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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inotropic support with digoxin is commonly used in patients with left ventricular volume overload due to ventricular septal defect (VSD). However, the hemodynamic consequences of inotropic agents with VSD have not been experimentally explored. We studied two inotropic agents, digoxin and amrinone, in chronically instrumented lambs with left ventricular volume overload due to a surgically created VSD. Intravenous digoxin (40 micrograms/kg) produced serum levels of 3.5 +/- 0.9 ng/ml (mean +/- SD) in seven lambs 60 min after administration, reduced the heart rate by 16% (172 to 149 beats/min, p less than 0.05), increased the stroke volume 16% (29.8 to 34.5 ml/beat, p less than 0.05) but did not significantly alter the systemic flow index (Qs), the pulmonary flow index (Qp), or the volume of left to right shunt (QL-R, 6.74 to 6.77 liter/min/m2). The mean left atrial pressure (LA) was unchanged (17.6 versus 17.1 mm Hg) following digoxin. Chronic digoxin use in four lambs for 4 days (25 +/- 8 micrograms/kg/8 h) produced trough serum levels of 1.2 +/- 0.2 ng/ml. There was no additional hemodynamic effect compared to acute digoxin, the Qp/Qs ratio was unchanged (3.10 versus 3.08) and evidence of left ventricular volume overload (LA - 14.0 versus 13.4) was unchanged. Amrinone lowered the systemic resistance index in a dose dependent fashion. The peak reduction of 20% (25.3 to 20.3 U/m2, p less than 0.01) occurred at 20 min after an intravenous (3 mg/kg) bolus in seven lambs. The Qs increased from 2.58 to 3.10 liter/min/m2 (p less than 0.01). The Qp was unchanged, thus the Qp/Qs ratio was lowered by 16% (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic consequences of inotropic support with digoxin or amrinone in lambs with ventricular septal defect. 404 55

In patients with ventricular or atrial septal defect, the ventricle which is chronically volume overloaded might not appropriately respond to increased demand for an augmentation in output and thereby might limit total cardiac function. In this study we simultaneously measured right and left ventricular response to exercise in 10 normal individuals, 10 patients with ventricular septal defect (VSD), and 10 patients with atrial septal defect (ASD). The normal subjects increased both right and left ventricular ejection fraction, end-diastolic volume, and stroke volume to achieve a higher cardiac output during exercise. Patients with VSD failed to increase right ventricular ejection fraction, but increased right ventricular end-diastolic volume and stroke volume. Left ventricular end-diastolic volume did not increase in these patients but ejection fraction, stroke volume, and forward left ventricular output achieved during exercise were comparable to the response observed in healthy subjects. In the patients with ASD, no rest-to-exercise change occurred in either right ventricular ejection fraction, end-diastolic volume, or stroke volume. In addition, left ventricular end-diastolic volume failed to increase, and despite an increase in ejection fraction, left ventricular stroke volume remained unchanged from rest to exercise. Therefore, cardiac output was augmented only by the heart rate increase in these patients. Right ventricular function appeared to be the major determinant of total cardiac output during exercise in patients with cardiac septal defects and left-to-right shunt.
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PMID:Radionuclide analysis of right and left ventricular response to exercise in patients with atrial and ventricular septal defects. 629 84

Between 1976 and 1981, 27 patients with complete transposition of the great arteries, ranging from one month to 2 1/2 years, underwent two-stage anatomic correction and 7 patients first-stage operation only. There were three early deaths after the first-stage and five after the second-stage operation and no late deaths. In seven patients the results of repeat cardiac catheterization including quantitative analysis of ventricular angiocardiograms at the different stages of the procedure were available. In these patients peak systolic pressure in the left ventricle rose to systemic levels after banding of the pulmonary artery. Left ventricular end-diastolic and stroke volumes decreased to normal levels without significant reduction of arterial oxygen saturation. One to 2 1/2 years after anatomic correction left and right ventricular function was normal, as judged by normal end-diastolic pressure, ejection fraction and ratio left ventricular muscle volume/end-diastolic volume. Minimal aortic regurgitation in five patients, mild mitral insufficiency in two and a small VSD in two contributed to elevated end-diastolic volumes of the left ventricle, observed in six patients, and of the right ventricle, found in two patients. The aortic and coronary anastomoses appeared to grow normally.
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PMID:Two-stage anatomic correction of complete transposition of the great arteries: ventricular volumes and muscle mass. 645 78

