[Method of evaluation of the right atrial function following complete right atrial bypass in tricuspid valve stenosis--ejection fraction of the right atrium].
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Atrial Function↗
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Significance of right atrial function during right sided inotropic stimulation of pig hearts in situ.
Cardiac adjustments to inotropic stimulation of the right side of the heart were examined in anaesthetised, open chest pigs by calcium chloride infusion (80 mumol.min-1) into the right coronary artery. At stable haemodynamic conditions and at constant heart rate, right ventricular (RV) pre-ejection segment length increased by 4.6 (2.7-7.2) % (median, 95 % confidence interval) (p less than 0.01), RV end diastolic pressure rose from 5.3 (3.4-7.7) to 6.0 (3.6-8.8) mm Hg (p less than 0.05), and stroke volume rose by 6.8 (4.2-10.8) % (p less than 0.001). When the effect of right atrial contraction on RV filling was excluded by simultaneous pacing of atria and ventricles, the RV pre-ejection segment length no longer increased, and stroke volume rose by only 3.5 (0.1-9.5) % (p less than 0.05) during right side inotropic stimulation. Right atrial inotropic stimulation improves right ventricular filling, and may cause redistribution of blood from the systemic to the pulmonary circulation. This redistribution would raise the pulmonary vascular pressures, and thereby also improve left ventricular filling. The improved right ventricular filling partly accounts for the rise in RV output.
Animals↗
[Hemodynamic evaluation of complete right heart bypass surgery for correction of tricuspid atresia - with special reference to postoperative hemodynamic evaluation and involvement of the right atrial function].
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Adolescent↗
[Assessment of right atrial and ventricular function by radionuclide ventriculography using continuous infusion of 81mKr].
The purpose of this study is to assess the right atrial and ventricular function by radionuclide ventriculography using continuous infusion of 81mKr in normal subjects and in patients with heart disease. 1) Reproducibility of RVEF measurement by continuous infusion of 81mKr was good (interobserver; gamma = 0.97, p less than 0.001, n = 20: intraobserver; gamma = 0.97, p less than 0.001, n = 20). This method had a excellent correlation with RVEF of 99mTc first-pass technique (gamma = 0.92, p less than 0.001, n = 20). 2) RVEF was measured in 10 normal volunteers, 76 patients with myocardial infarction (OMI), 20 patients with dilated cardiomyopathy (DCM), 5 patients with arrhythmogenic right ventricular dysplasia (ARVD) and 5 patients with primary pulmonary hypertension (PPH). In OMI and DCM, their RVEF was lower than that of normal volunteers and, in ARVD and PPH, lower than that of OMI and DCM. There was a significant inverse correlation between RVEF, mean pulmonary artery pressure and right ventricular end-diastolic volume index. 3) The effect of the location of right coronary artery (RCA) lesions on RVEF during exercise was also evaluated. Ten normal volunteers and 27 patients with OMI were studied at rest and during exercise. The patients with OMI were divided into two groups: those without proximal RCA lesions (non RCA group, n = 12) and those with proximal RCA lesions (RCA group, n = 15). Although there were no significant increases of RVEF during exercise in both group, the percent change in RVEF was less in RCA group than in non RCA group. These findings suggested that proximal RCA stenosis is a major determinant of exercise RVEF. 4) To assess the right atrial function, right atrial volume curve was measured in 10 normal volunteers, 32 patients with OMI and 4 patients with PPH. The curve was clearly divided into 4 phase; filling phase (312 +/- 40 msec), early ejection phase (276 +/- 53 msec), plateau an index of right atrial reservoir function, was 0.41 +/- 0.05 and Contractile Volume/Stroke Volume (Contr. V/SV), as an index of right atrial pump function, was 0.23 +/- 0.05 in normal volunteers. In OMI and PPH, atrial reservoir function decreased and atrial pump function increased. It was concluded that radionuclide ventriculography using continuous infusion of 81mKr was useful to assess the right heart function.
