood pressure in patients with hypertension and modified the cytokine profile in patients with heart failure. Measurement of serum 25-hydroxyvitamin D concentration usually provides the best assessment of an individual's vitamin D status. Serum levels below 20 ng/ml represent vitamin D deficiency, and levels above 30 ng/ml are considered optimal. Although the observational data linking vitamin D status to cardiovascular disease appear robust, vitamin D supplementation is not recommended as routine treatment for heart disease until definitive prospective, randomized trials can be carried out to assess its effects. However, such supplementation is often appropriate for other reasons and may be beneficial to cardiovascular health in certain patients.

Aspirin has been used for the prevention and treatment of cardiovascular disease (CVD) for several decades. The efficacy of aspirin for secondary prevention of cardiovascular disease is well established, but the clinical benefit of aspirin for primary prevention of CVD is less clear. The primary literature suggests that aspirin may provide a reduction in CVD events, but the absolute benefit is small and accompanied by an increase in bleeding. For aspirin to be beneficial for an individual patient, the risk of a future CVD event must be large enough to outweigh the risk of bleeding. The estimation of CVD risk is multifaceted and can involve numerous risk scores and assessments of concomitant comorbidities that confer additional CVD risk. Numerous guidelines provide recommendations for the use of aspirin for primary prevention, but they often contradict one another despite being based on the same clinical trials. Additional literature suggests that the presence of comorbidities that increase CVD risk, such as diabetes mellitus, asymptomatic peripheral arterial disease, or chronic kidney disease, does not ensure that aspirin therapy will be beneficial. Ongoing clinical trials may provide additional insight, but until more data are available, an individualized assessment of CVD risk with careful evaluation of risk and benefit should be performed before recommending aspirin therapy for primary prevention of CVD.

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