Ventricular Outflow Region Research Articles

Reappraisal of electrocardiographic criteria for localization of idiopathic outflow region ventricular arrhythmias.

Electrocardiographic (ECG) criteria have been proposed to localize the site of origin of outflow region ventricular arrhythmias (VAs). Many factors influence the QRS morphology of VAs and may limit the accuracy of these criteria. The purpose of this study was to assess the accuracy of ECG criteria that differentiate right from left outflow region VAs and localize VAs within the aortic sinus of Valsalva (ASV). One hundred one patients (mean age 52 ± 16 years; 55 [54%] women) undergoing catheter ablation of right ventricular outflow tract (RVOT) or ASV VAs with a left bundle branch block, inferior axis morphology were studied. ECG measurements including V2 transition ratio, transition zone index, R-wave duration index, R/S amplitude index, V2S/V3R index, V1-3 QRS morphology, R-wave amplitude in the inferior leads were tabulated for all VAs. Comparisons were made between the predicted site of origin using these criteria and the successful ablation site. Patients had successful ablation of 71 RVOT and 38 ASV VAs. For the differentiation of RVOT from ASV VAs, the positive predictive values and negative predictive values for all tested ECG criteria ranged from 42% to 75% and from 71% to 82%, respectively, with the V2S/V3R index having the largest area under the curve of 0.852. Morphological QRS criteria in leads V1 through V3 did not localize ASV VAs. The maximum R-wave amplitude in the inferior leads was the sole criterion demonstrating a significant difference between right ASV, right-left ASV commissure, and left ASV sites. ECG criteria for differentiating right from left ventricular outflow region VAs and for localizing ASV VAs have a limited accuracy.

Cardiac conotruncal malformations in a family of beagle dogs

To study forms of congenital heart disease present in a family of beagle dogs with a strong prevalence of ventricular septal defect and to document the pathological findings associated with the ventricular septal defects and investigate the mode of transmission. The animals were investigated by physical examination, radiography, electrocardiography and ultrasonography to diagnose the presence of congenital heart disease. Some animals were diagnosed at post-mortem examination and the dead animals underwent post-mortem examination to verify the presence of ventricular septal defect. An analysis of pedigree was undertaken and two of the affected animals were mated to investigate the mode of transmission. Among the 28 dogs evaluated clinically or by post-mortem examination, 14 cases of ventricular septal defect were identified. The post-mortem examination showed some abnormalities of the ventricular outflow region associated with malformation of conotruncal septum development. When two affected dogs were bred, congenital heart disease was present in all of the offspring. The congenital heart disease identified in this beagle family can be classified as conotruncal malformation, and an autosomal recessive mode of inheritance was suggested by pedigree analysis.

Development of a Signal-Averaged Vector-Projected 187-Channel High-Resolution Electrocardiogram for the Evaluation of the Spatial Location of High-Frequency Potentials and Abnormal Ventricular Repolarization

Noninvasive risk stratification is important for screening for lethal arrhythmia. We developed a 187-channel signal-averaged vector-projected high-resolution electrocardiograph (187-ch SAVP-ECG) for detecting abnormalities in the spatial location of ventricular high-frequency late potentials (HFLPs) and ventricular repolarization. The subjects consisted of 30 normal controls (CONTROL) and 13 patients with HFLPs (6 with myocardial infarction [MI], 6 with cardiomyopathy, and 1 with Brugada syndrome). The modified X, Y, Z-lead ECG and the synthesized signals from vector-projected 187-channel ECGs were amplified and passed through a digital filter. We calculated the integration of the HFLPs area between QRS(end) and 30 ms before QRS(end). The integrated HFLPs map was superimposed on the corrected recovery time (RTc) and Tpeak-end dispersion maps composed by 187-ch SAVP-ECG. All patients received an examination by 64-channel magnetocardiography (64-ch MCG) on the same day. The spatial distribution of HFLPs by the 187-ch SAVP-ECG map was in agreement with the location of increased RT dispersion in MI. The spatial distribution of HFLPs in DCM demonstrated a wide variety of patterns. Interestingly, the spatial distribution of HFLPs in cases with ARVC was located at around a right ventricular outflow region. The spatial distribution of HFLPs by 187-ch SAVP-ECG was in agreement with those determined by 64-ch MCG. The 187-ch SAVP-ECG might be useful for evaluating the spatial distribution of nonuniform conduction and ventricular repolarization heterogeneity.