Atrial Function, Right↗
Right atrial ischemia exacerbates hemodynamic compromise associated with experimental right ventricular dysfunction.
To determine the importance of right atrial function with acute right ventricular dysfunction, sequential right ventricular and right atrial ischemia were induced in 15 dogs. Right ventricular ischemia resulted in right ventricular free wall dyskinesia, right ventricular dilation by ultrasound, elevated right ventricular filling pressure and paradoxic septal motion. There were decrements in right ventricular systolic pressure (28.9 +/- 5.5 to 25.5 +/- 4.6 mm Hg) (p less than 0.05 for these and all subsequent values) and stroke work (5.66 +/- 0.94 to 2.66 +/- 0.62 g.m/m2), resulting in reductions in left ventricular preload, systolic pressure (123 +/- 11 to 97 +/- 12 mm Hg) and stroke volume (24.2 +/- 4.3 to 19.1 +/- 5.2 ml). Right atrial contractility was augmented, as indicated by increases in peak A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.22 +/- 0.02 to 1.46 +/- 0.3) and right atrial stroke work (0.11 +/- 0.02 to 0.25 +/- 0.05 g.m/m2). Right atrial ischemia depressed right atrial contraction, as indicated by decreased A wave amplitude (ratio of peak A wave to mean right atrial pressure 1.46 +/- 0.3 to 1.04 +/- 0.2) and stroke work (0.25 +/- 0.05 to 0.04 +/- 0.01 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
[Modified Fontan procedure, is the right atrial pump function necessary or not? Experimental approach using simulation model].
The effect of pulsatile pulmonary flow and the characteristics of pulmonary arterial pressure (PAP) trace were examined using a model simulating the right heart following the modified Fontan procedure. An inlet overflow tank (preload), valveless axial pulsatile pump, Windkessel model (afterload), and an outlet overflow tank (left atrium) were connected in series. Standard conditions were: flow 2.00 l/m, with 12 mmHg preload, 3.0 wood units resistance and left atrial pressure at 6 mmHg. The pump rate was set at 80 bpm. Simulated PAP and pulmonary flow (PF) waves produced by this model closely resembled those obtained from patients who had undergone the modified Fontan procedure. Parameters except preload were fixed and changes in PF were examined at varying preload of 8, 12, 15 and 17 mmHg. At the various preload levels, PF increased to values greater than the PF for the same conditions in the non-pulsatile state. With a preload value of 8 mmHg, PF increased from 1.10 l/m (non-pulsatile) to a maximum of 1.55 l/m at a peak PAP of 14 mmHg. With a preload of 12 mmHg, the PF increased from 2.00 l/m (non-pulsatile) to 2.65 l/m at 19 mmHg peak PAP. A preload of 15 mmHg resulted in an increase in PF from 2.65 l/m (non-pulsatile) to 3.30 l/m at 22 mmHg peak PAP, and when the preload was 17 mmHg the PF increased from 3.15 l/m (non-pulsatile) to 3.80 l/m at 25 mmHg peak PAP. The afterload of this model was fixed so the increase in PF with pulsation suggests a decrease in resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
Atrial Function, Right↗
Modulation of electrophysiological properties of neonatal canine heart by tonic parasympathetic stimulation.
