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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible reversal by calcium of the inhibitory action of verapamil on the atrioventricular (AV) node was investigated in anesthetized, atropinized dogs, with cardiac pacing. The His bundle potentials were recorded by endocavitory electrode and the AV node effective refractory period measured by the extrastimulus method. Calcium infusion was effective against the impairment of AV nodal conduction induced by verapamil, provided it remained moderate: the gradual rise in the plasma calcium concentration counteracted the effects of an infusion of verapamil on conduction time and effective refractory period in the AV node, as long as it did not exceed 5 mmol/L. However, beyond this level, calcium appeared less and less capable of reversing the effects of verapamil. Thus, the protective action of calcium had a bell-shaped dose-response curve, with the optimum at 5 mmol/L. This biphasic influence is consistent with the opposite opinions previously given concerning the antagonism between calcium and calcium blockers, depending on whether hypercalcemia brought into play was mild or major. In any case, the prominent role played by calcium in the slow inward current in the AV node accounts for the antagonism, observed in vivo, between calcium and verapamil. The pacemaker activity of the sinoatrial (SA) node was less influenced by both calcium blocker and calcium.
J Cardiovasc Pharmacol
PMID:Effect of gradual rise in plasma calcium concentration on the impairment of atrioventricular nodal conduction due to verapamil. 241 94

The effects of acute hypercalcaemia on arterial pressure and vascular tone have been poorly understood. We analysed the effect of a bolus of calcium chloride (15 mg . kg-1 iv) on arterial pressure, total peripheral resistance, and left ventricular function in 25 conscious dogs studied with or without pharmacological autonomic blockade. Without autonomic blocking drugs, the maximum response to calcium included increases of +139.4 kPa . s-1 (+1046 mmHg . s-1) in maximum rate of change of left ventricular pressure, +2.2 cm3 in stroke volume, +2.6 kPa (+ 19.2 mmHg) in aortic systolic pressure, and +0.6 kPa (+4.4 mmHg) in mean aortic pressure, but total peripheral resistance was unchanged. During beta-adrenergic blockade with propranolol, calcium again increased maximum rate of change of pressure and stroke volume, increased mean aortic pressure (2.2 kPa [+16.5 mmHg]), and increased resistance by 35%. When calcium was given during alpha-adrenergic blockade with phenoxybenzamine or phentolamine, mean aortic pressure did not rise, and resistance fell by 19%. The calcium-induced rise in resistance during beta-adrenergic blockade was abolished by surgical adrenalectomy. We conclude that excess extracellular calcium ion may influence vascular resistance by increasing autonomic nervous system excitation of alpha- and beta-adrenergic vascular receptors. A major mechanism by which the sympathetic nervous system effects occur is through increased release of catecholamines from the adrenal medulla.
Cardiovasc Res 1980 Sep
PMID:Role of the autonomic nervous system in the pressor response to calcium in conscious dogs. 611 96

To study the response of function in the regionally ischaemic left ventricle to increased and decreased concentrations of plasma ionised calcium, twenty-two anaesthetised dogs were placed on right heart bypass with constant mean aortic pressure and heart rate. Regional (sonomicrometry) and global left ventricular function were assessed before coronary artery ligation. Then, following ligation, function after 45 min stable ionised hypercalcaemia [( Ca2+] = 1.68 +/- 0.01 mmol x litre-1) and hypocalcaemia [( Ca2+] = 0.73 +/- 0.02 mmol x litre-1) were each compared to function during an immediately preceding normocalcaemic period. Control of cardiac output enabled paired comparisons to be made at matched preloads: systolic shortening from common end-diastolic chord lengths (n = 10), and stroke work at common left ventricular end-diastolic pressures (n = 22). With hypercalcaemia, systolic shortening in the ischaemic region (2.11 +/- 0.39 mm preligation) increased from -0.62 +/- 0.17 to -0.04 +/- 0.20 mm (P less than 0.01), whereas in the control region systolic shortening increased from 1.47 +/- 0.12 to 2.00 +/- 0.15 mm (P less than 0.01) reaching its preligation value (1.67 +/- 0.13 mm). Stroke work at a left ventricular end-diastolic pressure of 1.37 kPa increased (0.248 +/- 0.019 to 0.299 +/- 0.021 joules x beat-1, P less than 0.001) but not to preligation levels (0.364 +/- 0.016 joules x beat-1). Hypercalcaemia also increased myocardial oxygen consumption (by 1.0 +/- 0.3 cm3 x min-1 x 100 g-1, P less than 0.005) but not coronary blood flow. With hypocalcaemia, systolic shortening decreased in ischaemic and control regions, global function curves were markedly depressed, and myocardial oxygen consumption did not change but coronary blood flow increased. Thus hypercalcaemia improved function in ischaemic and control regions but improvement in the ischaemic region was small compared with the depression associated with ischaemia itself. Hypercalcaemia also improved global function, but not to preischaemic levels, at an increased oxygen cost.
Cardiovasc Res 1983 Jul
PMID:Global and regional function in the regionally ischaemic left ventricle related to plasma ionised calcium. 688 17

