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

The purpose of this study is to review the role of dopamine in hypertension and associated conditions. The analysis of literature indicates that present knowledge is mostly based on poor markers and indirect evidence of dopaminergic activity and only few molecular biological data. Alternative markers such as plasma dopamine sulfate emerge as a possible substitute for the low plasma free dopamine detectability, one of the main obstacles in understanding the relationship between circulating dopamine and its receptor actions in hypertension. Essential hypertension represents a heterogeneous entity: based on evidence in borderline and non-modulating hypertension, the tubular dopamine receptor defect may be compensated by increased dopamine synthesis (dopamine beta-hydroxylase suppression-mediated?) and release; alternatively, compatible with data in stable, salt-sensitive and low renin-hypertension, the receptor defect may be amplified by a deficient dopamine synthesis, basal and in response to salt and volume expansion. Secondary forms of hypertension (renovascular, renal, polycystic kidneys, mineralocorticoid, pheochromocytoma) associated conditions (renal and heart failure, diabetes, hypovolaemia, mastocytosis) or iatrogenic (cocaine abuse) are mostly reflected by increased dopamine indices, some of them proposed to be counteracting the activation of prohypertensive mechanisms. In conclusion dopamine should thus be monitored in hypertension while respecting several associated conditions affecting peripheral dopaminergic activity. Catecholamine synthesis and metabolism enzymes' and dopamine receptors' targeting are essential for advancing the understanding of dopamine's diagnostic and therapeutic implications.
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PMID:Peripheral dopamine in hypertension and associated conditions. 1048 70

Pheochromocytomas are rare neoplasias of the adrenal medulla which generally present with paroxysmal or sustained hypertension. Cardiogenic pulmonary edema is a common feature of these tumors, but few cases have been described with noncardiogenic pulmonary edema. We report a pheochromocytoma with the principle manifestation of noncardiogenic pulmonary edema and characterize a genetic lesion associated with the disorder. A 30-year-old man was admitted with abdominal pain and breathlessness. x-Ray examination of the chest revealed a massive, diffuse infiltration of the left lung without cardiomegaly. No paroxysmal blood pressure fluctuations or heart failure were evident during the entire course, and the infiltrate and dyspnea resolved in three days without inotropic or diuretic agents. Serum norepinephrine and epinephrine levels were elevated twenty and fifty times above normal, respectively. The patient was ultimately diagnosed with multiple endocrine neoplasia type 2A (MEN 2A). Mutations in the RET proto-oncogene have been described recently in patients with MEN 2A. Mutation analysis of selected RET exonic sequences identified a germline mutation at codon 634 in exon 11 of the RET proto-oncogene. The mutation introduces a transition encoding a non-conservative substitution from TGC (Cys) to CGC (Arg) and creates a novel restriction site recognized by HhaI. We further screened for this mutation among four of the proband's relatives by HhaI restriction analysis. One asymptomatic family member was identified who subsequently elected prophylactic total thyroid removal. Histological examination of this specimen confirmed the presence of medullary thyroid carcinoma.
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PMID:Noncardiogenic pulmonary edema as the chief manifestation of a pheochromocytoma: a case report of MEN 2A with pedigree analysis of the RET proto-oncogene. 1052 79

Heart failure is characterized by the inability of the myocardium to shorten sufficiently or to eject an adequate stroke volume to maintain normal perfusion of both the cardiac and the extracardiac organs. Irrespective of etiologic reasons, the depression of myocardial contractility represents one of the major mechanisms that contributes to low output in heart failure. Despite their intrinsic negative inotropic effects, beta-receptor-blocking agents have been used in numerous studies for treating the failing heart, especially in dilated cardiomyopathy and ischemic heart disease. In this regard, specific therapeutic aims of the use of beta-receptor-blocking agents in chronic heart failure have been described. e.g., reduction of an increased heart rate in tachycardia, blood pressure reduction in hypertensive heart failure, improvement of supraventricular and ventricular arrhythmias, depression of an increased sympathetic tone (e.g., in hyperthyrioidism, pheochromocytoma), increase in the amount of downregulated beta-receptors, and anti-ischemic effects in coronary artery disease. For chronic heart failure, therefore, some special indications may be established and may be individually used; for acute heart failure, only very rare indications are present (e.g., hypertensive crisis, life-threatening cardiac arrhythmias). The actual rationale for the use of beta-receptor blocking agents in heart failure is therefore analyzed with regard to pathophysiology, clinical effects, and clinical outcome of treated patients.
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PMID:Beta-blocking agents in heart failure: modern concepts and overview. 1152 16

