Transmural and vagal nerve stimulation of the right atrium of the cat.
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Animals↗
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Results for “Atrial Function, Right”
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Instantaneous dimensional changes of the right atrium of the cat.
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Animals↗
Endothelin A receptor blockade causes adverse left ventricular remodeling but improves pulmonary artery pressure after infarction in the rat.
BACKGROUND: Endothelin A (ETA) receptor antagonists have been shown to improve ventricular remodeling and survival in rats when started 10 days after infarction. Whether starting them earlier would have a more or less beneficial effect is uncertain. METHODS AND RESULTS: Rats surviving an acute myocardial infarction (MI) for 24 hours (n=403) were assigned to saline or the ETA receptor antagonist LU 127043 or its active enantiomer LU 135252 for 4 weeks. Chronic LU treatment had no effect on survival, with 46% of LU rats and 47% of saline-treated rats with large MI surviving to the end of the study. LU treatment led to scar thinning, further left ventricular (LV) dilatation, an increase in LV end-diastolic pressure, and an increase in wet lung weight (P<0.05). Despite this detrimental effect on LV function, LU led to a significant decrease in RV systolic (50+/-2 to 44+/-2 mm Hg, P<0.05 vs saline) and right atrial pressures. LU treatment also prevented the increase in pulmonary ET-1 found in saline-treated rats with large MI but did not modify the increase in cardiac ET-1 in hearts with large MI. CONCLUSIONS: The early use of the ETA receptor antagonists LU 127043 or its active enantiomer LU 135252 after infarction in the rat leads to impaired scar healing and LV dilatation and dysfunction. This is accompanied by a decrease in RV systolic and right atrial pressures and a decrease in pulmonary but not cardiac ET-1 levels. It would thus appear that the early use of ETA receptor antagonists after infarction may be detrimental.
Animals↗
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.
Adrenergic alpha-Agonists↗
[Effect of heart rate on cardiac hemodynamics in patients with aortic regurgitation].
We evaluated the effects of heart rate on cardiac hemodynamics in 10 patients with aortic regurgitation (AR, mean regurgitant fraction: 64.3%). Cardiac catheterization was performed in all patients, and the hemodynamic parameters were obtained by increasing heart rate (80.100.120.140) using right atrial pacing. Regurgitant fraction and total systemic resistance were improved up to 100/min, but aggravated on further increase in heart rate. Cardiac function curve was remarkably improved up to 100/min, but aggravated on further increase in heart rate. LV end-diastolic pressure-volume relation was moved toward the left lower direction up to 100/min, but toward the left upper direction on further increase in heart rate. Thus, it was concluded that in severe AR, cardiac function was improved up to 100/min, but aggravated on further increase in heart rate.
Aortic Valve Insufficiency↗
Reactivation of spontaneous activity of the right atrium in deep hypothermia and after unfreezing.
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Action Potentials↗
[Localization by micro-electrodes of the "pacemaker" region and excitation diffusion threshold in the right atrium of the rabbit].
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Animals↗
[Current status and indications for contrast echocardiography].
Due to newly developed techniques contrast echocardiography (CE) is less often applied today. As to reevaluate the usefulness and the indications for CE 7823 consecutive echocardiographic studies were analysed. In 638 (8%) of these studies CE was used. 379 patients showed signs of right ventricular overload, 58 due to a left-to-right shunt. Pressure overload due to pulmonary hypertension was found in 321 cases. CE enhanced doppler flow signals in tricuspid regurgitation and facilitated quantification of right heart dimensions. 259 patients were screened for patent foramen ovale (PFO), 94 after embolic events, and 165 because neurosurgical intervention in a sitting position was planned. So CE proved to be still indicated in the era of color flow doppler, especially for the detection of PFO.
Cardiac Volume↗
[An accurate formula for assessing the volume of the right ventricular outflow tract].