Gelfoam embolization of parathyroid adenomas causes temporary remission of hypercalcemia, but collateral circulation revascularizes the gland. Embolization with silicone permanently infarcts the gland, but is associated with all the risks of capillary bed occlusion. The staining of parathyroid adenomas with contrast material avoids the risks of particulate embolization and appears to produce permanent ablation. We carried out embolization or staining procedures in 14 parathyroid adenomas. In three of the four cases in which Gelfoam embolization was performed, hypercalcemia recurred within six months to two years; in the fourth case, in which persistent normocalcemia has been found, intense staining had been demonstrated before embolization. In eight of the remaining 10 cases, adequate staining was achieved, and normocalcemia has been maintained in all up to 36 months.
Cardiovasc Intervent Radiol 1980
PMID:The treatment of hyperparathyroidism by transcatheter techniques. 745 19

In lung cancer patients, hypercalcemia is a fairly common metabolic problem associated with malignancy. However, the occurrence of hypercalcemia in lung cancer patients means an ominous prognostic sign. As hypercalcemia often causes early death, quick diagnosis and treatment for hypercalcemia are required. A 69-year-old woman was admitted to our hospital with anorexia caused by hypercalcemia. On admission, serum level of PTH was elevated and PTHrP was normal. From the results of CT findings and transbronchial lung biopsy, the cause of the hypercalcemia was determined as lung cancer incidentally complicated with primary hyperparathyroidism. First, serum calcium level was returned to normal through hydration with saline and bisphosphonates. Next, left hemithyroidectomy for primary hyperparathyroidism was performed. Histologically, the tumor was diagnosed as parathyroid adenoma. Fifteen days later, left lower lobectomy for primary lung cancer was performed under a video-assisted thoracoscopic approach. Histologically, the tumor was diagnosed as a moderately differentiated adenocarcinoma. Four years and three months after the operation, the patient is alive and well with no sign of recurrence. When a lung cancer patient is complicated with hypercalcemia, we need to consider that primary hyperparathyroidism is a possible cause of the hypercalcemia.
Ann Thorac Cardiovasc Surg 2002 Jun
PMID:A case of lung cancer with hypercalcemia which was incidentally complicated with primary hyperparathyroidism due to parathyroid adenoma. 1247 97

The possible association of increased left ventricular ejection fraction (LVEF) in patients with increased serum Ca(2+) was observed in our clinic. Six patients with confirmed primary hyperparathyroidism and hypercalcaemia were studied prospectively. Tc-99m sestamibi gated SPECT was done pre- and postoperatively. The LVEF was abnormally high in all the patients pre-operatively, i.e. above the normal reference range (47-61%) as used in our clinic. It decreased in all of them postoperatively, yet in only three patients to values within the normal range. This was associated with normalisation of the serum Ca(2+) values. The median of the pre-operative LVEF was 74% and postoperative it was 61.5%. The median difference was 9% with a 95% CI for the median difference for paired data (6; 26). This was statistically significant. Increased LVEF was not previously described as part of the clinical picture of primary hyperparathyroidism. The in vivo effect of chronic hypercalcaemia on LV pump function my need to be revisited.
Cardiovasc J S Afr
PMID:Enhanced myocardial contractility associated with hypercalcaemia of hyperparathyroidism - a case study in six patients. 1284 99

