Left ventricular hypertrophy in primary hyperparathyroidism. Effects of successful parathyroidectomy

Piovesan, Alessandro; Molineri, Nadia; Casasso, Flavia; Emmolo, I; Ugliengo, Giuseppe; Cesario, Flora; Borretta, Giorgio

doi:10.1046/j.1365-2265.1999.00651.x

Cited by 206 publications

(183 citation statements)

References 32 publications

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“…This may be related to a regression of left ventricular hypertrophy, as demonstrated in a study using echocardiography to evaluate left ventricular hypertrophy in 43 patients with HPT compared to 43 age-and sex-matched controls. 31 This study found that the left ventricular mass index was statistically significantly higher in those with HPT than in the controls and that this correlated with PTH values. Furthermore, there was statistically significant decrease in left ventricular mass index six months after parathyroidectomy.…”

Section: Treatmentmentioning

confidence: 51%

Current Status and Treatment of Primary Hyperparathyroidism

Elaraj¹,

Clark²

2008

TPJ

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Section: Treatmentmentioning

confidence: 51%

Current Status and Treatment of Primary Hyperparathyroidism

Elaraj¹,

Clark²

2008

TPJ

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“…Stefenelli et al (8) have reported LV hypertropy, and valve and myocardial calcifications in a significant number of patients with mean serum calcium levels of 12 mg/dl. In contrast, patients who had a milder increase in serum Ca (11.1 -11.3 mg/dl) were found to have only LV hypertropy but no significant valvular or myocardial calcification (38,39). On the other hand, Längle et al did not find any direct correlation between the severity and the cardiovascular manifestations of PHPT; however, PTH-related skeletal manifestations and valvular calcifications were predictive factors for left ventricular hypertropy (37).…”

Section: Discussionmentioning

confidence: 82%

Increased intima-media thickness of the carotid artery wall, normal blood pressure profile and normal left ventricular mass in subjects with primary hyperparathyroidism

Nuzzo

Tauchmanovà

Fonderico

et al. 2002

European Journal of Endocrinology

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Objective: Despite the increasing evidence that primary hyperparathyroidism (PHPT) contributes to greater risk of cardiovascular morbidity and mortality, its exact role in the development of cardiovascular changes and its clinical significance are still controversial. Given the multiple influence of PHPT on the cardiovascular system, this study aimed to assess the effects of PHPT on blood pressure profile, and on features of the heart and arterial vessels in normotensive symptomless patients. Design: Twenty patients (8 males and 12 females) with a median age of 51.5 years (range 44 to 65 years) were evaluated and the results were compared with those of 20 controls matched for age, gender and body mass index. Patients' parathyroid hormone levels ranged from 172 to 454 pg/ml and Ca levels ranged from 11.4 to 13.5 mg/dl. Fasting levels of glucose, insulin, total and high density lipoprotein cholesterol and triglycerides were within the normal range in all subjects recruited. Methods: Twenty-four-hour blood pressure profile, left ventricle (LV) dimension and carotid artery anatomy were investigated, the latter two by ultrasonography. Results: No difference was found between the patients and controls in blood pressure profile, when the following parameters were considered: supine systolic/diastolic pressure, average 24-h systolic, diastolic and mean arterial pressure, day-time mean arterial pressure and fall in nocturnal blood pressure (217% and 2 18% respectively). Heart rate and all parameters of LV mass were similar in patients and controls. The only alteration found in patients was in significantly greater carotid intimal-medial thickness (IMT) ðP , 0:001Þ: Atherosclerotic plaques were more frequent in patients than in controls, with a difference reaching a trend (40% vs 10%, x 2 ¼ 4:8; P ¼ 0:091). Considering that the carotid IMT is considered to be a marker of systemic atherosclerosis, our finding suggests early atherosclerotic changes in PHPT. No correlation was found between the severity and cardiovascular manifestation of PHPT. Conclusions: Vascular changes may occur due to a combination of structural and functional impairments in PHPT patients, likely as a result of altered calcium metabolism and impaired equilibrium of other factors regulating vascular function. Both extent and duration of PHPT can play a relative role in the development of cardiovascular complications. Considering that PHPT is now recognized as a quite common and often symptomless endocrine disorder, the evidence of cardiovascular manifestation in normotensive patients, found by this morphological study, suggests a possible implication for the management of such patients. In this light, screening for abnormalities in cardiovascular system function should be recommended in all PHPT subjects.

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“…PTH was shown to act as a pro-hypertrophic factor by increasing protein synthesis in vitro (Schluter and Piper, 1998) and as a vasodilator by increasing the intracellular cAMP level, leading to a decrease in calcium influx (Clemens et al, 2001). The mass of the left ventricle was correlated with the PTH level in patients with end-stage renal disease and secondary hyperparathyroidism (Harnett et al, 1988) and in patients with primary hyperparathyroidism (Piovesan et al, 1999). However, no significant correlation between the left ventricular mass and PTH level was found in the general population (Saleh et al, 2003).…”

Section: Introductionmentioning

confidence: 94%

Parathyroid hormone accelerates decompensation following left ventricular hypertrophy

et al. 2010

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Abbreviations: FS, fractional shortening; LVH, left ventricular hypertrophy; LVIDs, left ventricular internal dimension at systole; LVPWs, left ventricular posterior wall thickness at systole; PTH, parathyroid hormone; TAB, transverse aortic banding AbstractParathyroid hormone (PTH) treatment was previously shown to improve cardiac function after myocardial infarction by enhancing neovascularization and cell survival. In this study, pressure overload-induced left ventricular hypertrophy (LVH) was induced in mice by transverse aortic banding (TAB) for 2 weeks. We subsequently evaluated the effects of a 2-week treatment with PTH or saline on compensated LVH. After another 4 weeks, the hearts of the mice were analyzed by echocardiography, histology, and molecular biology. Echocardiography showed that hearts of the PTH-treated mice have more severe failing phenotypes than the saline-treated mice following TAB with a greater reduction in fractional shortening and left ventricular posterior wall thickness and with a greater increase in left ventricular internal dimension. Increases in the heart weight to body weight ratio and lung weight to body weight ratio following TAB were significantly exacerbated in PTH-treated mice compared to saline-treated mice. Molecular markers for heart failure, fibrosis, and angiogenesis were also altered in accordance with more severe heart failure in the PTH-treated mice compared to the saline-treated mice following TAB. In addition, the PTH-treated hearts were manifested with increased fibrosis accompanied by an enhanced SMAD2 phosphorylation. These data suggest that the PTH treatment may accelerate the process of decompensation of LV, leading to heart failure.

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Left ventricular hypertrophy in primary hyperparathyroidism. Effects of successful parathyroidectomy

Cited by 206 publications

References 32 publications

Current Status and Treatment of Primary Hyperparathyroidism

Current Status and Treatment of Primary Hyperparathyroidism

Increased intima-media thickness of the carotid artery wall, normal blood pressure profile and normal left ventricular mass in subjects with primary hyperparathyroidism

Parathyroid hormone accelerates decompensation following left ventricular hypertrophy

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