Right ventricular ischemia diagnosed by an esophageal electrocardiogram and right atrial pressure tracing.
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Aged↗
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Efficacy and safety of right and left atrial ablations on the beating heart with irrigated bipolar radiofrequency energy: a long-term animal study.
OBJECTIVE: The Cox maze procedure is the most effective surgical treatment for atrial fibrillation; however, its complexity has limited its clinical utility. The purpose of this study was to simplify the procedure by using an irrigated bipolar radiofrequency ablation device on the beating heart without cardiopulmonary bypass. METHODS: Six domestic pigs underwent median sternotomy. The pulmonary veins were circumferentially ablated. Electrical isolation was confirmed by pacing. Eight lesions were performed epicardially, and three lesions were performed through purse-string sutures with one of the jaws of the device introduced into the right atrium. After 30 days, magnetic resonance imaging was performed to assess atrial function, pulmonary vein anatomy, and coronary artery patency. Cholinergic stimulation and burst pacing were administered to induce atrial fibrillation. Histologic assessment of the heart was performed after the animal was killed. RESULTS: A modified Cox maze procedure was successfully performed with the irrigated bipolar radiofrequency device with no deaths. In every instance, the pulmonary veins were electrically isolated. Cholinergic stimulation with burst pacing failed to produce atrial fibrillation. Imaging studies revealed tricuspid regurgitation without evidence of pulmonary vein stenosis, coronary artery stenosis, or intra-atrial thrombus. Total atrial ejection fraction was 16.9% +/- 7.5%, a significant reduction. Histologically, 99% of the lesions were transmural, and there was no evidence of coronary sinus injury. CONCLUSION: Lesions on both the right and left atria can be created successfully on the beating heart with irrigated bipolar radiofrequency. The great majority of lesions with this device were transmural. This device should not be used on valvular tissue.
Animals↗
Hemodynamic effects of atrial septal pacing in cardiac resynchronization therapy patients.
INTRODUCTION: Spontaneous or pacing-induced interatrial conduction delay may affect the outcome of heart failure patients treated with cardiac resynchronization therapy (CRT). The objective of this study was to evaluate the impact of the atrial pacing site (right atrial appendage, RAA; and low interatrial septum, LIS) during biventricular (BV) pacing on the left ventricular (LV) systolic function in candidates for CRT. METHODS AND RESULTS: Fifteen heart failure patients with left bundle branch block and LV ejection fraction < or =35% were enrolled. Electrodes were placed at the RAA, LIS, right ventricular apex, and LV free wall. A DDD protocol was tested, which consisted of 50 beats in AAI mode from the RAA followed by 50 beats in BV DDD mode with atrial pacing at the RAA (DDD_RAA) or at the LIS (DDD_LIS) at four AV delays. The average (+/-SD)%LV+dP/dtmax increase during DDD_RAA and DDD_LIS pacing with respect to baseline was 24 +/- 16% and 21 +/- 15%, respectively (P < 0.01), and average percentage change in aortic pulse pressure during DDD_RAA and DDD_LIS with respect to baseline (%PP) was 13 +/- 8% and 13 +/- 7% (ns). CONCLUSIONS: Our results show a significant hemodynamic improvement with both DDD_RAA and DDD_LIS biventricular pacing compared to AAI pacing. However DDD_LIS pacing was not superior to DDD_RAA pacing in acute hemodynamic responses.
Acute Disease↗
Early and late results of a protocol for simple transposition leading to an atrial switch (Mustard) repair.
Inferences: A treatment protocol for patients with simple transposition, consisting of initial balloon atrial septostomy and leading to a delayed atrial switch repair of the Mustard type, in good circumstances, results in survivorship at 1 month, 1 year, 10 years, and 20 years of 95% (95% confidence limits [CL] 90% to 97%), 90% (95% CL 84% to 94%), 83% (95% CL 74% to 90%), and 80% (95% CL 70% to 88%), respectively. Low birth weight adversely affects survivorship. Hypoxia or heart failure accounts for most deaths within the first month and before the atrial switch (Mustard) repair. Most of the few deaths late postoperatively are sudden and they appear to occur particularly in patients who have junctional rhythm. A progressive increase in the prevalence of junctional rhythm has been a risk of the atrial switch repair, and only 76%, 65%, 59%, 56%, and 53% of patients can be expected to be free of this by 1, 5, 10, 15, and 20 years after repair. Important right ventricular dysfunction late after an atrial switch repair, with its adverse affect on the patients' functional capacity, appears to be present in up to 10% of patients after the atrial switch repair, but may not be an immutable risk of this type of repair. About 90% of patients, essentially all of those who do not have right ventricular dysfunction, can be expected to be in New York Heart Association class I or II late postoperatively.
