Atrial natriuretic peptide levels during and after acute cardiac tamponade in dogs

The ability of the atrial wall to secrete atrial natriuretic peptide was studied in eight dogs during 2 h of cardiac tamponade and for 2 h after decompression of the pericardium. Cardiac tamponade was induced by instillation of 5% dextrose in water into the pericardial cavity until aortic systolic pressure was reduced by 30% to 35%. Heart rate, cardiac output and atrial, pericardial and aortic pressures were measured at 60 and 120 min of tamponade and at 5, 30, 60, 90 and 120 min after decompression. Blood samples were withdrawn at the same time for the determination of atrial natriuretic peptide and aldosterone levels. Aortic pressure decreased significantly during tamponade and increased after decompression to near control levels. Right and left atrial pressures as well as intrapericardial pressure increased significantly during tamponade and returned to control levels after decompression. The effective transmural pressure, which was reduced during tamponade, was increased significantly at 5 min after decompression. Cardiac output was significantly reduced during tamponade and returned to pretamponade levels after decompression. Over the total experimental period, no significant changes in the levels of atrial natriuretic peptide were observed, whereas aldosterone increased significantly. It is concluded that the increased atrial pressure observed during cardiac tamponade did not stimulate the secretion of atrial natriuretic peptide. Furthermore, atrial distension observed immediately after decompression was not sufficient or of long enough duration to induce measurable increases in atrial natriuretic peptide levels. Finally, the secondary hyperaldosteronism did not activate atrial natriuretic peptide secretion either during cardiac tamponade or after decompression.     

Atrial Appendage Thrombosis Risk Is Lower for Atrial Flutter Compared with Atrial Fibrillation

Background

The risk of stroke and thromboembolism in atrial fibrillation is established. However, the evidence surrounding the risk of thromboembolism in patients with atrial flutter is not as clear. We hypothesized that atrial flutter would have indicators of less risk for thromboembolism compared with atrial fibrillation on transesophageal echocardiography, thereby possibly leading to a lower stroke risk.

Atrial gradient as a potential predictor of atrial fibrillation

OBJECTIVES: We tested the utility and comparability of the atrial gradient and atrial ERP as early markers of electrical remodeling and a propensity to atrial fibrillation (AF). BACKGROUND: Pacing at physiologic rates from the left atrium alters the atrial gradient and is associated with atrial tachyarrhythmias. At these physiologic rates, there is no change in the atrial effective refractory period (ERP). METHODS: Sixty-one chronically instrumented mongrel dogs in complete heart block were paced from the left or right atrium at 400 to 900 bpm for 46 +/- 3 days. Dogs were monitored weekly and electrophysiologic studies conducted to determine changes in the atrial gradient, ERP, and rhythm. RESULTS: Rapid atrial pacing was associated with concordant decreases in atrial gradient, ERP, and occurrence of AF. Incidence of AF increased with increasing pacing rate. Although there ultimately was an equal incidence of AF with left atrial and right atrial pacing, the onset of AF occurred earlier with left atrial pacing. As expected, ERP decreased in both atria. Animals with long control ERP did not fibrillate. CONCLUSIONS: Rapid pacing induces changes in atrial gradient, which can be used as a noninvasive marker of electrical remodeling. AF is accompanied by decreases in atrial gradient and ERP, and the incidence is highest in dogs with short control ERP.     

Right Atrial Thrombi and Depressed Right Atrial Appendage Function After Cardioversion of Atrial Fibrillation