Multi-slice CT demonstration of sinus of Valsalva rupture

Aneurysms of the sinus of Valsalva are rare. We report here the case of a 56-year-old man with a ruptured aneurysm of sinus of Valsalva with flow into the right ventricle which was diagnosed non-invasively by 64-row multi-slice computed tomographic (CT) imaging. The right sinus of Valsalva aneurysm rupturing into the right ventricular outflow region might be silent or symptomless in many cases. The patient also had mild symptom. For anatomical demonstration, contrast-enhanced CT was performed. Although the ruptured sinus of Valsalva was initially diagnosed by echocardiography, CT images did give our surgeons a better three-dimensional appreciation when surgical repair was performed. Multi-slice CT imaging should be considered the technique of choice for both diagnosis and follow-up examination of the aneurysm of sinus of Valsalva and its rupture.

Effects of Low-Dose Quinidine on Ventricular Tachyarrhythmias in Patients With Brugada Syndrome

Quinidine is suggested as an effective agent to suppress ventricular fibrillation (VF) in the Brugada syndrome by inhibiting transient outward K(+) current (Ito) leading to the reduction and abbreviation of the disparity of repolarization in the right ventricular outflow region and ST segment elevation in the right precordial leads of electrocardiogram. We sought to assess the efficacy of low-dose (300-600 mg) quinidine sulfate on the prevention of ventricular fibrillation induction by programmed electrical stimulation (PES) and spontaneous ventricular fibrillation episodes during the subsequent follow-up period. Electrophysiologic study was performed in 14 patients with the Brugada syndrome (14 men, mean age 50 +/- 11 years, range 32-75) before and during the treatment with low-dose quinidine and evaluated the efficacy of the drug therapy. Ventricular fibrillation was induced in all the patients by programmed electrical stimulation at baseline. After oral quinidine administration (300 mg or 600 mg/d), programmed electrical stimulation was repeated. Ventricular fibrillation induction was prevented in 6 of 14 patients (44%). Serum quinidine concentration was higher in the patients with suppressed VF induction than those without (1.88 +/- 0.44 versus 1.31 +/- 0.43 microg/ml, respectively). After programmed electrical stimulation, 9 of 14 patients (64%), in whom four had implantable cardioverter defibrillator implantation, continued to receive quinidine. During a mean follow-up period of 31 months on quinidine, no side effects except one with diarrhea were observed (12.5%). There were no ventricular fibrillation recurrences in 3 of the 9 patients, who had frequent implantable cardioverter defibrillator discharges due to ventricular fibrillation attacks before treatment with quinidine. Low-dose quinidine has a potential as an adjunctive therapy for patients of the Brugada syndrome with frequent implantable cardioverter defibrillator discharges.

An Unusual Accessory Pathway: Anteroseptal to Ventricular Outflow Region Connection

Accessory pathways are typically located along the left or right atrioventricular junction. Distinct ventricular pre-excitation patterns determined by surface electrocardiography can provide reasonable pathway localization prior to invasive mapping and catheter ablation. We report an accessory pathway producing an unusual electrocardiographic appearance suggestive of ventricular outflow region pre-excitation. Pacing maneuvers and standard intracardiac recordings confirmed an atrial insertion immediately adjacent to the atrioventricular (AV) node and supported a ventricular insertion at the outflow tract region well away from the AV junction. The elimination of pathway conduction was achieved with radiofrequency (RF) energy at the atrial insertion after successful ice mapping excluded AV block at the target site. This is the second such pathway observed at our institution over a 20-year period.

Development of the cardiac coronary vascular endothelium, studied with antiendothelial antibodies, in chicken-quail chimeras.

The endothelium of the coronary vascular system has been described in the literature as originating from different sources, varying from aortic endothelium for the main coronary stems, endocardium for the intramyocardial network, and sinus venosus lining for the venous part of the coronary system. Using an antibody against quail endothelial cells (alpha-MB1), we investigated the development of the coronary vascular system in the quail (Hamburger and Hamilton stages 15 to 35) and in a series of 36 quail-chicken chimeras. In the chimeras, pieces of quail epicardial primordium and/or liver tissue were transplanted into the pericardial cavity of a chicken host. The results showed that the coronary vascular endothelial distribution closely followed the formation of the epicardial covering of the heart. However, pure epicardial primordium transplants did not lead to endothelial cell formation, whereas a liver graft with or without an epicardial contribution did have this capacity. The first endothelial cells were seen to reach the heart at the sinus venosus region, subsequently spreading through the inner curvature to the atrioventricular sulcus and the outflow tract and, last of all, over the ventricular surfaces. At these sites, the precursor cells and small vessels were seen to invade the sinus venosus wall, the ventricular and atrial myocardium, and the mesenchymal border of the aortic orifice. Connections with the endocardium of the heart tube were only observed in the right ventricular outflow region. Initially, the connections with the aortic endothelium were multiple, but later in development only two of these connections persisted to form the proximal part of the two main coronary arteries. Connections to the pulmonary orifice were never observed. Our transplantation data showed that the entire coronary endothelial vasculature originated from an extracardiac source. Moreover, using the developing subepicardial layer as a matrix, we showed that the endothelial cells reached the heart from the liver region. Ingrowth into the various cardiac segments was also observed. Implications for the relation to specific congenital cardiac malformations are discussed.

