Higher serum phosphorus levels are associated with a greater likelihood of with left ventricular remodeling.
The prevailing theory has been that serum phosphorus increases vascular and valvular calcification. Yet other processes involving phosphorus also may be contributing to cardiovascular damage and, in turn, heart failure, arrhythmias, and sudden cardiac death.
Investigators led by Geng-Ru Jiang, MD, of Xin Hua Hospital in Shanghai, China, studied left ventricular remodeling via transthoracic echocardiography in 296 hospitalized patients (average age 56.4) with pre-dialysis chronic kidney disease (CKD) who were free of symptomatic heart failure. Two-thirds of patients (68.6%) had hypertension, of whom 58% took antihypertensive medication; and 21.6% overall had diabetes. Most of the patients were never treated with phosphate binders or calcitriol, and received no treatment within 2 weeks of hospitalization.
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Serum phosphorus, assessed by tertiles from 1.04 to 2.02 mmol/L, independently predicted left ventricular mass index, along with gender, systolic blood pressure, and estimated glomerular filtration rate. It also predicted left ventricular end diastolic dimension, although not relative wall thickness. After multivariable analyses, serum phosphorus was significantly and independently associated with greater prevalence of left ventricular hypertrophy (LVH). In a fully adjusted model, each 1 mmol/L increase in serum phosphorus level was associated with a 2.4-fold increase in the odds of LVH. Compared with the 1st tertile of phosphorus level, the 3rd tertile was associated with a significant 2.5-fold increased odds of LVH.
Neither renal function decline nor systolic blood pressure solely explained changes to cardiac structure and function, although they no doubt contributed. Serum calcium and intact parathyroid hormone levels also did not account for the findings.
“These results suggest that serum phosphorus might be a mediator for left ventricular eccentric remodeling in CKD,” Dr Jiang and colleagues stated in the International Journal of Cardiology. Eccentric LVH possibly results from volume overload, whereas concentric LVH may result from afterload, such as hypertension, they explained.
The findings agree with observational studies in various populations linking serum phosphorus with increased left ventricular mass, the researchers noted.
As the current study was cross-sectional in design, it precludes the establishment of cause and effect. More research is needed to determine whether serum phosphorus directly or indirectly leads to left ventricular remodeling.
“Since left ventricular eccentric remodeling may predict a worse cardiovascular prognosis, and serum phosphorus levels may be modifiable, the causality of this association needs to be explored in both mechanistic studies and randomized controlled trials,” Dr Jiang and colleagues stated. Future research should explore the possible role of fibroblast growth factor 23 and the potential benefits of phosphate binders and a low phosphorus diet on cardiac structure and function.
