A. Karcic 1 , J. Dell'orfano 1 ; 1 Departments of Internal Medicine and Cardiology, State University of New York at Stony Brook and Nassau University Medical Center, East Meadow, NY LEARNING OBJECTIVE: 1. To understand that ischemic myocardium has a decreased capability to conduct pacemaker beats. CASE INFORMATION: A 73 years-old hypertensive man, had one year ago a pacemaker inserted for symptomatic sinus bradycardia (fainting spells). Coronary angiography performed at that time showed only mild nonobstructive coronary disease, The pacemaker was a dual chamber device, with leads in the night atrium and night ventricle, and it was functioning appropriately until a week ago, when the patient noticed chest pressure while shoveling snow. At that time his pulse rate, on self-exam was 40 bpm, so the patient went to see his internist, knowing that``there is something wrong with the pacemaker, since it was programmed to keep the heart rate above 60 bpm.'' During hospitalization the patient had slightly positive cardiac enzymes. The ECG revealed sinus bradycardia and inferior wall ST depressions with regular vertical pacemaker spikes at 60 bpm, but failure of these paced stimuli to``capture'' the myocardium and lead to ventricular beats. Coronary angiography revealed a 100% obstructed night coronary artery (RCA) as the cause of ECG changes and ischemia. Angioplasty was performed on the RCA, and a stent inserted to keep the vessel open. Several hours after the procedure a repeat ECG revealed no ST depressions, with all the pacemaker spikes 'capturing' the myocardium, and pacing the heart at the set rate of 60 bpm. DISCUSSION: Our patient had a complete RCA obstruction, leading to ischemia of the inferior areas of the heart, as seen on the ECG. It also caused ischemia of the myocardium where the night ventricular pacemaker lead was inserted. Ischemic myocardium (or dead myocardium Ð as a scar from an old myocardial infarction) has a decreased ability to conduct electrical stimuli, as those received from a pacemaker. It effectively acts as an obstacle to the conduction of these pacemaker beats to the surrounding healthy nonischemic myocardium. For at least some paced beats to be conducted through the ischemic myocardium, impulses at much higher energy levels need to be delivered by the pacemaker. This not only leads to faster pacemaker battery depletion, but also usually does not guarantee that all beats delivered by the pacemaker will be conducted, which is needed. The solution to this problem is relieving the ischemia, if possible (like in our patient), or by changing the position of the night ventricular lead, if it was located in myocardial scar tissue. (8 years), risk factor HIV positive hemophiliac husband, with history of recurrent respiratory infections, was admitted for worsening dyspnea of several months duration, and two weeks of abdominal and leg swelling and oliguria. On exam she was tachypneic with a blood pressure 100/60 mm Hg and pulse rate of 100/ min. Lungs were clear to auscultation, while a right-sided gallop was audible. The jugular veins were distended, the liver painfully enlarged, and there was bipedal pitting edema. EKG revealed an incomplete RBBB. Chest radiograph showed mild cardiomegaly, and a prominent pulmonary artery, with clear lungs. Sonogram of the heart revealed large right-sided chambers, paradoxical septal motion and pulmonary hypertension. VQ scan was low probability for pulmonary embolism. Finally a right-sided cardiac catheterization excluded a left to right shunt and revealed severe pulmonary hypertension, with preserved left ventricular function.