Key result
Elevated parathyroid hormone levels were independently associated with the presence of left ventricular hypertrophy in patients with stable coronary artery disease (OR 1.017; 95% CI 1.003-1.031; P=0.021).
Why the study?
Are elevated parathyroid hormone levels associated with left ventricular hypertrophy in patients with stable coronary artery disease?
Cross-Sectional (n=146)
Are elevated parathyroid hormone levels associated with left ventricular hypertrophy in patients with stable coronary artery disease?
Odds Ratio: 1.017 (95% CI 1.003–1.031)
p-value: p=0.021
In patients with stable coronary artery disease, elevated parathyroid hormone levels are independently associated with the presence of left ventricular hypertrophy.
Supports PTH-LVH association in stable CAD; hypothesis-generating, needs prospective trials before any clinical role.
BACKGROUND: Abnormalities of mineral metabolism and inflammation may affect the cardiovascular system. We have assessed the relationship of left ventricular hypertrophy (LVH) with inflammation and mineral metabolism. METHODS: LVH was measured in 146 outpatients with stable coronary artery disease (SCAD) using echocardiography. Calcidiol (a vitamin D metabolite), parathyroid hormone (PTH), fibroblast growth factor-23, high-sensitivity C-reactive protein, MCP-1 (monocyte chemoattractant protein-1), galectin-3, NGAL (neutrophil gelatinase-associated lipocalin), and sTWEAK (soluble TNF-related weak inducer of apoptosis) plasma levels were studied. RESULTS: LVH, defined as septal thickness ≥11 mm, was present in 19.9% of cases. These patients were older [75.0 (61.0-81.0) vs 64.0 (51.0-76.0) years; p=0.002], had higher prevalence of left ventricular ejection fraction (LVEF)>40%, and had higher PTH [84.7 (59.6-104.7) vs 63.2 (49.2-85.2) pg/ml; p=0.007], galectin-3 [9.6 (8.0-11.1) vs 8.3 (6.9-9.9) ng/ml; p=0.037], and NGAL (208.5±87.6 vs 173.9±73.4 ng/ml; p=0.031) plasma levels than those without LVH. Glomerular filtration rate was lower in patients with LVH than in those without it (65.1±20.0 vs 74.7±19.9 mL/min/1.73 m2; p=0.021). There were no significant differences in hypertension (79.3 vs 68.4%; p=0.363) or sex between both groups. Variables showing differences based on univariate analysis and hypertension were entered into a logistic regression analysis. Only age [odds ratio (OR) =1.052 (1.011-1.096); p=0.013], PTH plasma levels [OR=1.017 (1.003-1.031); p=0.021], and LVEF>40% [OR=7.595 (1.463-39.429); p=0.016] were independent predictors of LVH. CONCLUSIONS: In patients with SCAD, elevated PTH levels are independently associated with the presence of LVH. Further studies are needed to elucidate the role of PTH in the development of myocardial hypertrophy.
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Aceña et al. (2015) conducted a cross-sectional in Stable coronary artery disease (n=146). Elevated parathyroid hormone (PTH) levels vs. Lower PTH levels was evaluated on Presence of left ventricular hypertrophy (LVH) (OR 1.017, 95% CI 1.003-1.031, p=0.021). Elevated parathyroid hormone levels were independently associated with the presence of left ventricular hypertrophy in patients with stable coronary artery disease (OR 1.017; 95% CI 1.003-1.031; P=0.021).
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