Adult↗
Renal-endocrine adaptations to endogenous atrial natriuretic factor during tachycardia-induced reductions in renal perfusion pressure.
Atrial pressure, atrial natriuretic factor (ANF), the renin-angiotensin-aldosterone system, and renal hemodynamic functions were examined during and after right ventricular pacing in anesthetized dogs (n = 9). Mean arterial pressure, cardiac output, and renal blood flow decreased during tachycardia while right and left atrial pressures increased. ANF markedly increased during tachycardia but urinary and fractional excretion of sodium were unchanged from control. Plasma renin activity was not increased during pacing despite the decrease in renal perfusion pressure. After tachycardia and restoration of mean arterial pressure to control, ANF declined but remained elevated above control despite a return of atrial pressure to control level. After tachycardia, urinary and fractional sodium excretion increased significantly in the absence of an increase in glomerular filtration rate. These findings support the following conclusions: 1) tachycardia increases ANF in association with increased atrial pressure; however, an elevation of ANF persists following tachycardia despite the absence of the persistent stimulus of elevated atrial pressures; 2) the increase in ANF during tachycardia may contribute to the absence of a decrease in sodium excretion and activation of the renin-angiotensin system that occurs with reduction in renal perfusion pressure; and 3) tachycardia-induced natriuresis may be dependent on an increase in ANF and the maintenance of renal perfusion pressure.
Aldosterone↗
Effect of right atrial appendicectomy on the release of atrial natriuretic peptide in humans.
The present study evaluated the effect of right atrial appendicectomy on the release of atrial natriuretic peptide (ANP) and subsequent changes in postoperative haemodynamics in 20 men undergoing coronary artery bypass graft surgery. The right atrial appendix was removed in ten patients and saved in ten. Serum ANP, sodium levels and urinary sodium excretion were measured before and on days 1, 7 and 30 after surgery. Haemodynamic parameters were monitored before surgery and on day 30. Serum ANP levels fell significantly in patients undergoing appendicectomy (P < 0.05); haemodynamic parameters were unchanged. Hence, appendicectomy reduced serum ANP levels in the short term, though these tended to rise again with time; cardiac function was not affected by lowered levels of serum ANP. Consequently, saving the appendix in right atrial appendicectomy improves natriuresis and may decrease diuretic requirement.
Adult↗
Atrial flutter update.
Typical atrial flutter has long been considered a reentrant arrhythmia, but it is only recently that the full structure of the right atrial circuit was understood, leading to de devise of ablation techniques. Recognition of the role of functional block, based on anisotropic conduction was crucial to understanding of the flutter circuit. Anisotropy at the terminal crest creates a line of block that, with the orifices of superior and inferior vena cava, constitutes the posterior boundary of the flutter circuit. The anterior boundary is the tricuspid ring, and the circuit is a ring of myocardium made by the septal and anterior right atrial walls, linked on top by the right atrial roof and inferiorly by the inferior vena cava-tricuspid ring isthmus. This isthmus, a relatively narrow part of the circuit, has become the established target for typical flutter ablation. Complete, bidirectional isthmus block is the final goal of flutter ablation. This has to be assessed, after flutter interruption, by pacing both sides of the ablation line while recording electrogram sequences from the opposite right atrial wall and the isthmus itself. Success is great in terms of prevention of flutter recurrence, however a 30% incidence of atrial fibrillation during follow-up casts a large shadow on long-term prognosis. Understanding of the myocardial abnormalities underlying atrial flutter and fibrillation will be necessary to improve this long-term outlook.
Anticoagulants↗
Management of cardiomyopathy resulting from incessant supraventricular tachycardia in infants and children.
