Secondary hyperparathyroidism and cardiac hypertrophy in hemodialysis patients

Abstract

Echocardiographic assessment of left ventricular function was performed in 66, stable hemodialysis patients and 50 normal controls matched for sex, age and arterial blood pressure. On the basis of bone histology, hemodialysis patients were classified into two groups: (1) patients with normal bone resorption; and (2) patients with active secondary hyperparathyroidism characterized by an increased bone resorption. Left ventricular function of these two subgroups were compared together as well as with the echocardiographic characteristics of normal controls. In comparison with normal controls, hemodialysis patients with normal bone resorption had an increased left ventricular volume (P less than 0.001) and left ventricular mass (P less than 0.001) with a similar left ventricular mass-to-volume ratio. Their systolic arterial pressure--mass-to-volume ratio correlation was similar to that of normal controls, indicating an adequate myocardial hypertrophy. Patients with increased bone resorption had high parathormone and alkaline phosphatase levels; though the left ventricular dilation was similar to that of hemodialysis patients with normal bone resorption, the left ventricular mass was lower (P less than 0.001) and was similar to the left ventricular mass of normal controls. In addition, patients with increased bone resorption had a lower mass-to-volume ratio (P less than 0.001) and their systolic arterial pressure--mass-to-volume ratio correlation exhibited a significant downward shift (P less than 0.001), suggesting an inadequate myocardial hypertrophy. Patients with increased bone resorption and secondary hyperparathyroidism had an increased heart rate, a higher systolic arterial pressure and end-systolic stress. Furthermore, they had an increased velocity of fiber shortening (P less than 0.01) and shorter left ventricular ejection time (P less than 0.001). In summary, present data suggest the possibility that parathormone may exert myocardial effects in hemodialysis patients.

Beneficial Effects of Calcimimetics on Progression of Renal Failure and Cardiovascular Risk Factors

“…PTH is significantly correlated to left ventricular mass in patients with essential hypertension (48) as well as in patients with renal failure (49). Experimental studies documented that PTH activates protein kinase C of cardiomyocytes, leading to hypertrophic growth and reexpression of fetal-type proteins (50).…”

Impact of the Angiotensin II Receptor Antagonist, Losartan, on Myocardial Fibrosis in Patients with End-Stage Renal Disease: Assessment by Ultrasonic Integrated Backscatter and Biochemical Markers

“…Other factors have been reported to be responsible for the development of myocardial fibrosis in patients with ESRD, including hypervolemia (34), chronic anemia (35,36), uncontrolled arterial hypertension (37), a high i-PTH concentration (38), and hyperuricemia (39−41). The patients in our study were dialyzed in keeping with widely accepted criteria.…”

Calcium, Phosphorus, Parathyroid Hormone, and Cardiovascular Disease in Hemodialysis Patients: The USRDS Waves 1, 3, and 4 Study

“…A link between secondary hyperparathyroidism and cardiovascular disease in dialysis patients has been suspected for decades (1)(2)(3). As in other types of cell, high levels of parathyroid hormone (PTH) seem to damage cardiac myocytes, possibly through a calcium ionophore effect (4).…”