Search PubMedSearch

Biomedical subjects

A V Mehta

Publications and source records attributed to A V Mehta.

At least 19 recordsLinked to original sources

Ventricular septal defect in the first year of life.

Of approximately 22,000 live births in the region under study during the last 4 years, ventricular septal defect (VSD) was identified as the primary or isolated congenital heart lesion in 124 infants who were followed up from birth for a minimum of 1 year (incidence, 5.7 per 1,000 live births). Doppler color flow mapping was performed in 93 of 124 patients; 47 had a muscular VSD and 46 had a perimembranous VSD. Only 1 patient had 2 muscular VSDs. None had a subpulmonic type of defect. Of 124 patients, 14 were lost to follow-up. Spontaneous closure was seen in 18 patients (42%) in the muscular group, in 9 (23%) in the perimembranous group and in 10 patients (37%) in the unclassified group by the end of the first year. The overall rate of spontaneous closure was 34% by the end of the first year. Congestive heart failure developed in 2 of 46 patients with muscular VSD and in 12 of 47 patients with perimembranous VSD. In the first year, 2 patients with muscular VSD as opposed to 5 with perimembranous VSD required surgery. Doppler color flow mapping is a valuable aid in the diagnosis of VSD and may be one reason for the observed increase in the incidence of VSD. The overall prognosis appeared much better in the muscular than the perimembranous type of VSD.

Female

Efficacy and safety of intravenous and oral nadolol for supraventricular tachycardia in children.

The efficacy and safety of oral nadolol in supraventricular tachycardia were evaluated prospectively in 27 children (median age 5.5 years). Fifteen patients had an unsuccessful trial of digoxin therapy. Intravenous nadolol was given to seven patients during electrophysiologic study; five of these had an excellent response and two had a partial response (25% decrease in tachycardia rate). Six of these patients had a similar response to oral nadolol. Twelve patients received both propranolol and nadolol. Among six patients, intravenous propranolol was successful in four and unsuccessful in two; all six had a similar response to oral nadolol. With oral propranolol, tachycardia was well controlled in four patients and persistent in two; five of five patients had a similar response to oral nadolol. Twenty-six patients were treated with oral nadolol; the arrhythmia was well controlled in 23, 2 had recurrent tachycardia and 1 patient had tachycardia at a 25% slower rate. The effective dose of nadolol ranged between 0.5 and 2.5 mg/kg body weight once daily (median dose 1 mg/kg per day). During follow-up (3 to 36 months), compliance and tolerance were excellent; excluding 2 patients with reactive airway disease who developed wheezing, only 3 (12%) of 24 had side effects necessitating a change in drug therapy. Once a day nadolol is a safe and effective agent in the management of supraventricular tachycardia in children. Its long-term efficacy can be predicted by the short-term response to intravenous nadolol or propranolol during programmed electrophysiologic study.

Administration, Oral

Pharmacokinetics of nadolol in children with supraventricular tachycardia.

The pharmacokinetics of intravenous and oral nadolol, a long-acting beta-adrenoceptor blocking agent, were investigated in six children receiving the drug for treatment of supraventricular tachycardia. In the youngest patient (age 3 months), no distribution phase was seen. In children younger than 22 months of age, nadolol is more rapidly eliminated (t1/2 = 4.3 hours or less) than in older children, in whom elimination is more similar to that in adults (t1/2 approximately 7.3-15.7 hours). After intravenous administration, nadolol displayed two-compartment pharmacokinetics with a distribution phase (t1/2 = 0.2-1.1 hours) followed by elimination. Large changes in nadolol pharmacokinetics may occur during the first year of life. Nadolol should be used cautiously in infants.

Adolescent

Currarino-Silverman syndrome (pectus carinatum type 2 deformity) and mitral valve disease.

