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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Blood pressure, left ventricular mass and platelet cytosolic free calcium concentrations were measured in 23 patients with untreated primary hyperparathyroidism, 30 normotensive control subjects and 23 control subjects matched for age, sex and blood pressure. In 12 patients measurements were repeated after parathyroidectomy. 2. Patients with primary hyperparathyroidism had significantly elevated blood pressures (139 +/- 6/86 +/- 3 mmHg, mean +/- SEM) compared with control subjects (125 +/- 2/78 +/- 1 mmHg), but high values persisted after hypercalcaemia was corrected. 3. Despite chronic extracellular hypercalcaemia, intracellular free calcium levels were lower in patients with hyperparathyroidism than in controls matched for age, sex and blood pressure (median concentrations 81.5 nmol/l vs 93 nmol/l, 95% confidence interval 0.1 to 20.1; P less than 0.05) and values tended to increase after parathyroidectomy. 4. Left ventricular mass index was increased in the primary hyperparathyroid group as compared with control subjects matched for age, sex and blood pressure (123 g/m2 vs 100 g/m2, 95% confidence interval -36.1 to -3.1; P = 0.03). Parathyroidectomy resulted in a small reduction of the left ventricular mass index (123.5 g/m2 vs 104 g/m2, 95% confidence interval 46.5 to 2.5; P = 0.1) but no change in blood pressure. 5. Hypertension and left ventricular hypertrophy in primary hyperparathyroidism are associated with relatively low levels of free calcium in platelets.
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PMID:Blood pressure, left ventricular mass and intracellular calcium in primary hyperparathyroidism. 215 37

Left ventricular hypertrophy (symmetric, asymmetric, or hypertrophic cardiomyopathy) is an almost invariable accompaniment of primary hyperparathyroidism. Five of 18 patients with hypertrophic cardiomyopathy had raised serum concentrations of parathyroid hormone with normal serum calcium concentrations. Left ventricular hypertrophy did not occur in any of the six patients with hypercalcaemia alone. These relations suggest that parathyroid hormone rather than a rise in the extracellular calcium concentration is associated with a spectrum of left ventricular hypertrophy. All patients with increased circulating parathyroid hormone concentrations should have echocardiographic examination of the left ventricle. Conversely, parathyroid hormone concentrations should be measured in all patients with left ventricular hypertrophy from an unknown cause, especially those with hypertrophic cardiomyopathy.
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PMID:Cardiac hypertrophy, hypertrophic cardiomyopathy, and hyperparathyroidism--an association. 293 35

Comparing patients with primary hyperparathyroidism (PHP) to a normocalcemic control population, those with PHP have a higher incidence of cardiovascular disease and cardiac abnormalities. This study aimed at correlating cardiac findings (valvular and myocardial calcification, myocardial hypertrophy) with clinical data (age, sex, clinical manifestation, nephrolithiasis, nephrocalcinosis, hypertension, skeletal abnormalities, hypercalcemic syndrome) and biochemical data (serum calcium, serum phosphate, serum iPTH level, serum creatinine). A group of 132 consecutive patients with surgically verified PHP (94 women, 38 men; ages 15-86, mean age 57 +/- 16 years) were included in this study. Blood chemistry, clinical presentation, radiography, and echocardiography were carried out in all patients for univariate and multivariate analyses of all parameters. There was no statistical correlation between clinical symptoms, biochemical data, and cardiac calcific alterations. Typical skeletal manifestations (osteolysis/subperiostal resorption) and valvular calcifications were significantly correlated to left ventricular hypertrophy (p = 0.005). Cardiac abnormalities such as calcific myocardial deposits or mitral and aortic valvular calcifications do not correlate with laboratory findings and clinical presentation at the time of diagnosis. There was no biochemical or clinical variable that could predict the frequency or severity of valvular sclerosis or calcific deposits in the myocardium. However, PHP-related skeletal abnormalities and valvular calcification were predicting factors for left ventricular hypertrophy, a reversible cardiac manifestation of PHP. Myocardial hypertrophy is more often found with classic symptomatic PHP with osseous abnormalities.
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PMID:Primary hyperparathyroidism and the heart: cardiac abnormalities correlated to clinical and biochemical data. 772 54

