In the Journals

Vitamin D supplementation fails to reduce major adverse CV events

JoAnn E. Manson
JoAnn E. Manson

Vitamin D supplementation did not reduce individual CVD endpoints, all-cause mortality or major adverse CV events, according to a meta-analysis published in JAMA Cardiology.

“The findings suggest that in the general ‘usual risk’ population not selected for vitamin D deficiency, vitamin D supplementation does not appear to confer cardioprotection,” JoAnn E. Manson, MD, DrPH, FAHA, chief of the division of preventive medicine at Brigham and Women’s Hospital and professor of medicine and the Michael and Lee Bell Professor of Women’s Health at Harvard Medical School, told Cardiology Today. “Thus, in general community settings, routine vitamin D supplementation is unlikely to have significant CVD benefit. Patients with known vitamin D deficiency, however, should obviously be treated, given that correcting deficiency is known to be important for bone health.”

Vitamin D vs. placebo

Researchers analyzed data from 21 randomized clinical trials that assessed vitamin D supplementation of at least 1 year and its effect on CV outcomes. There were 83,291 patients (mean age, 66 years; 74% women) who were assigned vitamin D (n = 41,669) or placebo (n = 41,622).

The primary endpoint was a composite of major adverse CV events, which was defined in each trial. Secondary endpoints included stroke/cerebrovascular accident, MI, all-cause mortality and CVD mortality.

Of the trials in this meta-analysis, four trials had prespecified CVD as a primary endpoint.

Vitamin D supplementation did not reduce individual CVD endpoints, all-cause mortality or major adverse CV events, according to a meta-analysis published in JAMA Cardiology
Source: Shutterstock

Compared with placebo, vitamin D supplementation was not linked to reduced major adverse CV events (RR = 1; 95% CI, 0.95-1.06; I2 = 11%). This was also seen for secondary endpoints including stroke-cerebrovascular accident (RR = 1.06; 95% CI, 0.98-1.15; I2 = 0%), MI (RR = 1; 95% CI, 0.93-1.08; I2 = 0%), all-cause mortality (RR = 0.97; 95% CI, 0.93-1.02; I2 = 0%) and CV mortality (RR = 0.98; 95% CI, 0.9-1.07; I2 = 2%).

Results were consistent by baseline 25-hyddroxyvitamin D level, formulation, sex, vitamin D dosage and the presence or absence of concurrent calcium administration.

“Additional randomized trials designed to test CVD endpoints and relevant biological pathways would be welcome,” Manson said in an interview. “Also, additional research on the role of vitamin D supplementation in preventing heart failure is needed. In VITAL, heart failure is being examined as an ancillary study outcome, and the results are expected to be reported soon.”

Research beyond CV outcomes

Arshed A. Quyyumi
Arshed A. Quyyumi

“The report by Barbarawi et al in this issue of JAMA Cardiology supports efforts aimed at curbing wasteful spending on vitamin D testing and treatment in populations not at risk for deficiency and/or for the purpose of preventing CVD morbidity and mortality,” Arshed A. Quyyumi, MD, FRCP, tenured professor of medicine in the division of cardiology at Emory University School of Medicine and co-director of the Emory Clinical Cardiovascular Research Institute, and Ibhar Al Mheid, MD, assistant professor in the division of hospital medicine at Emory University School of Medicine, wrote in a related editorial. “At the same time, it also should be emphasized that vitamin D therapy in patients with chronic kidney disease and hyperparathyroidism is definitely indicated, and such therapy has established cardiovascular benefits including blood pressure reduction, reduced electrolyte derangements, and overall reduced cardiovascular mortality rates in patients on hemodialysis.” – by Darlene Dobkowski

For more information:

JoAnn E. Manson, MD, DrPH, FAHA, can be reached at Brigham and Women’s Hospital, Harvard Medical School, 900 Commonwealth Ave., 3rd Floor, Boston, MA 02215; email: jmanson@rics.bwh.harvard.edu.

Disclosures: Manson reports she received funding from the NIH to conduct the VITAL trial. Vitamin D pills used in the study were donated by Pharmavite LLC and omega-3 supplements were donated by Pronova BioPharma and BASF. The authors of the study and of the editorial report no relevant financial disclosures.

