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PubMedDate not supplied

Prospective evaluation of the balloon-to-annulus ratio for valvuloplasty in the treatment of pulmonic stenosis in the dog.

BACKGROUND: In dogs, treatment of pulmonic valve stenosis (PS) with pulmonary balloon valvuloplasty (PBV) is a viable method to decrease the pressure gradient across the valve. However, to the authors' knowledge, the variables that influence the selection of the correct balloon size for the procedure have not been explored. Moreover, the lesions caused by the procedure have not been detailed. HYPOTHESIS: Variables that influence the measurement of the annulus could affect selection of the balloon size. We sought to determine the effects of treatment when the balloon-to-annulus ratio (BAR) was or > 1.3, but within the recommended range of 1.2-1.5, regardless of whether dilation was performed with single or double balloon technique. ANIMALS: Twenty-five Beagles with PS were studied. METHODS: Inter- and intra-observer variability, echocardiography versus angiocardiography, and systolic versus diastolic timing were evaluated for the BAR. Assessment of right ventricular (RV) pressure, Doppler gradient, stenotic valve area, and RV wall thickness were compared before and 1, 90, and 180 days after treatment. Postmortem examination of the heart was done. RESULTS: Significant correlations existed in measurement of the annulus; however, variation existed that would change balloon size. Improvement in the degree of PS was significant regardless of the BAR or single or double ballooning. In the most severely affected dogs, continued improvement was noted on day 90. Postmortem examination revealed tears in the commissures and the valve leaflets. CONCLUSIONS: Multiple factors influenced determination of the BAR and a range of 1.2-1.5 was effective without detrimental consequences. Dogs with severe PS had continued decrease in RV pressure 3 months after treatment.

Animals↗
PubMed1975

First heart sound and ejection sounds. Echocardiographic and phonocardiographic correlation with valvular events.

To provide additional information on the relation of valvular events to the principal components of the first heart sound (s1), combined echocardiograms and phonocardiograms were recorded in 49 subjects, chosen because of audible splitting of S1 or a combination of S1 and an ejection sound. The subjects included 14 normal persons, 16 patients with a variety of predominantly right-sided heart conditions, 7 with mitral stenosis, 3 with pulmonary stenosis and 9 with aortic valve disease or systemic hypertension. A precise relation was found between completion of closure of the atrioventricular (A-V) valves manifested in the echocardiogram and the high-frequency components of S1 (M1 and T1). The average time from the Q wave of the electrocardiogram to M1 was 0.06 plus or minus 0.003 second and the Q-T1 interval was 0.09 plus or minus 0.002 second. In mitral stenosis the Q-M1 interval was delayed to 0.10 plus or minus 0.005 second, resulting in some instances in reversed splitting of S1. In pulmonary stenosis, the ejection sound occurred 0.10 plus or minus 0.003 second from the Q wave. In 7 of the 16 patients with various right-sided abnormalities, but without valvular stenosis, an ejection sound of pulmonary origin occurred 0.18 plus or minus 0.012 second from the Q wave. In the nine patients with aortic valve disease or systemic hypertension, the time from the Q wave to the aortic ejection sound was 0.13 plus or minus 0.004 second. With only two exceptions the ejection sounds of aortic and plumonary origin coincided exactly with achievement of a fully opened position of the respective semilunar valve. Our findings support the postulate that M1, T1 and the ejection sounds occur in association with closing or opening of valves with consequent sudden deceleration or acceleration of a column of blood that, in turn, results in vibrations of the cardiohemic system and audible sounds.

Adolescent↗
PubMed1983

Pulmonary atresia with and without ventricular septal defect: a different etiology and pathogenesis for the atresia in the 2 types?

In 15 of 20 hearts of neonates with pulmonary atresia and intact septum (PA-IVS) and in 4 with critical pulmonary stenosis, the pulmonary valve consisted of 3 fused cusps. One of the 11 patients with a ventricular septal defect (PA-VSD) had a well-developed pulmonary root; in 8 the pulmonary trunk arose from a dimple. Two had a bicuspid valve. In 10 of the 20 patients with PA-IVS and in those with critical stenosis, the diameter of the pulmonary trunk was normal or larger than normal. The authors believe that this is related to flow through an initially patent pulmonary valve and, perhaps more importantly, to poststenotic dilatation. In all hearts with PA-VSD, the pulmonary trunk was very small. In the patients with PA-IVS and a normal-sized pulmonary trunk and in 3 with critical pulmonary stenosis, the morphology of the ductus arteriosus was normal, suggesting that even in the former the valve was patent before birth, allowing forward flow. In all patients with small pulmonary trunk, the ductus was long, tortuous, and originated from the aortic arch in a proximal position, suggesting that reversal of flow had occurred early in development. The authors postulate that in patients with ventricular septal defect (VSD), the pulmonary ostium becomes atretic early in development, at or shortly after partitioning of the truncoconal part of the heart has taken place but before closure of the ventricular septum. In patients with intact ventricular septum, on the other hand, atresia very likely occurs sometime after cardiac septation has been completed. In these cases the pulmonary atresia may be due to a prenatal inflammatory process, rather than representing a true congenital malformation.

Heart Septal Defects, Ventricular↗
PubMed1983

Severe congestive heart failure in mild pulmonic stenosis due to dysplastic pulmonary valve associated with cardiomyopathy.

Congestive heart failure has never been described in patients with dysplastic stenotic pulmonary valve without associated shunt lesions. We describe two patients with mild pulmonic stenosis due to valvular dysplasia associated with cardiomyopathy who developed severe congestive heart failure. Since the small pressure gradients across the pulmonary valve cannot cause this complication, we suggest that it resulted from the associated hypertrophic non-obstructive cardiomyopathy. The presence of cardiomyopathy may alter the clinical presentation and prognosis of patients with dysplastic pulmonary valve. In some cases, like our two cases, the cardiomyopathy rather than the valvular lesion should be considered the main disease.

Cardiomegaly↗