Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We encountered a patient with pheochromocytoma associated with a catecholamine-induced cardiomyopathy that developed recurrently bilateral and unilateral pulmonary edema. The diagnosis of pheochromocytoma was made by elevated plasma catecholamine levels and the intense tumor [123I]MIBG uptake and was confirmed at the time of surgery. The patient showed reduced myocardial [123I]MIBG uptake with left ventricular dysfunction, and endomyocardial biopsy findings were consistent with the diagnosis of catecholamine-induced cardiomyopathy. After tumor resection, plasma levels of catecholamine were normalized, and pulmonary edema never recurred, although cardiac dysfunction did not show an improvement on echocardiography. Myocardial and lung [123I]MIBG uptake increased when compared to uptake levels on preoperative scans, but myocardial uptake was still below normal. These findings indicated that over-secreted catecholamines influenced both the heart and lungs. Pheochromocytoma can induce cardiac and lung injuries, and [123I]MIBG scanning may contribute not only to tumor characterization but also to assessing and monitoring the influence of catecholamines on the heart and lungs.
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PMID:Iodine-123-MIBG imaging in pheochromocytoma with cardiomyopathy and pulmonary edema. 870 74

The clinical signs and pathology in an outbreak of toxicity in feedlot cattle attributed to the ingestion of toxic levels of the ionophore antibiotic salinomycin over an extended period of 11 weeks are described. Thirty-nine out of 380 cattle developed signs consistent with cardiac failure and 8 of these died. Clinical signs included dyspnoea, tachypnoea, tachycardia and exercise intolerance. Two cattle were necropsied and in one there were macroscopic lesions suggestive of congestive heart failure, namely pulmonary oedema, hydrothorax and hepatomegaly. Histopathology revealed a chronic cardiomyopathy characterised principally by extensive myocardial fibre atrophy with multifocal hypertrophy and interstitial and replacement fibrosis. Hepatic and pulmonary lesions were consistent with those of congestive cardiac failure. The myocardial lesions in this outbreak were similar to those encountered in cases of a chronic toxicity associated with the ingestion of litter derived from poultry rations containing ionophores (ionophore-associated poultry litter toxicity). Hence, the clinical and pathological findings in this outbreak indicate that in cattle, the prolonged ingestion of ionophores over several weeks may result in the development of chronic myocardial lesions comparable to those of IAPLT but significantly different from those encountered in the more traditional acute outbreaks of ionophore toxicity as described in the literature.
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PMID:A chronic cardiomyopathy in feedlot cattle attributed to toxic levels of salinomycin in the feed. 878 18

The direct toxic effect of alcohol and its metabolite acetaldehyde has been demonstrated both in laboratory animals and in humans. Alterations in the mitochondrial ultrastructure and the dilatation of the sarcoplasmatic reticulum have been shown after an acute infusion of alcohol in the heart. These changes correlate with decreased mitochondrial function, defects in protein synthesis and the occurrence of arrhythmias. The risk of developing alcoholic cardiomyopathy is related to both the mean daily alcohol intake and the duration of drinking, but there is much individual susceptibility to the toxic effect of alcohol. Most patients, in whom alcoholic cardiomyopathy develops, have been drinking over 80 g/d for more than 5 years. The clinical diagnosis of alcoholic cardiomyopathy reflects the coexistence of global myocardial dysfunction in a heavy drinker in whom no other cause for myocardial disease was found. In studies focussing on alcoholic cardiomyopathy the surprising histologic findings in endomyocardial biopsy in about 30% of all cases was myocarditis with a lymphocytic infiltrate in association with myocyte degeneration or focal necrosis. In myocarditis, the network of microtubules and intermediate filaments is also disrupted by the inflammatory reaction which involves resident cells (myocytes, fibroblasts, endothel cells) and systemic cells (granulocytes, macrophages, monocytes, lymphocytes). Changes in the cardiac cytoskeleton and the extracellular matrix may affect contractile function, since the cytoskeleton organizes the intra- and intercellular architecture. After all, in patients with alcohol abuse and myocarditis the immune functioning appears to be compromised. Several studies suggest that heavy drinking alters both lymphocyte and granulocyte production and function. Alcohol consumption per se might harm the immune system. Furthermore, the myocardial damage due to alcohol consumption could initiate autoreactive mechanisms comparable to those in viral or idiopathic myocarditis. Patients with alcohol abuse and myocarditis have a poor prognosis: signs of biventricular failure including tachycardia, hepatomegaly, and peripheral and lung edema are observed. These symptoms are as nonspecific as are various echocardiographic and electrocardiographic changes such as atrial and ventricular arrhythmias which may be associated both with myocarditis, alcoholic cardiomyopathy and acute effects of drinking without hemodynamic alterations. For the management of patients with alcohol abuse the prevention of further alcohol intake is mandatory to reverse the myocardial damage and the unfavorable predisposition for infection. Specific treatment of myocarditis is the second important option, and treatment of heart failure by reducing the size of the dilated heart and alleviating the signs and symptoms of heart failure is a logical third step.
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PMID:[Alcohol and myocarditis]. 880 5

