The effect of stretch of the right strium on arterial pressure and renal function in the dog.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
BACKGROUND: It is critical to repair atrial septal defects during childhood to minimize long-term morbidity and mortality. However, only a few studies have examined factors that predict a favorable outcome. OBJECTIVE: To examine prognostic variables in the repair of atrial septal defects. METHODS: Retrospective analysis of children who underwent repair of atrial septal defects between 1957 and 1981. RESULTS: There were 70 girls and 57 boys with a mean age of 9.3 years at the time of surgery (range 4 months to 20 years). The most common presenting symptoms were fatigue and dyspnea. Before surgery, 74% were in New York Heart Association functional class I, 70% had echocardiographic evidence of right ventricular hypertrophy, and 55% had cardiomegaly on chest radiographs. The average mean pulmonary arterial pressure was 17.1 mm Hg. The only factor significantly related to poor outcome was pulmonary hypertension. Age at surgery did not influence long-term results. Ninety-four percent of patients were in functional class I at follow-up. CONCLUSIONS: Repair of atrial septal defects is safe before age 21, but it should be done as early as possible in order to minimize the long-term complications of chronic left-to-right shunting.
Dramatic changes occur in the circulation of the newborn during the transition from fetal to neonatal life. Closure of the foramen ovale and ductus arteriosus, decrease in pulmonary vascular resistance, and improvement in right ventricular compliance are among these changes. These physiological-anatomical events were characterized by means of two-dimensional, Doppler and color flow echocardiography. Forty-five full-term infants (22 male, 23 female) were studied at a mean age of 4.2 hours (T1), 25.5 hours (T2), 49.8 hours (T3), and 73.8 hours (T4) by two-dimensional, Doppler and color flow echocardiography. At T1, T2, T3, and T4, the ductus arteriosus was patent by color flow echocardiography in 100%, 34%, 22%, and 11%, respectively. Conversely, patency of the ductus by Doppler alone was detected in 100% (T1), 13% (T2, T3), and 11% (T4). Reversal of flow in the descending aorta, reflective of diastolic ductal filling, was not sensitive in detecting ductal patency (T1 50%, T2 3%, T3 and T4 0%). The patency of the foramen ovale was noted to decrease over the course of the study. Right ventricular compliance was quantitatively assessed by pulsed-Doppler diastolic properties (E-to-A ratio). This changed significantly from T1 to T4 (0.90 to 0.97) reflecting improving compliance of the right ventricle. The ratio of acceleration to ejection time, a Doppler estimation measure of pulmonary vascular resistance, increased from 0.28 to 0.33 (T1 to T4) reflecting a decrease in pulmonary vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of TCV-116 ((+/-)-1-(cyclohexyloxycarbonyloxy) ethyl 2-ethoxy-1-[[2'-(1 H-tetrazol-5-yl)biphenyl-4-yl] methyl]-1 H-benzimidazole-7-carboxylate, CAS 145040-37-5) on the cardiovascular system and renal function were investigated in rats, guinea pigs, and dogs. TCV-116 at doses of 3 mg/kg (i.d.) and higher markedly increased renal blood flow in anesthetized dogs. TCV-116 at 30 mg/kg (i.d.) had no effect on heart rate, left ventricular systolic pressure, its dp/dtmax, or cardiac output in anesthetized dogs. Furthermore, TCV-116 at 10 and 30 mg/kg (p.o.) had little effect on cardiac output, right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure or respiration in conscious dogs. In isolated guinea pig perfused heart, CV-11974 even at a dose of 0.1 mg/ heart had no effect on cardiac function. In isolated guinea-pig atria, CV-11974, the active metabolite of TCV-116, even at 10(-4) mol/l had no effect on the spontaneous beating rate of the right atria or the contractile force of electrically-paced left atria. No significant effect of TCV-116 on urinary volume or urinary excretion of sodium and potassium was observed in rats (at 30, 100 or 300 mg/kg p.o.). These findings suggest that TCV-116 exerts no any additional pharmacological effects on cardiac and respiratory functions in dogs or on renal function in rats, other than an increase in renal blood flow in anesthetized dogs thought to be due to its inhibitory effect on the renin-angiotensin system.
