Relation between Serum Levels of Vitamin D and Echocardiographic Determinants of Systolic and Diastolic Functions in Patients with and Without Cardiorenal Syndrome

Abstract

SUMMARY V itamin D is a fat-soluble vitamin, it can be ingested as cholecalciferol (vitamin D3) or ergocalciferol (vitamin D2) and also the body can also synthesize it (from cholesterol) when sun exposure is adequate. This is followed by subsequent activation in Liver and kidneys to produce active form of vitamin D3. It has skeletal and non-skeletal functions such as regulation of cell proliferation and differentiation, regulation of hormone secretion, regulation of immune function and blood pressure regulation. The effect of Vitamin D on CV disease had several mechanisms including elevated PTH and Calcium-phosphate metabolism. Moreover, Vitamin D could directly suppress renin gene expression and thus decreasing the pro- remodeling of Angiotensin II on the cardiomyocytes. Renal dysfunction is a common and progressive complication of chronic heart failure, with a clinical course that typically fluctuates with the patient’s clinical status and treatment. Despite growing recognition of the frequent presentation of combined cardiac and renal dysfunction, or “Cardiorenal syndrome” its underlying pathophysiology is not well understood, and no consensus regarding its appropriate management has been achieved. Vitamin D deficiency is highly prevalent in HF patients (especially those with cardiorenal syndromes) and has been shown to be associated with increased CVD diseases, including LVH and heart failure. Our study included 90 patients of all age groups and both sexes, admitted to Ain-Shams University hospital. The study included 3 groups of patients: Group 1: Systolic dysfunction and renal insufficiency (30 patients), Group 2: Systolic dysfunction only (30 patients). Group 3: Renal insufficiency only (30 patients), In addition 10 healthy controls were taken as a reference for comparing echocardiographic data and laboratory results. Patients were subjected to full comprehensive echocardiography and KFT with estimation of creatinine clearance, and measurement of Vitamin D level that was statistically studied against echocardiographic parameters of cardiac systolic and diastolic function. It is thought that vitamin D deficiency could be a result to impaired vitamin D metabolism (including decreasing sun exposure, intestinal absorption, hepatic and renal activation of vitamin D) in patient with heart failure, in addition, our study confirmed that vitamin D deficiency (<20ng/ml) itself induce adverse remodeling changes due to loss of protective effect of Vitamin D against LV hypertrophy and /or Hypertension. Compared to patients with normal vitamin D level, patients with vitamin D deficiency (defined as having vitamin D level <20 ng/ml) had significantly higher ventricular thickness (IVS, PW and mean wall thickness) and higher LV mass which seems to be linked eventually to worse outcomes. The Worsening Diastolic function is still a matter of conflict but, at least in our study, Vitamin D deficiency was not associated with worse LV diastolic dysfunction or abnormal LAV index. Due to highly significant negative correlation between mean wall thickness and Vitamin D level (P value < 0.001), a Roc curve was done revealing a sensitivity of 80% and a specificity of 72% for the mean wall thickness (≥ 10 mm) to identify patient with vitamin D deficiency. We do recommend monitoring of vitamin D level in patients with heart failure especially those with coexisting renal impairment and /or LV hypertrophy with subsequent correction of vitamin D deficiency if its level is < 20 Ug/ml to improve heart failure outcomes.