Patients with primary hyperparathyroidism (PHPT) show a high incidence of left ventricular hypertrophy, cardiac calcific deposits in the myocardium, and/or aortic and mitral valve calcification and thus may carry an increased risk of death from circulatory diseases. This prospective study was designed to assess an effect of parathyroidectomy on cardiac abnormalities of patients with PHPT. Echocardiography was used to evaluate the mechanical performance of the heart muscle, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications within 12 and 41 months after parathyroidectomy. In a blinded fashion, aortic and mitral value calcifications were determined in 46% and 39% of patients with PHPT. Calcific deposits in the myocardium were found in 74% of patients. Follow-up studies after parathyroidectomy disclosed no evidence of progression of these calcifications. Before operation left ventricular hypertrophy was detected in 82%. After parathyroidectomy and 41 months of normocalcemia and normal PTH concentrations, a regression of hypertrophy of the interventricular septum and the posterior wall by -6% and -19% (P < 0.05) was observed. Subgroup analysis disclosed the most impressive long-term reduction of left ventricular hypertrophy in patients without a history of hypertension (-11% and -21%; P < 0.05 and P < 0.005); no changes were determined in 9 patients who developed secondary hyperparathyroidism after operation. The present data show a high incidence of left ventricular hypertrophy and aortic and/or mitral valve calcifications in patients with PHPT. Follow-up at 1 year and at 41 months after successful parathyroidectomy disclose regression of hypertrophy. Our results give evidence that parathyroid hormone per se plays an important role in the maintainance of myocardial hypertrophy. Post-surgical restoration of normocalcemia and normalization of parathyroid hormone valvular sclerosis persists without evidence of progression. We further conclude that patients with PHPT and parathyroidectomy are at low risk for the development of severe aortic and mitral valve stenosis within this period of time.
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PMID:Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up. 898 42

A 72-year-old woman presented to hospital with rapidly progressive dyspnea and chest pain on exertion. Physical findings included a grade 3/6 systolic murmur increased by the Valsalva manoeuvre. Transthoracic echocardiography revealed concentric left ventricular hypertrophy, systolic anterior motion of the mitral valve and critical dynamic outflow tract obstruction. The myocardium was strikingly heterogeneous with hyperdynamic left ventricular systolic function. Laboratory findings included severe hypercalcemia secondary to primary hyperparathyroidism. The patient's outcome was unfavourable with nephrogenic diabetes insipidus, pancreatitis, shock, severe acidosis and death. Postmortem examination confirmed the presence of severe concentric left ventricular hypertrophy, a narrowed left ventricular outflow tract and localized endocardial fibrosis of the left interventricular septum. Microscopic findings showed diffuse calcium deposits of the myocardium, coronary arteries, kidneys and lungs. This appears to be the first report of two-dimensional and Doppler echocardiographic findings in hypercalcemic cardiomyopathy mimicking obstructive hypertrophic cardiomyopathy.
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PMID:Hypercalcemic cardiomyopathy associated with primary hyperparathyroidism mimicking primary obstructive hypertrophic cardiomyopathy. 985 22

In recent decades, primary hyperparathyroidism (pHPT) has changed its clinical presentation from a disease with bone and renal involvement to a frequently asymptomatic disorder detected on routine biochemistry. Nevertheless, it remains unclear whether patients with untreated mild asymptomatic hyperparathyroidism are at risk for other complications such as increased morbidity and mortality from cardiovascular diseases. There are limited data on the incidence of cardiovascular abnormalities in mild pHPT. However, pHPT has been associated with increased risk of death from cardiovascular disease, hypertension, left ventricular hypertrophy (LVH), valvular and myocardial calcifications, impaired vascular reactivity, alterations in cardiac conduction, impaired glucose metabolism, dyslipidaemia, and alterations in body composition. The nature of some of these associations is in question, because cure of pHPT does not lead to improvement of the cardiovascular disorder e.g. hypertension. In contrast, currently available data suggest that LVH, impaired glucose metabolism and dyslipidaemia may improve after surgery and that successful parathyroidectomy could decrease the excess mortality in patients with pHPT due to cardiovascular disease.
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PMID:Parathyroid adenomas and cardiovascular risk. 1279 Jul 92