The effects of tonic right and left vagal stimulation (RVS and LVS) on electrophysiological properties of the immature myocardium and specialized conduction system were evaluated in 11 neonatal canines pretreated with propranolol (1 mg/kg iv). Electrophysiological studies were performed by recording intracardiac electrograms from multiple endocardial catheters during programmed electrical stimulation. Assessments were made of sinus node function, intra-atrial, atrioventricular (AV) nodal and His-Purkinje conduction, and atrial and ventricular refractoriness in the control state and during RVS and LVS at 4-12 Hz. Vagal stimulation prolonged the sinus cycle length; RVS produced a 38% increase and LVS a 25% increase at 8 Hz (P less than 0.01). There were no changes in the intra-atrial or His-Purkinje conduction times. Comparable increases occurred during RVS and LVS in the paced cycle length resulting in AV nodal Wenckebach, the AV nodal conduction time at a paced cycle length of 340 ms, and the effective and functional refractory periods of the AV node, suggesting symmetrical influences of the right and left vagus on neonatal AV nodal function. Right atrial effective and functional refractory periods shortened significantly during vagal stimulation (ERP, 36% RVS and 23% LVS; FRP, 27% RVS and 15% LVS), and in 5 of 11 neonates, a sustained regular atrial tachyarrhythmia was induced during atrial extra-stimulation. Small yet significant increases were observed in the right ventricular ERP and FRP during vagal stimulation. This study provides information regarding the functional integrity of the parasympathetic nervous system and its potential role as a modulator of the electrophysiological properties of the newborn heart.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Assessment of superior vena caval blood flow velocity in ischemic heart disease.
In order to evaluate the right atrial function in patients with ischemic heart-disease, we studied the superior vena caval blood flow velocity using pulsed Doppler echocardiography. The subjects included 31 patients with anteroseptal infarction (ANT), 23 with inferior or inferoposterior infarction (INF + POS), 27 with effort angina pectoris (EAP) and 15 with vasospastic angina pectoris (VAP). The systolic peak flow velocity (PFVs) was significantly reduced only in INF + POS compared with those in ANT, EAP and VAP (36.8 +/- 1.8 cm/sec vs 46.9 +/- 2.1 cm/sec, 46.4 +/- 2.1 cm/sec and 42.6 +/- 1.9 cm/sec, p less than 0.05, respectively). No significant difference in diastolic peak flow velocity (PFVd) was found between the 4 groups. PFVs/PFVd was significantly reduced only in INF + POS compared with those in ANT, EAP, and VAP (1.39 +/- 0.05 vs. 1.75 +/- 0.08, 1.76 +/- 0.09, and 1.62 +/- 0.09, p less than 0.05, respectively). These results suggested that INF + POS caused impairment of the right atrial reservoir function.
Analysis of Variance↗
The relationship between atrial pressure, atrial dimensions and atrial natriuretic factor during pacing tachycardia in dogs.
Acute supraventricular tachycardia is known to increase the plasma level of atrial natriuretic factor (ANF). The purpose of these experiments was to investigate if such an increase in plasma-ANF could be ascribed to changes in atrial pressure and atrial dimensions. Eight anaesthetized dogs were instrumented with atrial pressure catheters and sonomicrometers to measure left and right auricular and atrial free wall dimensions. An acute increase in atrial rate from 150 to 200 min-1 for 10 min did not change plasma-ANF or atrial haemodynamic variables. A further increase in atrial rate to 250 or 300 min-1 increased right and left atrial intracavitary pressures (P less than 0.01), both auricular diameters and right atrial free wall segment length (P less than 0.05). Left atrial free wall segment length remained unchanged. Plasma-ANF increased in all dogs (P less than 0.01). The change in plasma-ANF correlated well with changes in atrial pressures as well as with changes in atrial dimensions. These results support the hypothesis that release of ANF during acute atrial tachycardia may in part be attributed to atrial dilatation.
Animals↗
Right atrial predominance of atrial natriuretic peptide secretion in isolated perfused rat atria.
In order to investigate the regulatory mechanism for the atrial release of atrial natriuretic peptide (ANP), a perfused rabbit atrial model was devised. In the present experiments, the effect of a reduction in atrial distension on the immunoreactive ANP (irANP) secretion was investigated and compared in the perfused right and left atria of rats. Elevations in right and left atrial pressure resulted in proportional increases in the volume of atrial distension-reduction which was larger in the right than in the left atria. The basal rate of irANP secretion was higher in the right than in the left atria. Increases in the volume of atrial distension-reduction resulted in proportional increases in irANP secretion in both atria. Increment in irANP secretion in response to a reduction in atrial distension was significantly higher in the right than in the left atria. Higher rate of irANP secretion in response to unit volume change was observed in the right atria. Increases in the volume of atrial distension-reduction resulted in accentuated irANP responses in the right atrium. IrANP content was significantly higher in the right than in the left atria. The results suggest that the right atrium is a predominant site in ANP secretion in rats.
