Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the history of a 60-year-old patient with a multiple myeloma and Staphylococcus aureus associated sepsis to whom adenosine in a dose of 6 mg was administered, when a regular, narrow QRS complex tachycardia at a heart rate of 120 beats/minute started. Adenosine led to a complete AV-block and revealed atrial flutter. Atrial flutter waves persisted for about 15 seconds and were followed by atrial and ventricular asystole for about 20 seconds. Repeated nonsustained polymorphic ventricular tachycardias followed and after about 90 seconds sinus rhythm was restored.
Acta Cardiol 2003 Aug
PMID:Enlarged effects of adenosine in a septic patient with multiple myeloma and atrial flutter. 1294 44

A 48-year-old male patient presented with dyspnea on exertion. Patient was found to have pulmonary hypertension. Myocardial biopsy showed amyloidosis and further work-up revealed Salmon-Durie stage 1A multiple myeloma. Patient had no other clinical manifestations of amyloidosis. It is possible that the pulmonary hypertension is caused by amyloid deposition into pulmonary arteries as the arterial amyloid deposition is common in AL amyloidosis. Treatment with sildenafil led to hemodynamic and symptomatic improvement.
Int J Cardiol 2007 Jan 31
PMID:Pulmonary hypertension as a dominant clinical picture in a case of amyloidosis and smoldering multiple myeloma. 1704 43

The Brugada syndrome is an inherited channelopathy associated with a high propensity of ventricular tachyarrhythmias and sudden cardiac death in individuals with structurally normal hearts. Recent data are indicative of mild structural changes, mainly involving the right ventricle, in patients with Brugada syndrome. We present the case of a patient with cardiac amyloidosis due to multiple myeloma who presented with pre-syncopal episodes and intermittent Brugada-like ECG pattern.
Int J Cardiol 2010 Nov 19
PMID:Cardiac amyloidosis and Brugada-like ECG pattern. 1974 May 56

Amyloidosis is a systemic disease that is a consequence of extracellular deposition of insoluble fibrils composed of subunits of low molecular weight (5-25 kD) derived from a variety of plasma proteins. Identification of the amyloidogenic protein determines the type of amyloidosis. In primary systemic amyloidosis (classically called AL amyloidosis), the amyloid protein is composed of light chains resulting from plasma-cell dyscrasia. Cardiac manifestations are the most common clinical presentation of this type of amyloidosis, occurring in 50% of patients. The authors describe two cases in which hospitalization was due to decompensated heart failure, which were similar in their etiology (multiple myeloma/amyloid cardiomyopathy) and evolution (sudden death). The authors wish to draw attention to an entity that is rarely encountered in clinical practice and that requires a high index of suspicion.
Rev Port Cardiol 2010 Nov
PMID:Behind heart failure syndrome: remember AL amyloidosis. Two case-reports. 2130 62

A 61-year-old man with chronic chest pain was referred for a myocardial perfusion scan. Following dipyridamole infusion, 99mTc-MIBI was injected and the reconstructed images showed decreased activity in the anteroseptal wall, which prompted the supervising physician to review the cinematic data. Reviewing the cinematic images revealed abnormal 99mTc-MIBI uptake by the ribs, clavicles, and more intensely in the sternum. The next morning, whole-body planar imaging was performed 20 minutes after injection of 99mTc-MIBI at rest, which again revealed widespread abnormal 99mTc-MIBI uptake. Subsequently, a skull X-ray showed multiple areas of osteolysis, typical of punched-out lesions. In view of this evidence, the patient underwent bone marrow aspiration, which revealed marked plasmocytosis and confirmed the diagnosis of multiple myeloma. Our case indicates a false positive perfusion defect induced by sternal sestamibi uptake secondary to sternal tumoral involvement. As the sternum is in close proximity to the myocardium, the effects of its unusual radiotracer uptake on the pattern of myocardial perfusion can be significant. The interpretation of a myocardial perfusion scan should not be limited to the heart and, as the ultimate goal is the patient's wellbeing, any available information should be interpreted.
Hellenic J Cardiol
PMID:False perfusion defect on myocardial perfusion SPECT induced by sternal tumoral uptake. 2147 28

A 62-year-old woman with multiple myeloma and light-chain amyloidosis with significant heart involvement developed an in-hospital cardiac arrest. After cardiopulmonary resuscitation, a stable sinus rhythm without any cerebral damage was restored, and the patient was admitted to the coronary care unit. A cardioverter-defibrillator was implanted, and it successfully intervened in two sustained ventricular tachycardia episodes and one ventricular fibrillation episode, which were recorded during hospitalization. After achieving discrete cardiac compensation, the patient was transferred to the emergency medicine department where she underwent chemotherapy for multiple myeloma. The patient died 40 days after admission from refractory heart failure. In the literature, there are studies that describe the use of cardioverter-defibrillator implantation in cardiac amyloidosis; however, at present, there is no evidence of a beneficial effect on survival with the use of this intervention. A high index of suspicion for amyloid heart disease and early diagnosis are critical to improving outcomes.
Exp Clin Cardiol 2013
PMID:Cardioverter-defibrillator implantation in myeloma-associated cardiac amyloidosis. 2429 34

