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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both calcium and vitamin D play important roles in cardiac muscle contraction and performance. In this cross-sectional study, we evaluated the status of serum calcium, PTH and 25(OH)D(3) and their correlation with left ventricular Function and NYHA Functional class in 95 heart failure patients referred to Shahid Chamran Hospital, Isfahan, Iran, by colorimetric, immunoradiometric, and Immunochemiluminescent assays, echocardiography and interview respectively. The study was performed between Oct 2007 and Feb 2008. Twenty eight women and 67 men of functional classes 1, 2, or 3 participated in the study. Mean (SD) of age of the participants was 62(11) years. Mean (SD) serum calcium and 25(OH)D(3) were 2.41(0.16) mmol/L and 56.78(51.33) nmol/L, respectively. The overall prevalence of low vitamin D status was 84.2%. There was no correlation between serum calcium and 25(OH)D(3) with LVEF. Interestingly, patients with hyperparathyroidism (serum PTH>65 ng/L) had lower LVEF (27% versus 32.5% p = 0.03). NYHA functional class was worse in patients with hyperparathyroidism (p = 0.08). Hypovitaminosis D is very prevalent in heart failure patients. Hyperparathyroidism in these patients may adversely affect cardiac function. Vitamin D3 might serve as an adjunctive treatment for heart failure patients.
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PMID:Calcium and vitamin D status in heart failure patients in Isfahan, Iran. 1969 Aug 19

We report the radiographic, echocardiographic and cardiac CT appearances of 'porcelain heart' in an 85-year-old woman who presented with progressive heart failure. The extensive myocardial calcification was secondary to hyperparathyroidism with renal failure.
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PMID:"Porcelain heart" cardiomyopathy secondary to hyperparathyroidism: radiographic, echocardiographic, and cardiac CT appearances. 2103 Mar 32

Left ventricular hypertrophy (LVH) is a cardiovascular complication highly prevalent in patients with chronic kidney disease (CKD) and end-stage renal disease. LVH in CKD patients has generally a negative prognostic value, because it represents an independent risk factor for the development of arrhythmias, sudden death, heart failure and ischemic heart disease. LVH in CKD patients is secondary to both pressure and volume overload. Pressure overload is secondary to preexisting hypertension, but also to a loss of elasticity of the vessels and to vascular calcifications, leading to augmented pulse pressure. Anemia and the retention of sodium and water secondary to decreased renal function are responsible for volume overload, determining a hyperdynamic state. In particular, the correction of anemia with erythropoietin in CKD patients is advantageous, since it determines LVH reduction. Other risk factors for LVH in CKD patients are documented: some are specific to CKD, as mineral metabolism disorders (hypocalcemia, hyperphosphatemia, low serum vitamin D levels and secondary hyperparathyroidism), others are non-traditional, such as increased asymmetric dimethylarginine, oxidative stress, hyperhomocysteinemia and endothelial dysfunction that, in turn, accelerates the process of atherogenesis, triggers the inflammation and pro-thrombotic state of the glomerular and the vascular endothelium and aggravates the process of both CKD and LVH.
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PMID:Hypertension, left ventricular hypertrophy and chronic kidney disease. 2111 11

Chronic kidney disease has been increasingly recognized as a risk factor for incident heart failure. Despite advances in chronic heart failure treatment, the prognosis remains poor. The annual mortality from all cardiovascular causes in the end stage renal disease population is significantly higher than the general population, accounting for more than half of all deaths in this group. The mechanisms underlying the enhanced susceptibility to myocardial ischemia in chronic kidney disease are not well defined. Traditional cardiovascular risk factors, although common in chronic kidney disease, do not exert the same impact as in the general population. The presence of "renal-specific" non-traditional risk factors including endothelial dysfunction, inflammation, oxidative stress, anaemia, proteinuria and changes in vitamin D metabolism (encompassing the complex interactions of calcium and phosphate metabolism, hyperparathyroidism and vascular calcification) play an important role in cardiovascular disease progression. An increased understanding of the array of metabolic changes/adaptations occurring in uraemic heart disease have allowed one to consider optimal management strategies and to develop new strategies for future management of uraemic heart disease.
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PMID:Risk factors and metabolic mechanisms in the pathogenesis of uraemic cardiac disease. 2119 37