Adrenomedullin (AM), identified from pheochromocytoma and having 52 amino acids, elicits a long-lasting vasodilatation and diuresis. AM is mainly mediated by the intracellular adenylate cyclase coupled with cyclic adenosine monophosphate (cAMP) and nitric oxide (NO) -cyclic guanosine monophosphate (cGMP) pathway through its specific receptor. The calcitonin receptor-like receptor (CLCR) and receptor-activity modifying protein (RAMP) 2 or RAMP3 models have been proposed as the candidate receptor. AM is produced mainly in cardiovascular tissues in response to stimuli such as shear stress and stretch, hormonal factors and cytokines. Recently established AM knockout mice lines revealed that AM is essential for development of vitelline vessels of embryo. Plasma AM levels elevate in cardiovascular diseases such as heart failure, hypertension and septic shock, where AM may play protective roles through its characteristic biological activities. Human AM gene delivery improves hypertension, renal function, cardiac hypertrophy and nephrosclerosis in the hypertensive rats. AM decreases cardiac preload and afterload and improves cardiac contractility and diuresis in patients with heart failure and hypertension. Advances in gene engineering and receptor studies may contribute to further understandings of biological implication and therapeutic availability of AM.
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PMID:A review of the biological properties and clinical implications of adrenomedullin and proadrenomedullin N-terminal 20 peptide (PAMP), hypotensive and vasodilating peptides. 1175 55

Pheochromocytoma is a rare catecholamine secreting tumor that accounts for about 0.04% of cases of hypertension. Other less common cardiovascular manifestations such as arrhythmias, angina pectoris, acute myocardial infarction, dilated cardiomyopathy, acute heart failure, and cardiogenic shock have occasionally been reported. We describe the case of a 32-year-old previously healthy male patient who died of cardiogenic shock within 10 hours of admission. Postmortem examination showed a catecholamine cardiomyopathy and a pheochromocytoma of the right adrenal gland. Pheochromocytoma with predominant epinephrine or dopamine secretion may take a hypotensive course. Sudden excessive catecholamine release can, as in the described case, cause cardiogenic shock.
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PMID:A rare cause of cardiogenic shock: catecholamine cardiomyopathy of pheochromocytoma. 1211 3

Adrenomedullin (ADM) release is enhanced in pheochromocytoma, chronic heart failure (HF), hypertension and renal diseases. This study was designed to test the hypothesis that ADM secretion increases also in response to acute stimuli, such as static effort and to compare plasma ADM response to this stimulus in patients with chronic HF and healthy persons. Eight male HF patients (II/III class NYHA) and eight healthy subjects (C) performed two 3-min bouts of static handgrip at 30% of maximal voluntary contraction, alternately with each hand without any break between the bouts. At the end of both exercise bouts and in 5 min of the recovery period, plasma ADM and catecholamines were determined. In addition, heart rate, blood pressure, and stroke volume (SV) were measured. The baseline plasma ADM and noradrenaline levels were higher, whilst plasma adrenaline and SV were lower in HF patients than in C group. The 1st exercise bout caused an increase in plasma ADM from 3.32 +/- 0.57 to 4.98 +/- 0.59 pmol l(-1) (p<0.01) in C and from 6.88 +/- 0.58 to 7.80 +/- 0.43 pmol x l(-1) (p<0.02) in HF patients. The 2nd exercise bout did not produce further elevation in plasma ADM and during recovery the hormone concentration declined to pre-exercise or lower values. There were no differences between groups in exercise-induced increases in plasma ADM. Plasma ADM correlated with SV (r = -0.419) and with noradrenaline concentrations (r = 0.427). It is concluded that static exercise causes the short-lasting increase in plasma ADM concentration which is similar in healthy subjects and in patients with mild heart failure.
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PMID:Effect of static handgrip on plasma adrenomedullin concentration in patients with heart failure and in healthy subjects. 1212 Aug 96

In this case report, we present the successful therapy of severe cardiac failure in pituitary adrenal insufficiency. A previously healthy 56-year-old-man in pituitary coma due to an atypical variant of multiple endocrine adenomatosis (pituitary adenoma and pheochromocytoma) suffered from cardiac failure resistant to catecholamine and standard hydrocortisone therapy. After two bolus injections of dexamethasone (2 x 24 mg) mean arterial pressure and cardiac function dramatically improved, probably due to restoration of permissive effects on catecholamine action and reversal of pathophysiological mechanisms of cardiac failure. We conclude that in patients with severe cardiovascular failure in pituitary coma the administration of potent glucocorticoids may be more effective in reversing cardiovascular failure than standard dosages of hydrocortisone.
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PMID:Cardiac failure and multiple organ dysfunction syndrome in a patient with endocrine adenomatosis. 1236 15