BACKGROUND: It has been shown that cardioversion of atrial fibrillation may result in left atrial chamber and appendage dysfunction and cause new thrombi in the left atrium. The aim of this prospective study was to investigate right atrial appendage function and assess the incidence of new right atrial thrombi after electrical cardioversion. METHODS: Transthoracic echocardiography was performed in 25 patients 4 h before and at 24 h and 7 days after electrical cardioversion to determine right and left atrial mechanical function (internal atrial defibrillation, n = 16; external electrical cardioversion, n = 9), as assessed by peak A wave velocities derived from the transtricuspid and transmitral velocity profiles. In addition, transesophageal echocardiography was performed 4 h before and 24 h after cardioversion to evaluate postcardioversion thrombus formation in the right and left atrial chambers and to assess right and left atrial appendage function. The degree of spontaneous echo contrast was noted, and peak emptying velocities of the appendages were measured before and after cardioversion. RESULTS: Peak emptying velocities of both the right atrial appendage (mean +/- SD, 0.23 +/- 0.1 vs 0.32 +/- 0.11 m/sec; P = 0.02) and the left atrial appendage (0.3 +/- 0.15 vs 0.4 +/- 0.15 m/sec; P = 0.01) were significantly lower 24 h after cardioversion compared with 4 h before cardioversion, respectively. The degree of spontaneous echo contrast increased in the left atrium after cardioversion from 1.0 +/- 1.2 to 1.9 +/- 2.1 (P = 0.02), and in the right atrium, it increased from 0.8 +/- 1.1 to 1.2 +/- 1.1 (P = 0.1) after cardioversion. Peak A wave transtricuspid velocity increased from 0.26 +/- 0.05 m/sec at 24 h to 0.38 +/- 0.06 m/sec (P = 0.001) after 7 days; respective values for transmitral peak A wave velocity were 0.39 +/- 0.15 and 0.54 +/- 0.16 m/sec (P = 0.009). No thrombi were found in either the right or left atrium before cardioversion. In two patients, new thrombi in the right atrium were detected 24 h after internal atrial defibrillation. Thrombi were located at the superior rim of the fossa ovalis in both patients with patent foramen ovale. Another patient had developed a thrombus in the left atrial appendage. CONCLUSIONS: Electrical cardioversion may not only cause left atrial chamber and appendage dysfunction and left atrial thrombi but also lead to depressed right atrial appendage function and the generation of new thrombi in the body of the right atrium.     

Correlation of Left Atrial Diameter by Echocardiography and Left Atrial Volume by Computed Tomography

Introduction: For patients undergoing catheter ablation of atrial fibrillation (AF), left atrial size is a predictor of recurrence of AF during follow-up. For this reason, major clinical trials have used a left atrial diameter (LAD) of more than 5.0 or 5.5 cm, assessed by echocardiography, as an exclusion criterion for patients deemed candidates for ablation of AF. However, whether LAD accurately reflects true left atrial size has not been systematically investigated. Therefore, the purpose of this study was to test the hypothesis that LAD, measured by echocardiography, accurately correlates to left atrial volume measured by computed tomography (CT).
Methods and Results: We included 50 patients (mean age 56 ± 12 years, five female) with symptomatic AF (40% paroxysmal, 60% persistent), referred for catheter ablation. In each patient, transthoracic echocardiography was performed. Additionally, all patients underwent CT using a 64-slice CT scanner. Left atrial volume was calculated by manually tracing left atrial area on each CT cross-sectional image. Patients had a mean LAD measured by echocardiography of 4.5 ± 0.7 cm, ranging from 2.9 to 5.7 cm. Left atrial volume measured by CT ranged from 67 mL to 270 mL with a mean value of 146 ± 49 mL. A poor correlation was noted between LAD and left atrial volume, r = 0.49 (P < 0.001).
Conclusion: LAD measured by echocardiography correlates poorly with left atrial volume measured by CT in patients with AF. As a result, selecting patients with AF for treatment with catheter ablation should not be based on an echocardiographic-derived LAD alone.     

Blade and balloon atrial septostomy for left heart decompression in patients with severe ventricular dysfunction on extracorporeal membrane oxygenation