BACKGROUND: Radiofrequency ablation is considered to be the treatment of choice in patients with ventricular dysfunction related to incessant supraventricular tachycardia. However, reservations regarding its use in infants and children prompted us to try alternative strategies for this group. METHODS AND RESULTS: Eight children (age range: 1 day to 10 years) were diagnosed to have tachycardia-related ventricular dysfunction in the past 6 years. They presented with symptoms of palpitation, dyspnea and/or generalized swelling over the body of 3 months to 2 years'duration. The cardiothoracic ratio at presentation was 64% (52%-70%) and ejection fraction was 22.2% (15%-45%). In 7 patients tachycardia was diagnosed to be ectopic atrial and in 1 it was permanent junctional reciprocating tachycardia. Six of these children were managed with intravenous/oral amiodarone in combination with digoxin (3) and/or propranolol (2). In one child addition of amiodarone to digoxin and propranolol led to polymorphic ventricular tachycardia, and amiodarone was withdrawn. Only one child underwent radiofrequency ablation as the first choice because regular follow-up was not possible due to logistic reasons. Sinus rhythm with normalization of ventricular function was achieved in 6 of the 7 children treated medically. One child continued to have frequent episodes of tachycardia and underwent successful radiofrequency ablation of a high right atrial ectopic focus. Two out of the 6 patients on amiodarone could be managed with only digoxin and propranolol after their ventricular function had returned to normal. A third patient relapsed on stopping amiodarone and underwent successful radiofrequency ablation of a left atrial ectopic tachycardia. CONCLUSIONS: Short-term amiodarone in combination with digoxin/propranolol is a safe and effective treatment strategy for infants/children with tachycardiomyopathy. Control of tachycardia is achieved in the majority, leading to recovery of ventricular function. This approach may avoid unnecessary ablations in children or at least postpone it till the procedure would be safer.
Amiodarone↗
Ultrastructure and possible function of an atrial paraganglion not directly related to atrial ganglion in the albino mouse.
The ultrastructure of a paraganglion found in right atrium of albino mouse close to the superior cava vein is described. A capillary, which occupied the central part of the paraganglion, was surrounded by three chromaffin cells. Two other chromaffin cells were also present, but neither nerve fibers nor nerve endings were seen. The possible physiological role of paraganglia is discussed.
Albinism↗
Right ventricular filling following balloon pulmonary valvuloplasty.
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Catheterization↗
Enalapril as initial and sole treatment in severe chronic heart failure with sodium retention.
Five patients, who had never received any drug treatment but who had severe chronic congestive heart failure with salt and water retention, were studied before and after a single dose of enalapril (10 mg orally). Three patients continued on enalapril as monotherapy (10 mg b.d. orally) for one month. Central haemodynamics, body fluid volumes, renal function and plasma hormones were measured at rest. The initial mean right atrial pressure was 13 +/- 4 mm Hg, pulmonary wedge pressure 29 +/- 4 mm Hg and cardiac index 1.8 +/- 0.21/min/m2. Enalapril, given acutely, caused only small changes. Two patients were withdrawn after the single dose of enalapril and treated with diuretics for clinical reasons. The remaining three patients each lost more than 4 kg in weight after one month of treatment with enalapril alone. Total body exchangeable sodium and total body water were reduced but central haemodynamics were unchanged. Although enalapril was of some benefit when given alone to patients with severe congestive heart failure, all five patients were finally treated with diuretics for clinical reasons. Enalapril is not recommended as the initial and only therapy for patients with severe congestive heart failure.
Adult↗
Effect of whiskey on atrial vulnerability and "holiday heart".
Vulnerability to atrial fibrillation and flutter was examined in 11 alcohol abusers who did not have cardiomyopathy or manifest heart failure. Atrial extrastimulation was done with rapid pacing (drive cycle length 500 ms) to facilitate induction of atrial vulnerability, seen in four alcohol abusers. The remaining seven were retested 30 minutes after drinking 60 to 120 ml of 86 proof whiskey (ethanol blood levels were 49 to 101 mg/100 ml but pulmonary capillary wedge pressure remained normal in all) and atrial fibrillation or flutter was induced in three of the drinkers. Three nondrinkers, symptomatic with sinus bradycardia but not in heart failure, were found not to be vulnerable to atrial fibrillation or flutter, but flutter was induced in two of the three after drinking whiskey. Whiskey did not alter atrial functional refractory periods (mean +/- standard error of the mean 297 +/- 14 to 290 +/- 12 ms) or widen the dispersion among three disparate right atrial sites (57 +/- 13 to 47 +/- 12 ms). Thus, whiskey enhanced vulnerability to atrial fibrillation and flutter in patients without heart failure or cardiomyopathy, substantiating the "holiday heart" syndrome.
Adult↗
Elevation of the tumor marker CA125 in right heart failure.
Carbohydrate antigen 125, known as a marker for ovarian cancer, has been reported to be elevated in heart failure caused by left ventricular dysfunction. A case of elevated carbohydrate antigen 125 in isolated right heart failure due to atrial septal defect with preserved left ventricular function is reported.
