Right heart bypass operations.
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OBJECTIVES: We sought to assess the right heart's response to percutaneous device closure of moderate sized atrial septal defects (ASDs) in adults over a one-year follow-up period. BACKGROUND: Percutaneous ASD device closure is a safe and effective means of reducing or eliminating interatrial shunting. The response of the adult's right heart to device closure is incompletely understood. METHODS: Forty consecutive patients had 40 device implantations (32 with the CardioSeal implant and 8 with the Amplatzer device). The patients were assessed with echocardiography, chest radiography and electrocardiography before the procedure and at 1, 6 and 12 months. RESULTS: The mean ASD size was 13+/-4 mm, and the device size ranged from 33 to 40 mm for CardioSeal and 12 to 36 mm for Amplatzer. At one month, heart size (49% vs. 46%), four-chamber right ventricular (RV) size (45 vs. 41 mm), paradoxical septal motion (60% vs. 5%), QRS duration (125 vs. 119 ms), PR interval (181 vs. 155 ms) and echocardiographically determined pulmonary artery systolic pressure decreased significantly and was maintained at 12-month follow-up. At six months, right atrial length decreased from 50 to 47 mm. At one year, 29% of patients had persistent RV enlargement. CONCLUSIONS: Right heart morphology undergoes rapid improvement within one month of defect closure, with associated mechanoelectrical benefit. A small number of patients had persistent RV enlargement or pulmonary hypertension, or both, at one year. Our data support the application of transcatheter methods in achieving excellent hemodynamic and anatomic outcomes.
INTRODUCTION: Early reports suggested that some patients with "atrial fibrillation/flutter" might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. METHODS AND RESULTS: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12-lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra-atrial conduction block during sinus rhythm, suggesting functional intra-atrial block as a mechanism for simultaneous atrial fibrillation/flutter. CONCLUSION: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.
INTRODUCTION: Currently, surgery- and catheter-mediated ablation is applied when drug refractoriness of atrial fibrillation is evident, although little is known about the long-term incidence of new atrial arrhythmia and the preservation of sinus node function. METHODS AND RESULTS: To address this issue, 30 patients with successful corridor surgery for lone paroxysmal atrial fibrillation and normal preoperative sinus node function were followed in a single outpatient department. Five years after surgery, the actuarial proportion of patients with recurrence of atrial fibrillation arising in the corridor was 8% +/- 5%, with new atrial arrhythmias consisting of atrial flutter and atrial tachycardia in the corridor 27% +/- 8%, and with incompetent sinus node requiring pacing therapy 13% +/- 6%. Right atrial transport was preserved in 69% of the patients without recurrence of atrial fibrillation and normal sinus node function. Stroke was documented in two patients. CONCLUSIONS: Corridor surgery for atrial fibrillation is a transient or palliative treatment instead of a definitive therapy for drug refractory atrial fibrillation. This observation strongly affects patient selection for this intervention and constitutes a word of caution for other, nonpharmacologic interventions for drug refractory atrial fibrillation.
The response of several parameters of left ventricular function to right atrial pacing was compared in 21 patients with idiopathic mitral valve prolapse and 10 normal patients. An inability to appropriately lower left ventricular end-diastolic pressure with increasing rates was demonstrated in the mitral valve prolapse group. This abnormality was not related to mitral regurgitation or factors other than ventricular performance per se.
The influence of continuous positive pressure breathing (cm H2O) on the breathing mechanics, central venous pressure, and transmural pressure in the right atrium, were studied in anaesthetised cats separately during inspiration and expiration. It's shown that hemodynamics effects are directly connected with the influence of increased intrathoracic pressure during whole breathing cycles in contrast with the phase changes in natural expiration and inspiration. The inversion of relation of intrathoracic and central venous pressure due to displacement of the mechanical respiratory characteristics became the factors defining the fall of the right atrium filling pressure.
The essence of the Ebstein's malformation is that the tricuspid valve leaflets do not attach normally to the valve annulus, and the effective orifice is displaced downward into the right ventricular cavity at the junction of the inlet and trabecular components of the right ventricle. Only the septal and posterior leaflets are displaced and divide the right ventricle into two portions. The inlet portion is usually integrated functionally with the right atrium ("atrialized portion"), while the other, including the trabecular and outlet portions, constitutes the functional right ventricle. The proximal atrialized right ventricle often has a wall thinner than the distal functional right ventricle, due to partial congenital absence of myocardium. An atrial septal defect is present in more than one-third of hearts, and the majority of the remainder has a patent foramen ovale resulting in a right-to-left shunt. The downward displacement of the septal tricuspid valve leaflet is associated with discontinuity of the central fibrous body and septal atrioventricular ring, thus creating a potential substrate for accessory atrioventricular connections and ventricular pre-excitation making the patient at risk of sudden death. Angiography has demonstrated that a significant number of patients with Ebstein's anomaly also have morphofunctional abnormalities of the left ventricle, which may be explained by increased fibrosis in the left ventricular wall and ventricular septum as demonstrated by histological studies. Regarding embryology, the leaflets and tensile apparatus of the tricuspid valve are believed to be formed mostly by a process of delamination of the inner layers of the inlet zone of the right ventricle. The downward displacement of the leaflets in Ebstein's anomaly suggests that delamination from the inlet portion failed to occur.