We treated a patient with refractory biventricular heart failure, dilutional hyponatremia and prerenal azotemia, by means of ultrafiltration. After ultrafiltration, gas exchange and cardiac output improved, with concomitant reduction of systemic and pulmonary vascular resistances. Despite a decrease of right atrial and wedge pressure, atrial natriuretic factor rose and plasma renin activity decreased.
Left ventricular hypertrophy (LVH) is the major adaptation of the heart to a prolonged increase in the left ventricular afterload in hypertension. However, the structure and function of the right ventricle have received little attention. The present study was designed to assess right ventricular structural changes in patients with established essential hypertension. To accomplish this, M-mode echocardiograms were obtained from 15 healthy normotensive subjects and 35 patients with essential hypertension-15 with normal left ventricles and 20 with clear-cut echocardiographic evidence of LVH. In comparison with the normotensive subjects, right ventricular wall thickness was increased almost twofold in the hypertensive patients with LVH (7.0 +/- 2.1 mm vs 3.7 +/- 0.8 mm; p less than 0.001); there was a significant, direct correlation between right and left ventricular wall thickness in the entire patient population (r = 0.65; p less than 0.001). Furthermore, the left atrial emptying index was significantly reduced in all patients with hypertension regardless of whether LVH was present (p less than 0.001) and suggests early diastolic functional involvement of the left ventricle in hypertension. We therefore conclude that right ventricular hypertrophy is associated with LVH in patients with hypertension, although the changes of LVH are frequently more obvious to the clinician.
BACKGROUND: Data in normal human subjects on the factors affecting pulmonary artery systolic pressure (PASP) are limited. We determined the correlates of and established a reference range for PASP as determined by Doppler transthoracic echocardiography (TTE) from a clinical echocardiographic database of 102 818 patients, of whom 15 596 (15%) had a normal Doppler TTE study. METHODS AND RESULTS: A normal TTE was based on normal cardiac structure and function during complete Doppler TTE studies. The PASP was calculated by use of the modified Bernoulli equation, with right atrial pressure assumed to be 10 mm Hg. Among TTE normal subjects, 3790 subjects (2432 women, 1358 men) from 1 to 89 years old had a measured PASP. The mean PASP was 28.3+/-4.9 mm Hg (range 15 to 57 mm Hg). PASP was independently associated with age, body mass index (BMI), male sex, left ventricular posterior wall thickness, and left ventricular ejection fraction (P<0.001). The estimated upper 95% limit for PASP among lower-risk subjects was 37.2 mm Hg. A PASP >40 mm Hg was found in 6% of those >50 years old and 5% of those with a BMI >30 kg/m(2). CONCLUSIONS: Among 3790 echocardiographically normal subjects, PASP was associated with age, BMI, sex, wall thickness, and ejection fraction. Of these subjects, 28% had a PASP >30 mm Hg, and the expected upper limit of PASP may include 40 mm Hg in older or obese subjects. These findings support the use of age- and BMI-corrected values in establishing the expected normal range for PASP.
This report details the clinical, hemodynamic, and morphologic data from four patients 59 to 77 years old (mean 66) with a primary restrictive cardiomyopathy. All patients had symptoms of congestive heart failure, jugular venous distention, and murmurs of mitral and tricuspid regurgitation. Four patients required pacemakers, three for the brady-tachy syndrome and one for complete heart block. Chest x-ray demonstrated cardiomegaly in all four patients and pulmonary congestion and/or pleural effusions in three. Echocardiographic examination documented left atrial enlargement in all patients, along with normal left ventricular internal dimensions. Global left ventricular systolic function was normal in all, and left and right ventricular filling pressures were elevated and similar in three. A dip and plateau pattern was present in the pressure tracings of two of three patients. Unlike previous reports of restrictive cardiomyopathy, in our four patients there was no specific morphologic cause noted at necropsy. Pathologic evaluation demonstrated biatrial dilatation in all patients, with thrombi present in the atrial appendages in three. Normal ventricular cavity size and mild right ventricular hypertrophy were present in all patients and mild-to-moderate left ventricular hypertrophy was present in two. There were no significant pericardial, endocardial, or valvular abnormalities and no infiltrative myocardial disorders were present. Light and electron microscopic studies demonstrated only interstitial fibrosis of the myocardium. A restrictive hemodynamic profile may be observed in the absence of specific infiltrative disorders and affected patients may exhibit a prolonged clinical course of 4 to 14 years (mean 9). However, in these patients congestive heart failure responded poorly to medical therapy or surgical correction of valvular regurgitation, which is common in this disorder.