Aged↗
Contribution of beta 1- and beta 2-adrenoceptors of human atrium and ventricle to the effects of noradrenaline and adrenaline as assessed with (-)-atenolol.
1. (-)-Atenolol was used as a tool to assess the function of beta 1- and beta 2-adrenoceptors in human heart. Right atrial and left ventricular preparations from patients undergoing open heart surgery were set up to contract isometrically. Membrane particles were prepared for beta-adrenoceptor labelling with [3H]-(-)-bupranolol and adenylate cyclase assays. 2. The positive inotropic effects of (-)-noradrenaline were antagonized to a similar extent by (-)-atenolol in atrial and ventricular preparations. (-)-Atenolol consistently antagonized the effects of (-)-adrenaline to a lesser extent than those of (-)-noradrenaline in atrial preparations. In ventricular preparations (-)-atenolol antagonized the effects of low concentrations of (-)-adrenaline to a lesser extent than those of high concentrations. 3. pKB values (M) of (-)-atenolol, estimated with non-linear analysis from the blockade of the positive inotropic effects of the catecholamines, were 7.4 for beta 1-adrenoceptors and 6.0 for beta 2-adrenoceptors. 4. (-)-Atenolol inhibited the binding of [3H]-(-)-bupranolol to ventricular beta 1-adrenoceptors with a pKD (M) of 5.9 and to ventricular beta 2-adrenoceptors with a pKD of 4.6. 5. (-)-Atenolol inhibited the catecholamine-induced adenylate cyclase stimulation in the atrium and ventricle with pKB values of 5.8-6.4 for beta 1- and pKB values of 4.7-5.7 for beta 2-adrenoceptors. The binding and cyclase assays suggest a partial affinity loss for (-)-atenolol inherent to membrane preparations. 6. beta 1-Adrenoceptors mediate the maximum positive inotropic effects of (-)-noradrenaline in both the atrium and ventricle of man. beta 2-Adrenoceptors appear to be capable of mediating maximal positive inotropic effects of (-)-adrenaline in atrium. In contrast, ventricular beta 2-adrenoceptors mediated only submaximal effects of (-)-adrenaline.
Adenylyl Cyclase Inhibitors↗
Carcinoid heart disease: relationship of circulating vasoactive substances to ultrasound-detectable cardiac abnormalities.
Cardiac ultrasound investigation of 68 prospectively studied patients with histologically proven midgut carcinoid tumors showed right heart disease in 66%. The abnormal findings included morphologic and functional aberrations of the tricuspid valve in 52% and 83%, respectively, right atrial and ventricular enlargement in 53% and 30%, and paradoxical systolic septal contractions in 19%. The patients with the most pronounced right heart disease had significantly higher (p less than .01) plasma levels of the tachykinins neuropeptide K and substance P as well as higher (p less than .001) urinary excretion of the serotonin metabolite 5-hydroxyindoleacetic acid. These patients also had the most extensive tumor disease. The occurrence of echocardiographic abnormalities of the left heart was similar to that in healthy individuals of the same age, but abnormalities were less frequent among the patients with severe right heart disease. Electrocardiographic changes were nonspecific. Right heart disease thus seems to be present more often than previously reported in patients with malignant midgut carcinoid tumors. The severity of cardiac involvement does not seem to be related to the duration of carcinoid disease but more to the extent of the disease, i.e., higher plasma levels of serotonin and tachykinins.
Adult↗
Effects of extreme lateral posture on hemodynamics and plasma atrial natriuretic peptide levels in critically ill patients.
