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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular performance was studied in three patients with heart failure due to amyloid deposits. The diagnosis of amyloidosis was proved by cardiac biopsy in two patients and by rectal biopsy in the third. One patient had myelomatosis, but the other two had no other identifiable disease. The investigative technique allowed simultaneous measurements of pressure and volume in the left ventricle. The functional defect with slow cardiac filling at high pressure and greatly reduced left ventricular contraction differed from that of constrictive pericarditis and other heart muscle disease. These features of a "stiff heart" are probably unique to amyloidosis and should make possible positive recognition of the condition on the basis of echocardiographic, angiographic and hemodynamic findings.
Am J Cardiol 1975 Oct 06
PMID:The functional defect in amyloid heart disease. The "stiff heart" syndrome. 119 48

Four monoclonal antibodies for a calcium-dependent protease inhibitor protein were produced by fusing Sp2/0 myeloma cells with spleen cells from a Balb/C mouse immunized with purified bovine heart inhibitor. Each of the monoclonal antibodies was highly specific for the inhibitory protein as revealed by electro-blot analysis. The antibodies recognized different antigenic sites on CNBr peptides prepared from the purified inhibitor protein. Immunofluorescent microscopy of sections from bovine heart ventricles treated with each of the antibodies demonstrated the same fluorescent pattern. Fluorescence was observed at or near the sarcolemma of the myocytes, and along the Z-discs of relaxed myofibrils within the myocytes. Contracted myofibrils did not appear to bind antibody. Immunostaining of glycerinated relaxed cardiac myofibrils revealed staining at the Z-discs. One of the antibodies could also stain the Z-disc region of bovine skeletal muscle myofibrils.
J Mol Cell Cardiol 1985 Sep
PMID:Subcellular localization of bovine heart calcium-dependent protease inhibitor. 390 Apr 27

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.
Cardiol Clin 1984 Nov
PMID:Cardiac effects of noncardiac neoplasms. 640 9

The authors report 11 cases cardiac amyloidosis discovered on autopsy. The routine examination of the artrial of 20 patients over the age of 60 revealed the presence of these deposits in 10 per cent of cases. Three cases of secondary amyloidosis were discovered with minimal cardiac involvement. There was one case of senile amyloidosis and five cases of primary amyloidosis, two of which were associated with multiple myeloma. The clinical manifestations of these last six cases were cardiac decompensation (congestive in one case) and angina with normal coronary arteries, but involvement of the small vessels. Two cases of anterior pseudo-sequelae are reported and there were 4 cases of disturbances of intraventricular conduction and one case of atrial fibrillation. Amyloid deposits are rarely localized to the heart alone. Associated immunological disorders were present in 3 of the 6 cases. The authors compare this series to a review of the literature.
Ann Cardiol Angeiol (Paris)
PMID:[Cardiac amyloidosis. Report of 11 autopsy cases and review of the literature]. 663 97

A high cardiac output state, with or without congestive heart failure, has recently been recognized in patients with multiple myeloma. This case report deals with a 62-year-old man with multiple myeloma refractory to treatment, a high cardiac output state, and life-threatening pulmonary edema. In addition, a brief review of the literature is presented.
Clin Cardiol 1994 Dec
PMID:High cardiac output state in patients with multiple myeloma: case report and review of the literature. 786 42

The authors report the case of a 36-year-old male who, following investigations for dyspnea, othopnea and peripheral cyanosis, was found to have metastatic intracardiac plasmacytoma. Diagnosis was made initially with transesophageal echocardiography and emergent cardiac surgery was performed. Postoperative transthoracic and transesophageal echocardiograms revealed residual masses in the right and left atrium. The patient was subsequently treated with systemic chemotherapy and was symptom-free within three months of treatment, with rapid decline of paraproteins in the serum and urine. This case of intracardiac metastatic plasmacytoma is deemed unique because cardiac involvement with multiple myeloma has not been studied in detail, largely due to the rarity of such a presentation.
Can J Cardiol 1994 Oct
PMID:An unusual case of metastatic intracardiac plasmacytoma. 795 22

We report the case of an adult West Indian patient who presented with heart failure 20 years after an initial diagnosis of pulmonary sarcoidosis. Endomyocardial biopsy revealed AL type amyloid which was later found to be secondary to an underlying multiple myeloma.
Int J Cardiol 1993 Sep
PMID:Sarcoid, amyloid and heart failure. 828 46

Cardiac injury is a frequent characteristic in primary, senile and myeloma related amyloidosis, but it is unusual in secondary amyloidosis. We report a patient with complete atrioventricular block and polymorphic ventricular tachycardia as the initial manifestation of secondary amyloidosis. Necropsy demonstrated amyloidosis deposits in the specific conduction system.
Rev Esp Cardiol 1999 Dec
PMID:[A complete atrioventricular block and polymorphic ventricular tachycardia as the initial manifestation of secondary amyloidosis]. 1065 64

We present the case of a 43-year-old male who was initially evaluated for angina pectoris and dyspnea. His CK, CK-MB, and cTnI were all elevated following a blood transfusion and he underwent coronary arteriography, which demonstrated no luminal obstructions. After several months, he was transferred to Mayo Clinic where diagnoses of fulminant cardiac amyloidosis and systemic multiple myeloma were established. The cTnI remained elevated despite normalization of the CK and CK-MB. Despite aggressive treatment, the patient died. Postmortem analysis demonstrated amyloid cardiac deposition including involvement of the coronary microvasculature. Electron microscopy revealed myocyte compression injury from amyloid infiltration. We believe this is the first report of elevated troponin I in a patient with cardiac amyloidosis. The electron microscopy in our case confirms cardiac damage as the mechanism for cTnI elevation. This observation strengthens our knowledge about the specificity of cTnI for the detection of cardiac injury.
Clin Cardiol 2002 Jan
PMID:Cardiac amyloidosis presenting with elevations of cardiac troponin I and angina pectoris. 1180 38

Non bacterial thrombotic endocarditis is characterized by the presence of non infected vegetation in aortic or mitral valves associated with systemic arterial emboli. Non-bacterial thrombotic endocarditis is a common complication of neoplastic diseases: adenocarcinoma of the lung, another adenocarcinomas, myeloma, lymphoma, leukemia, carcinoma of the pancreas, breast, cervix, colon and stomach. We report a case of non-bacterial thrombotic endocarditis localized in the aortic and mitral valves and systemic emboli as the first manifestation of adenocarcinoma of the lung.
Arch Cardiol Mex
PMID:[Non-bacterial thrombotic endocarditis as paraneoplastic manifestation of pulmonary adenocarcinoma]. 1261 39


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