Background Ibrutinib is a Bruton's tyrosine kinase (BTK) inhibitor approved for second-line treatment for mantle cell lymphoma (MCL), chronic lymphocytic leukemia (CLL), and Waldenström macroglobulinemia. Ibrutinib use has been linked to increased incidence of atrial fibrillation and hypertension in multiple studies. Other forms of cardiac toxicities have also been reported in isolated case reports. Bradycardia and asystole have not been associated with ibrutinib use in the past. Case Report We present a case of a 76-year-old female with no prior cardiac history, who initiated treatment with ibrutinib for relapsing mantle cell lymphoma and was noted to have symptomatic bradycardia, greater than 20 second long pauses on her cardiac monitor requiring placement of a permanent pacemaker. Conclusion This is the first case associating bradycardia and asystole with tyrosine kinase inhibitor use. Irreversible inhibition of certain cardioprotective tyrosine kinases has been a growing topic of research in oncology therapeutics.
A 45-year-old Caucasian man presented to the hospital with a 3-month history of fatigue, bilateral upper and lower limb paresthesias and gradually worsening ascending paralysis. A few weeks later, he developed acute renal failure requiring haemodialysis. Investigations revealed presence of myeloperoxidase (MPO) perinuclear antineutrophil cytoplasmic antibodies (ANCA). Renal biopsy was conclusive for rapidly progressive glomerulonephritis with crescents. Treatment for ANCA positive vasculitis was initiated with pulsed steroids, cyclophosphamide and plasmapheresis. The hospital course took an unexpected turn when the patient developed acute chest pain with an EKG consistent with inferior ST elevation myocardial infarction (STEMI). Urgent left heart catheterisation revealed distal occlusions in multivessel coronary distribution. Coronary involvement is rare in ANCA vasculitis and STEMI has not been reported in MPO-ANCA positive vasculitis, to the best of our knowledge.
A 60-year-old woman was admitted with progressively worsening dyspnea on exertion associated with intermittent lightheadedness and palpitations. On physical examination, a 3/6 diastolic decrescendo murmur was audible along the left sternal border. The murmur was most prominently heard in the left third intercostal space at end expiration with the patient in the sitting position. In addition, bounding carotid and femoral pulses were present, and the pulse pressure was wide. Careful examination of her eyes revealed alternating constriction and dilation of the pupils occuring in synchrony with the patient's heartbeat, a rarely reported finding known as "Landolfi's sign" (Figure 1, Video S1 available online). Figure 2 is a still frame of the long-axis parasternal view on 2-dimensional color flow transthoracic echocardiography showing significant aortic regurgitation as depicted by the arrow. Figure 3 is a still frame of 2-dimensional-guided pulsed-wave Doppler from the suprasternal view demonstrating diastolic flow reversal at the level of the aortic arch-descending aorta junction (arrow), thus confirming severe aortic regurgitation. "Landolfi's sign," described by Michel Landolfi (La Semaine Medicale, July 28, 1909), is believed to be a result of an exaggeration of the physiologic circulatory hippus in the iridial vessels due to high pulse pressure and large stroke volume, thereby resulting in systolic constriction and diastolic dilation of the pupil. "Landolfi's sign," "Corrigan's pulse" (bounding carotid pulsation), "Watson's waterhammer pulse" (forceful extremity pulsation), "Quincke's sign" (alternating flushing and blanching of fingernail beds), "de Musset's sign" (rhythmic head bobbing), "Becker's sign" (prominent retinal artery pulsations), "Müller's sign" (systolic bobbing of the uvula), and "Duroziez's sign" (audible diastolic murmur over femoral artery) are important manifestations of the hyperdynamic circulatory state seen in clinically significant aortic regurgitation.
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