Vasodilator drugs are generally classified according to their prevalent site of action: arteriolar vasodilators (e.g. phentolamine, hydralazine, nifedipine) which reduce peripheral resistance and, therefore, increase stroke volume and cardiac output; venodilators (e.g. nitrates), which decrease filling pressure, redistributing intravascular blood volume from the central to the peripheral reservoirs and therefore relieve signs and symptoms of congestion; "balanced" vasodilators (e.g. nitroprusside, prazosin, captopril) which present both effects. Vasodilator therapy is indicated in heart failure caused by impaired contractility (congestive cardiomyopathy, ischemic heart disease) and volume overload (mitral and aortic regurgitation, ventricular septal defect). Hemodynamic studies of acute pharmacological effects are necessary for a correct drug choice, even if they are not always predictive of the long-term efficacy. Non-invasive studies (in particular echocardiography) don't seem actually adequate for vasodilator therapy evaluation. Finally it is not known if vasodilator treatment influence prognosis of chronic heart failure (especially survival), but there is evidence that it can lessen symptoms and increase effort tolerance.
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PMID:Vasodilators in left ventricular failure. 651 Jun 23

The ratio of pulmonary to systemic flow (Qp/Qs) was noninvasively evaluated by duplex Doppler echocardiography in 22 patients with atrial septal defects (ASDs). Right and left ventricular stroke volumes (RSV, LSV) were determined from the recordings of ejection blood flow velocity and diameter at the level of the pulmonary and aortic orifices in each ventricular outflow tract. The ratio RSV/LSV, determined by the duplex Doppler echocardiography, was compared with Qp/Qs by oximetry. The RSV/LSV for 10 normal subjects was 0.99 +/- 0.05 (mean +/- SD), whereas the RSV/LSV for patients with ASD, 2.26 +/- 0.63, was significantly higher than that for normal subjects (p less than .01). In patients with ASD, a fairly good correlation was found between RSV/LSV and Qp/Qs (r = .92, p less than .01; y = 1.11x - 0.30), and this high correlation was found even in patients with complications such as pulmonary hypertension, mitral and tricuspid regurgitation, Eisenmenger complex, and ventricular septal defect. We also found that semilunar valve regurgitation modified the value of RSV/LSV in accordance with the degree of regurgitation. These findings indicate that, with a few limitations, the Doppler index RSV/LSV is clinically useful in the estimation of the magnitude of the shunt flow in patients with ASD and that the limitations could be overcome by additional Doppler examination.
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PMID:Noninvasive evaluation of the ratio of pulmonary to systemic flow in atrial septal defect by duplex Doppler echocardiography. 668 49

We studied the acute effects of increasing hemoglobin concentration and hematocrit on the pulmonary and systemic circulations of nine infants with large left-to-right shunts. After isovolemic exchange transfusion, which was designed to raise hemoglobin but keep blood volume constant, a consistent rise in systemic and pulmonary vascular resistances occurred. This rise was comparable to those previously found in isolated circulations showing a linear relation between hematocrit and loge of the vascular resistance. These changes in resistance were accompanied by decreases in systemic and pulmonary blood flow and a marked decline in left-to-right shunt. Despite the decrease in systemic blood flow, there was no decline in systemic oxygen transport, and there may have been a marginal decrease in left ventricular stroke work. These observations help explain why the newborn with a large ventricular septal defect and a high hemoglobin concentration does not have clinical signs of a large left-to-right shunt, and also suggest that the postnatal decline in hematocrit has a substantial role in the normal fall in pulmonary vascular resistance after birth.
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PMID:Physiologic effects of increasing hemoglobin concentration in left-to-right shunting in infants with ventricular septal defects. 705 57

We reviewed the records of 217 children whose first episode of supraventricular tachycardia occurred before 18 years (median age 24 months). There were 112 males and 105 females. Of the 49 with congenital heart disease, SVT began before any operation in 26 and greater than 2 weeks postoperatively in 23. Wolf-Parkinson-White syndrome was present on surface ECG in 47/217 (22%). Congestive heart failure accompanied the first episode of SVT in 38% of the patients who were 4 months of age or younger, and in only 19% of those over 4 months (P less than 0.001). Treatment was successful in stopping SVT within 48 hours in 90/142 (63%). Successful short-term treatment included digoxin 57/184 (68%), cardioversion 12/20 (60%), vagal maneuvers 12/19 (63%), phenylephrine 3/9, and overdrive pacing 4/5. SVT recurred at least once in 83% of all patients. On follow-up (mean 4.6 years), episodes of SVT were still present in 56%. Three patients died--two from incessant SVT and one from a CVA after VSD repair. We conclude that long-term status was difficult to predict, but SVT was present in fewer patients whose age at onset was less than 4 months and in those with unoperated CHD. Early recurrence was not a poor prognostic sign. We recommended treatment for at least one year in all patients with SVT, whether or not the first episode terminates spontaneously.
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PMID:Supraventricular tachycardia in children: clinical features, response to treatment, and long-term follow-up in 217 patients. 722 88

