Abstract

There is suggestive evidence that chronic elevations of parathyroid hormone (PTH), associated with poor vitamin D status or low calcium intake, can increase risk for insulin resistance, weight gain, hypertension, and left ventricular hypertrophy, while stimulating production of acute phase reactants. New evidence that elevated PTH is prognostic for increased vascular mortality in very elderly subjects, prompts an examination of the possible impact of PTH on risk for arrhythmias. The cardiac effects of PTH are mediated by G protein-coupled receptors that activate phospholipase C (PLC). Catecholamines, angiotensin II, and endothelin have been shown to be arrhythmogenic for ischemic myocardium in animal studies; the receptors mediating this effect are all likewise linked to activation of PLC. Thus, it is reasonable to presume that a sufficient concentration of PTH can be arrhythmogenic in the ischemic heart. The extent to which this effect can be evoked by the high-normal PTH levels prevalent in many elderly subjects, can be assessed in epidemiological studies.

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