Extracorporeal membrane oxygenation (ECMO) is used as circulatory support or bridge to transplantation in patients with severe left ventricular (LV) dysfunction. Left heart decompression is needed to reduce pulmonary edema, prevent pulmonary hemorrhage, and reduce ventricular distention that may aid in recovery of function. We reviewed our experience from November 1993 to December 1997 with 10 patients having severe LV dysfunction (7 myocarditis, 3 dilated cardiomyopathy) who required circulatory support with ECMO and who underwent left heart decompression with blade and balloon atrial septostomy (BBAS). Patients ranged in age from 1 to 24 years (median, 3 years). Indications for BBAS included left atrial/left ventricular distension (10), pulmonary edema/hemorrhage (9), or severe mitral regurgitation (2). BBAS was performed electively in eight patients and urgently in two patients. BBAS was performed while on ECMO in seven patients and pre-ECMO in three. A femoral venous approach was used in all patients. ECMO patients were fully heparinized. Transseptal puncture was required in nine patients while one patient had a patent foramen ovale. Blade septostomy was performed in all patients. Enlargement of the defect was then performed by stationary balloon dilation in nine and Rashkind balloon atrial septostomy in one. Balloon diameters ranged from 10 to 20 mm. Sequential balloon inflations were performed in some patients. Adequacy of the atrial septal defect (ASD) was confirmed by pressure measurement and echocardiography. Adequate left heart decompression was achieved in all patients. Pulmonary edema improved in nine of nine patients. Left atrial mean pressure fell from a mean of 30.5 mm Hg, (range, 12–50 mm Hg) to 16 mm Hg (range, 9–24 mm Hg). Left atrial to right atrial pressure gradient fell from a mean of 20 mm Hg pre-BBAS to 3 mm Hg post-BBAS. ASDs ranged in size from 2.5 to 8 mm (mean, 5.9 mm). Complications included needle perforation of the left atrium without hemodynamic compromise (one), ventricular fibrillation requiring defibrillation (one), and hypotension following BBAS which responded to volume infusion (two). Duration of ECMO ranged from 41 hr to 704 hr (mean, 294 hr). Seven patients survived and four patients had recovery of normal LV function. Of those who recovered, two had no ASD at follow-up while two ASDs are patent 14 days and 3 months post-BBAS. Three patients underwent successful cardiac transplantation. Three patients died, all of whom had multisystem organ failure with or without sepsis. A patent ASD was noted at transplant (three) or autopsy (two). No patient required a second BBAS. BBAS alleviates severe left atrial hypertension and pulmonary edema. In addition, BBAS avoids the potential bleeding complications of surgical left heart decompression. Stationary balloon dilation of the atrial septum is an effective alternative to Rashkind balloon septostomy in older patients. BBAS achieves left heart decompression that may permit recovery of LV function or allow extended ECMO support as a bridge to transplant. Cathet. Cardiovasc. Intervent. 46:179–186, 1999. © 1999 Wiley-Liss, Inc.     

Stenting of a restrictive foramen ovale in a patient with hypoplastic left heart syndrome

Neonates with a severely restrictive foramen ovale and hypoplastic left heart syndrome (HLHS) present as an emergency. We report the case of a newborn in whom left atrial decompression was successfully achieved by stent implantation into the foramen ovale on the first day of life.     

Atrial dysfunction as a marker of iron cardiotoxicity in thalassemia major

We measured left atrial size and function from biplane MRI data in 62 adults with thalassemia major. Age-adjusted left atrial ejection fraction was depressed in 7 out of 20 subjects having T2* < 10 ms. Left atrial size, left ventricular size and cardiac output fell with cardiac iron loading, representing increased cardiac or peripheral vascular stiffness.     

Atrial septal aneurysm with right-to-left interatrial shunting

Interatrial shunting in the presence of an atrial septal aneurysm is an uncommon but well recognized abnormality. Previous case reports have demonstrated that elevated right atrial pressure secondary to pulmonary embolism or right ventricular infarction may cause right-to-left interatrial shunting in the presence of an atrial septal aneurysm. We describe a unique situation in which an atrial septal aneurysm was associated with a right-to-left shunt secondary to severe systemic hypotension and normal right atrial pressure. In this patient, we used midodrine, an oral alpha-1 agonist, to increase systemic arterial pressure, decrease the severity of the shunt, and treat the severe hypoxemia. This case establishes that right-to-left interatrial shunting can result from a decrease in left ventricular afterload with normal right atrial pressure. Oral alpha-1 agonist therapy can be used successfully to treat patients such as ours and possibly others with similar functional abnormalities.     

