Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors describe a case of 44-year-old woman with severe cardiac failure due to chronic hypocalcemia caused by primary hypoparathyroidism with coexisting Fahr's disease. This type of cardiomyopathy was refractory to conventional therapy. Spectacular clinical improvement and normalisation of echocardiographic left ventricular parameters were observed following supplementation with calcium and alphacalcidol. The effects of calcium ions and parathyroid hormone on myocardial contractility, ECG changes and serum CK activity are discussed.
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PMID:[Hypocalcemic cardiomyopathy--a reversible type of cardiac failure in a patient with primary hypoparathyroidism and coexisting Fahr's disease]. 1450 39

The parathyroid hormone-related peptide (PTHrP) was initially identified in the early eighties, as the humoral mediator causing hypercalcaemia associated with malignancy. However, recently PTHrP was also shown to mediate a wide range of local paracrine/autocrine and intracrine functions in various tissues under physiological and pathological conditions. Indeed, PTHrP is a polyhormone, which can act through different receptors, including the type 1 parathyroid hormone (PTH) receptor 1 (PTH-1R). In the cardiovascular system, PTHrP appears to have potent effects on vascular smooth muscle cells and cardiomyocytes, where it participates in different pathological conditions, such as ischemia and heart failure. Therefore, it is conceivable that further studies on the regulation of PTHrP expression, characterization of its autocrine/paracrine/intracrine functions and definition of its intracellular signal transduction pathways in cardiomyocytes and cardiac vascular smooth muscle cells can elucidate the potential role of PTHrP in cardiovascular pathophysiology.
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PMID:Parathyroid hormone-related peptide and cardiovascular system. 1459 5

The reduction of cardiovascular disease risk in kidney failure involves treatment of modifiable risk factors and provision of proven interventions to patients with established disease. Volume status management is key to blood pressure control. Statins are the agents of choice for the treatment of dyslipidemia. Target hemoglobin levels should be achieved using intravenous iron and erythropoietic agents. Combinations of calcium and noncalcium-containing phosphorus binders and vitamin D and its analogues should be used to attain target parathyroid hormone, phosphorus, and calcium phosphorus product levels. beta Blockers and aspirin are recommended in patients with ischemic heart disease and angiotensin-converting enzyme inhibitors (or angiotensin II receptor blockers), and beta blockers are recommended in patients with heart failure with reduced ejection fraction. In patients who require revascularization, studies suggest a survival benefit of coronary artery bypass graft surgery over percutaneous transluminal coronary angioplasty and coronary artery stenting.
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PMID:Treating the Patient with Kidney Failure to Reduce Cardiovascular Disease Risk. 1521 21

Inflammation in vascular (mostly arterial) walls and heart valves triggered by the trans-endothelial influx of LDL particles and the action of subsequently modified (e.g., by oxidation) LDL particles can trigger true bone formation by valvar fibroblasts, by a subpopulation of re-differentiation-competent VSMCs (vascular smooth muscle cells) or by vascular pericytes. Vascular ossification can lead to heart failure and death. Elderly osteoporotic women who need osteogenic drugs to restore their lost skeletal bone are paradoxically prone to vascular ossification-the "calcification paradox." The recent introduction into the clinic of a potently osteogenic parathyroid hormone peptide, Lilly's rhPTH-(1-34)OH (Forteotrade mark), to reverse skeletal bone loss raises the question of whether this and other potently osteogenic PTHs still in clinical trial might also stimulate vascular ossification in such osteoporotic women. Indeed the VSMCs in human and rat atherosclerotic lesions hyperexpress PTHrP and the PTHR1 (or PTH1R) receptor as do maturing osteoblasts. And the evidence indicates that endogenous PTHrP with its NLS (nuclear/nucleolar localization sequence) does stimulate VSMC proliferation (a prime prerequisite for atheroma formation and ossification) via intranuclear targets that inactivate pRb, the inhibitory G1/S checkpoint regulator, by stimulating its hyperphosphorylation. But neither externally added full-length PTHrP nor the NLS-lacking PTHrP-(1-34)OH gets into the VSMC nucleus and instead they inhibit proliferation and calcification by only activating the cell's PTHR1 receptors. No PTH has an NLS and, as expected from the observations on the externally added PTHrPs, hPTH-(1-34)OH inhibits calcification by VSMCs and cannot stimulate vascular ossification in a diabetic mouse model. Encouraging though this may be for osteoporotics with their "calcification paradox," more work is needed to be sure that the skeletally osteogenic PTHs do not promote vascular ossification with its cardiovascular consequences.
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PMID:Osteogenic PTHs and vascular ossification-Is there a danger for osteoporotics? 1578 90