Severe congestive heart failure and cardiogenic shock don't resemble a homogeneous clinical picture, but a syndrome that is based on very different etiologies. What all the etiologies have in common is the inadequate peripheral O2-supply to essential organs with or without signs of severe pulmonary congestion up to pulmonary edema. For prognosis and therapy is a fast diagnostical clarification of the causes crucial. The therapeutical procedure for the various etiologies may be diametrically opposed. For the therapy is it also dicisive to distinguish between acute myocardial failure, e.g. acute myocardial infarction, and the development of myocardial failure from a longer existing consistent congestive heart failure (cardiomyopathy). Whenever possible, next to symptomatically therapy of cardiogenic shock the basic conditions of the disease should be cured (e.g., PTCA, lysis with acute myocardial infarction, lysis in acute pulmonary embolism). In myogenic cardiogenic shock the use of positive-inotropic substances with and without simultaneous vasodilatory effects, if necessary in combination with other vasodilators, may be life-saving. Up until now there still doesn't exist an alternative to the catecholamines in the acute phase, initially they should be used as a first-line-therapy to stabilize the hemodynamics. The insertion of a Swan-Ganz-catheter for invasive therapy-monitoring, especially for the regulation of the therapy is a "condition sine qua non" for every patient with unstable hemodynamics. Because of the prompt beta-receptor-down-regulation during shock, caused by endogenous catecholamines, successful therapy with exogenous catecholamines is limited (adrenaline, dopamine, dobutamine), on account of the acceleration and intensification of the beta-receptor-down-regulation process. Possible beta-receptor independent alternatives are beta 2-agonists (dopexamine), PDE-III-inhibitors (amrinone, milrinone, enoximone) as well as H2-receptor agonists (impromidine, arpromidine) and finally the calcium-sensitisers (pimobendane). First results give rise to optimism to effectively reduce the mortality of congestive heart failure. The combination of these new pharmacological possibilities with interventional transcutaneous applicable assist-systems (aortic counterpulsationpump IABP, hemopump, transcutaneous heart-lung-machine) as well as the transitory application of an artificial heart (Novacor) can possibly increase the success of these therapeutic strategies. So far there are no convincing results shown in the world literature.
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PMID:[Pharmacotherapy of severe heart failure with inodilators--new approaches]. 902 10

