Cardiac Abnormalities in Patients with Primary Hyperparathyroidism: Implications for Follow-Up
Thomas Stefenelli,
Claudette Abela,
Herbert Frank,
Janette Koller-Strametz,
Sebastian Globits,
Jutta Bergler-Klein and
Bruno Niederle
Department of Cardiology (T.S., H.F., J.K-S., S.G.,
J.B-K.) and the Department of Surgery, Division of General Surgery
(C.A., B.N.), University of Vienna Medical School, Austria
Address correspondence and requests for reprints to: Thomas Stefenelli, MD, FACC, Associate Professor for Internal Medicine, Department of Cardiology, University of Vienna, Währinger Cpürtel 18-20, A-1090-Vienna, Austria.
Patients with primary hyperparathyroidism (PHPT) show a highincidence
of left ventricular hypertrophy, cardiac calcificdeposits in the
myocardium, and/or aortic and mitral valve calcificationand thus may
carry an increased risk of death from circulatorydiseases. This
prospective study was designed to assess an effectof parathyroidectomy
on cardiac abnormalities of patients withPHPT. Echocardiography was
used to evaluate the mechanical performanceof the heart muscle, the
thickness of the left ventricular wall,myocardial calcific deposits,
and valvular calcifications within12 and 41 months after
parathyroidectomy.
In a blinded fashion, aortic and mitral valve calcificationswere
determined in 46% and 39% of patients with PHPT. Calcificdeposits in
the myocardium were found in 74% of patients. Follow-upstudies after
parathyroidectomy disclosed no evidence of progressionof these
calcifications. Before operation left ventricular hypertrophywas
detected in 82%. After parathyroidectomy and 41 months of
normocalcemiaand normal PTH concentrations, a regression of
hypertrophy ofthe interventricular septum and the posterior wall by
-6% and-19% (P < 0.05) was observed. Subgroup
analysis disclosedthe most impressive long-term reduction of left
ventricularhypertrophy in patients without a history of hypertension
(-11%and -21%; P < 0.05 and P <
0.005); no changes were determinedin 9 patients who developed
secondary hyperparathyroidism afteroperation.
The present data show a high incidence of left ventricular hypertrophy
andaortic and/or mitral valve calcifications in patients with PHPT.
Follow-upat 1 year and at 41 months after successful parathyroidectomy
discloseregression of hypertrophy. Our results give evidence that
parathyroidhormone per se plays an important role in the maintainance
ofmyocardial hypertrophy. Post-surgical restoration of normocalcemia
andnormalization of parathyroid hormone valvular sclerosis persists
withoutevidence of progression. We further conclude that patients with
PHPTand parathyroidectomy are at low risk for the development of
severeaortic and mitral valve stenosis within this period of time.
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