An incomplete pacemaker lead fracture causing inappropriate pacing inhibition due to oversensing of the minute ventilation sensor pulses.

Cardiac pacemakers using rate response technologies represent the effectiveness of increasing the heart rate and cardiac output during exercise. Minute ventilation (MV) sensors are popular and estimate rates using transthoracic impedance by emitting very low amperage short electrical current pulses between the pacemaker lead tip and pulse generator. We present a case of an incomplete pacemaker lead fracture developing inappropriate pacing inhibition due to oversensing caused by the electrical current emitted by the MV sensor. A permanent pacemaker replacement was performed, resulting in no further abnormal findings such as inappropriate pacing inhibition. .

The utility of atrial pacing for identifying the electrical breakthrough sites between the left atrium and pulmonary veins.

BACKGROUND: Circumferential pulmonary vein (PV) isolation for atrial fibrillation (AF) is occasionally difficult to achieve because electrical breakthrough sites (EBSs) between the left atrium (LA) and PVs cannot be identified during ablation especially in the carina regions. METHODS: The left PVs (Lt.PVs) of 60 AF patients and the right PVs (Rt.PVs) of 37 patients undergoing PV isolation were studied. When PV isolation was not achieved after the initial circumferential PV isolation, atrial pacing was repeatedly performed from the distal coronary sinus (CSd) and high right atrium (HRA), and the time interval from the stimulus to the earliest PV potential (stimulus-PV interval) was measured using circular mapping catheters at each PV until PV isolation was achieved. When PV isolation was achieved via local Radiofrequency (RF) deliveries, those regions were diagnosed as final EBSs. We classified the final EBSs into six segments for each PV (anterior and posterior PV walls of the roof, carina, and bottom) and investigated the relationship between the final EBSs and stimulus-PV intervals. RESULTS: For Lt.PVs, the stimulus-PV intervals during CSd pacing were significantly shorter than during HRA pacing at the Lt.PV anterior carina and bottom (90±28 ms vs. 125±26 ms, P<0.001 and 84±20 ms vs. 148±24 ms, P=0.028, respectively), but there was no significant difference in the Lt.PV roof and any posterior segments. For Rt.PVs, the stimulus-PV interval from both pacing sites exhibited no significant difference between either segment. CONCLUSIONS: This pacing method may help to identify whether EBSs are located in the anterior Lt.PVs. Improved recognition of EBSs through pacing from different sites would be helpful for achieving PV isolation.

Change in filling pattern with preload reduction reflects left ventricular relaxation.

BACKGROUND: The early diastolic mitral valve pressure gradient and the rate of left ventricular filling are determined by the rate of left ventricular relaxation and left atrial pressure at the time of mitral valve opening. Accordingly, we hypothesized that the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved systolic function. METHODS: We evaluated the relationship between the logistic time constant of left ventricular relaxation and left ventricular filling pattern calculated from the time derivative of left ventricular volume using a microtipmanometer and a conductance catheter in 26 consecutive patients with preserved left ventricular ejection fraction (>45%). Left ventricular filling patterns were determined from the maximal rates of early diastolic left ventricular filling (E velocity) and atrial filling (A velocity) before and after preload reduction by inferior venal caval occlusion. RESULTS AND CONCLUSIONS: There was no significant relationship between the logistic time constant of left ventricular relaxation and the E/A velocity ratio at baseline. However, the time constant was correlated with the E/A velocity ratio after venal caval occlusion (r=-0.47, p=0.02). Furthermore, the time constant was correlated with %E/A velocity change, which was defined as the rate of change of E/A before and after caval occlusion divided by E/A after caval occlusion, more significantly (r=-0.67, p<0.01) than with the E/A velocity ratio after caval occlusion. Thus, the left ventricular filling pattern with preload reduction can be used to estimate left ventricular relaxation in patients with preserved left ventricular ejection fraction.

Two cases of giant aneurysm in coronary-pulmonary artery fistula associated with atherosclerotic change.

Giant sacclar aneurysm in a coronary-pulmonary artery fistula is extremely rare. In this article, we presented two cases of giant aneurysms in coronary-pulmonary artery fistula with atherosclerosis.

Combined angiotensin receptor blocker and ACE inhibitor on myocardial fibrosis and left ventricular stiffness in dogs with heart failure.

