PURPOSE: The mechanisms underlying increased cardiovascular risk in primary hyperparathyroidism (pHPT) have not been fully defined. Recently, this issue has become the subject of renewed interest due to the increasing evidence that the endothelium and vascular wall are targets for parathyroid hormone (PTH). The aim of this study was to measure regional coronary flow reserve (CFR) to determine whether the vascular damage induced by pHPT extends to affect the coronary microvascular function. METHODS: A total of 22 pHPT patients without a history of coronary artery disease and 7 age-matched control subjects were recruited. Dipyridamole myocardial blood flow (MBF) was assessed using 99mTc-sestamibi by measuring first-transit counts in the pulmonary artery and myocardial count rate from G-SPECT images. Baseline MBF was estimated 2 h later according to the same procedure. Regional CFR was defined as the ratio between dipyridamole and baseline MBF using a 17-segment left ventricular model. RESULTS: Three pHPT patients showed reversible perfusion defects and were excluded from the analysis. In the remaining 19, CFR was significantly lower with respect to the control subjects (1.88±0.64 vs. 3.36±0.66, respectively; p<0.01). Moreover, patients studied for more than 28 months from pHPT diagnosis showed lower CFR values than the others (1.42±0.18 vs. 2.25±0.64, respectively; p<0.01). Consequently, the time from diagnosis to the nuclear study showed a reasonable correlation with the degree of CFR impairment (Spearman's rho -0.667, p<0.02). CONCLUSION: pHPT is associated with a significant dysfunction of the coronary microcirculation. This disorder might contribute to the high cardiovascular risk of conditions characterized by chronic elevations in serum PTH levels.
PURPOSE: The mechanisms underlying increased cardiovascular risk in primary hyperparathyroidism (pHPT) have not been fully defined. Recently, this issue has become the subject of renewed interest due to the increasing evidence that the endothelium and vascular wall are targets for parathyroid hormone (PTH). The aim of this study was to measure regional coronary flow reserve (CFR) to determine whether the vascular damage induced by pHPT extends to affect the coronary microvascular function. METHODS: A total of 22 pHPT patients without a history of coronary artery disease and 7 age-matched control subjects were recruited. Dipyridamole myocardial blood flow (MBF) was assessed using 99mTc-sestamibi by measuring first-transit counts in the pulmonary artery and myocardial count rate from G-SPECT images. Baseline MBF was estimated 2 h later according to the same procedure. Regional CFR was defined as the ratio between dipyridamole and baseline MBF using a 17-segment left ventricular model. RESULTS: Three pHPT patients showed reversible perfusion defects and were excluded from the analysis. In the remaining 19, CFR was significantly lower with respect to the control subjects (1.88±0.64 vs. 3.36±0.66, respectively; p<0.01). Moreover, patients studied for more than 28 months from pHPT diagnosis showed lower CFR values than the others (1.42±0.18 vs. 2.25±0.64, respectively; p<0.01). Consequently, the time from diagnosis to the nuclear study showed a reasonable correlation with the degree of CFR impairment (Spearman's rho -0.667, p<0.02). CONCLUSION: pHPT is associated with a significant dysfunction of the coronary microcirculation. This disorder might contribute to the high cardiovascular risk of conditions characterized by chronic elevations in serum PTH levels.
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