DISCUSSION: PPH is a diagnosis of exclusion. In order for it to be diagnosed, no cause for the pulmonary hypertension should be found. Frequently, in HIV positive patients, pulmonary hypertension develops secondary to HIV related cardiomyopathy and left ventricular failure. Early reports of PPH in HIV involved hemophiliacs receiving large amounts of factor VIII concentrates, which over a period of time can cause pulmonary vascular insults leading to PPH. Only later came reports of non-hemophiliac HIV positive patients with PPH. Intravenous drug users can develop pulmonary hypertension as tale emboli cause pulmonary fibrosis and vascular disease. Progressive pulmonary thromboembolism has also been reported to cause pulmonary hypertension in HlV positive patients. While mild and moderate pulmonary hypertension can develop in many cardiac and pulmonary diseases, it is proposed that a genetic predisposition (rare familial PPH), in concord with pulmonary vascular insults (shear stress, chronic hypoxia and chronic inflammation), leads to severe and fatal PPH. Patients with AIDS have a multitude of pulmonary vascular insults (infections, emboli, hypoxia etc.), but only 0.5% of them develop severe PPH. Our patient for example had frequent bronchitis. It appears that PPH in patients with HIV is multifactorial in origin, rather than being merely a coincidental finding. As a conclusion, one could mention that pulmonary hypertension in HIV which is labeled as primary may in fact be secondary to a multitude of factors that may remain unrecognized, year old woman with a history of smoking and hypertension was admitted to the hospital with syncope. She was found to have episodes of significant sinus bradycardia for which she needed a pacemaker. A dual chamber pacemaker was inserted, with pacemaker leads placed in the right atrium and right ventricular apex. ECG, fluoroscopy and a chest radiograph confirmed the correct position of the leads, while postoperative pacemaker interrogation revealed that the right atrial and right ventricular pacing and sensing thresholds were within normal limits. Initially after the procedure the patient was feeling fine, but the same night she started complaining of persistent, rhythmic, frequent and annoying contractions on the right side of her upper abdomen, feeling somewhat like hiccups. There was nothing the patient could do in order to bring upon or abort these symptoms. After having interrogated the pacemaker, the cardiologist abandoned right atrial pacing and the symptoms resolved completely. DISCUSSION: This patient had right hemidiaphragmatic contractions that were induced by pacemaker beats. The diaphragm is a muscle and hence can be stimulated by electrical stimuli from the pacemaker. In order to understand how a pacemaker induces diaphragmatic contractions, one should recall that the right phrenic nerve traverses the right atrium (atrial electrode location), and the left phrenic nerve the right ventricular apex (ventricular electrode location). If the pacemaker stimuli are of adequately high energy, not only the surrounding myocardium wall be paced, but the paced beats will also be conducted through the overlying right or left phrenic nerve to cause contractions of the right or left hemidiaphragm respectively. In our patient the right hemidiaphragm was paced, telling us that the right phrenic nerve was paced via the right atrial electrode. Frequently there is a therapeutic window that enables us to pace the myocardium without pacing the overlying phrenic nerve. This is due to the fact that usually lower energy levels are needed to pace the myocardium. Gradual decrease of pacemaker energy output below that needed to pace the phrenic nerve, but still high enough to pace the myocardium is the perfect solution for this problem. If such a therapeutic window does not exist, the culprit electrode must be abandoned (atrial), or a new one can be placed in a different location (ventricular).