Effect of different location of atrial lead position on nearfield and farfield electrograms in dual chamber pacemaker-defibrillators.

The normal functioning of dual chamber pacemaker-cardioverter defibrillator (AV pacer/ICD) may be affected by oversensing of the farfield R wave (FFRW) by the atrial channel. This study aimed to investigate whether placement of the AV pacer/ICD's atrial lead at a lateral (LAT) wall location compared to a medial (MED) location i.e. the appendage of the right atrium, would reduce the amplitude of FFRWs but not the nearfield atrial electrograms (AEGMs) during sinus rhythm (SR) and ventricular fibrillation (VF). In 17 patients, real time electrograms were recorded during SR and induced VF through the atrial lead initially at the MED and subsequently at the LAT location. In 10 patients the electrograms in SR were also recorded on a computerized data acquisition and recording system at different band-pass filter settings. Although FFRWs were recorded both at MED and LAT locations, they were much smaller, 3.5+/-4.1mm during SR and 1.7+/-2.2mm during VF at the LAT location. At 30-500Hz band-pass filter, lower amplitudes of FFRWs 0.14+/-0.09 mV were recorded at the LAT location. The V/A ratios of the amplitudes of FFRWs and AEGMs were smaller at the LAT location during SR and VF. The nearfield AEGMs were of similar amplitudes at the MED and LAT locations. These data indicate that lower amplitudes of FFRWs are recorded by placement of the atrial lead at the lateral wall of the right atrium. Oversensing of FFRWs may be prevented to improve functioning of the AV pacer-ICD.

Feasibility, safety, and determinants of extraction time of percutaneous extraction of endocardial implantable cardioverter defibrillator leads by intravascular countertraction method.

Previous studies of the removal of implantable cardioverter defibrillator (ICD) leads have been restricted to case reports or small series. In this report, we describe our experience in ICD lead extraction by intravascular countertraction method using Cook's extraction kit. A total of 47 high-voltage (HV) leads, 3 rate sensing (S) leads, and 2 subcutaneous arrays were removed from 42 patients (33 men, 9 women; mean age 59 years [range 14 to 81]). One HV superior vena cava (SVC) lead and 11 HV right ventricular (RV) leads were explanted by manual traction only and defined in the "lead removal" category. One S lead was removed using a femoral venous approach. The remaining 37 leads were explanted by SVC approach using extraction sheaths and defined in the "lead extraction" category. Twenty leads were extracted for "infectious" (group A) and 17 leads for "noninfectious" (group B) etiologies for which extraction times of 27.0+/-18.0 and 27.0+/-15.0 minutes (mean+/-SD), respectively, were not different. Although extraction time, 34.0+/-11.0 minutes, for leads implanted for >48 months was longer than 23.0+/-16.0, 28.0+/-18.0, and 24.0+/-14.0 minutes, for leads with implant durations of 12, 24, and 48 months, respectively, such differences were not statistically significant. The extraction time, however, was directly related to the degree of fibrosis around the lead, 39.0+/-15.0 minutes for leads with severe fibrosis compared with 13.0+/-6.0 minutes for the leads with mild fibrosis (p<0.001). Patient's age, sex, or history of coronary artery bypass graft surgery did not significantly affect extraction time. All except the initial 2 lead extractions were performed in the electrophysiology laboratory. No mortality or serious complications associated with the procedure using these methods were observed.

Insertion-deletion polymorphism of the ACE gene modulates reversibility of endothelial dysfunction with ACE inhibition.

BACKGROUND: The aim of this study was to examine whether angiotensin-converting enzyme (ACE) inhibition improves coronary endothelial dysfunction in patients with atherosclerosis and its risk factors and whether this was related to the ACE insertion-deletion (I/D) polymorphism. METHODS AND RESULTS: In 56 patients with atherosclerosis or its risk factors, we studied endothelium-dependent responses with acetylcholine and endothelium-independent function with sodium nitroprusside, before and after ACE inhibition with enalaprilat. Enalaprilat did not alter either resting coronary tone or vasodilation with sodium nitroprusside. However, it potentiated the coronary microvascular and epicardial responses with acetylcholine; coronary blood flow increased from 82+/-7 to 90+/-8 mL/min (P=0.05) after enalaprilat. Patients with depressed endothelial function (P<0.001) and those with ACE DD or ID genotypes (P=0.002) but not those homozygous for the I allele had the greatest improvement by multivariate analysis. Similarly, acetylcholine-mediated epicardial vasomotion improved in segments that initially constricted (endothelial dysfunction): from -10.1+/-1% to -1.4+/-2% (P<0.001) after enalaprilat. No augmentation was observed in segments that dilated (normal endothelial dysfunction) with acetylcholine. Patients with the D allele, hypercholesterolemia, and smokers (all P<0.05) had greater improvement. CONCLUSIONS: Acute ACE inhibition improves coronary epicardial and microvascular endothelium-dependent vasomotion in patients with atherosclerosis or its risk factors who have endothelial dysfunction and presence of the D allele.

