Symptomatic bradycardia is effectively treated with the implantation of a cardiac pacemaker. Although a highly successful therapy, during recent years there has been a focus on the negative effects associated with long-term pacing of the apex of the right ventricle (RV). It has been shown in both experimental and clinical studies that RV pacing leads to ventricular dyssynchrony, similar to that of left bundle branch block, with subsequent detrimental effects on cardiac structure and function, and in some cases adverse clinical outcomes such as atrial fibrillation, heart failure and death. There is substantial evidence that patients with reduced left ventricular function (LVEF) are at particular high risk of suffering the detrimental clinical effects of long-term RV pacing. The evidence is, however, incomplete, coming largely from subanalyses of pacemaker and implantable cardiac defibrillator studies. In this group of patients with reduced LVEF and an expected high amount of RV pacing, biventricular pacing (cardiac resynchronization therapy) devices can prevent the negative effects of RV pacing and reduce ventricular dyssynchrony. Therefore, cardiac resynchronization therapy has emerged as an attractive option with promising results and more clinical studies are underway. Furthermore, specific pacemaker algorithms, which minimize RV pacing, can also reduce the negative effects of RV stimulation on cardiac function and may prevent clinical deterioration.

A 64-year-old man with history of hyperlipidemia and type 2 diabetes mellitus presented with sudden onset of atypical chest pain and dyspnea at rest. He denied palpitations or dizziness. Examination revealed blood pressure of 132/ 81 mm Hg and a heart rate of 153 bpm. The ECG showed a wide-QRS-complex tachycardia compatible with a sustained monomorphic ventricular tachycardia ( Figure 1). An amiodarone drip was started, and the tachycardia abruptly terminated during the infusion. In the ECG performed shortly after (Figure 2), normal sinus rhythm with T-wave inversion (transient) in the lateral leads (I, aVL) was evident, probably related to cardiac memory phenomenon. There was no evidence of further arrhythmias while the patient was maintained on oral amiodarone treatment. A chest x-ray showed moderate cardiomegaly and an abnormal left mediastinal contour owing to a bulge in the surface of the left ventricle ( Figure 3A and 3B). A transthoracic echocardiogram was performed, demonstrating a normal-size left ventricle, with mild septal hypertrophy, normal systolic function of both ventricles, and no pericardial effusion. A coronary angiography excluded any occlusive disease but revealed a cardiac mass with multiple "feeding" collaterals from the left anterior

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