Decompression of the left ventricle in the recovery period during myocardial revascularization

Effective left heart decompression is essential for the reduction of myocardial oxygen consumption during recovery from an induced ischemic insult. During the early postischemic recovery phase of patients undergoing aorto-coronary bypass surgery, left ventricular, left atrial and aortic pressures were measured in non-vented hearts and in 2 types of left ventricular decompression. The following findings were made: Total cardiopulmonary bypass with effective decompression of the left ventricle decreases peak systolic left ventricular pressure, thereby reducing oxygen consumption of the myocardium. In this way adequate conditions are provided for recovery of the myocardium after unclamping of the aorta. The best method for decompression appears to be the placing of a large-lumen cannula in the left ventricle and allowing the blood to pour freely from the vent. The zero or near zero left ventricular filling pressure achieved with total cardiopulmonary bypass but without ventricular decompression does not prevent the chamber from producing isometric pressure work with peak systolic pressure reaching 80 to 90 torr. The hazard of air embolism may be reduced by precautionary measures. Left atrial monitoring permits recognition of pressure decreases to negative values. Active suction of the blood from the left ventricle is dangerous and should be avoided.     

Atrial septal aneurysm and stroke: a transesophageal echocardiographic study

The prevalence and morphologic characteristics of atrial septal aneurysms identified by transesophageal echocardiography in 410 consecutive patients are described. Two groups of patients were compared: Group I consisted of 133 patients referred for evaluation of the potential source of an embolus and Group II consisted of 277 patients referred for other reasons. An atrial septal aneurysm was diagnosed by transesophageal echocardiography in 32 (8%) of the 410 patients. Surface echocardiography identified only 12 of these aneurysms. Atrial septal aneurysm was significantly more common in patients with stroke (20 [15%] of 133 vs. 12 [4%] of 277) (p less than 0.05); right to left shunting at the atrial level was demonstrated in 70% of patients in Group I and 75% of patients in Group II by saline contrast echocardiography. Four patients in Group I had an atrial septal defect with additional left to right flow. There was no difference between the two groups in aneurysm base width, total excursion or left atrial or right atrial excursion. However, Group I patients had a thinner atrial septal aneurysm than did Group II patients. It is concluded that an atrial septal aneurysm occurs commonly in patients with unexplained stroke, is more frequently detected by transesophageal echocardiography than by surface echocardiography and is usually associated with right to left atrial shunting. Treatment (anticoagulant therapy vs. surgery) of atrial septal aneurysm identified in stroke patients can be determined only by long-term follow-up studies.     

Inverted Left Atrial Appendage Bonded to Atrial Septum

Inverted left atrial appendage (LAA) is a rare surgical complication. Our patient, a boy aged 2 years, was diagnosed with a partial atrioventricular defect with mild regurgitation of the left atrioventricular valve and a large primum atrial septal defect. Direct postoperative transesophageal echocardiography revealed a new left atrial mass attached to the atrial septum, without left ventricle inflow obstruction. Out of concern about the nature of this mass, we chose surgical direct examination. Intraoperatively, we diagnosed it as an inverted LAA accidentally attached to the atrial septum suture line. Awareness of this condition can avoid unnecessary diagnostic and therapeutic procedures.     

Atrial enlargement as a consequence of atrial fibrillation. A prospective echocardiographic study

To test the hypothesis that atrial enlargement can develop as a consequence of atrial fibrillation, left and right atrial dimensions were measured echocardiographically at two different time points in patients with atrial fibrillation. Patients were selected who initially had normal atrial sizes and who had no evidence of significant structural or functional cardiac abnormalities other than atrial fibrillation either by history or two-dimensional and Doppler echocardiography. Fifteen patients were studied (12 men and three women; mean age, 67.3 years). Average time between studies was 20.6 months. Three orthogonal left atrial dimensions and two right atrial dimensions were measured, and all were found to increase significantly between studies. Also, highly significant increases in calculated left atrial volume (from 45.2 to 64.1 cm3, p less than 0.001) and right atrial volume (from 49.2 to 66.2 cm3, p less than 0.001) were observed. The relative extents of left and right atrial volume increase did not differ, and left ventricular size did not change significantly between studies. These results indicate that atrial enlargement can occur as a consequence of atrial fibrillation. The maintenance of sinus rhythm, therefore, may prevent atrial enlargement and its adverse clinical effects.     