Practical application of formulae for separate assessment of the volumes of inlet and outlet sections of the right ventricle derived previously by the authors has shown that the formula for right ventricular outlet section determining it as a curved truncated cone with nonparallel bases does not take into account a narrowing in the middle third of the outlet portion during the right ventricular systole and/or supraventricular crest hypertrophy. In the specified formula right ventricular outlet portion volume is determined as a sum of the volumes of two truncated cones with a borderline in the middle of the outlet portion long axis. The most reliable difference from the main formula was obtained in the control group where the borderline of outlet portion division coincided with the area of the maximal stenosis of outlet portion stenosis in the systole. In other groups (patients with some congenital heart diseases) the maximal stenosis zone is located lower. Hence, the specified formula helps reduce the overvaluing of the right ventricular outlet portion volume; to make the estimation more accurate, the borderline between the cones should be carried out at the site of this portion maximal stenosis.
Cardiac Volume↗
Effects of ramipril on renal function during progressive overpacing-induced heart failure in dogs.
OBJECTIVE: To investigate the effects of preventive angiotensin converting enzyme inhibitor treatment with ramipril in dogs with progressively severe experimentally induced heart failure. ANIMALS: 20 dogs. PROCEDURES: Dogs were randomly allocated to receive no treatment (control) or ramipril (0.125 mg/kg, PO, daily) for 7 weeks. Physical examination, repetitive catheterization of the right side of the heart, and echocardiography were performed before the study (day 0) and weekly for 7 weeks. Renal plasma flow (RPF) as determined by para-aminohippuric acid clearance and glomerular filtration rate (GFR) as determined by creatinine and iohexol clearances were measured on day 0 and at weeks 4 and 7. RESULTS: Overpacing induced a progressive increase in right atrial pressure (RAP) and pulmonary artery pressure, occluded (PAPO), with a decrease in systemic arterial pressure. There were progressive alterations of echocardiographic indices of diastolic and systolic ventricular function. The RPF and GFR decreased before cardiac output decreased, and filtration fraction increased. The logarithm of the urinary sodium-to-potassium concentration ratio (log(10)[Na(+)/K(+)]) decreased. Significant effects of ramipril included a delay in clinical signs of heart failure, a late decrease in RAP and PAPO, and increases in the sodium excretion fraction and log(10)(Na(+)/K(+)). There was a satisfactory agreement between the creatinine and iohexol clearance measurements. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that, in this rapid-evolving, dilated cardiomyopathy, activation of the renin-angiotensin system contributes to the pathophysiology of heart failure late in the disease and essentially by an activation of renal salt and water retention.
Angiotensin-Converting Enzyme Inhibitors↗
Electrophysiologic consequences of the arterial switch repair of d-transposition of the great arteries.
Electrophysiologic studies were performed at 12.7 +/- 4 months postoperatively in 20 patients who had the arterial switch repair at 1 to 120 days (mean 13 +/- 26 [SD]) for d-transposition of the great arteries. Preoperative electrocardiograms (ECGs) at rest revealed an ectopic atrial rhythm in one patient. Postoperative rest ECGs revealed transient postoperative ectopic atrial or junctional rhythms in two patients, intermittent ectopic atrial rhythms in two and right bundle branch block in nine with a normal QRS axis. In addition, ambulatory monitor recordings revealed infrequent premature ventricular complexes in five patients. Catheter endocardial mapping revealed sinus rhythm in 18 patients and ectopic atrial rhythm in 1 patient. Atrial activation after the switch repair was comparable with normal atrial activation. Activation of all low atrial sites was significantly earlier after the switch repair than after the Mustard repair. Mild abnormalities of sinus node function were present and consisted of slight prolongation of corrected sinus node recovery time in six patients and slightly increased sinoatrial conduction time in four. The ratio of sinus node recovery time to sinus cycle length was normal in all 20 patients. Atrial effective and functional refractory periods were normal in all patients and no atrial arrhythmias could be induced by programmed stimulation. Atrioventricular (AV) node conduction was excellent with normal AV node effective and functional refractory periods. The only electrophysiologic abnormality of His-Purkinje function was distal right bundle branch block in nine patients. Programmed stimulation of the ventricle produced repetitive ventricular responses in four patients: bundle branch reentry in three and intraventricular reentry in one.(ABSTRACT TRUNCATED AT 250 WORDS)
Ambulatory Care↗
Pitfalls in creation of left atrial pressure-area relationships with automated border detection.