An American Cocker Spaniel with low plasma taurine concentration (< 2 nmol/mL) was presented with dyspnoea associated with pulmonary oedema and a left ventricular shortening fraction of 9%. Emergency therapy with furosemide, dobutamine, nitroglycerine and oxygen supplementation led to a good response. Chronic therapy was started with enalapril, furosemide, digoxin and taurine. Improvement in all echocardiographic indices were noted over a 22 week follow-up, most notably an increase in left ventricular shortening fraction to 20%, a decrease of E-point septal separation from 14 mm to 7 mm and marked left ventricular remodelling. This degree of improvement in myocardial function may represent a direct link between dilated cardiomyopathy in the American Cocker Spaniel and plasma taurine deficiency. Alternatively, this response may reflect a breed-related cardiomyopathy with a natural history and therapeutic response not commonly seen in the more common large breed cardiomyopathy presentations.
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PMID:Dilated cardiomyopathy in an American cocker spaniel with taurine deficiency. 946 19

The current interest in understanding the role of stress-induced cytokines in heart failure relates to the observation that many of the untoward pathophysiologic responses of the failing circulation might be explained by these compounds. These small molecules appear to cause left ventricular dysfunction, precipitate pulmonary edema, cause cardiomyopathy, reduce peripheral organ perfusion, induce ventricular remodeling, activate the fetal gene program in animal models, and cause anorexia and cachexia. Thus, the elaboration of cytokines, similar to the upregulation of neurohormones, may represent a biochemical mechanism that is responsible for producing symptoms and remodeling in heart failure patients. To better understand how cytokines play a role in heart failure, it is important to delineate the concept of cytokine bioactivity in this setting.
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PMID:Cytokines and heart failure. 1042 71

We report a patient with primary aldosteronism (PA) complicated with hypertrophic nonobstructive cardiomyopathy (HNCM) who underwent resection of a left adrenal tumor. Amrinone was administered to improve the features of congestive heart failure induced by retention of body fluid. Maintaining adequate preload and afterload and preventing excessive increases in contractility are important in the anesthetic management of patients with hypertrophic obstructive cardiomyopathy (HOCM). Although the preoperative diagnosis may be HNCM, stenosis of the left ventricular outflow tract may occur due to hemodynamic changes during surgery. Therefore amrinone is not often used for patients with HNCM. We inserted a pulmonary arterial catheter (Swan-Ganz CCO Thermodilution Catheter) and measured the cardiac output continuously to monitor hemodynamic changes. The symptoms of pulmonary edema were diminished one month after the surgery. These findings suggest that the increased blood volume induced by PA is a main factor aggravating preoperative congestive heart failure with HNCM.
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PMID:[General anesthesia for a patient with primary aldosteronism complicated with hypertrophic nonobstructive cardiomyopathy]. 1058 55

With the advent of smaller biphasic transvenous implantable cardioverter defibrillators (ICDs) and the experience gained over the years, it is now feasible for electrophysiologists to implant them safely in the abdominal or pectoral area without surgical assistance. Throughout the years, general anesthesia has been used as the standard technique of anesthesia for these procedures. However, use of local anesthesia combined with deep sedation only for defibrillation threshold (DFT) testing might further facilitate and simplify these procedures. The purpose of this study was to test the feasibility of using local anesthesia and compare it with the standard technique of general anesthesia, during implantation of transvenous ICDs performed by an electrophysiologist in the electrophysiology laboratory. For over 4 years in the electrophysiology laboratory, we have implanted transvenous ICDs in 90 consecutive patients (84 men and 6 women, aged 58 +/- 15 years). Early on, general anesthesia was used (n = 40, group I), but in recent series (n = 50, group II) local anesthesia was combined with deep sedation for DFT testing. Patients had coronary (n = 58) or valvular (n = 4) disease, cardiomyopathy (n = 25) or no organic disease (n = 3), a mean left ventricular ejection fraction of 35%, and presented with ventricular tachycardia (n = 72) or fibrillation (n = 16), or syncope (n = 2). One-lead ICD systems were used in 74 patients, two-lead systems in 10 patients, and an AVICD in 6 patients. ICDs were implanted in abdominal (n = 17, all in group I) or more recently in pectoral (n = 73) pockets. The DFT averaged 9.7 +/- 3.6 J and 10.2 +/- 3.6 J in the two groups, respectively (P = NS) and there were no differences in pace-sense thresholds. The total procedural duration was shorter (2.1 +/- 0.5 hours) in group II (all pectoral implants) compared with 23 pectoral implants of group I (2.9 +/- 0.5 hours) (P < 0.0001). Biphasic devices were used in all patients and active shell devices in 67 patients; no patient needed a subcutaneous patch. There were six complications (7%), four in group I and two in group II: one pulmonary edema and one respiratory insufficiency that delayed extubation for 3 hours in a patient with prior lung resection, both probably related to general anesthesia, one lead insulation break that required reoperation on day 3, two pocket hematomas, and one pneumothorax. There was one postoperative arrhythmic death at 48 hours in group I. No infections occurred. Patients were discharged at a mean time of 3 days. All devices functioned well at predischarge testing. Thus, it is feasible to use local anesthesia for current ICD implants to expedite the procedure and avoid general anesthesia related cost and possible complications.
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PMID:Electrophysiologist-implanted transvenous cardioverter defibrillators using local versus general anesthesia. 1066 58