Cardiovascular diseases are the leading cause of death in patients on haemodialysis. Cardiovascular mortality rate in these patients is approximately 9% per year, with the highest prevalence of left ventricular hypertrophy, ischemic heart disease and congestive heart failure being the most frequent cardiovascular complications. Risk factors for cardiac failure include hypertension, disturbed lipid metabolism, oxidative stress, microinflammation, hypoalbuminemia, anaemia, hyperhomocysteinemia, and increased concentration of asymmetric dimethylarginine, increased shunt blood flow and secondary hyperparathyroidism. Diagnostic strategy for early detection of patients with increased risk for the development of asymptomatic disturbances of systolic and diastolic left ventricular function should include echocardiografic examination, tests for determining coronary vascular disease, as well as tests of myocardial function (BNP, Nt-proBNP). Early detection of patients with a high risk of congestive heart failure enables timely implementation of adequate therapeutic strategy to provide high survival rate of HD patients.
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PMID:[Heart failure in haemodialysis patients: evaluation and treatment]. 2162 74

Secondary hyperparathyroidism (SHPT) may contribute to the systemic illness that accompanies chronic heart failure (CHF). Healthy elderly with vitamin D deficiency who did not develop hyperparathyroidism (functional hypoparathyroidism, FHPT) had lower mortality than those who did. This study was designed to examine determinants of the PTH response in the vitamin D insufficient CHF patients. Sixty five vitamin D insufficient males with NYHA class II and III and 20 control subjects age >/=55 years were recruited. Echocardiography, physical performance, NT-pro-BNP, PTH, 25-hydroxyvitamin D (25(OH)D), adiponectin and bone activity surrogate markers (OPG, RANKL, OC, beta-CTx) were assessed. Increased NYHA class was associated with SHPT, while physical performance was inferior compared to FHPT. SHPT was associated with lower left ventricular ejection fraction (LVEF) and flow mediated dilatation, but with higher left heart dimensions, left ventricular mass index and right ventricular systolic pressure. CHF patients with SHPT had increased NT-pro-BNP, adiponectin and bone markers, but decreased 25(OH)D compared to those with FHPT. Independent determinants for SHPT in CHF patients with vitamin D insufficiency were LVEF, adiponectin and beta-CTx, irrespective of renal function and serum vitamin D levels. In conclusion, increased PTH levels, but not low vitamin D, demonstrated close relation to CHF severity.
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PMID:Parathyroid hormone response to vitamin D insufficiency in elderly males with chronic heart failure. 2177 17

Animal and human studies support a clinically relevant interaction between aldosterone and parathyroid hormone (PTH) levels and suggest an impact of the interaction on cardiovascular (CV) health. This review focuses on mechanisms behind the bidirectional interactions between aldosterone and PTH and their potential impact on the CV system. There is evidence that PTH increases the secretion of aldosterone from the adrenals directly as well as indirectly by activating the renin-angiotensin system. Upregulation of aldosterone synthesis might contribute to the higher risk of arterial hypertension and of CV damage in patients with primary hyperparathyroidism. Furthermore, parathyroidectomy is followed by decreased blood pressure levels and reduced CV morbidity as well as lower renin and aldosterone levels. In chronic heart failure, the aldosterone activity is inappropriately elevated, causing salt retention; it has been argued that the resulting calcium wasting causes secondary hyperparathyroidism. The ensuing intracellular calcium overload and oxidative stress, caused by PTH and amplified by the relative aldosterone excess, may increase the risk of CV events. In the setting of primary aldosteronism, renal and faecal calcium loss triggers increased PTH secretion which in turn aggravates aldosterone secretion and CV damage. This sequence explains why adrenalectomy and blockade of the mineralocorticoid receptor tend to decrease PTH levels in patients with primary aldosteronism. In view of the reciprocal interaction between aldosterone and PTH and the potentially ensuing CV damage, studies are urgently needed to evaluate diagnostic and therapeutic strategies addressing the interaction between the two hormones.
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PMID:Aldosterone and parathyroid hormone: a precarious couple for cardiovascular disease. 2233 95