To obtain insight into the hemodynamics of abnormal cardiac development, a chick embryo model was recently developed in which a spectrum of double outlet right ventricle was induced with all-trans-retinoic acid. In Hamburger and Hamilton (HH) stage 34 white Leghorn chick embryos, we simultaneously measured dorsal aortic flow velocities with a 20 MHz pulsed Doppler velocity meter and vitelline artery blood pressures with a servonull system. These measurements were performed in embryos treated at HH stage 15 with 1 microgram of all-trans-retinoic acid (n = 47), or with the solvent DMSO (n = 15), and in control embryos (n = 21). After the wave form recordings were collected, all embryos were examined histologically. Embryos treated with all-trans-retinoic acid showed in 15 cases hearts with a rightward positioned aorta with an additional subaortic ventricular septal defect and 32 cases without septation abnormalities of the heart. The hemodynamic data were correlated with the morphology. Statistical comparison was performed between control and experimental values. There was no significant discrepancy in hemodynamics of sham-operated and control embryos. Heart rate, peak systolic and mean velocities, peak systolic and mean blood flows, and peak acceleration and stroke volume were reduced in embryos treated with all-trans-retinoic acid (p < 0.01). Furthermore, in the presence of a subaortic ventricular septal defect the diameter of the dorsal aorta was reduced. Pressure readings were not statistically significant. Our findings suggest that the hemodynamic changes are the result of a decrease in cardiac contraction force.
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PMID:Hemodynamic changes in HH stage 34 chick embryos after treatment with all-trans-retinoic acid. 749 57

Left ventricular function and the extent of pulmonary vascular disease were studied in 18 children with Down's syndrome and 20 children without Down's syndrome who underwent corrective surgery for ventricular septal defect (VSD) and severe pulmonary hypertension. This study was conducted between 1985 and 1993. All patients underwent routine cardiac catheterization preoperatively and postoperatively (mean, 11.4 months after surgery). Left ventricular function was estimated using cineangiographic levograms. In both groups, the pulmonary-to-systemic arterial pressure ratio (Pp/Ps) and pulmonary vascular resistance (PVR) were significantly lower after surgery (P < 0.05). Postoperative improvement was more remarkable in the non-Down group (P < 0.05). Left ventricular end-diastolic volume (percent of normal) (LVEDV%N) was significantly lower after surgery in both groups (P < 0.01). The left ventricular stroke work-to-end-diastolic volume ratio (LVSW/EDV) was significantly higher after surgery in the non-Down group only (P < 0.01). Postoperative left ventricular ejection fraction (LVEF) was significantly lower in the Down group than in the non-Down group (P < 0.01). Some degree of irreversible pulmonary vascular disease was present after repair of VSD in patients with Down's syndrome. In the Down group, there were no significant changes in left ventricular function after surgery, despite the relief of volume overload. These results suggest that early diagnosis and surgical repair are key elements in the management of patients with Down's syndrome and VSD.
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PMID:Comparison of hemodynamic data before and after corrective surgery for Down's syndrome and ventricular septal defect. 767 86

The effects of Amrinone on cardiac function soon after extracorporeal circulation (ECC) were studied in 5 patients including mitral valvuloplasty, VSD closure, Fontan operation and coronary AV fistel closure. In all patients, left ventricular volume load decreased postoperatively. To evaluate the efficacy, we obtained left ventricular pressure-volume loops (P-V loop) before and after ECC and after intravenous administration of Amrinone (1 mg/kg) following ECC. P-V loops were produced by measuring left ventricular pressure using a Miller catheter which was retrogradely advanced from the ascending aorta into the left ventricle and by measuring left ventricular diameter to calculate left ventricular volume with Teichholtz' formula. Although no apparent difference of Emax was recognized before and after ECC, Emax increased from 3.2 +/- 2.5 mmHg/cm3 to 5.9 +/- 4.7 mmHg/cm3 after the administration of Amrinone. The left ventricular "systolic" pressure-volume area (PVA) which is the sum of stroke work (SW) and elastic potential energy decreased from 34.4 +/- 16.4 gm to 30.9 +/- 17.8 gm after Amrinone. No difference was also recognized in left ventricular end-diastolic pressure. Ejection fraction increased from 50 +/- 17.5% to 56.1 +/- 17.3%. These results suggested that Amrinone could improve the left ventricular function without prominent change in myocardial oxygen consumption immediately after open heart surgery.
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PMID:[Effects of amrinone on left ventricular function following open heart surgery--analysis with left ventricular pressure volume loops]. 779 1


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