Comparison of M mode echocardiography and pathologic findings in the hypoplastic left heart syndrome

John L. Bass, Giora Ben-Shachar, Jesse E. Edwards

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3 Scopus citations

Abstract

The M mode echocardiograms and pathologic specimens from 18 infants with the hypoplastic left heart syndrome were compared to determine the accuracy with which the echocardiogram reflects the state of the mitral valve, left ventricle and aortic valve, and its limitations in establishing this diagnosis. Mitral valve echoes were recorded in 7 of the 11 cases with an anatomic mitral valve orifice diameter greater than 3 mm. Ventricular septal echoes were found only in the seven cases in which the mitral valve was recorded. Differences between echocardiographic and anatomic left ventricular internal dimensions were not statistically significant in this small group. When aortic valve echoes were recorded, this valve was always patent in the anatomic specimen. The aortic valve was atretic in 9 of the 11 cases in which no aortic valve echoes were present. The echocardiographic and anatomic aortic root dimensions had a statistically significant correlation (p < 0.05), but there was considerable scatter in the data. None of the 18 infants met all of the previously proposed criteria for the echocardiographic diagnosis of hypoplastic left heart syndrome. An echocardiographic left ventricular dimension of 10 mm or greater was present in five cases (28 percent), and an aortic root dimension of 10 mm or greater in six (33 percent). The most reliable echocardiographic finding was excursion of 5 mm or less of the anterior leaflet of the mitral valve or inability to detect the mitral valve. Noninvasive findings are not always sufficient to establish the diagnosis of hypoplastic left heart syndrome, and further studies may be necessary in some patients.

Original languageEnglish (US)
Pages (from-to)79-86
Number of pages8
JournalThe American Journal of Cardiology
Volume45
Issue number1
DOIs
StatePublished - Jan 1980

Bibliographical note

Funding Information:
From the Department of Pathology, United Hospitals-Miller Division, St. Paul, and the Departments df Pediatric Cardiology and Pathology, University of Minnesota, Minneapolis. This study was supported by Public Health Service Research Grant 5 ROl HL05694 and Training Grants TO1 HL05996 and T32 HL07359 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland and by the Dwan Family Fund, Minneapolis, Minnesota. Manuscript received June 12, 1979; revised manuscript received August 21, 1979, accepted September 10, 1979.

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