Creation of pressure-area relationships (loops) with automated border detection (ABD) involves correction for the variable inherent delay in the ABD signal relative to the pressure recording. This article summarizes (1) the results of in vitro experiments performed to define the range of, and factors that might influence, the ABD delay; (2) the difficulties encountered in evaluating a thin-walled structure like the left atrium in the dog model; and (3) the solutions to some of the difficulties found. The in vitro experiments showed that the ABD delay relative to high-fidelity pressure recordings ranges from 20 to 34 msec and 35 to 57 msec at echocardiographic frame rates of 60/sec and 33/sec, respectively. The delay was not influenced significantly by the type of transducer used, distance from the target area, or size of the target area. The delay in the ABD signal, relative to the echocardiographic image, ranges from nil to less than one frame duration, whereas it is delayed one to two frame durations relative to the electrocardiogram processed by the imaging system. In the dog model, inclusion of even small areas outside the left atrium rendered curves with apparent physiologic contour but inappropriately long delays of 90 to 130 msec. To exclude areas outside the left atrial cavity, time-gain compensation and lateral gain compensation were used much more extensively than during left ventricular ABD recording. By changing the type of sonomicrometers used in our experiments, we were able to record simultaneously ABD and ultrasonic crystal data. However, both spontaneous contrast originating from a right-sided heart bypass pump and electronic noise from the eletrocautery severely interferred with ABD recording.
Animals↗
Fracture and migration of a pacemaker atrial lead retention wire found by fluoroscopic screening in an asymptomatic patient.
We present the case of a woman who had an Accufix atrial "J" pacemaker lead implanted in 1990. Subsequently, Telectronics Pacing Systems recalled two models of the atrial leads after problems with fracture and malfunction were reported. One of these models was used in our case. Fifty-two months after implantation, following recommended fluoroscopic screening, our patient was found to have a complete fracture of the "J" retention wire with one fragment protruding from the sheath in the right atrium and another fragment of the wire lodged in the right ventricle. The pacemaker had continued to function normally and there was no clinical evidence to suggest such a potentially disastrous fracture. Our report emphasizes the importance of fluoroscopic screening of all patients with atrial leads involved in the recall.
Aged↗
Mechanism of adenosine-induced elevation of pulmonary capillary wedge pressure in humans.
BACKGROUND: Continuous intravenous administration of adenosine to humans often results in a paradoxical rise in pulmonary capillary wedge pressure (PCWP), whereas arterial resistance is lowered and cardiac output and heart rate increase. This is believed to be due to diastolic stiffening of the ventricle or to a negative inotropic effect. In the present study, we tested these and other mechanisms by using pressure-volume (PV) analysis and echocardiography. METHODS AND RESULTS: Fifteen patients with normal rest left ventricular function underwent cardiac catheterization and received adenosine at a rate of 140 micrograms/kg per minute IV for 6 to 10 minutes. PV relations were measured in 9 patients (without coronary artery disease) using the conductance catheter method. In 6 additional patients with coronary artery disease, echocardiograms were used to assess wall thickness and function, and aortic and coronary sinus blood, lactate, oxygen, and adenosine levels were measured. Adenosine increased PCWP by 19% (+2.6 mm Hg) in both patient groups while lowering arterial load by 30% and increasing cardiac output by 45% (all P < .001). There was no significant effect of adenosine on mean linear chamber compliance or monoexponential elastic stiffness, as the diastolic PV relation was unchanged in most patients. Diastolic wall thickness also was unaltered. Thus, the PCWP rise did not appear to be due to diastolic stiffening. Adenosine induced a rightward shift of the end-systolic PV relation (ESPVR) (+12.7 +/- 3.7 mL) without a slope change. This shift likely reflected effects of afterload reduction, as other indexes (stroke work-end-diastolic volume relation and dP/dtmax at matched preload) were either unchanged or increased. Furthermore, this modest shift in ESPVR was more than compensated for by vasodilation and tachycardia, so reduced systolic function could not explain the increase in PCWP. There also was no net lactate production to suggest ischemia. Rather than arising from direct myocardial effects, PCWP elevation was most easily explained by a change in vascular loading, as both left ventricular end-diastolic volume and right atrial pressure increased (P < .05). This suggests that adenosine induced a redistribution of blood volume toward the central thorax. CONCLUSIONS: PCWP elevation in response to adenosine primarily results from changes in vascular loading rather than from direct effects on cardiac diastolic or systolic function.