OBJECTIVE: To quantify the hemodynamic effects of turning critically ill, mechanically ventilated patients to the extreme left and right lateral postures. DESIGN: Prospective investigation. SETTING: Eight-bed intensive care unit in a university hospital. PATIENTS: Twelve consecutive patients presenting with severe respiratory failure and requiring continuous positive inotropic support. INTERVENTIONS: All patients were mechanically ventilated and placed in a kinetic treatment system. They were positioned in the supine, left dependent, and right dependent postures, resting for 15 min in each position. MEASUREMENTS AND RESULTS: Hemodynamic measurements, assessments of right ventricular function, and determinations of intrathoracic blood volume were performed in three different positions. Concentrations of atrial natriuretic peptide in plasma were quantified. In three patients, the findings were controlled by transesophageal echocardiography. Cardiac index [median (range) 5.5 (3.2-8.1) vs 4.3 (3.2-7.5) l/min per m2, p < 0.01], intrathoracic blood volume [1125 (820-1394) vs 1037 (821-1267) ml/m2, p < 0.01], and right ventricular end-diastolic volume [130 (83-159) vs 114 (79-155) ml/m2, p < 0.05] increased significantly in the left dependent position compared to supine. Mean arterial pressure did not change. Atrial natriuretic peptide levels rose from 140 to 203 pg/ml. In the right dependent position, we found a marked decrease in the mean arterial pressure [85 mmHg (supine) to 72 mmHg (right dependent), p < 0.01]. Cardiac index and intrathoracic blood volume were unchanged, but right ventricular end-diastolic volume decreased from 114 to 102 ml/m2 (p < 0.05). Additionally, atrial natriuretic peptide levels decreased significantly (median delta value: 37 pg/ml). In echocardiographic controls we found an increase in right ventricular end-diastolic diameters in the left dependent position and shortened diameters in the right dependent position. CONCLUSIONS: Extreme lateral posture affects the cardiovascular system in critically ill, mechanically ventilated patients: in the left dependent position a "hyperdynamic state" is reinforced, while the right decubitus position impairs right ventricular preload and predisposes to hypotension. Echocardiography and changes in plasma atrial natriuretic peptide values indicate that these findings are due to altered distensibility of the right ventricle caused by regional intrathoracic gravitational changes. We conclude that the duration and the angle of lateral posture should be restricted in hemodynamically unstable patients.
Acute Disease↗
Estimation of the right ventricular volume overload in children with atrial septal defect by body surface mapping.
To investigate the possibility of estimating the right ventricular volume overload in atrial septal defect (ASD) by body surface mapping (BSM), 45 children with ASD were included in the present study. The breakthrough minimum (BTM) appeared later and more leftward in ASD subjects than in the normal controls. Neither the length of the delay in the appearance of the BTM nor the extent of its leftward deviation was significantly correlated with the pulmonary and systemic flow volume ratio (Qp/Qs), obtained by cardiac catheterization. Therefore neither could be used as the parameter of the right ventricular volume overload. sigma R, Rmax (D3 + D4) + magnitude of S max (H4 + H5) and "T dep", the sum of the absolute values of the departure indices (DIs) in the G4, G5, H4 and H5 leads, and the DIs in the J5, J6, K5, and K6 leads in T departure Map, correlated with the Qp/Qs significantly (r = 0.62, 0.68, 0.69, respectively). Accordingly, they might be useful for estimating the right ventricular volume overload. The subjects were divided into 3 groups according to their Qp/Qs. Discriminant analysis between these 3 groups was then performed, using Rmax (D3), magnitude of S max (H4), and T dep as the variables. The accuracy of this discrimination was 82.2%. The results suggest the possibility of estimating the severity of ASD by BSM.
Adolescent↗
Chronic hemodynamic overload of the atria is an important factor for gap junction remodeling in human and rat hearts.
OBJECTIVES: The expression and distribution of connexins is abnormal in a number of cardiac diseases, including atrial fibrillation, and is believed to favor conduction slowing and arrhythmia. Here, we studied the role of atrial structural remodeling in the disorganization of gap junctions and whether redistributed connexins can form new functional junction channels. METHODS: Expression of connexin-43 (Cx43) was characterized by immunoblotting and immunohistochemistry in human right atrial specimens and in rat atria after myocardial infarction (MI). Gap junctions were studied by electron and 3-D microscopy, and myocyte-myocyte coupling was determined by Lucifer yellow dye transfer. RESULTS: In both chronically hemodynamically overloaded human atria in sinus rhythm and in dilated atria from MI-rats, Cx43 were dephosphorylated and redistributed from the intercalated disc to the lateral cell membranes as observed during atrial fibrillation. In MI-rats, the gap junctions at the intercalated disc were smaller (20% decrease) and contained very little Cx43 (0 or 1 gold particle vs. 42 to 98 in sham-operated rats). In the lateral membranes of myocytes, numerous connexon aggregates comprising non-phosphorylated Cx43 were observed. These connexon aggregates were in no case assembled into gap junction plaque-like structures. However, N-cadherin was well organized in the intercalated disc. There was very little myocyte-myocyte coupling in MI-rat atria and no myocyte-fibroblast coupling. Regression of the atrial remodeling was associated with the normalization of Cx43 localization. CONCLUSION: Structural alteration of the atrial myocardium is an important factor in the disorganization of connexins and gap junction. Moreover, redistributed Cx43 do not form junction channels.
Animals↗