A practical guide to managing cardiopulmonary toxicities of tyrosine kinase inhibitors in chronic myeloid leukemia.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of chronic myeloid leukemia (CML) but their use was associated with a range of serious cardiopulmonary toxicities including vascular adverse events, QT prolongation, heart failure, pleural effusion, and pulmonary arterial hypertension. Dedicated clinical management guidelines for TKI-induced toxicities are not available. This review aims to discuss TKI-associated cardiopulmonary toxicities and proposes a practical guide for their management.

Endomyocardial fibrosis in a non-tropical patient who presented with chest pain mimicking ACS and left ventricular thrombus, case report.

Endomyocardial fibrosis (EMF) is a disease known to cause restrictive cardiomyopathy. It shows a high prevalence in tropical countries. Several triggering factors have been proposed. However, the pathogenesis is still a mystery. The disease is progressive, and the outcome is generally unfavorable. The most common symptom is heart failure. However, an atypical presentation may be expected. Our case presented with symptoms suggestive of ischemia and missed diagnosis initially as ischemic cardiomyopathy. This report aims to increase the attention and awareness of this disease. We present a case of a 53-year-old man referred to the emergency department for sudden chest pain, left-sided and non-radiating lasted for several minutes, awoke him from sleep with no associated symptoms. He is known to have Diabetes type-2 and hypertension on oral therapy. Cardiac markers were within the normal limit. The patient was discharged home with an appointment at the cardiology outpatient clinic. Echocardiography was done and revealed mildly reduced left ventricular (LV) systolic function, Ejection Fraction of 46%, asymmetric LV hypertrophy affecting the apical segments with aneurysm, and calcified apical thrombus. CT coronary angiography was done with non-significant Left Anterior Descending artery lesions and left ventricular hypertrophy affecting the apex with calcified apical thrombus. Further investigation by cardiac MRI revealed apical thrombus and late apical uptake suggesting Endomyocardial Fibrosis of possible eosinophilic etiology. The patient continued to have attacks of similar chest pain, for which stress cardiac MRI was done and was negative for ischemia. Another diagnostic workup was done, including hematological and serological tests such as Antinuclear Antibodies and Schistosoma Antibodies. The patient was kept on valsartan and Bisoprolol with oral anticoagulant (vitamin K antagonist) and Rosuvastatin. EMF may have a heterogeneous presentation and should be considered in a patient with calcific apical thrombus without previous history of cardiac problem, even in the non-tropical region.

Relapsed Brucellosis Manifested as Endocarditis with Vegetation on the Implantable Cardioverter Defibrillator Lead.

Implantable cardioverter defibrillator lead endocarditis due to Brucella melitensis is a rare and life-threatening complication of brucellosis. Successful management requires a combination of medical treatment and device extraction. We present a case of relapsing brucellosis manifested as infective endocarditis colonizing the lead of the implantable cardioverter defibrillator with formation of vegetation on the lead. A 63-year-old male presented to the rehabilitation unit with hypotension. No other signs of infection were noted. The patient had a history of drinking unpasteurized milk since childhood and a previous episode of Brucella infective endocarditis. A transthoracic echocardiography showed an oscillating vegetation on the lead of the tip of the right atrial ICD, and the blood cultures were positive for Brucella melitensis. Surgical removal of the device was infeasible, and medical management was the only feasible option in this case.