BACKGROUND: Cardiopulmonary involvement in patients with systemic sclerosis (SSc) carries a poor prognosis, mainly due to pulmonary hypertension and right-heart failure. To date, right ventricular (RV) involvement has not been studied in detail. We therefore assessed RV function in patients with SSc and related the findings to the clinical features of the disease. METHOD: Twenty-six consecutive patients (21 women) with SSc (mean age, 56 +/- 15 years [+/- SD]) and 25 healthy, age-matched control subjects (21 women) were studied. Doppler echocardiography including Doppler tissue imaging was used to evaluate cardiac function. Pulmonary function was also studied. RESULTS: Compared with control subjects, RV free wall thickness (5.8 +/- 1.7 mm vs 3.7 +/- 1.1 mm, p < 0.001) and right atrial (RA) systolic area (15.9 +/- 3.7 cm2 vs 13.0 +/- 2.3 cm2, p < 0.01) were increased in patients with SSc, while the global early diastolic/atrial component velocity ratio was reduced (1.2 +/- 0.4 vs 1.7 +/- 0.6, p < 0.01). The global isovolumic relaxation time (IVRT) [64 +/- 23 ms vs 39 +/- 13 ms, p < 0.001] and regional IVRT (83 +/- 40 ms vs 46 +/- 24 ms, p < 0.001) were prolonged in patients vs control subjects, whereas the RV global filling time was reduced (454 +/- 122 ms vs 548 +/- 104 ms, p < 0.01). RV systolic function and pulmonary pressures at rest were similar in the two groups, but the pulmonary artery acceleration time was reduced (119 +/- 34 ms vs 141 +/- 29 ms, p < 0.05) in patients compared to control subjects. Left ventricular function did not differ between the two groups. CONCLUSION: Patients with SSc exhibit altered RV diastolic function together with an increase in RV wall thickness and RA area. These findings appear to be early markers of RV disturbance, probably in response to intermittent pulmonary arterial hypertension.
We present the case of a patient with cardiac arrest and resuscitation in whom, consistent with direct cardiac compression, large aortic-to-right atrial systolic pressure gradients occurred. Forward blood flow during CPR was sufficient for the patient to maintain consciousness. Although aortic-to-right atrial diastolic gradients adequate to maintain coronary perfusion in experimental models were generated, in our patient, cardiac function could not be restored and the resuscitation was ultimately unsuccessful.
BACKGROUND: Thyroid hormone level abnormalities commonly exist in severe heart failure and may be of prognostic value. The therapeutic potential of using thyroid hormone for cardiogenic shock resulting from progressive heart failure has not been previously delineated. We sought to evaluate the role of an intravenous infusion of thyroxine as an adjunct to conventional inotropic agents and intra-aortic balloon counterpulsation in patients with severe heart failure with cardiogenic shock. METHODS AND RESULTS: We studied 10 consecutive patients with severe systolic heart failure that progressed to a cardiogenic shock state unresponsive to conventional pharmacological inotropic measures. Intravenous thyroxine (20 micrograms/h) was used as an adjunctive salvage measure after the failure of conventional pharmacological and mechanical support by intra-aortic balloon pump. The invasive hemodynamic profile (right atrial pressure, pulmonary capillary wedge pressure, cardiac index, mean arterial pressure), overall clinical status, core temperature, renal function, and tachyarrhythmias were compared before and sequentially at 6, 24, and 36 hours after the initiation of thyroxine administration. Long-term outcome was also defined. All patients had statistically significant improvements in cardiac index, pulmonary capillary wedge pressure, and mean arterial pressure at 24 and 36 hours post-initiation of thyroxine. No sustained tachyarrhythmias were seen during the thyroxine infusion. In 9 of 10 patients who underwent left ventricular assist device placement and/or heart transplantation, the use of thyroxine served as an effective adjunctive measure to allow transitioning to definitive surgical therapy. The 6-month and 1-year cohort survival rates, achieved by the transition to surgical therapy, were 90% and 80%, respectively. CONCLUSION: The beneficial hemodynamic properties of intravenous thyroid hormone can be effectively used in otherwise terminal situations of cardiogenic shock, and in such situations, the use of thyroid hormone can serve as a pharmacological adjunct to a definite surgical intervention. Further studies in larger numbers of patients might be warranted to confirm these findings.