RUPTURED CONGENITAL ANEURYSM OF THE RIGHT SINUS OF VALSALVA INTO THE RIGHT VENTRICLE: WITH SPECIAL REFERENCE TO PATHOANATOMIC AND HEMODYNAMIC CHARACTERISTICS IN SYMPTOMLESS CASES

Clinical features of 19 cases with congenital aneurysm of the right sinus of Valsalva rupturing into the right ventricular outflow region (Type 1) were analysed in relation to their pathoanatomic lesions and hemodynamic alterations. Sixteen cases were operated with one surgical death. All were catheterized together with ascending aortographic study. Rupture of the aneurysm in many cases was silent or symptomless and progressive heart failure was not quite common. Symptomatology of the patients did not seem to be related entirely to status of the pathoanatomical lesions or hemodynamic alterations. Time of the rupture, and inherent right ventricular characteristics, tolerating volume overload rather well, might be, in part, responsible for its better prognosis in some cases. However, all patients with ruptured aneurysm of the sinus of Valsalva should be treated surgically. Bacterial endocarditis is a serious complication leading to death.

Surgical Treatment of Ebstein's Anomaly: Early and Late Results in Seven Consecutive Cases

The surgical treatment of Ebstein's anomaly is discussed on the basis of our experience with 7 patients who underwent operation at this clinic during the last ten years. The age of the patients (2 males, 5 females) ranged from 17 to 47 years (mean 27 years) at the time of operation. Two patients were in functional class II and five in classes III or IV (N.Y.H.A.). The Wolff-Parkinson-White syndrome was concomitant in 2/7 cases and patent foramen ovale or atrial septal defect (ASD) with right-to-left shunt was present in 6/7 cases. The valvular anomaly was typical in 5 patients and stenosis of displaced tricuspid leaflets into right ventricular outflow region was detected in two patients. Tricuspid valve replacement (TVR) with disc valve prosthesis was performed in 5 patients (Björk-Shiley model in 4 cases, Kay-Shiley model in one) and tricuspid valve commissurotomy in two patients. All six patients with interatrial communication underwent closure of this communication simultaneously. One patient had concomitant epicardial mapping and attempted division of the anomalous conduction pathways was unsuccessful. This patient died on the 14th postoperative day from ventricular fibrillation. No other early or late mortality was recorded. Life-long anticoagulation therapy was introduced in all 5 patients with TVR. Thrombotic malfunction of the prosthetic valves necessitated re-operation and new prosthetic valve replacement in two patients 15 and 16 months after the first TVR. One of these patients had recurrent prosthetic thrombosis twice which was successfully treated with streptokinase. The other patient's prosthesis is functioning well 18 months after re-operation. All 6 long-term survivors were improved and remained in good condition, in functional class I, 1, 3, 3, 8, 9, and 10 years, respectively, after operation.

Multiple conduction defects with markedly prolonged ventricular depolarization in cardiomyopathy

Electrophysiologic investigation of a diffuse and bizarre conduction abnormality in a patient with cardiomyopathy revealed profound slowing of the impulse in the right ventricular outflow region. The resultant 220 msec QRS duration is the longest reported in right bundle branch block.

Endocardial cushion defects: Specific diagnosis by angiocardiography ∗

1. 1. The anatomy and embryology of endocardial cushion defects are reviewed. 2. 2. Angiocardiographic deformities of the left ventricular outflow region and of the mitral valve are described which we believe to be characteristic and diagnostic of endocardial cushion defects. This method appears to be the most accurate single diagnostic technic available for the identification of these lesions. 3. 3. This study is based on a review of 16 cases of cushion defects and over 200 left ventricular angiocardiograms in a wide variety of congenital cardiac disorders.