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Impairment of endothelium-independent vasodilation in patients with hypercalcemia
T Neunteufl1, R Katzenschlager, C Abela
1Department of Cardiology, University of Vienna, Austria.
Insights
Primary hyperparathyroidism (PHPT) impairs endothelium-independent vasodilation, affecting vascular smooth muscle function. Endothelium-dependent dilation remained similar, suggesting arterial media involvement in PHPT-related vascular changes.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Vascular Biology
Background:
- Primary hyperparathyroidism (PHPT) is linked to increased myocardial ischemia risk.
- The impact of PHPT on vascular function, specifically endothelium-dependent and independent vasodilation, is not well understood.
- This study investigates potential preclinical vascular disease in PHPT patients.
Purpose of the Study:
- To determine if endothelium-dependent, flow-mediated dilation (FMD) is impaired in PHPT patients.
- To assess if endothelium-independent, nitroglycerin-induced dilation (NMD) is impaired in PHPT patients.
- To explore the relationship between PHPT, serum calcium levels, and arterial reactivity.
Main Methods:
- Twenty-six PHPT patients and 26 normocalcemic controls were studied.
- Brachial artery FMD and NMD were measured using high-resolution ultrasound.
- Coronary artery disease (CAD) was ruled out in all participants.
Main Results:
- NMD was significantly impaired in PHPT patients compared to controls (p=0.012).
- FMD did not differ significantly between the groups (p=NS).
- The FMD/NMD ratio was significantly lower in PHPT patients (p=0.0009), associated with serum calcium levels.
Conclusions:
- PHPT patients exhibit impaired endothelium-independent vasodilation, suggesting altered arterial media function.
- Endothelium-dependent dilation was preserved, unlike in advanced atherosclerosis.
- Arterial reactivity changes in PHPT may primarily involve the arterial media, not the endothelium.
Objective:
Patients with primary hyperparathyroidism (PHPT) and/or hypercalcemia are at increased risk for myocardial ischemia. Whether PHPT is associated with altered endothelium-dependent dilation, vascular smooth muscle cell function, or both is unknown. This study was performed to test the hypothesis that endothelium-dependent, flow-mediated dilation (FMD) and/or endothelium-independent, nitroglycerin-induced dilation (NMD) is impaired in the preclinical phase of vascular disease in patients with PHPT.
Methods:
Twenty-six PHPT patients (mean +/- SD; age 55 +/- 15 y, serum calcium 3.00 +/- 0.37 mmol/l, serum phosphate 0.79 +/- 0.21 mmol/l, iPTH 249 +/- 262 pg/ml) with no evidence of coronary artery disease (CAD) as well as 26 normocalcemic control subjects (CTL; age 51 +/- 12 y) were studied. FMD following reactive hyperemia and NMD after 0.8 mg nitroglycerin (NTG) were assessed in the brachial artery by using high resolution ultrasound (7 MHz).
Results:
NMD was impaired in PHPT patients compared to CTL (11.9 +/- 3.9% vs. 15.6 +/- 5.7%; p = 0.012). FMD was similar in both study groups (11.6 +/- 4.6% vs. 12.6 +/- 4.9; NS). The ratio of FMD to NMD was significantly different between PHPT patients and CTL (0.98 +/- 0.19 vs 0.81 +/- 0.25, p = 0.0009). On multiple stepwise regression analysis serum calcium was independently associated with the FMD/NMD ratio (r = 0.34, p = 0.017).
Conclusions:
Endothelium-independent vasodilation is impaired in PHPT patients without clinical evidence of coronary artery disease compared to normocalcemic CTL, while endothelium-dependent dilation was similar in both study groups. Thus, altered arterial reactivity in the course of PHPT may predominantly involve the arterial media and not the endothelium as observed previously in patients with various stages of atherosclerosis.