Our purpose was to reexamine the relationship of the fall in cardiac output and blood pressure which occurs during positive end-expiratory pressure (PEEP) to changes in transmural right atrial and left atrial filling pressures. Closed-chest dogs, half with pulmonary edema, were studied during spontaneous breathing and inspiratory positive-pressure breathing (IPPB) with 0-15 cmH2O PEEP. Mean esophageal pressure accurately reflected changes in pericardial pressure and was used to estimate extracardiac pressure. We found that cardiac output fell approximately 50% and blood pressure fell 20% during 15 cmH2OPEEP in spite of well maintained transmural right atrial and left atrial (or pulmonary artery wedge) pressures suggesting a primary or reflex depression of atrial or ventricular function.
Changes in contractile function following exposure to iron (Fe) salts were evaluated in isolated isometrically contracting rabbit left atrial strips and right ventricular papillary muscles. Fe acutely depressed myocardial contractility as evidenced by dose-related declines in developed force and maximal rate of force development. There were no significant changes in duration of contraction or resting force. The tissue Fe content was increased nearly 3-fold after a 60 min exposure to Fe and subsequently was not decreased by repeated washing or by treatment with deferoxamine. Isoproterenol, but not deferoxamine, reversed the Fe-mediated impairment of myocardial contractility. These findings suggest that in cases of severe acute iron poisoning, depression of cardiac contractility might occur which may be improved by treatment with isoproterenol.
BACKGROUND: Ectopic atrial tachycardia (EAT) is a reversible cause of cardiomyopathy but may be quite difficult to control with conventional therapy. Transcatheter ablation with radiofrequency current was tested as an alternative to medical or surgical treatment of this condition. METHODS AND RESULTS: Twelve young patients (aged 10 months to 19 years) with drug-resistant EAT were treated with direct transcatheter ablation of the ectopic focus using radiofrequency (RF) energy. All had depressed left ventricular contractility by echocardiographic criteria, involving shortening fractions of 10-26% (median, 20%; normal, 28-35%). The EAT was mapped to the left atrium in seven cases and to the right atrium in five. Local atrial activation at the ectopic site preceded the onset of the surface P wave by 20-60 msec (median, 42 msec). Tachycardia terminated 0.5-13.0 seconds (median, 2.0 seconds) into a successful RF application. The ablation effectively eliminated EAT in 11 of 12 patients (92%), all of whom were discharged in sinus rhythm without medications after a median hospital stay of 48 hours. Ablation was unsuccessful in one patient with diffuse dysplasia of the anterior right atrium, who eventually did well after surgical resection of abnormal atrial tissue. Transient depression of sinus node function was noted in one patient who had successful ablation of an EAT focus in close proximity to the sinus node, although normal sinus node function returned within 72 hours. No other complications were encountered. During follow-up (3-21 months; median, 13 months), one patient had recurrence of a slower and less-sustained EAT that was successfully eliminated at a second ablation session. All others remained in sinus rhythm, and all 12 subjects recovered normal ventricular function. CONCLUSIONS: RF ablation appears to be a safe and effective therapeutic option for drug-resistant ectopic atrial tachycardia and may be the preferred first-line therapy for those patients with depressed ventricular function.
BACKGROUND: The effects of mechanical left ventricular assist on the nonassisted right ventricle have not been fully elucidated. Current information indicates that the right ventricle benefits from a lower left atrial pressure; however, ventricular septal shifting and increased venous return caused by left ventricular assist impair right ventricular function. Acute intraoperative alterations in mitral and tricuspid valve regurgitation (MR and TR, respectively) may occur as a result of mechanical left ventricular assist but have not yet been documented. METHODS AND RESULTS: Eight patients undergoing implantation of a left ventricular assist device (LVAD) as a bridge to transplantation were studied during surgery by transesophageal echocardiography. MR was present in seven of eight patients, and TR was present in eight of eight patients before LVAD implant (mean MR jet area, 10.6 +/- 2.4 cm2, mean TR jet area, 4.8 +/- 1.0 cm2). Immediately after LVAD placement, MR was still present in seven of eight patients, and TR was present in eight of eight patients (mean MR jet area, 4.2 +/- 0.9 cm2; mean TR jet area, 8.4 +/- 1.9 cm2) (P < .05 preimplant versus postimplant jet area). These changes in MR and TR were associated with a decrease in left ventricular end-systolic dimension (62 +/- 4 versus 48 +/- 3 mm) and an increase in right ventricular end-systolic dimension (31 +/- 4 versus 40 +/- 5 mm) (P < .05 preimplant versus postimplant end-systolic dimension). No patients developed progressive right ventricular failure during 70 to 279 days of LVAD support. CONCLUSIONS: Mechanical left ventricular assist causes an acute decrease in preexisting MR. However, left ventricular assist may acutely worsen TR, presumably by shifting the ventricular septum leftward and increasing venous return to the right ventricle.