Currarino-Silverman syndrome is a rare disorder characterized by premature fusion of manubrio-sternal joint and the sternal segments, resulting in a high carinate chest deformity; it is frequently associated with congenital heart disease. Among the various heart lesions reported in this syndrome, mitral valve disease and coarctation of the aorta have not yet been described (to our knowledge). Our report consists of five children with this syndrome, four of whom had mitral valve disease, with an associated coarctation of the aorta in one patient. The fifth patient had an innocent heart murmur.

Aortic Coarctation

Percutaneous transluminal balloon angioplasty of stenotic standard Blalock-Taussig shunts: effect on choice of initial palliation in cyanotic congenital heart disease.

To date, attempted balloon dilation of stenotic standard Blalock-Taussig shunts has been largely disappointing. It has been suggested that this may be due to the use of balloons of insufficient diameter. Balloon dilation of stenotic Blalock-Taussig shunts was attempted with use of relatively large balloons in five patients (11 to 67 months old) with cyanotic heart disease who were becoming progressively cyanotic and polycythemic (hemoglobin 17.9 +/- 1.1 g/dl) because of discrete shunt stenosis at the site of pulmonary anastomosis. Balloon diameters selected were equal to or within 1 mm of the unobstructed proximal shunt diameter. Before balloon dilation the diameter at the site of the stenosis was 2.8 +/- 0.8 mm (range 1.7 to 4); after balloon dilation it was 5.7 +/- 1.1 mm (range 4.5 to 7.5). The diameter increased in all patients (range 2.0 to 3.5 mm); the mean increase was 2.8 +/- 0.2 mm (p less than 0.005). Expressed as a percent, the increase in diameter at the stenosis ranged from 80% to 182.4% (mean 108.2 +/- 16.8%). Before balloon dilation the systemic oxygen saturation was 72.8 +/- 9.2% (range 55% to 80%) and after balloon dilation it was 83.6 +/- 2.9% (range 80% to 87%). A satisfactory increase (range 6% to 25%) in blood oxygen saturation was seen in all patients; the mean increase was 10.8 +/- 3.2% (p less than 0.01). At follow-up, the oxygen saturation by pulse oximetry was 85.8 +/- 2.9% (mean 5.8 +/- 1.7 months after balloon dilation) and the hemoglobin was 15.6 +/- 1.9 g/dl (mean 6.6 +/- 1.5 months after balloon dilation).(ABSTRACT TRUNCATED AT 250 WORDS)

Anastomosis, Surgical

Urokinase treatment of neonatal aortoiliac thrombosis caused by umbilical artery catheterization: a case report.

Umbilical artery catheterization is known to be associated with aortoiliac thrombosis in approximately 1% of newborns in whom catheters are placed. We describe a case of catheter-associated aortoiliac thrombosis in a newborn who was successfully treated by urokinase infusion. The infant was monitored by imaging studies followed by ultrasonography. The use of real-time ultrasonography enabled us to image this infant's aortoiliac thrombosis in an accurate, noninvasive manner and monitor the effectiveness of thrombolytic therapy. The fibrinolytic state was achieved with a combination of intravenous and intraarterial infusions of urokinase. Frequent measurement of prothrombin time, activated partial thromboplastin time, fibrinogen, and thrombin time was used to guide fibrinolytic therapy. We reviewed the literature for similar cases of aortoiliac thrombosis in newborns; some were managed by medical means, others by operation. The success rate of the two approaches appeared to be approximately equal. Therefore we recommend the less invasive approach first--urokinase therapy--to be followed by surgical intervention if thrombolysis is unsuccessful.

Aorta, Thoracic

Palliative percutaneous balloon valvuloplasty in a cyanotic child with tetralogy of Fallot.

We have presented the case of an 8-month-old child who had tetralogy of Fallot with severe pulmonary stenosis and minimal infundibular stenosis. Because of the relatively small annulus (10 mm) and young age of the infant, total correction was deferred, and a percutaneous palliative pulmonary balloon valvuloplasty was done. At the end of the procedure, he had neither cyanosis nor signs of congestive heart failure, and after four months of follow-up, he had only mild cyanosis with activities.