Atrial Tachycardia Confined Within the Left Atrial Appendage

AT Confined Within the LAA. Left atrial tachycardias are often seen following catheter ablation of persistent atrial fibrillation (AF). We report here an unusual case where AF was converted to sinus rhythm following catheter ablation, but ongoing atrial tachycardia confined within the left atrial appendage (LAA) was observed. Although the LAA tachycardia was dissociated from the atrium in sinus rhythm, bidirectional conduction between the left atrium and the LAA was, however, demonstrated after tachycardia termination. (J Cardiovasc Electrophysiol, Vol. 21, pp. 933‐935, August 2010)     

Atrial fibrillation and atrial enlargement in patients with mitral stenosis

The present study was designed to assess the relative contribution of atrial fibrillation and left atrial pressure to changes in the size of the left and right atria in patients with mitral stenosis. The study included 155 subjects, 102 of whom underwent prospective echocardiography and Doppler cardiography, and 69 of whom underwent cardiac catheterization. The size of the atria was determined by two-dimensional echocardiography. There were no significant hemodynamic differences between patients with mitral stenosis who were in either sinus rhythm or atrial fibrillation. The left atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (37.6 +/- 10.8 cm2) than in patients in sinus rhythm (27.8 +/- 7.7 cm2) or normal subjects (15 +/- 3.3 cm2). The size of the right atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (21.7 +/- 5.2 cm2) than in patients in sinus rhythm (13.4 +/- 3.9 cm2) or normal subjects (13.8 +/- 3.7 cm2). Multiple regression analysis showed that the severity of mitral stenosis accounted for 38%, age for 7%, and atrial fibrillation for 11% of the change in the size of the left atrium. Atrial fibrillation accounted for 24%, age for 11, and mitral valve area for 3% of the change in the size of the right atrium. The analysis suggests that the onset of left atrial dilatation in mitral stenosis is the result of an early increase in left atrial pressure. Atrial fibrillation, which develops irrespective of the severity of the mitral stenosis, contributes to a further enlargement of the left and right atria.     

Atrial fibrillation in congestive cardiomyopathy: Echocardiographic and hemodynamic correlates

Previous studies have suggested an unexpectedly low incidence of atrial fibrillation in patients with congestive cardiomyopathy. To further investigate the incidence of chronic atrial fibrillation in these patients and its relationship to left atrial dimension and pressure, we retrospectively examined M-mode echocardiographic and cardiac catheterization data from 54 patients with idiopathic (n = 29) and ischemic (n = 25) congestive cardiomyopathy. The incidence of atrial fibrillation (17%) was surprisingly low given the degree of left atrial enlargement (51 ± 5 mm; mean ± SD) and left atrial hypertension (19 ± 8 mm Hg). In addition, there were no significant differences in left atrial pressure or left atrial dimension between those congestive cardiomyopathy patients in sinus rhythm and those in atrial fibrillation, nor was there a higher incidence of secondary mitral regurgitation in patients in atrial fibrillation. Comparisons were also made between congestive cardiomyopathy patients and 21 patients with primary mitral valve disease and atrial fibrillation. Left atrial pressure was not significantly different between these groups. However, the mean left atrial dimension of the patients with mitral valve disease (56 ± 8 mm) was greater (P < 0.01) than that of patients with idiopathic (51 ± 6 mm) or ischemic (50 ± 4 mm) cardiomyopathy in sinus rhythm and also greater (P = 0.07) than left atrial dimension (51 ± 6 mm) of congestive cardiomyopathy patients in atrial fibrillation. Furthermore, massive enlargement of the left atrium (greater than 60 mm) was a common feature of mitral valve disease (33% incidence) but occurred only rarely in congestive car-diomyopathy (5% incidence). We conclude that while left atrial volume and pressure loads may be important contributors to the pathogenesis of atrial fibrillation, these factors are not sufficient to produce the arrhythmia in most patients with congestive cardiomyopathy. Other variables such as disease duration or the degree of atrial fibrosis or inflammation may also be important in determining which patients with left atrial enlargement will develop atrial fibrillation. Furthermore, massive left atrial enlargement (left atrial dimension > 60 mm) is rarely associated with ischemic or idiopathic congestive car-diomyopathy and suggests underlying primary mitral valve disease.     

