ABSTRACT
Bortezomib (Velcade(R)) came into the spotlight as a target therapy for multiple myeloma. It acts through reversible inhibition of intracellular proteasomes, which triggers apoptosis, with relative selectivity for malignant cells. It has been hypothesized that the accumulation of damaged proteins in myocytes impairs cardiac function. Cardiotoxicity is a rare side effect of bortezomib treatment. We report a case of reversible systolic heart failure that probably occurred after bortezomib treatment in a patient with multiple myeloma. Patients being treated with bortezomib who have previously had cardiac comorbidities should undergo routine cardiac monitoring.
Subject(s)
Humans , Apoptosis , Comorbidity , Heart Failure , Heart Failure, Systolic , Multiple Myeloma , Muscle Cells , BortezomibABSTRACT
BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.
Subject(s)
Humans , Antifibrinolytic Agents , Fibrinogen , Fibrinolytic Agents , Myocardial Infarction , Plasma , Protein C , Protein S , Thrombolytic Therapy , Tissue Plasminogen Activator , Urokinase-Type Plasminogen ActivatorABSTRACT
BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.