Catheterization

Ectopic automatic atrial tachycardia in children: clinical characteristics, management and follow-up.

Ectopic automatic atrial tachycardia, an uncommon type of supraventricular tachycardia in children and adults, has been reported to be resistant to medical therapy, and surgical or cryoblation has been recommended. This report describes 10 infants and children (median age 6 months; range birth to 7.5 years) with automatic atrial tachycardia and their management and follow-up. Digoxin alone was unsuccessful in controlling tachycardia in all 10 patients but decreased the tachycardia rate by 5 to 20% in 8. Intravenous (0.1 mg/kg body weight per dose) and oral propranolol successfully suppressed tachycardia in three of five patients and oral propranolol successfully controlled tachycardia in two of five other patients. Class I antiarrhythmic agents--quinidine (three patients), procainamide (four patients) and phenytoin (three patients)--did not control tachycardia in any patients but made the tachycardia rate worse in three patients. Intravenous (5 mg/kg per dose) and oral amiodarone suppressed tachycardia in three of four patients and oral amiodarone suppressed it in another patient. Thus, intravenous propranolol and amiodarone were effective in acutely suppressing automatic ectopic atrial tachycardia and predicted the response to long-term oral therapy. One patient had persistent tachycardia after surgical ablation of the high right atrial ectopic focus, and another patient had unsuccessful catheter ablation of the high right atrial ectopic focus (25 J). During follow-up (10 to 28 months), ectopic atrial tachycardia resolved completely in four patients and was well controlled in four patients.

Administration, Oral

Oncocytic cardiomyopathy of infancy with Wolff-Parkinson-White syndrome and ectopic foci causing tachydysrhythmias in children.

Two female infants, ages 6 months and 13 months, were first seen in the newborn period with supraventricular tachycardia associated with Wolff-Parkinson-White syndrome. One infant had echocardiographic and angiographic evidence of diffuse cardiomyopathy and died suddenly at home. The other infant was seen initially at 13 months of age with refractory ventricular tachycardia and died following surgical resection of arrhythmogenic foci on the left and right ventricles. Autopsy showed diffuse patchy oncocytic cardiomyopathy in both instances. Serial histologic sections of the cardiac conduction system showed oncocytic involvement of the atrioventricular (AV) node, His bundle, and bundle branches. Both infants had interruption of the anulus fibrosus by oncocytic cells at several sites, resulting in multiple accessory AV and nodoventricular connections. Additionally, patient No. 1 had an accessory AV connection by oncocytic cells in the fatty fibrous tissue of the left AV sulcus. To our knowledge, this is the first report of multiple accessory AV connections of oncocytic cells seen during histologic study. In addition, both infants had oncocytic involvement of the exocrine and endocrine glands. This report discusses the clinicopathologic correlations in these two patients, the literature on oncocytic cardiomyopathy, and the types of dysrhythmias found in these patients and their management.

Cardiomyopathies

Recurrent obstruction after subclavian flap repair of coarctation of the aorta in infants. Can it be predicted or prevented?

Recoarctation is a problem in some patients after subclavian flap aortoplasty. To investigate the reason for recoarctation, we reviewed the records of 26 infants who underwent subclavian flap repair for symptomatic coarctation of the aorta at less than 3 months of age between June, 1979, and December, 1983. Age at repair ranged from 2 to 65 days (median 16 days) and weight from 2.1 to 4.9 kg (median 3.4 kg). In 14 patients the coarctation was associated with significant intracardiac defects (complex in six). There were two intraoperative deaths and one early death (surgical mortality 12%). The survivors were followed from 6 weeks to 66 months (median 12 months). Five survivors (22%), all operated on at less than 14 days of age, developed severe recoarctation 6 weeks to 6 months (median 5 months) after repair. The obstruction appeared to be due to lumen obliteration by shelf-life posterior wall tissue. Morphometric analysis of preoperative angiograms showed no correlation between recoarctation and distance between the left subclavian artery and the site of coarctation, length of the isthmus, diameter of the isthmus, combined cross-sectional area of the left subclavian artery and isthmus, or the ratio of the combined cross-sectional area of the left subclavian artery and isthmus to the cross-sectional area of the descending thoracic aorta. Recoarctation did not correlate with weight at operation, but it correlated significantly with age at aortoplasty (p = 0.02). The results suggest that intrinsic abnormalities of the periductal aortic wall are responsible for recoarctation after subclavian flap aortoplasty. Particular attention to this abnormal tissue at repair may prevent early recurrence in young infants.