Angiotensin receptor blocker (ARB) and angiotensin-converting enzyme (ACE) inhibitor (ACEI) each act in a different manner to prevent myocardial fibrosis and left ventricular (LV) stiffness in animals with pathways in the heart for generating ANG II as well as ACE. A model of pacing-induced congestive heart failure (CHF) was used to test the central hypothesis that ARB + ACEI prevents myocardial fibrosis and decreases LV stiffness to a greater extent than ARB or ACEI alone. Thirty-five dogs were assigned to the following treatment protocols on the 8th day of a 4-wk pacing schedule: 1) rapid ventricular pacing, 2) ARB (candesartan cilexetil, 1.5 mg.kg(-1).day(-1)) with pacing, 3) ACEI (enalapril, 1.9 mg.kg(-1).day(-1)) with pacing, 4) ARB (candesartan cilexetil, 0.75 mg.kg(-1).day(-1)) + ACEI (enalapril, 0.95 mg.kg(-1).day(-1)) with pacing, and 5) sham operation. The LV stiffness coefficient was significantly increased after rapid pacing but was significantly lower with ARB + ACEI than with ARB or ACEI alone. The collagen volume fraction and mRNA levels of collagen I and III, which were increased by rapid pacing, were significantly lower with ARB + ACEI than with ARB or ACEI alone. Thus ARB + ACEI prevents myocardial fibrosis and decreases LV stiffness during the progression of CHF compared with ARB or ACEI alone.

Candesartan prevents myocardial fibrosis during progression of congestive heart failure.

BACKGROUND: The goal of this study was to determine whether an Angiotensin II receptor antagonist, candesartan, prevents myocardial fibrosis more effectively than enalapril in animals with a non-ACE pathway during the progression of congestive heart failure (CHF). METHODS AND RESULTS: Dogs were randomly assigned to one of four groups: (1) rapid ventricular pacing (240 bpm); (2) concomitant candesartan cilexetil (1.5 mg/kg/d) and rapid pacing; (3) concomitant enalapril (1.9 mg/kg/d) and rapid pacing; (4) sham-operated control. The expression of collagen type I & III mRNA and the collagen volume fraction, which were significantly increased in the pacing-only group, were suppressed by both treatments; it was lower in the candesartan than the enalapril group. Although there were no differences in the LV stiffness coefficient (beta) among all pacing groups, the absolute changes in beta from the control values were smaller in the candesartan group, but not the enalapril group, compared with the rapid-pacing-only group. CONCLUSIONS: The present study demonstrates that in animals with a non-ACE pathway, candesartan suppressed myocardial fibrosis during the progression of CHF in comparison with enalapril. Furthermore, candesartan prevented an increase in LV stiffness. These findings imply potential clinical applications for candesartan in the management of CHF to prevent myocardial fibrosis. Further prospective evaluation and clinical study will be necessary before deciding on the net benefits of candesartan in comparison to enalapril.

Addition of angiotensin II receptor antagonist to an ACE inhibitor in heart failure improves cardiovascular function by a bradykinin-mediated mechanism.

Whether cardiovascular responses to bradykinin are augmented by additional treatment with angiotensin II receptor antagonism (ATRA) to angiotensin-converting enzyme inhibition (ACEI) in congestive heart failure (CHF) is unknown. To clarify the level and functional effects of endogenous bradykinin in CHF with combined ATRA and ACEI, 35 dogs were assigned to the following treatment protocols: 1). rapid ventricular pacing (240 bpm), 2). concomitant ATRA (TCV116, 1.5 mg x kg-1.day-1) and rapid pacing, 3). concomitant ACEI (enalapril 1.9 mg x kg-1.day-1) and rapid pacing, 4). concomitant combined ATRA (TCV116, 0.75 mg x kg-1.day-1) and ACEI (enalapril 0.95 mg x kg-1.day-1) and rapid pacing, and 5). sham-operated control. Plasma bradykinin levels were increased and B(2) receptors were synergistically upregulated in CHF groups treated with combined ATRA and ACEI compared with those treated with ATRA or ACEI alone. HOE-140 (0.3 mg/kg), a bradykinin B(2) receptor antagonist, produced an increase in total systemic resistance and a decrease in left ventricular contractility in CHF with combined therapy compared with either monotherapy. Thus, endogenous bradykinin partially contributes to the synergistic improvement of cardiovascular function in CHF with additional treatment with ATRA to ACEI.

Infected papillary fibroelastoma attached to the atrial septum.

A 61-year-old woman had intermittent fever of 2 months' duration following a dental extraction. On admission, her body temperature was 39.2 degrees C. A mid-systolic murmur was heard at the apex on ausculation. A 2-dimensional echocardiogram revealed a mobile, heavy stick-like mass with vegetation (5.0 x 1.5 cm) attached to the left atrial septum. Multiple blood cultures grew Streptococcus constellatus. On diagnosis of an infected left atrial myxoma, antibiotics were administered daily and 4 weeks later, the left atrial tumor was resected. The tumor was 5.3cm long, 1.5cm in diameter at the inter-atrial wall and had vegetation on the free edge. On microscopic examination, colonies of Gram-positive cocci were found in the thrombus, on the papillary fibroelastoma. After treatment with antibiotics for a further 4 weeks, the patient was discharged. This is the first report of infected papillary fibroelastoma.