Although systemic hypertension is a common clinical disorder, hypertensive emergencies are unusual in clinical practice. Situations that qualify as hypertensive emergencies include accelerated or malignant hypertension, hypertensive encephalopathy, acute left ventricular failure, acute aortic dissection, pheochromocytoma crisis, interaction between tyramine-containing foods or drugs and monoamine oxidase inhibitors, eclampsia, drug-induced hypertension and possibly intracranial hemorrhage. It is important to recognize these conditions since immediate lowering of systemic blood pressure is indicated. The diagnosis of hypertensive emergencies depends on the clinical manifestations rather than on the absolute level of the blood pressure. Depending on the target organ that is affected, the manifestations of hypertensive emergencies can be quite expressive, yet variable. Thus, the physician has to make the clinical diagnosis urgently in order to render appropriate therapy. Several parenteral drugs can quickly and effectively lower the blood pressure in hypertensive emergencies. Intravenous fenoldopam, a selective dopamine (DA1) receptor agonist, offers the advantage of improving renal blood flow and causing natriuresis. Intravenous nicardipine may be beneficial in reserving tissue perfusion in patients with ischemic disorders. Whereas trimethaphan camsilate is the drug of choice for managing acute aortic dissection, hydralazine remains the drug of choice for the treatment of eclampsia. The alpha-adrenoceptor, phentolamine, is useful in patients with pheochromocytoma crisis. Enalaprilat is the only ACE inhibitor available for parenteral use and may be particularly useful in treating hypertensive emergencies in patients with heart failure. However, ACE inhibitors may cause a precipitous fall in blood pressure in patients who are hypovolemic. Although useful as adjunctive therapy in hypertensive crises, diuretics should be used with caution in these patients because prior volume depletion may be present in some conditions such as malignant hypertension. The treating physician should be familiar with the pharmacological and clinical actions of drugs which are indicated for and useful in the treatment of hypertensive emergencies. Once the patient's situation has stabilized, the patient may be switched to an oral medication and the physician should discuss long term follow up plans. With appropriate clinical diagnosis, hypertensive emergencies can be successfully treated and the complications can be prevented with timely intervention.
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PMID:Hypertensive emergencies. Etiology and management. 1472 43

Adrenomedullin (ADM) is a 52-amino acid peptide with structural homology to calcitonin gene-related peptide (CGRP) initially isolated from human pheochromocytoma. ADM is synthesized by many mammalian tissues including the adrenal medulla, endothelial and vascular smooth muscle cells, myocardium and central nervous system. ADM binds to plasma membrane receptors composed of calcitonin receptor-like receptor (CRLR), a member of serpentine receptor superfamily, and receptor activity modifying protein (RAMP) type 2 or 3. ADM has also some affinity for CGR(1) receptor composed of CRLR and RAMP1. ADM dilates blood vessels in both endothelium-dependent and independent manner and decreases systemic arterial pressure. Intrarenally administered ADM increases natriuresis by vascular and tubular mechanisms. In addition, ADM inhibits migration and proliferation of vascular smooth muscle cells and attenuates myocardial remodelling by inhibiting protein synthesis in cardiomyocytes and proliferation of cardiac fibroblasts. ADM is expressed in various tissues from early stage of embryogenesis and is also synthesized in placenta, uterus and fetal membranes. Plasma ADM level is increased in arterial hypertension, acute coronary syndromes, heart failure, renal diseases and septic shock, being involved in the pathophysiology of these disorders. Experimental ADM treatment is beneficial in arterial and pulmonary hypertension, heart failure, septic shock and ischemia/reperfusion injury. Proadrenomedullin N-terminal peptide (PAMP) is another product of ADM gene which is co-secreted by ADM-producing tissues, with some effects similar and some opposite to ADM.
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PMID:Adrenomedullin--what do we know 10 years since its discovery? 1504 74

Pheochromocytoma is a rare neuroendocrine tumor that secretes high levels of catecholamines and usually causes paroxysmal or sustained hypertension. Various forms of myocardial damage have also been reported, including cardiomyopathy, myocardial infarction, arrhythmias, and angina. When patients present with severe unexplained heart failure, exploring all causes for the source of cardiomyopathy is essential, especially if the cause is reversible. The authors describe the case of a young man who presented to the hospital with acute heart failure who was later diagnosed with a pheochromocytoma.
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PMID:Pheochromocytoma presenting as heart failure. 1603 Apr 12


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