JoAnn E. Manson
JoAnn E. Manson

Vitamin D supplementation did not reduce individual CVD endpoints, all-cause mortality or major adverse CV events, according to a meta-analysis published in JAMA Cardiology.

“The findings suggest that in the general ‘usual risk’ population not selected for vitamin D deficiency, vitamin D supplementation does not appear to confer cardioprotection,” JoAnn E. Manson, MD, DrPH, FAHA, chief of the division of preventive medicine at Brigham and Women’s Hospital and professor of medicine and the Michael and Lee Bell Professor of Women’s Health at Harvard Medical School, told Cardiology Today. “Thus, in general community settings, routine vitamin D supplementation is unlikely to have significant CVD benefit. Patients with known vitamin D deficiency, however, should obviously be treated, given that correcting deficiency is known to be important for bone health.”

Vitamin D vs. placebo

Researchers analyzed data from 21 randomized clinical trials that assessed vitamin D supplementation of at least 1 year and its effect on CV outcomes. There were 83,291 patients (mean age, 66 years; 74% women) who were assigned vitamin D (n = 41,669) or placebo (n = 41,622).

The primary endpoint was a composite of major adverse CV events, which was defined in each trial. Secondary endpoints included stroke/cerebrovascular accident, MI, all-cause mortality and CVD mortality.

Of the trials in this meta-analysis, four trials had prespecified CVD as a primary endpoint.

Vitamin D supplementation did not reduce individual CVD endpoints, all-cause mortality or major adverse CV events, according to a meta-analysis published in JAMA Cardiology
Source: Shutterstock

Compared with placebo, vitamin D supplementation was not linked to reduced major adverse CV events (RR = 1; 95% CI, 0.95-1.06; I2 = 11%). This was also seen for secondary endpoints including stroke-cerebrovascular accident (RR = 1.06; 95% CI, 0.98-1.15; I2 = 0%), MI (RR = 1; 95% CI, 0.93-1.08; I2 = 0%), all-cause mortality (RR = 0.97; 95% CI, 0.93-1.02; I2 = 0%) and CV mortality (RR = 0.98; 95% CI, 0.9-1.07; I2 = 2%).

Results were consistent by baseline 25-hyddroxyvitamin D level, formulation, sex, vitamin D dosage and the presence or absence of concurrent calcium administration.

“Additional randomized trials designed to test CVD endpoints and relevant biological pathways would be welcome,” Manson said in an interview. “Also, additional research on the role of vitamin D supplementation in preventing heart failure is needed. In VITAL, heart failure is being examined as an ancillary study outcome, and the results are expected to be reported soon.”

Research beyond CV outcomes

Arshed A. Quyyumi
Arshed A. Quyyumi

“The report by Barbarawi et al in this issue of JAMA Cardiology supports efforts aimed at curbing wasteful spending on vitamin D testing and treatment in populations not at risk for deficiency and/or for the purpose of preventing CVD morbidity and mortality,” Arshed A. Quyyumi, MD, FRCP, tenured professor of medicine in the division of cardiology at Emory University School of Medicine and co-director of the Emory Clinical Cardiovascular Research Institute, and Ibhar Al Mheid, MD, assistant professor in the division of hospital medicine at Emory University School of Medicine, wrote in a related editorial. “At the same time, it also should be emphasized that vitamin D therapy in patients with chronic kidney disease and hyperparathyroidism is definitely indicated, and such therapy has established cardiovascular benefits including blood pressure reduction, reduced electrolyte derangements, and overall reduced cardiovascular mortality rates in patients on hemodialysis.” – by Darlene Dobkowski

For more information:

JoAnn E. Manson, MD, DrPH, FAHA, can be reached at Brigham and Women’s Hospital, Harvard Medical School, 900 Commonwealth Ave., 3rd Floor, Boston, MA 02215; email: jmanson@rics.bwh.harvard.edu.

Disclosures: Manson reports she received funding from the NIH to conduct the VITAL trial. Vitamin D pills used in the study were donated by Pharmavite LLC and omega-3 supplements were donated by Pronova BioPharma and BASF. The authors of the study and of the editorial report no relevant financial disclosures.