Adenosine↗
Progressive left ventricular dysfunction and remodeling after myocardial infarction. Potential mechanisms and early predictors.
BACKGROUND: Left ventricular enlargement and the development of chronic heart failure are potent predictors of survival in patients after myocardial infarction. Prospective studies relating progressive ventricular enlargement in individual patients to global and regional cardiac dysfunction and the onset of late chronic heart failure are not available. It was the aim of this study to define the relation between left ventricular dilatation and global and regional cardiac dysfunction and to identify early predictors of enlargement and chronic heart failure in patients after myocardial infarction. METHODS AND RESULTS: Left ventricular volumes, regional area shrinkage fraction in 18 predefined sectors (gated single photon emission computed tomography), global ejection fraction, and hemodynamics at rest and during exercise (supine bicycle, 50 W, 4 minutes, Swan-Ganz catheter) were assessed prospectively 4 days, 4 weeks, 6 months, and 1.5 and 3 years after first myocardial infarction. Seventy patients were assigned to groups with progressive, limited, or no dilatation. Patients without dilatation (n = 38) maintained normal volumes and hemodynamics until 3 years. With limited dilatation (n = 18), left ventricular volume increased up to 4 weeks after infarction and stabilized thereafter; depressed stroke volume was restored 4 weeks after infarction and then remained stable at rest. Wedge pressure during exercise, however, progressively increased. With progressive dilatation (n = 14), depressed cardiac and stroke indexes were also restored by 4 weeks but progressively deteriorated thereafter. Area shrinkage fraction as an estimate of regional left ventricular function in normokinetic sectors at 4 days gradually deteriorated during 3 years, but hypokinetic and dyskinetic sectors remained unchanged. Global ejection fraction fell after 1.5 years, whereas right atrial pressure, wedge pressure, and systemic vascular resistance increased. By multivariate analysis, ejection fraction and stroke index at 4 days, ventriculographic infarct size, infarct location, and Thrombolysis in Myocardial Infarction trial grade of infarct artery perfusion were significant predictors of progressive ventricular enlargement and chronic dysfunction. CONCLUSIONS: Almost 26% of patients may develop limited left ventricular dilatation within 4 weeks after first infarction, which helps to restore cardiac index and stroke index at rest and to preserve exercise performance and therefore remains compensatory. A somewhat smaller group (20%) develops progressive structural left ventricular dilatation, which is compensatory at first, then progresses to noncompensatory dilatation, and finally results in severe global left ventricular dysfunction. In these patients, depression of global ejection fraction probably results from impairment of function of initially normally contracting myocardium. Early predictors from multivariate analysis allow identification of patients at high risk for progressive left ventricular dilatation and chronic ventricular dysfunction within 4 weeks after acute infarction.
Aged↗
Acute myocardial beta-adrenergic receptor dysfunction after cardiopulmonary bypass in patients with cardiac valve disease. Duke Heart Center Perioperative Desensitization Group.
BACKGROUND: Patients with cardiac valve disease (CVD) frequently have congestive heart failure (CHF) and chronic myocardial beta-adrenergic receptor (beta AR) desensitization. Cardiac surgery requiring cardiopulmonary bypass (CPB) is associated with increased plasma catecholamine concentrations, which might worsen myocardial beta AR function. We therefore tested the hypothesis that acute beta AR dysfunction occurs during CPB in patients with CVD. METHODS AND RESULTS: After informed consent, 50 patients were enrolled. Right atrial biopsy samples were obtained at initiation and conclusion of CPB to assess beta AR density and adenylyl cyclase (AC) activity. Plasma catecholamine concentrations increased 3-fold during CPB (P < 0.01). Although beta AR density remained constant, isoproterenol-stimulated AC activity decreased significantly (approximately 30%; P < 0.005). AC activity decreased 22% and 24% with direct G protein (NaF) or AC (manganese) activation, respectively. Patients with or without preoperative CHF exhibited similar degrees of acute myocardial beta AR dysfunction during CPB. CONCLUSIONS: Acute myocardial beta AR dysfunction occurs during CPB in patients with severe CVD requiring surgical correction, with or without preexisting CHF. The primary underlying mechanism involves functional uncoupling of the beta AR signal transduction pathway at the level of the AC moiety. This information should facilitate development of agents designed to prevent acute myocardial beta AR dysfunction during CPB, potentially leading to improved outcome in this high-risk population.
