The association of serum vitamin D concentration and ventricular dysfunction among patients with acute coronary syndrome
Therapeutics and Clinical Risk Management 20 October 2017 Volume 2017:13 Pages 1455—1461. DOI https://doi.org/10.2147/TCRM.S144437
Khademvatani K, Mohammadzad MS, Yekta Z, Hadizadeh O
Department of Cardiology, Shohada Hospital, 2Department of Community and Preventive Medicine, Urmia University of Medical Sciences, Urmia, Iran
Frequently used features
More blood was pumped by those getting 800,000 IU of vitamin D after heart failure – RCT Oct 2013
Cardiovascular category starts with the following
- Overview Cardiovascular and vitamin D
- Hypertension and vitamin D
- Overview Metabolic Syndrome and vitamin D
- Overview Stroke and vitamin D
- Peripheral arterial disease risk is 1.5X higher if low vitamin D – meta-analysis March 2018
- Peripheral Arterial Disease 3.7 X more likely in diabetics with low vitamin D – June 2019
- Heart attack ICU costs cut in half by Vitamin D – Oct 2018
- Heart Failure and Vitamin D meta-analyses - 2016, 2019
- Cardiovascular death 1.5X more likely if less than 20 ng of Vitamin D – 22nd meta-analysis Nov 2019
- Vitamin D supplementation reduces many Cardiovascular Disease markers– meta-analysis July 2018
- Cardiovascular Prevention with Omega-3 (finally using high doses) – Sept 2019
- Higher Omega-3 index (4 to 8 percent) associated with 30 percent less risk of coronary disease (10 studies) July 2017
A poor Vitamin D Receptor can block Vitamin D in blood from getting to tissues
- Heart Failure 15X more likely if poor VDR, even if good level of vitamin D (China) – March 2019
- Coronary Artery Disease without diabetes 5 times more likely if VDR gene problems – meta-analysis May 2016
- Cholesterol is needed to produce both Vitamin D and Cortisol
- Overview Cholesterol and vitamin D
- Statins and vitamin D statins often reduce levels of vitamin D
- Statin side-effects are reduced by Vitamin D – US patent Application – April 2019
Objective: To determine if vitamin D deficiency was associated with higher odds of left ventricular dysfunction among patients with acute coronary syndrome (ACS) and, if so, to determine whether this association was mediated by increased inflammation as measured by C-reactive protein (CRP) and white blood cell count (WBC).
Methods: This was a cross-sectional study of 170 participants with ACS. Multiple logistic regression was used to examine the association between the outcome of ventricular performance and serum vitamin D concentrations. We also determined whether CRP and WBC meet standard criteria as the mediators between left ventricular ejection fraction and vitamin D deficiency.
Results: Participants with vitamin D deficiency were more likely to have ventricular dysfunction (OR: 2.12, 95% CI: 1.2–5.23). WBC counts did not meet one of the criteria for mediation. However, the WBC was an effect modifier such that the association of vitamin D deficiency and ventricular dysfunction was only present among participants with WBC more than 11,000.
Conclusion: This study found that vitamin D deficiency was associated with higher odds of ventricular dysfunction. Further longitudinal and experimental studies are necessary to confirm this finding and to determine if there is a role for vitamin D supplementation therapy in preventing ventricular dysfunction in select patient populations.
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