Chondrosarcoma is a malignant bone tumour common in adults, third to myeloma and osteosarcoma, but is exceptionally rare in children. Here we discuss a 9-year-old girl presenting with occlusive right pulmonary artery neoplastic embolus, resulting from a primary right proximal humerus chondrosarcoma. To the best of our knowledge, this the first pediatric and only second overall case reported in the United States of a neoplastic pulmonary embolus resulting from a primary chondrosarcoma.
Cardiol Young 2015 Feb
PMID:Chondrosarcoma presenting with pulmonary embolism in a 9-year-old girl: a case report. 2466 27

Bortezomib is a proteasome inhibitor used to treat multiple myeloma and mantle cell lymphoma. Traditionally, bortezomib was thought to have little cardiovascular toxicity; however, there is increasing evidence that bortezomib can lead to cardiac complications including left ventricular dysfunction and atrioventricular block. We present the case of a 66-year-old man with multiple myeloma and persistent asymptomatic elevations of cardiac biomarkers who developed complete heart block and evidence of myocardial scar after his eighth cycle of bortezomib, requiring permanent pacemaker placement. In addition to discussing the cardiovascular complications of bortezomib therapy, we propose a potential role for biomarkers in the prediction and monitoring of bortezomib cardiotoxicity.
Case Rep Cardiol 2016
PMID:Bortezomib-Induced Complete Heart Block and Myocardial Scar: The Potential Role of Cardiac Biomarkers in Monitoring Cardiotoxicity. 2694 19

The clinical manifestations of anti-cancer drug associated cardiac side effects are diverse and can range from acutely induced cardiac arrhythmias to severe contractile dysfunction, and potentially fatal heart failure. Anthracyclines and trastuzumab cardiac toxicity have been well described and left ventricular ejection fraction (LVEF) evaluation is commonly performed before their use. Bortezomib (Velcade), a potent, specific and reversible proteasome inhibitor is approved for treatment of multiple myeloma (MM). The incidence of cardiac failure associated with bortezomib therapy in clinical trials remains incidental. Acute exacerbation of pre-existing congestive cardiac failure has been associated with this therapy but de novo cardiomyopathy has been reported in only one patient receiving bortezomib for small cell lung cancer. As a result, cardiac evaluation is not normally ordered before its use. We describe a 50-year-old female with newly diagnosed MM and no risk factors for cardiac disease that unexpectedly developed florid heart failure after 2 cycles of bortezomib and low-dose dexamethasone. 2-D echocardiogram showed dilated cardiomyopathy with severely decreased LVEF; no changes consistent with amyloid deposits or myocardial scarring were described. Coronary angiogram ruled out coronary artery disease. The mechanism of bortezomib-induced cardiomyopathy has been postulated to be through fluid retention. Based on literature review we hypothesize that the disruption of the ubiquitin-proteasome system by bortezomib may cause cardiomyopathy and severe cardiac failure. As Bortezomib is a new and promising therapy for MM patients, we recommend routinely monitoring cardiac parameters in patients undergoing this treatment.
Cardiol Res 2010 Dec
PMID:Bortezomib-induced Severe Congestive Heart Failure. 2835 72

The use of proteasome inhibitors (PI) as targeted chemotherapeutics have significantly improved survival in patients with multiple myeloma (MM). However, rare and serious cardiovascular complications have occurred as a result of their use, most commonly congestive heart failure, hypertension, and arrhythmias. MM occurs in an aged population with many concurrent cardiovascular risk factors. The primary disease process also contributes to cardiovascular complications. Furthermore, many MM patients have prior exposure to cardiotoxic chemotherapy such as anthracyclines. Because of these occurrences, the identification, prevention, and management of cardiovascular complications is made increasingly difficult. Various clinical studies and case reports have documented cardiotoxicity among all 3 of the currently approved PIs, bortezomib, carfilzomib, and ixazomib. Carfilzomib has shown the highest rates of cardiotoxicity, whereas there is conflicting evidence regarding bortezomib's role in producing cardiotoxicity. However, various case reports have documented the existence of adverse cardiac effects. Higher frequencies of complications have also been seen in "real-life" populations with cardiovascular co-morbidities who were originally excluded from clinical studies. Ixazomib, the most recently approved PI, has also been proposed to cause cardiotoxicity, elucidating a possible class effect. PIs are thought to cause cardiotoxicity through the unfolded protein response, leading to apoptosis in cardiac myocytes. Apremilast and rutin have been used in an animal model to reverse this signaling. Standardized guidelines identifying patients at greatest risk, to prevent and manage complications, have not yet been developed. Efforts have been made to prioritize patients older than 60 years with anthracycline exposure, cardiovascular risk factors, or amyloidosis. Withholding medication, using slower-infusion times, limiting fluids and providing supportive therapy have been successful. Screening echocardiograms have not been proven effective.
Cardiol Rev
PMID:Cardiovascular Complications of Proteasome Inhibitors Used in Multiple Myeloma. 2907 85


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