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Pacemaker implantation can be associated with several complications, including myocardial perforation with or without pericardial effusion, venous thrombosis, vegetations of the tricuspid valve (TV) or pacing lead, and tricuspid regurgitation (TR). The TR is thought to be derived from deformity or perforation of the TV by the pacing lead or secondary to atrioventricular discordance with asynchronous ventricular pacing. Severe TR can be deleterious to the patient because it raises the central venous pressure by increasing the right sided preload. Chronically, the increase in right sided blood volume can result in an increase in the right atrial pressure leading to a decrease in venous return and low cardiac output. Severe TR from leaflet adhesion to the pacemaker lead has not been reported before. With the aging of the population and the expanding use of pacemakers and implantable cardioverter defibrillators (ICD) in clinical practice, this complication may be seen more frequently. We present a patient diagnosed with severe TR, years after his pacemaker implantation. His TR was thought to be caused by adhesion of the tricuspid valve to his pacemaker lead.

Amiodarone is increasingly prescribed for patients with ventricular and supraventricular tachyarrhythmias. Many adverse effects have been reported due to this drug and include injury to the liver, thyroid, cornea, skin, and neuromuscular system. Pulmonary toxicity is one of the more serious side effects of this anti-arrhythmic drug and is potentially fatal. Since the first case of amiodarone-induced pneumonitis was described in the early 1980s, amiodarone pneumonitis has been recognized as a distinctive and not uncommon form of drug-induced lung injury. On the other hand, amiodarone-induced pulmonary toxicity resulting in alveolar hemorrhage is rare. The authors report a patient with amiodarone-induced alveolar hemorrhage and review the literature.

AH is a rare complication of treatment with GP IIb/IIIa inhibitors. Its incidence ranged from 0.14% in patients treated with abciximab to 0.33% in those receiving eptifibatide. Compared to a control group, patients treated with GP IIb/IIIa inhibitors had a statistically increased risk for AH.

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