Ventricular arrhythmia and cardiomyopathy often coexist. Many patients with abnormal ventricular function have either documented premature ventricular contractions (PVCs) or nonsustained ventricular tachycardia and have an increased risk of sudden death from ventricular fibrillation. Tachycardia is a treatable cause of cardiomyopathy. The culprit arrhythmia may be atrial tachycardia, atrial fibrillation, or another supraventricular arrhythmia. The syndrome of PVCs giving rise to ventricular dysfunction was recently described. Thus, a conundrum exists for clinicians in determining which abnormality (PVCs or cardiomyopathy) came first and gave rise to the other. Solving this dilemma is important because radiofrequency ablation for frequent PVCs can completely reverse the cardiomyopathy and normalize systolic ventricular function. In this article, we describe the present evidence for the syndrome of PVCs that can be ablated as a cause for cardiomyopathy. We include a case example and discussion to illustrate this concept and provide a stepwise approach to determining whether PVCs cause cardiomyopathy or vice versa.

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Thromboangiitis obliterans, or Buerger’s disease, is a relatively rare nonatherosclerotic, segmental inflammatory and obliterative vascular disease that affects the small- and medium-sized arteries, veins, and nerves. In the acute phase, the lesion presents as an inflammatory, nonsuppurative panarteritis or panphlebitis with vascular thrombosis without necrosis. In the late stage of the disease, the thrombus becomes organized leading to varying degrees of recanalization and subsequent gangrene and amputation. There have been rare reports of thromboangiitis obliterans with involvement of the gastrointestinal trace and even more unusual is the occurrence of this manifestation of disease in women. Here, we report a case of a 45-year-old female patient with a history of thromboangiitis obliterans who presented with ischemic colitis.

First report of t(8;21)(q22;q22) in a patient with CLL. RUNX1‐RUNX1T1 fusion gene resulting from the translocation may have played a role in the prolymphocytic transformation.