Primary hyperparathyroidism (pHPT), caused by solitary parathyroid adenomas in 85% of cases and diffuse hyperplasia in most of the remaining cases, overproduces parathyroid hormone (PTH), which mobilizes calcium to the blood stream. Renal stones, osteoporosis and diffuse symptoms of hypercalcaemia, such as constipation, fatigue and weakness are well-known complications. However, in Western Europe and North America, patients with pHPT are nowadays usually discovered during an early, asymptomatic phase of the disease. It has been reported that patients suffering from symptomatic pHPT have increased mortality, mainly due to an overrepresentation of cardiovascular death. pHPT is reported to be associated with hypertension, disturbances in the renin-angiotensin-aldosterone system, and structural and functional alterations in the vascular wall. Recently, studies have indicated an association between pHPT and heart disease, and studies in vitro have produced a number of theoretical approaches. An increased prevalence of cardiac structural abnormalities such as left ventricular hypertrophy (LVH) and valvular and myocardial calcification has been observed. Associations have been found between PTH and LVH, and between LVH and serum calcium. LV systolic function does not seem to be affected in patients with pHPT, whereas any influence on LV diastolic performance needs further evaluation. The aim of this review is to clarify the connection between pHPT and cardiac disease.
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PMID:Primary hyperparathyroidism and heart disease--a review. 1547 92

Long-term follow-up is initially considered appropriate for the majority of patients with primary hyperparathyroidism (PHPT) having small increases in calcium levels (< 2.8 mmol/l) and lacking the 'classical' symptoms of PHPT. The supportive reasoning is that many such patients never progress to more severe biochemical or clinical disease. There are, however, arguments in favour of early surgical treatment of such patients but adequately powered studies have not been carried out in this subgroup of patients to asses the impact of PHPT on their quality of life, cardiovascular risk and bone density. Progressive loss in bone mineral density and an increased risk of bone fracture become increasingly significant in an ageing population. Left ventricular hypertrophy, an increased risk of arrhythmia and/or myocardial infarction in addition to changes in atherogenic lipid profile and impaired glucose tolerance may translate into an increased risk of premature death in this group of patients. Changes in the quality of life identified using standardized questionnaires are sometimes recognized by patients only in retrospect (i.e. after resolution of symptoms following successful parathyroidectomy). In addition, many series fail to assess and record accurately such symptoms. Multicentre cohort studies of patients with asymptomatic PHPT randomized to immediate or delayed surgical treatment could address some of the debated issues highlighted in this review. Until such studies are set up, most surgeons would consider that parathyroid surgery should represent the first choice of treatment for all patients, but many physicians would favour a long-term follow-up. Nevertheless, the threshold for referral for surgical treatment has been lowered since the introduction of scan-directed minimally invasive parathyroidectomy, which enables the experienced parathyroid surgeon to successfully treat patients with PHPT with a minimum of complications as a day-case operation. In the context of improved surgical treatment, we need more data on the benefits or otherwise in so-called asymptomatic patients with a thorough assessment of their bone quality, cardiovascular risk and quality of life.
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PMID:Asymptomatic hyperparathyroidism--need for multicentre studies. 1765 48

Data concerning the cardiovascular manifestations of primary hyperparathyroidism (PHPT) are inconsistent, which is due, in part, to the decrease in disease severity over the last several decades. In areas where patients tend to be more symptomatic, data support the presence of cardiovascular findings including myocardial and vascular calcification as well as increased cardiovascular mortality. Data from the cohorts in whom the disease is characterized by mild hypercalcemia, suggest that clinically overt cardiovascular manifestations are unusual in PHPT. Recent data, however, support the presence of subtle cardiovascular manifestations in mild disease, such as changes in endothelial function as well as increased vascular stiffness and perhaps diastolic dysfunction. Left ventricular hypertrophy is a more consistent finding across a spectrum of disease severity, though this finding may be related to hypertension, which has long been associated with PHPT.
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PMID:Cardiovascular aspects of primary hyperparathyroidism. 1909

Left ventricular hypertrophy is a common complication of primary hyperparathyroidism. Numerous disturbances of myocardial physiology have been described as a result of excess parathyroid hormone action. In this brief communication, another phenotype of the hyperparathyroid heart is proposed, the 'pseudo-myocardial infarction hyperparathyroid heart'.
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PMID:The hyperparathyroid heart mimicking acute myocardial infarction. 1957 90


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