Radiofrequency catheter ablation of atrioventricular nodal reentrant tachycardia after orthotopic heart transplantation.

Patients with orthotopic heart transplantation may develop a variety of arrhythmias. Successful radiofrequency catheter ablation for tachyarrhythmias from manifest and concealed accessory bypass tracts in transplant patients has been previously reported. We present a patient with orthotopic heart transplantation who developed typical atrioventricular nodal tachycardia, which was successfully treated by radiofrequency catheter ablation.

Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability.

OBJECTIVES: We investigated whether glutathione (GSH), a reduced thiol that modulates redox state and forms adducts of nitric oxide (NO), improves endothelium-dependent vasomotion and NO activity in atherosclerosis. BACKGROUND: Endothelial dysfunction and reduced NO activity are associated with atherosclerosis and its clinical manifestations such as unstable angina. METHODS: In the femoral circulation of 17 patients with atherosclerosis or its risk factors, endothelium-dependent vasodilation with acetylcholine (ACH), and endothelium-independent vasodilation with nitroglycerin and sodium nitroprusside were studied before and after GSH. In 10 patients, femoral vein plasma cyclic guanylate monophosphate (cGMP) levels were measured during an infusion of ACH before and after GSH. Femoral artery flow velocity was measured using a Doppler flow wire and the resistance index (FVRI) calculated as mean arterial pressure divided by flow velocity. RESULTS: Glutathione strongly potentiated ACH-mediated vasodilation; at the two doses, FVRI decreased by 47% and 56% before, and by 61% and 67% after GSH (p = 0.003). Glutathione also elevated cGMP levels in the femoral vein during ACH infusion from 17.6 +/- 3 to 23.3 +/- 3 pmol/ml (p = 0.006). Augmentation of ACH responses was only observed in patients with depressed endothelial function. Glutathione did not influence endothelium-independent vasodilation with either NO donor. CONCLUSIONS: Thiol supplementation with GSH selectively improves human endothelial dysfunction by enhancing NO activity.

Acute myocardial infarction with normal coronary artery: a case report and review of literature.

A 17-year-old girl with no risk factors for coronary artery disease had acute myocardial infarction. She received thrombolytic therapy with tissue-type plasminogen activator. An extensive workup for the cause of myocardial infarction revealed protein S deficiency. Angiography showed normal coronary arteries. We speculate that the cause of myocardial infarction was coronary spasm or thrombus formation, which was successfully dissolved by thrombolytic therapy. This is the eighth case report of acute myocardial infarction in a patient with normal coronaries and protein S deficiency. We reviewed the literature concerning myocardial infarction and normal coronaries and protein S deficiency. This case report and review of the literature suggest the need to extend the concept of classic risk factors for coronary artery disease in young patients with myocardial infarction and normal coronary arteries.

Echocardiographic diagnosis of pericardial cyst.

A 52-year-old woman was seen with atypical chest pain. A routine chest roentgenogram revealed an enlarged cardiac silhouette. Results of transthoracic echocardiography performed using the standard views was normal. Because of the discrepancy between the findings of chest roentgenogram and transthoracic echocardiography, a biplane transesophageal echocardiogram was obtained and revealed the presence of a pericardial cyst.

Myocardial stunning following respiratory arrest.

Myocardial stunning is defined as a prolonged myocardial dysfunction with gradual return of contractile activity after a brief episode of severe ischemia. Usually it is seen in patients with myocardial infarction following treatment with thrombolytic agents, in patients with angina, and in patients recovering from cardiopulmonary bypass surgery. We report an interesting case of myocardial stunning following respiratory arrest.