There are three injectable and one oral bone-building (i.e., bone anabolic) parathyroid hormone (PTH) peptides. One of the four, Lilly's injectable teriparatide (Forteo), is currently being used, and the other three are in clinical trials. They are being used or assessed only for treating postmenopausal osteoporosis. However, their potential clinical targets now extend far beyond osteoporosis. They can accelerate the mending of even severe non-union fractures; they will probably be used to strengthen the anchorage of pros-theses to bone; they have been shown to treat psoriasis that has resisted other treatments; they can increase the size of haematopoietic stem cell proliferation and accelerate the endogenous repopulation or repopulation by donor transplants of bone marrow depleted by chemotherapeutic drugs; and they may prevent vascular ossification. Leptin, a member of the cytokine superfamily has a PTH-like osteogenic activity and may even partly mediate PTH action. But leptin has two drawbacks that cloud its therapeutic future. First, apart from directly stimulating osteoblastic cells, it targets cells in the hypothalamic ventromedial nuclei and through them it reduces oestrogenic activity by promoting osteoblast-suppressing adrenergic activity. Second, it stimulates vascular and heart valve ossification, which leads to such events as heart failure and diabetic limb amputations.
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PMID:Parathyroid hormone and leptin--new peptides, expanding clinical prospects. 1583 57

In the cardiovascular system, parathyroid hormone-related peptide (PTHrP) is expressed in various cells such as cardiac vascular smooth muscle cells, coronary endothelial cells and cardiomyocytes and acts as an autocrine/paracrine substance. We compared PTHrP levels in 35 consecutive patients with severe CHF (33 male, mean age 66.2 +/- 8.9 years) with 26 normal controls (24 male, mean age 63.1 +/- 8.6 years). PTHrP levels were reduced in severe CHF patients (11.10 +/- 1.37 fmol/ml) compared with the controls (20.62 +/- 3.30 fmol/ml, p = 0.005). PTHrP values decreased as a function of New York Heart Association classification. These results suggest that PTHrP levels decrease in proportion to the severity of heart failure and could potentially be used to monitor progression of disease non-invasively.
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PMID:Parathyroid hormone-related protein is reduced in severe chronic heart failure. 1650 Jul 29

We report a 61-year-old woman who was admitted to our hospital in August 2004 with severe hypercalcemia and osteoporosis. Although she was found to have hypercalcemia five years earlier, she has never been treated. The patient was transferred to our hospital for further management of a recently-identified left neck mass. Serum calcium level was 15.0 mg/dL and intact parathyroid hormone (PTH) 3,321 pg/mL. (99m)Tc-methoxyisobutylisonitrile (MIBI) scintigraphy showed marked accumulation in the left neck. We diagnosed the tumor as parathyroid gland tumor and it was enucleated surgically. Although serum Ca level returned to normal after surgery, the patient suffered multiple rib fractures, complicated with marked paradoxical breathing. Internal fixation of the thorax was necessary due to deterioration of the heart failure. Progression of severe osteoporosis was associated with multiple fractures of the ribs and other serious complications including congestive heart failure occurred after surgery, reflecting the extreme difficulty in treating this patient.
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PMID:[Primary hyperparathyroidism complicated with flail chest due to severe osteoporosis]. 1658 22