Animals↗
Newborn cardiorenal dynamics: a state of atrial natriuretic peptide unresponsiveness.
The newborn has an attenuated response to saline fluid challenge. We studied the response of endogenous atrial natriuretic peptides (ANF) to 10% body weight graded isotonic saline volume expansion (VE) in 14 anesthetized neonatal lambs which were either 1 day old or 7 days old. Plasma ANF values were unchanged at 3.3% and 10% VE compared with control values (56 +/- 28 vs. 66 +/- 17 and 66 +/- 37 pg/ml, not significant) in the 1-day-old lambs, whereas values increased significantly at both 3.3% and 10% VE (47 +/- 40 vs. 99 +/- 57 and 96 +/- 73, P = 0.022 and P = 0.018, respectively) in the 7-day-old lambs. No relationship existed between right atrial (RAP) or pulmonary capillary wedge pressures (PCWP) and plasma ANF in the 1-day-old lambs; however, a significant correlation existed (RAP, P = 0.015; PCWP, P = 0.022) in the 7-day-old lambs. In general, renal function was improved in the 7-day-old lambs compared with the 1-day-old lambs, but only changes in fractional sodium excretion were significantly different (P = 0.017). We speculate that ANF unresponsiveness in the 1-day-old lamb is related to physiological transitions during the birth process and that the maturation of the renal response to VE may require maturation of the atrial mechanism which permits ANF secretion.
Aging↗
Effects of arginine vasopressin and extracellular osmolarity on atrial natriuretic peptide release by superfused rat atria.
This study investigated the characteristics of atrial natriuretic peptide (ANP) release from superfused sliced atria and ventricles of rats. Right atria spontaneously released more immunoreactive ANP (Ir-ANP: pg/min per mg tissue) (32 +/- 3) than did left atria (11 +/- 2) or right ventricles (1.5 +/- 0.5). Addition of 10(-9) to 10(-5) M of arginine vasopressin (AVP) to the superfusing fluid or increasing its osmolarity (290 to 490 mOsM) resulted in a significant increase of the Ir-ANP outflow from right atria. The effect of AVP was prevented by a specific V1 receptor antagonist, ([d(ch2)5Tyr(Me)]AVP). Superfusion with indomethacin (10(-5) M) did not alter spontaneous release but inhibited the peak levels of Ir-ANP induced by AVP (10(-5) M). Moreover, DDAVP, a specific V2 receptor agonist, did not induce Ir-ANP release. Ca(2+)-free medium alone or plus 1 mM EGTA induced a significant increase in basal Ir-ANP outflow. The Ir-ANP released chromatographed similarly to the standard alpha-rANP. These results suggest a specific stimulatory effect of AVP and osmolarity and a negative influence of extracellular Ca2+ on atrial spontaneous Ir-ANP release. It appears that the effect of AVP could be mediated by prostaglandin synthesis.
Animals↗
Plasma atrial natriuretic factor in patients with acute myocardial infarction.