Age Factors

Successful percutaneous balloon valvuloplasty of the aortic valve in an infant.

Percutaneous balloon aortic valvuloplasty was attempted in an eight-month-old infant with severe aortic valve stenosis. The procedure resulted in a fall in the resting transvalvular systolic pressure gradient from 106 mmHg to 40 mmHg and no aortic regurgitation. Clinical and Doppler echocardiography findings suggest persistent improved status 3 1/2 months after the procedure.

Angioplasty, Balloon

Heart block and atrioventricular septal defect.

The cardiac conduction system was examined in 2 hearts which had repair of atrioventricular septal defect. The first was from a child known to have had a prolonged P-R interval and the second was from a girl who developed complete heart block before submission to surgery. The atrioventricular conduction axis was histologically discontinuous in the first case, but preserved and surrounded by hemorrhage in the second case. This study draws attention to the inherent vulnerability of the cardiac conduction axis which must also be recognized before surgical intervention.

Child

M-mode echocardiographic findings in children with idiopathic restrictive cardiomyopathy.

The M-mode echocardiographic findings in five pediatric patients, ages 4-15 years, with primary idiopathic restrictive cardiomyopathy, diagnosed by cardiac catheterization, and of 12 normal children (control group) are presented. The M-mode echocardiographic findings in patients with restrictive cardiomyopathy were (1) normal left and right ventricular end-diastolic dimension, (2) normal left ventricular posterior wall and interventricular septal thickness (three patients) or mild concentric hypertrophy (two patients), (3) normal opening and closing velocity of the mitral valve, (4) consistently enlarged left atrium (more than 40 mm) in all, and (5) right ventricular systolic time intervals compatible with pulmonary artery hypertension. The left ventricular ejection phase parameters (systolic time intervals, shortening fraction, and mean velocity of circumferential fiber shortening) were normal. Left ventricular relaxation phase parameters (diastolic function) were abnormal. The isovolumic relaxation time index was prolonged, 68 +/- 40 ms (+/- SD), in the study group as compared with 11 +/- 6 ms (+/- SD) in the control group (P less than 0.001). Percent relaxation of left ventricular posterior wall endocardium at 50% of diastole was decreased, 58 +/- 4% (+/- SD), in the study group as compared with 85 +/- 6% (+/- SD) in the control group (P less than 0.005). We conclude that M-mode echocardiography provides a relatively useful and specific noninvasive method for the diagnosis of primary restrictive cardiomyopathy in pediatric patients.

Adolescent

Induction of nonsustained atrial flutter by programmed atrial stimulation in children: incidence, mechanisms, and clinical implications.

Nonsustained atrial flutter was induced by programmed atrial extrastimulation in 6 (4%) of 137 children with preoperative congenital heart defects, who underwent electrophysiologic evaluation as part of cardiac catheterization. None of these patients had ECG or clinical evidence of arrhythmias. Atrial reentry was induced by programmed atrial extrastimulation in these six patients at coupling intervals slightly longer than the coupling interval at which flutter was induced. The flutter cycle length was similar to the atrial refractory periods. The duration ranged between 0.4 second and 60 seconds. The PA interval and the duration of the P wave were normal in all of the patients. Five of the six had normal PR intervals. It is concluded that nonsustained atrial flutter may be induced by programmed atrial extrastimulation in dysrhythmia-free children. The cycle length is determined by atrial refractoriness and, contrary to adults with clinical atrial flutter, prolonged PA and P wave duration are not predisposing factors.

Adolescent