Atrial Myxoma in a Patient with Hypertrophic Cardiomyopathy

Atrial myxoma is the most common primary cardiac tumor. Patients with atrial myxoma typically present with obstructive, embolic, or systemic symptoms; asymptomatic presentation is very rare. To our knowledge, isolated association of atrial myxoma with hypertrophic cardiomyopathy has been reported only once in the English-language medical literature. We report the case of an asymptomatic 71-year-old woman with known hypertrophic cardiomyopathy in whom a left atrial mass was incidentally identified on cardiac magnetic resonance images. After surgical excision of the mass and partial excision of the left atrial septum, histopathologic analysis confirmed the diagnosis of atrial myxoma. The patient was placed on preventive implantable cardioverter-defibrillator therapy and remained asymptomatic. The management of asymptomatic cardiac myxoma is a topic of debate, because no reports definitively favor either conservative or surgical measures.Key words: Abnormalities, multiple/diagnosis; cardiomyopathy, hypertrophic/diagnosis/physiopathology; heart atria/pathology; heart neoplasms/diagnosis/pathology/surgery; myxoma/diagnosis/pathology/surgery; risk factorsPrimary cardiac tumors are rare entities, with a prevalence on autopsy of less than 1%.¹ Approximately three quarters of primary heart tumors are benign, and approximately 75% of those are myxomas. The remainder are lipomas, papillary fibroelastomas, and rhabdomyomas.² Cardiac myxomas usually develop in the atria—the vast majority in the left atrium, specifically from the interatrial septum at the border of the fossa ovalis.³ Patients with atrial myxoma typically present with cardiovascular symptoms such as heart failure and pulmonary hypertension, secondary to mitral valve obstruction. They can also present with neurologic deficits, transient or permanent visual loss, or involvement of internal viscera secondary to embolic phenomena. Constitutional symptoms include fatigue, fever, erythematous rash, arthralgia, myalgia, and weight loss.³ An asymptomatic presentation is extremely rare. Hypertrophic cardiomyopathy (HCM) is often diagnosed incidentally, and it can also present with obstructive symptoms similar to those of myxoma.⁴ We describe and discuss the case of an asymptomatic elderly patient with known HCM and an incidentally diagnosed atrial myxoma.     

Simultaneous Right and Left Atrial Appendage Thrombus in a Patient with Atrial Fibrillation: A Lesson to Remember

We report a case of simultaneous right and left atrial appendage thrombi in a 76‐year‐old‐man with atrial fibrillation. Although transesophageal echocardiography is considered a routine diagnostic procedure, complete and comprehensive visualization of both atrial appendages is of paramount importance, particularly with the introduction of new therapeutic options like left atrial appendage exclusion devices. We expect to raise awareness among clinicians of the prevalence and implications of bilateral atrial appendage thrombi in common clinical practice.     

Efficacy of Atrial Antitachycardia Functions for Treating Atrial Fibrillation: Observations in Patients with a Dual-Chamber Defibrillator

In patients with conventional indication for ICD implantation, atrial fibrillation may occur in more than 50% during the life-span of the device and may lead to severe adverse events. Dual chamber defibrillators with atrial antitachycardia functions, including prevention algorithms, arrhythmia detection capability and atrial therapy options (antitachy pacing and cardioversion) have been recently introduced. The aim of this review is to examine the effectiveness of these new devices and to identify patients who may benefit. We recently studied 112 patients who received the device because of life-threatening ventricular arrhythmias. Fifty-five percent of them had atrial fibrillation prior to implantation. During the follow-up (one year on average), 27% had at least one episode of sustained atrial tachyarrhythmia. Effectiveness of atrial antitachy pacing was 71% on regular atrial tachycardia and 36% on irregular atrial tachyarrhythmias. Atrial shock efficacy was over 90% when adequately programmed. Interestingly, near half of the episodes started as regular atrial tachycardia and accelerated and became less organized in few minutes. Early delivery of antitachy pacing may increase success rate and decrease the need for atrial shock. Furthermore, it may prevent atrial remodeling and reduce atrial fibrillation burden.Based on our experience, we recommend that all patients with a class I indication for defibrillator implantation (related to risk of ventricular arrhythmias) who have a history of or are at risk of developing atrial tachyarrhythmias should receive a dual chamber defibrillator equipped with atrial antitachycardia functions. Furthermore, patients either with a history of heart failure, with poor functional capacity (functional class III or IV), depressed left ventricular ejection fraction, a need for monitoring of atrial rhythm, or in whom there is some concern about appropriate detection of ventricular arrhythmias, may benefit from a single device capable of managing ventricular and supraventricular arrhythmias.