Aged↗
Evaluation of acute dual-chamber pacing with a range of atrioventricular delays on cardiac performance in refractory heart failure.
OBJECTIVES: This study evaluated how variations in atrioventricular (AV) delay affect hemodynamic function in patients with refractory heart failure being supported with intravenous inotropic and intravenous or oral inodilating agents. BACKGROUND: Although preliminary data have suggested that dual-chamber pacing with short AV delays may improve cardiac function in patients with heart failure, detailed Doppler and invasive hemodynamic assessment of patients with refractory New York Heart Association class IV heart failure has not been performed. METHODS: Nine patients with functional class IV clinical heart failure had Doppler assessment of transvalvular flow and right heart catheterization performed during pacing at AV delays of 200, 150, 100 and 50 to 75 ms. RESULTS: Systemic arterial, pulmonary artery, right atrial and pulmonary capillary wedge pressures, cardiac index, systemic and pulmonary vascular resistances, stroke volume index, left ventricular stroke work index (SWI) and arteriovenous oxygen content difference demonstrated no significant changes during dual-chamber pacing with AV delays of 200 to 50 to 75 ms. There were also no changes in the Doppler echocardiographic indexes of systolic or diastolic ventricular function. The study was designed with SWI as the outcome variable. Assuming a clinically significant change in the SWI of 5 g/min per m2, a type I error of 0.05 and the observed standard deviation from our study, the observed power of our study is 85% (type II error of 15%). CONCLUSIONS: Changes in AV delay between 200 and 50 ms during dual-chamber pacing do not significantly affect acute central hemodynamic data, including cardiac output and systolic or diastolic ventricular function in patients with severe refractory heart failure due to dilated cardiomyopathy.
Aged↗
Negative dromotropism of adenosine under beta-adrenergic stimulation with isoproterenol.
Adenosine depresses atrioventricular (AV) nodal function by binding to specific A1 receptors which activate the acetylcholine, adenosine-regulated potassium current. In addition, adenosine can act to antagonize the effects of beta-adrenergic stimulation on AV nodal function. To assess the negative dromotropic effects of adenosine under beta-adrenergic stimulation, 15 patients were studied during clinical electrophysiologic study. During high right atrial pacing at a cycle length of 400 to 600 ms, adenosine was injected intravenously at an initial dose of 0.5 mg followed by a stepwise increment of 0.5 or 1.0 mg given at 5-minute intervals until a maximal dose of 12 mg was achieved or AV block developed. Intravenous isoproterenol (1 to 3 micrograms/min) was then infused to accelerate sinus rate by 20 to 30% during which intravenous injection of incremental doses of adenosine as described was repeated. The AV nodal conduction time (AH interval) was measured at each dose of adenosine. Dose-response curves of AV nodal conduction time (expressed as percent increase in AH interval) were studied during the control state and during isoproterenol infusion. The dose of adenosine required to produce AV nodal Wenckebach block, the increase in the AH interval by 50% (ED50) and the maximal response (Emax) were 3.4 +/- 0.9 mg, 1.8 +/- 0.9 mg and 60 +/- 4%, respectively, in the control state, and 3.7 +/- 0.8 mg, 2.0 +/- 0.7 mg and 56 +/- 4%, respectively, during isoproterenol infusion. No significant changes in ED50, Emax and the dose of adenosine yielding AV nodal Wenckebach block could be demonstrated between the control state and during isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine↗