To examine whether atrial natriuretic factor (ANF) is secreted adequately in the early phase of myocardial infarction, plasma ANF concentration and clinical parameters, including hemodynamic variables, were studied in 118 patients with acute myocardial infarction (AMI). The patients were divided into 2 subgroups according to the absence (group A, n = 41) or presence (group B, n = 77) of a history of valvular heart disease, previous myocardial infarction, hypertension, or renal failure. Although no significant difference in atrial pressure after the infarction was found between the 2 groups, the plasma ANF level was significantly lower in group A than in group B (76 +/- 6 vs. 185 +/- 26 pg/ml; mean +/- SEM, p < 0.01). Plasma ANF was correlated with pulmonary capillary wedge pressure in group B (r = 0.54, p < 0.001), whereas no relationship with hemodynamic parameters was observed in group A. In 56 of the 118 patients (group A, n = 18; group B, n = 38), the pulmonary arterial plasma level was significantly higher in group A (p < 0.05), whereas the difference was not significant in group B. Seven of the 8 expired cases among these 56 patients had peripheral plasma ANF levels of more than 150 pg/ml, which were higher than those in pulmonary arterial plasma. These observations suggest firstly that the plasma level of ANF is lower in patients with a new onset of myocardial infarction compared to those with a history of cardiac or renal diseases, and secondly that stimulated ANF release originates not only from the right side of the heart, but also from additional site(s), particularly in patients with chronic ventricle overload and a poor prognosis.
Atrial Function, Right↗
Human atrial natriuretic factor and renin-aldosterone in paracetamol induced fulminant hepatic failure.
It has been postulated that deficiency of a putative natriuretic factor, or resistance to such a factor, may contribute to sodium retention in fulminant hepatic failure. Levels of plasma human atrial natriuretic factor (h-ANF), plasma renin activity, and aldosterone concentration were measured in 33 patients with fulminant hepatic failure due to paracetamol overdose, and 12 healthy control subjects. Levels of h-ANF were raised only in patients with evidence of severe renal impairment (serum creatinine greater than 300 mumol/l and urine output less than 100 ml/24 hours). h-ANF values were median 4.15, range 2-9 pmol/l and 10.1, 1-25 pmol/l for the control and severe renal impairment groups respectively (p less than 0.001). In the latter plasma renin activity was raised compared to that in control subjects (median 19.8, range 1.04-41.7 and 2.86, 1.87-5.9 pmol/l/h respectively, p less than 0.02). Plasma aldosterone concentration was also raised in patients (2176, 199-6894 pmol/l compared to 368, 133-578 pmol/l in control subjects, p less than 0.01). Haemodialysis induced changes in circulating h-ANF which correlated with volume and right atrial pressure changes (p less than 0.001 and p less than 0.05 respectively). In six patients with no or mild renal failure infusion of 900 ml 5% human albumin solution caused a significant increase in plasma h-ANF (p less than 0.05) without natriuresis or diuresis, a finding compatible with the hypothesis that there may be resistance to h-ANF in this group. The present findings indicate that there is no deficiency of h-ANF in fulminant hepatic failure and that known mechanisms of h-ANF release are not impaired.
Acetaminophen↗
Atrial natriuretic peptide responses during anaesthesia in patients with refractory cardiomyopathies.
In patients with congestive heart failure, the release of atrial natriuretic peptide (ANP) is decreased. This study sought to determine the extent of ANP, sympathetic and haemodynamic responses to acutely increased atrial pressure in patients with cardiomyopathies undergoing orthotopic cardiac transplantation. Haemodynamic variables, plasma ANP, norepinephrine, and epinephrine concentrations were measured in 17 patients at five times before and after induction of anaesthesia using either ketamine 1.5 micrograms.kg-1 or sufentanil 3.6 +/- 0.3 micrograms.kg-1. Preinduction values in the ketamine and sufentanil groups were not significantly different. Compared with preinduction values, increases in mean arterial pressure (26%), pulmonary capillary wedge pressure (90%), right atrial pressure (107%), and heart rate (24%) occurred in the ketamine group while cardiac index decreased by 19% (P less than 0.05). Haemodynamic variables in the sufentanil group did not change at any of the times studied. Plasma concentrations of atrial natriuretic peptide were not different within or between treatment groups. Following tracheal intubation plasma norepinephrine levels increased by 116% in the ketamine group (P less than 0.05), but did not change in the sufentanil group. Plasma norepinephrine concentrations differed significantly between the ketamine and sufentanil groups. There were no differences in epinephrine concentrations in either group. Despite the anticipated haemodynamic and catecholamine differences found between the ketamine and sufentanil groups, the levels of plasma ANP were similar. Based upon these results, it is concluded that ANP exerts little influence in the control of fluid volume or blood pressure in patients with refractory cardiomyopathy.