1. We investigated the affinity of SB 207710 for sinoatrial 5-HT4 receptors and the density of right atrial 5-HT4 receptors with [125I]-SB 207710 in right atria of new-born piglets. 2. SB 207710 (1-100 nM) antagonized the 5-HT-evoked tachycardia surmountably with a pKB of 9.8. 3. [125I]-SB 207710 (5-1500 pM) labelled a small population of saturable binding sites with a pKD of 10.1 and with 5-HT4 receptor characteristics. The density of atrial binding sites with 5-HT4 receptor characteristics was 174 and 22 times lower respectively than those of atrial beta 1- and beta 2-adrenoceptors, labelled with (-)-[125I]-cyanopindolol. 4. We suggest that the small 5-HT4 receptor population may in part explain why the maximal tachycardia caused by 5-HT is smaller than that caused by catecholamines.
Chronic atrial fibrillation can be eliminated by an atrial compartment operation, but additional partition on the right atrium impairs the recovery of right atrial mechanical function. Thus, it is important to appropriately divide the atria for both maintaining sinus rhythm and maximizing atrial mechanical function.
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Background-We studied atrial activation during induced atrial flutter in the canine sterile pericarditis model to test the hypothesis that the atrial flutter reentrant circuit includes a septal component. Methods and Results-We studied 10 episodes of induced, sustained (>5 minutes) atrial flutter in 9 dogs. In all episodes, the reentrant circuit included a septal component. In 6 episodes, there were 2 reentrant circuits, one in the right atrial free wall and the second involving the atrial septum, Bachmann's bundle, and the right atrial free wall; both circuits shared a pathway in the right atrial free wall (figure-of-eight). The direction (superior or inferior) of the septal wave front of the second circuit correlated with the direction (clockwise or counterclockwise, respectively) of the right atrial free-wall circuit. A line of functional block in the right atrial free wall was part of both reentrant circuits. In the other 4 atrial flutter episodes, only 1 reentrant circuit was present, with activation in an inferior-to-superior direction in the septum and a superior-to-inferior direction in the right atrial free wall in 2 episodes and in the opposite direction in the other 2 episodes. In all atrial flutter episodes, the flutter wave polarity in ECG lead II was determined by the direction of activation in the left atrium; polarity was positive when the direction was superior to inferior and negative when the direction was inferior to superior. Conclusions-In this model of atrial flutter, the reentrant circuit (1) always included a septal component, (2) did not always require a right atrial free-wall reentrant circuit, (3) demonstrated figure-of-eight reentry when a reentrant circuit was present in the right atrial free wall, and (4) was associated with a line of functional block in the right atrial free wall.
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An alternative technique for orthotopic heart transplantation is described. The principle consists of total excision of the recipient's right atrium with donor heart implantation performed using bicaval anastomoses; the left atrium is done in the standard fashion. This approach is technically simple and preserves the anatomic and physiologic function and integrity of the right atrium, especially the conduction system.
Optimization of right atrial (RA) mechanics is important for maintaining right ventricular (RV) filling and global cardiac output. However, the impact of pericardial restraint on RA function and the compensatory role of the right atrium to changes in RV afterload remain poorly characterized. In eight open-chest sheep, RA elastance (contractility) and chamber stiffness were measured (RA pressure-volume relations) at baseline and during partial pulmonary artery (PA) occlusion. Data were collected before and after pericardiotomy. With the pericardium intact and partial PA occlusion, RA elastance increased by 28% (P < 0.04), whereas RA stiffness tended to rise (P = 0.08). However, after pericardiotomy, there was a significant fall in both RA elastance (54%, P < 0.04) and stiffness (39%, P < 0.04), and subsequent PA occlusion failed to induce a change in elastance (P > 0.19) or stiffness (P > 0.84). After pericardiotomy, RA elastance and stiffness fell dramatically, and the compensatory response of the right atrium to elevated RV afterload was lost. The ability of the right atrium to respond to changes in RV hemodynamics is highly dependent on pericardial integrity.
PURPOSE OF REVIEW: Because the right side of the heart supplies blood to the pulmonary circulation, its integrity is required for both adequate respiratory and circulatory function. By reducing pulmonary perfusion, right-sided heart failure may compromise arterial oxygenation and left ventricular filling, and monitoring of right-sided heart function at the bedside in critically ill patients is fundamental. Two recent clinical commentaries have focused on the invaluable help provided by echocardiography for this purpose. RECENT FINDINGS: Bedside echocardiography has supplanted invasive procedures as the best tool to evaluate right-sided heart function. Although not recent, this technique, previously reserved for cardiologists, has recently gained a larger acceptance in respiratory intensive care units. Echocardiographic examination detects excessive right ventricular afterload, visualized by septal dyskinesia, and its usual consequence, right ventricular enlargement, which impairs left ventricular filling. SUMMARY: Monitoring of right-sided heart function is essential in a clinical setting associated with hemodynamic instability, such as severe sepsis or acute coronary artery obstruction, and also in that it is associated with increased pulmonary vascular resistance, as in massive pulmonary embolism or acute respiratory failure. Moreover, use of mechanical ventilation requires regular evaluation of its effects on the right side of the heart.
Cardiac lipomas are rare tumors. They usually remain asymptomatic for a long time and cause angina, arrhythmia, dysfunction of the ventricles or valves, and peripheral embolization during the later stages of development. There is little or no information about right-to-left interatrial shunt with normal pulmonary artery pressure, produced as a consequence of the infiltration of the atrial septum, the right atrial wall, and the myocardium because of the presence of fat in patients with platypnea-orthodeoxia syndrome. We present a patient with this syndrome who was identified through transesophageal echocardiography. The study showed a massive right-to-left shunt without pulmonary hypertension, produced by an important cardiac infiltration of adipose tissue that created a narrow passage in the right atrium, and a redirection of the flow to a patent foramen ovale, explaining the pathophysiology of the syndrome.