This 8-week study investigated the effects of increasing dietary Ca2+ content from 1.0% to 3.0% and hypercalcemia induced by oral 1alpha-OH vitamin D3 (1OH-D3, 1.2 microg/kg), on arterial tone in NaCl-hypertensive rats. The high-Ca2+ diet completely prevented the increase in blood pressure induced by the 6.0% NaCl chow, while plasma total Ca2+ and body weight were not different from controls. The 1OH-D3 treatment moderately elevated plasma total Ca2+ and attenuated the NaCl-induced rise in blood pressure, but also impaired weight gain. The tone of isolated mesenteric arterial rings was examined at the end of study. The endothelium-independent relaxations to nitroprusside, isoproterenol, and cromakalim were impaired in NaCl-hypertension. Experiments with NG-nitro-l-arginine methyl ester and tetraethylammonium in vitro suggested that both the nitric oxide- and hyperpolarization-mediated components of endothelium-dependent relaxation to acetylcholine were reduced in NaCl-hypertensive rats. All of the impaired relaxations in NaCl hypertension were normalized by concomitant Ca2+ supplementation. The 1OH-D3 treatment did not affect vascular relaxation, but it attenuated maximal contractile responses induced by norepinephrine and KCl by more than 50%. The reduced vasoconstrictor responses could not be explained by increased apoptosis in the vessel wall, but calcification may have played a role, since moderate signs of medial or adventitial calcification were observed in the aortic preparations after the 1OH-D3 treatment. In conclusion, a high-Ca2+ diet, which did not cause hypercalcemia, normalized blood pressure and endothelium-dependent and endothelium-independent vasorelaxation in NaCl-hypertensive rats. In contrast, chronic hypercalcemia induced by 1OH-D3 was associated with moderately lowered blood pressure, possibly because of reduced vasoconstrictor responses in arterial smooth muscle.
J Cardiovasc Pharmacol 2003 Sep
PMID:Vascular influences of calcium supplementation and vitamin D-induced hypercalcemia in NaCl-hypertensive rats. 1296 Jun 76

We present two patients who were diagnosed with symptomatic sinus node dysfunction in the setting of hypercalcemia secondary to hyperparathyroidism. An extensive review of the literature has not revealed previous reports of this pathologic process.
J Cardiovasc Pharmacol Ther 2004 Jun
PMID:Sinus node dysfunction secondary to hyperparathyroidism. 1530 50

We report a case of gene-positive long-QT syndrome (KCNH2) in a patient with concomitant Williams Syndrome. The hypercalcemia that developed in association with Williams Syndrome pseudo-normalized the QTc interval on surface ECG, concealing the clinical and electrocardiographic manifestations of the disease. Initiation of medical therapy for hypercalcemia unmasked the prolonged QT interval, allowing for the diagnosis of long-QT syndrome to be made.
J Cardiovasc Electrophysiol 2008 Dec
PMID:Congenital long-QT syndrome concealed by hypercalcemia in Williams Syndrome. 1866 76

A 47-year-old man presented with multiple lung metastases from parathyroid carcinoma that caused hyperparathyroidism and refractory hypercalcemia. Lung radiofrequency (RF) ablation was repeated to decrease the serum calcium and parathyroid hormone levels and improve general fatigue. Pulmonary resection was combined for lung hilum metastases. The patient is still alive 4 years after the initial RF session. He has received 20 RF sessions for 50 lung metastases during this period.
Cardiovasc Intervent Radiol 2010 Jun
PMID:A case report of 20 lung radiofrequency ablation sessions for 50 lung metastases from parathyroid carcinoma causing hyperparathyroidism. 1988 31


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