The increasing prevalence of chronic kidney disease (CKD) in the United States demands a closer evaluation of and attention to associated morbidities, and, particularly, the rising mortality related to cardiovascular disease in all age groups. Patients with CKD demonstrate an increased risk of coronary artery disease due to calcium deposition and subsequent arterial stiffening, in addition to left ventricular dysfunction with associated heart failure and arrhythmias. While clearly impacted by the traditional risk factors for development of cardiovascular disease (CVD), patients with CKD are also affected by non-traditional risk factors, including calcium overloading related to aggressive management of secondary hyperparathyroidism. Recent data have shown that a substantial number of patients with CKD are deficient in vitamin D on a nutritional basis, in addition to the known decrease in the kidney-produced active metabolite during progressive CKD. Historically, vitamin D has been described as an endocrine hormone that regulates blood calcium and parathyroid hormone levels. It has become increasingly clear, through the recognition of a vitamin D receptor in most tissues, that vitamin D possesses functions well beyond calcium homeostasis, such that a deficiency may contribute to the development of CVD. In this brief review, the role of vitamin D activation through its vitamin D receptor will serve as an introduction to the magnitude of the nutritional deficits in children, adults, and those with CKD. As therapeutic entities in the management of renal osteodystrophy, vitamin D analogues play an important role in cardiovascular health that continues to evolve. Preliminary studies indicate that vitamin D therapy for control of secondary hyperparathyroidism may confer cardioprotection and reduce mortality. Attention to care of osteodystrophy in CKD must take into account heart health as well.
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PMID:Renal osteodystrophy in children: a systemic disease associated with cardiovascular manifestations. 1662 9

Heart failure is thought to be more common and of greater severity in African-Americans (AAs). Potential mechanisms remain uncertain. The importance of micronutrient deficiencies in the pathophysiologic expression of congestive heart failure (CHF) in AAs remains to be explored, including hypovitaminosis D, which can promote secondary hyperparathyroidism (SHPT), together with hypozincemia and hyposelenemia, the 2 most crucial trace minerals integral to diverse biologic functions. Serum parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), Zn, and Se were monitored in 30 AAs hospitalized during June through December 2005, with decompensated failure and reduced ejection fraction (EF) (<35%) of predominantly nonischemic origin treated with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB), furosemide, and spironolactone. Based on their symptomatic status before hospitalization, 15 patients were stratified as having protracted (>or=4 weeks) CHF, whereas 15 patients had short-term (1-2 weeks) CHF. These hospitalized patients were compared with 10 AA outpatients with stable, similarly treated compensated failure and comparable EF, and 9 AA normal volunteers without cardiovascular disease. Serum PTH was elevated in all patients with protracted CHF and in 60% of patients with short-term CHF, but not in compensated patients or normal volunteers. However, serum 25(OH)D was reduced in all patients with >or=4 weeks and 80% with either 1-2 weeks CHF or compensated failure compared with volunteers. Serum Zn was below normal in 11 of 15 patients with protracted CHF, in 8 of 15 patients with shorter duration CHF, and in 5 of 10 patients with compensated failure. Serum Se was reduced in all patients with >or=4 weeks, 60% with short-term CHF, and 90% of compensated patients. Concomitant to hypovitaminosis D, hypozincemia, and hyposelenemia, SHPT is a covariant of CHF in housebound AAs.
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PMID:Micronutrients in African-Americans with decompensated and compensated heart failure. 1716 51

Chromogranin A (CgA), one component of the granin family, represents the major soluble protein co-stored and co-released with catecholamines, within chromaffin cells secretory granules. It is considered a diagnostic and prognostic marker of several diseases, including a variety of tumours and cardiac heart failure. It also represents a precursor of biologically active fragments, generated after proteolytic cleavage at the level of the multiple pairs of dibasic sites which enrich its sequence. CgA, and its derived fragments show an old evolutionary history being ubiquitously present throughout the animal word, from mammals to invertebrates. Their biological functions include control of hormone production, and several paracrine and autocrine actions mainly attributed to its derived peptides. Two N-terminal fragments, named vasostatins 1 (VS-1: CgA(1-76)) and vasostatin 2 (VS-2: CgA(1-113)) due to their ability to dilate pre-constricted vessels, exert a large spectrum of homeostatic actions, including antifungal and antimicrobial effect, modulation of cell adhesion, and inhibition of parathyroid hormone secretion. Recently, on isolated heart preparations from eel, frog and rat they were shown to act as negative inotropic agents able to counteract the effects of beta-adrenergic stimulation. This short note introduces the abstracts of the contributions at the "International Workshop on Vasostatins and Chromogranin A-derived peptides" (Island of Capri, Italy; September 2005). The Workshop was focused on recent findings on the role of vasostatins (VSs) in cardiovascular and gastrointestinal systems, extracellular fluids composition, and innate immunity. Particular attention has been given to the still elusive mechanism of action of these peptides.
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PMID:New biological aspects of chromogranin A-derived peptides: focus on vasostatins. 1730 79


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