Adult↗
Superior vena cava flow and tricuspid anular motion after cardioversion of atrial fibrillation, and role of right atrial relaxation on systolic venous return.
To determine whether atrial relaxation or systolic descent of the tricuspid anulus is the predominant factor determining systolic venous return, 22 patients with atrial fibrillation were studied. Venous return (i.e., superior vena cava (SVC) flow) was measured using pulsed Doppler echocardiography. Systolic descent of the tricuspid anulus (i.e., total excursion of tricuspid anulus during systole) was also measured using echocardiography. Serial examinations were performed before and after cardioversion of atrial fibrillation in 15 patients. In 11 patients, both the total excursion of the tricuspid anulus and SVC flow were examined in relation to the ratio of the preceding to the pre-preceding RR interval (R2/R1). Systolic forward flow of SVC increased as the ratio of late diastolic to total excursion of the tricuspid anulus (i.e., right atrial systolic function) increased. It correlated significantly with the ratio of late diastolic to total excursion of the tricuspid anulus but not with total excursion. Total excursion of the tricuspid anulus correlated significantly with R2/R1, but systolic forward flow of SVC did not. These results indicate that atrial relaxation rather than systolic descent of the tricuspid anulus was the predominant factor determining systolic forward flow in the SVC.
Atrial Fibrillation↗
Preexisting cardiopulmonary disease attenuating the atrial natriuretic peptide response. Results in patients with acute respiratory failure.
The purpose of this study was to evaluate the pathophysiologic role of atrial natriuretic peptide (ANP) as a pulmonary artery vasodilator in patients with acute respiratory failure receiving artificial ventilation. Twenty-one consecutive patients were studied, 12 without and 9 with preexisting cardiopulmonary disease. Pulmonary artery plasma ANP levels were significantly higher than the levels obtained in the superior vena cava and radial artery. Plasma ANP levels correlated significantly with the plasma levels of its second messenger, guanosine 3',5'-cyclic monophosphate (cGMP). In the 12 patients without prior cardiopulmonary disease, plasma ANP levels correlated significantly with mean pulmonary arterial pressure (MPAP). This correlation was not found in the nine patients with preexisting cardiopulmonary disease. The cGMP/ANP ratio, indicating the biologic effect of ANP, was also higher in the patients without preexisting cardiopulmonary disease. These results are compatible with clearance and vasodilator activity of ANP in the pulmonary vascular bed, but only in patients without preexisting cardiopulmonary disease.
Acute Disease↗
Right ventricular myocardial function after atrial switch operation for transposition of the great arteries.
Postoperative right ventricular (RV) myocardial function was evaluated in 6 patients who underwent atrial switching for simple transposition of the great arteries (TGA). The average age at study was 5.5 years. RV function was evaluated at rest and during administration of methoxamine by cardiac catheterization and RV angiography. The data were compared with left ventricular function in a control group, which consisted of 6 patients, 3 with functional murmur and 3 with pulmonary valvar stenosis. During stress, the TGA group showed a significant increase in end-diastolic pressure, minute work index and end-diastolic and end-systolic volume indexes, along with a significant decrease in ejection fraction. The control group also showed an increase in these variables except for ejection fraction during stress, which did not change. The slope of the work-function curve for the TGA group was lower than that for the control group (p = 0.02). The TGA group had a lower slope of the peak systolic pressure-volume relation than the control group (p = 0.005). There was no significant correlation between the slope of the peak systolic pressure-volume relation and age at repair or study. This study shows that RV pump dysfunction observed in postoperative TGA patients may be caused by depressed myocardial function.
Cardiac Catheterization↗