The prevalence of cardiomyopathy in Irish wolfhounds was evaluated by retrospective review of the results of cardiovascular examinations carried out in 500 dogs presented for veterinary services at the author's practice. Abnormalities were found in 209 (41.8%) of the dogs examined. Dilated cardiomyopathy (DCM) was diagnosed in 121 (24.2%) of the dogs and was accompanied by atrial fibrillation in 106 dogs. Seventeen dogs were suffering from advanced congestive heart failure (CHF), and 55 dogs were suffering from mild to moderate CHF as a result of DCM. Congestive heart failure was most commonly characterized by mild to severe pleural effusion due to right-sided heart failure in addition to pulmonary edema. Rhythm disturbances without evidence of DCM were detected in 48 dogs. Forty dogs had echocardiographic abnormalities without signs of DCM. Soft to moderate mitral regurgitations were diagnosed in 13 (2.6%) of these 40 dogs examined. In 39 dogs that died as a result of DCM, the median survival time from the time of diagnosis was 5.1 months, and in 59 dogs with DCM that are still alive, the median survival time is 15.7 months.
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PMID:The prevalence of cardiomyopathy in the Irish wolfhound: a clinical study of 500 dogs. 1073 Jun 22

From 1994 to 1999, 16 captive African hedgehogs (Atelerix albiventris), from among 42 necropsy cases, were diagnosed with cardiomyopathy. The incidence of cardiomyopathy in this study population was 38%. Fourteen of 16 hedgehogs with cardiomyopathy were males and all hedgehogs were adult (>1 year old). Nine hedgehogs exhibited 1 or more of the following clinical signs before death: heart murmur, lethargy, icterus, moist rales, anorexia, dyspnea, dehydration, and weight loss. The remaining 7 hedgehogs died without premonitory clinical signs. Gross findings were cardiomegaly (6 cases), hepatomegaly (5 cases), pulmonary edema (5 cases), pulmonary congestion (4 cases), hydrothorax (3 cases), pulmonary infarct (1 case), renal infarcts (1 case), ascites (1 case), and 5 cases showed no changes. Histologic lesions were found mainly within the left ventricular myocardium and consisted primarily of myodegeneration, myonecrosis, atrophy, hypertrophy, and disarray of myofibers. All hedgehogs with cardiomyopathy had myocardial fibrosis, myocardial edema, or both. Other common histopathologic findings were acute and chronic passive congestion of the lungs, acute passive congestion of the liver, renal tubular necrosis, vascular thrombosis, splenic extramedullary hematopoiesis, and hepatic lipidosis. This is the first report of cardiomyopathy in African hedgehogs.
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PMID:Cardiomyopathy in captive African hedgehogs (Atelerix albiventris). 1102 39


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