Treadmill exercise test was performed for the evaluation of exercise tolerance after mitral valve replacement. The duration of maximum exercise tolerance in TR free group had no significant difference as compared with TR combined group. Preoperative RV function in TR combined group was kept relatively good as shown in cardiac index, pulmonary arterial and right atrial pressure. As hemodynamics was improved by TAP (TVR), it may not occur the difference in exercise tolerance between the groups. The duration of maximum exercise tolerance with MS group showed shorter tolerance than that of MR group. This difference in MS group might be considered due to the limitation of LV dilatation by rheumatic cardiac damage. Exercise tolerance after MVR was significantly lowered by atrial fibrillation, cardio-thoracic ratio over 60% and pulmonary vascular resistance over 3.0 Runits.m2.
Although atrial morphologic changes are well documented, the description of early atrial function is limited. We used videomicroscopic methods to define the function of the contracting atrium in stage 16 to 24 white Leghorn chick embryos. We exposed the embryo in ovo (right side up) and imaged the ventricle, then repositioned the embryo (left side up) and imaged the atrium (n greater than or equal to 8 per stage). We traced the atrial endocardial border and then measured atrial perimeter (mm) and cross-sectional area (mm2). A 20-MHz pulsed Doppler velocity meter was used to measure atrioventricular blood velocity during atrial imaging in an additional six stage 21 embryos. Data were tested by analysis of variance and regression analysis. Mean heart rate change after repositioning was -4 +/- 1%. Atrial maximum and minimum area increased linearly versus embryo stage (y = 0.10x - 1.41, r = 0.89, p less than 0.05 and y = 0.05x - 0.67, r = 0.82, p less than 0.05, respectively). Shortening fraction (percentage of reduction) of atrial perimeter and area decreased from 32.3 +/- 2.0% to 27.5 +/- 1.8% (p less than 0.05) and 56.2 +/- 3.0% to 47.7 +/- 2.0% (p less than 0.05), respectively, from stage 16 to 24. During atrial contraction, the velocity of circumferential wall shortening increased linearly with stage (y = 0.22x - 2.08, r = 0.81, p less than 0.01); however, the velocity of lengthening was similar between stages (p = 0.45). Simultaneous atrial imaging and pulsed Doppler velocity measurement showed that passive atrioventricular flow occurred late in atrial lengthening and active atrioventricular flow occurred during atrial contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of the study was to evaluate segmental and global right ventricular function at rest and during stress in patients having a systemic morphologically right ventricle. We studied 17 patients after atrial correction for transposition, 13 with congenitally corrected transposition, and 11 age-matched controls using cardiovascular magnetic resonance at rest and during stress with dobutamine given at 15 micrograms per kilogram per minute. Blood was drawn to obtain levels of brain natriuretic peptide. Right ventricular ejection fraction was calculated, and wall-motion and wall-thickening were assessed, in 4 segments of a midventricular slice. The findings for the systemic right ventricle were compared to the left ventricle in controls. Patients with transposition showed a decreased ejection fraction at rest (57 percent versus 69 percent, p equal to 0.005), decreased wall motion of the anterior, lateral and septal wall (p less than 0.01, p less than 0.01, and p less than 0.01) and decreased thickening of the lateral wall (p less than 0.01). Patients with congenitally corrected transposition showed normal ejection fraction, wall thickening, and wall motion at rest. During dobutamine stress, we found no significant differences in wall motion and thickening between the two groups. Ejection fraction, also increased to comparable values during stress, at 67 percent versus 66 percent, p not being significant. In both groups, we observed similarly increased levels of brain natriuretic peptide (p equal to 0.02 and 0.03, respectively). We conclude that only patients with transposition showed segmental wall motion and wall thickening abnormalities at rest. After dobutamine stress, however, segmental and global right ventricular dysfunction was similar in both groups.