Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47-year-old male with histiocytic lymphoma and no previous history of heart disease developed significant fluctuations of blood pressure, electrocardiographic evidence of myocardial ischemia, and life-threatening arrhythmia after the first dose of BACOP (bleomycin, adriamycin, cyclophosphamide, Oncovin, and prednisone) chemotherapy. The presence of pheochromocytoma was suspected, and it was demonstrated by elevated urinary metanephrines, catecholamines, and vanillylmandelic acid, and finally confirmed on autopsy. The possible role of chemotherapeutic agents in stimulating excessive catecholamine release, thus causing transient cardiac injury, is suggested.
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PMID:Acute cardiac toxicity of antineoplastic agents as the first manifestation of pheochromocytoma. 36 Dec 18

A young woman with hypoplastic right heart syndrome developed a carotid body tumor at age 28. High altitude habitation is known to predispose to hyperplastic and neoplastic carotid bodies; emphysema and congenital cyanotic heart disease have recently been shown to induce hyperplasia of this oxytrophic tissue. Therefore, a link between congenital cyanosis and carotid body tumor is suggested by this patient. Carotid bodies are nonchromaffin paraganglionic analogues of the adrenal medulla. Congenital cyanosis has an association with pheochromocytoma. In the cyanotic milieu carotid body tumor may be a histological analogue of pheochromocytoma.
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PMID:Cyanotic heart disease: "low altitude" risk for carotid body tumor? 62 92

Phaeochromocytoma is rare and usually presents as paroxysmal or sustained hypertension; none the less, it can also cause severe acute pulmonary oedema in normotensive individuals. Six patients with phaeochromocytoma presenting in Cornwall and West Devon between 1982 and 1986 are described. Five of them died of pulmonary oedema within 24 hours of the onset of symptoms. At necropsy all five had normal sized hearts and in the four hearts examined by histology there was evidence of catecholamine induced heart disease in the form of focal myocardial necrosis. The sixth patient presented with arterial spasms and pulmonary oedema. Surgical removal of the causative tumour was successful in this patient.
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PMID:Phaeochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure. 233 95

Authors report a case of a patient with abdominal pheochromocytoma who presented recurrent episodes of acute pulmonary edema. No cardiopathy was detected either by clinical examination or by electrocardiogram, echograms or invasive cineventricleangiograma. They concluded that a non cardiogenic etiology is possible for the referred clinical manifestations.
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PMID:[Acute pulmonary edema secondary to pheochromocytoma. A case report]. 259 2

Catecholamine-induced cardiopathy accompanied with pheochromocytoma in a 28-year-old female including two other cases are reported and the relationship between pheochromocytoma and cardiac change was also discussed. In the first case, catecholamine in the tumor tissue showed extremely high values; 94.22 micrograms/g of adrenaline and 6,332.42 micrograms/g of noradrenaline. Histologically, myocardial degeneration and inflammatory cell infiltration between myocardial fibers were noted. In the second case, hypertrophied heart showed focal degeneration of myocardial fibers with a few inflammatory cells in the stroma. The third case showed increase of heart weight, but neither myocardial degeneration nor inflammatory infiltration was noted except for moderate myocardial hypertrophy. Although the cause of difference in degree of myocardial changes is not yet clear, it may be attributed to the blood catecholamine level and/or duration of disease and/or area examined. A relative hypoxia theory is accepted for the mechanism of catecholamine-induced cardiopathy. This theory is supported by more severe lesions being noted near to the cardiac apex corresponding to peripheral coronary circulation.
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PMID:Catecholamine-induced cardiopathy accompanied with pheochromocytoma. 295 67

During the years 1956-1982, 64 pheochromocytoma patients were operated upon without mortality. Twenty-eight patients had sustained hypertension and 29 paroxysmal hypertension only. In two patients high blood pressure was not related to pheochromocytoma and five subjects were normotensive. In two women the pheochromocytoma demonstrated malignancy by widespread metastases. Sixteen patients also had neuroectodermal manifestations other than pheochromocytoma. Preoperatively, heart disease was found in most of the hypertensive patients aged 50 years or more at operation, but was uncommon in the others. In these subjects, heart disease persisted after surgery. Young subjects with sustained hypertension were not less affected by preoperative cerebrovascular accidents than older subjects. After surgery, hypertension persisted in 12 patients, and was easily controlled by drug therapy in eight. Nine patients died 7 months-18 years after surgery. In no case was the death directly associated with the pheochromocytoma disease. Three died from other neuroectodermal abnormalities. The 55 surviving patients have been followed up for a mean of 12 years after surgery. During the observation time the survival of the pheochromocytoma patients was similar to that of the normal population. At the end of the study, 44 out of the 55 surviving patients were free from symptoms.
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PMID:Long-term results in 64 patients operated upon for pheochromocytoma. 336 15

Clinically significant cardiovascular abnormalities may occur as secondary manifestations of noncardiac neoplasms. The principal cardiac effects of noncardiac tumors include the direct results of metastases to the heart or lungs, the indirect effects of circulating tumor products (causing nonbacterial thrombotic endocarditis, myeloma-associated amyloidosis, pheochromocytoma-associated cardiac hypertrophy and myofibrillar degeneration, and carcinoid heart disease), and the undesired cardiotoxicities of chemotherapy and radiotherapy.
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PMID:Cardiac effects of noncardiac neoplasms. 640 9

Sudden onset of pulmonary edema after administration of intravenous propranolol hydrochloride developed in a patient with pheochromocytoma but without clinical or histological evidence of heart disease. Previous cases of pulmonary edema have been reported in association with oral propranolol therapy but have failed to document histological absence of cardiac pathology. The mechanism for the development of pulmonary edema may have been a propranolol-induced beta 1- and beta 2-blockade that led to unopposed alpha effects and sudden elevation of afterload. This case underlines the caution that should be used in the administration of propranolol when the diagnosis of pheochromocytoma is considered.
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PMID:Propranolol-induced pulmonary edema and shock in a patient with pheochromocytoma. 669 55

Pheochromocytoma is a rare neuroendocrine tumor. We report a case of pheochromocytoma-induced cardiomyopathy in an 18-year old white female. A review of the literature indicated that this is the most dramatic reversal of pheochromocytoma cardiomyopathy reported. With aggressive medical management, there was complete recovery of the hemodynamic, echocardiographic, and electrocardiographic abnormalities within 14 days. This case emphasizes the importance of aggressive and appropriate medical therapy in pheochromocytoma heart disease.
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PMID:Acute reversal of pheochromocytoma-induced catecholamine cardiomyopathy. 755 49

Pheochromocytoma is the most frequent cause of adrenal sudden death, which is the unique sign in 1.5% of cases. After a short review of the literature, we report a case of a 36 years old asymptomatic woman, who died suddenly and unexpectedly while receiving preoperative treatment. Gross examination did not allow to reveal any cause of death. Microscopy revealed signs of acute myocardial ischemia, in the lack of any coronary and catecholaminic heart disease. Azan-Mallory trichromic stain was found to be necessary in revealing myocardial lesions. A plausible death pathway is the following: a single catecholaminic peak might have induced myocardic vessel spasm, which in turn could be responsible for a lethal arrhythmia; the dramatic pressure drop can be the effect of pump failure or of a paradoxical disproportionate beta stimulation.
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PMID:[Pheochromocytoma and sudden death: a case of hyperacute myocardial ischemia]. 761 1


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