A synchronized dyshomeostasis of extra- and intracellular Ca(2+), expressed as plasma ionized hypocalcemia and excessive intracellular Ca(2+) accumulation, respectively, represents a common pathophysiologic scenario that accompanies several diverse disorders. These include low-renin and salt-sensitive hypertension, primary aldosteronism and hyperparathyroidism, congestive heart failure, acute and chronic hyperadrenergic stressor states, high dietary Na(+), and low dietary Ca(2+) with hypovitaminosis D. Homeostatic responses are invoked to restore normal extracellular [Ca(2+)](o), including increased plasma levels of parathyroid hormone and 1,25(OH)(2)D(3). However, in cardiomyocytes these calcitropic hormones concurrently promote cytosolic free [Ca(2+)](i) and mitochondrial [Ca(2+)](m) overloading. The latter sets into motion organellar-based oxidative stress, in which the rate of reactive oxygen species generation overwhelms their detoxification by endogenous antioxidant defenses, including those related to intrinsically coupled increments in intracellular Zn(2+). In turn, the opening potential of the mitochondrial permeability transition pore increases, allowing for osmotic swelling and ensuing organellar degeneration. Collectively, these pathophysiologic events represent the major components to a mitochondriocentric signal-transducer-effector pathway to cardiomyocyte necrosis. From necrotic cells, there follows a spillage of intracellular contents, including troponins, and a subsequent wound healing response with reparative fibrosis or scarring. Taken together, the loss of terminally differentiated cardiomyocytes from this postmitotic organ and the ensuing replacement fibrosis each contribute to the adverse structural remodeling of myocardium and progressive nature of heart failure. In conclusion, hormone-induced ionized hypocalcemia and intracellular Ca(2+) overloading comprise a pathophysiologic cascade common to diverse disorders and that initiates a mitochondriocentric pathway to nonischemic cardiomyocyte necrosis.
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PMID:Disturbances in calcium metabolism and cardiomyocyte necrosis: the role of calcitropic hormones. 2282 13

The symptoms and signs constituting the congestive heart failure (CHF) syndrome have their pathophysiologic origins rooted in a salt-avid renal state mediated by effector hormones of the renin-angiotensin-aldosterone and adrenergic nervous systems. Controlled clinical trials, conducted over the past decade in patients having minimally to markedly severe symptomatic heart failure, have demonstrated the efficacy of a pharmacologic regimen that interferes with these hormones, including aldosterone receptor binding with either spironolactone or eplerenone. Potential pathophysiologic mechanisms, which have not hitherto been considered involved for the salutary responses and cardioprotection provided by these mineralocorticoid receptor antagonists, are reviewed herein. In particular, we focus on the less well-recognized impact of catecholamines and aldosterone on monovalent and divalent cation dyshomeostasis, which leads to hypokalemia, hypomagnesemia, ionized hypocalcemia with secondary hyperparathyroidism and hypozincemia. Attendant adverse cardiac consequences include a delay in myocardial repolarization with increased propensity for supraventricular and ventricular arrhythmias, and compromised antioxidant defenses with increased susceptibility to nonischemic cardiomyocyte necrosis.
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PMID:Mineralocorticoid receptor antagonism confers cardioprotection in heart failure. 2311 91

Secondary hyperparathyroidism is an almost inevitable complication of advanced kidney failure. The introduction of the calcimimetic cinacalcet for the treatment of secondary hyperparathyroidism in patients on dialysis was based on its ability to reduce elevated levels of parathyroid hormone (PTH). Subsequent clinical studies confirmed the beneficial effects of cinacalcet on biochemical parameters reflecting mineral disturbances and bone disease. In this review we summarise the impact of cinacalcet on biochemical, intermediate and clinical outcomes. We also present previously unpublished mineral metabolism data from 144 Dutch dialysis patients treated with cinacalcet who participated in the pan-European ECHO observational study. Although secondary hyperparathyroidism tended to be more severe in our Dutch cohort, compared with the entire ECHO cohort, cinacalcet was nevertheless effective in reducing PTH in these patients. Two recent clinical studies evaluated, respectively, the efficacy of cinacalcet in improving the intermediate endpoint of cardiovascular calcifications (ADVANCE trial), and its impact on clinical outcomes, including all-cause mortality and cardiovascular events (EVOLVE trial). The ADVANCE trial provided evidence that cinacalcet may indeed improve calcification in both large arteries and cardiac valves. The EVOLVE trial, however, did not meet its clinical primary endpoint (time to all-cause mortality, myocardial infarction, hospitalisation for unstable angina, heart failure or a peripheral vascular event), although secondary and sensitivity analysis suggested a beneficial effect. The clinical implications of these important studies are also addressed in this review.
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PMID:Cinacalcet for secondary hyperparathyroidism: from improved mineral levels to improved mortality? 2403 60


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