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Biomedical subjects

C E Clark

Publications and source records attributed to C E Clark.

At least 55 records · Page 3Linked to original sources
PubMed1978

Abnormal right ventricular size and ventricular septal motion after atrial septal defect closure: etiology and functional significance.

Postoperative echocardiogram often demonstrate persistent right ventricular dilatation and paradoxic ventricular septal motion after repair of an atrial septal defect. To determine the prevalence, causes and significance of these echocardiographic abnormalities, 31 patients were studied with catheterization and echocardiography before and after repair of an atrial septal defect. Before operation, every patient manifested right ventricular dilatation, and all but one had abnormal septal motion. After operation, right ventricular dilatation was noted in 24 (77%) and abnormal septal motion in 21 (68%) patients despite the absence of residual left to right shunting in 30 (97%). These echocardiographic abnormalities could be correlated with age at operation and length of postoperative follow-up study but did not correlate with the degree of preoperative right ventricular enlargement or with shunt size or right ventricular pressure before or after operation. There was no associated functional deficit as demonstrated by the normal maximal oxygen consumption in all 13 patients who underwent treadmill exercise testing 5 to 38 months after operation; these patients included 9 with persistent right ventricular enlargement and abnormal septal motion.

Adolescent↗
PubMed1978

Prevalence and characteristics of disproportionate ventricular septal thickening in patients with coronary artery disease.

Echocardiographic or necropsy studies were performed in 151 patients with coronary artery disease. Prevalence of disproportionate septal thickening (septal to free wall ratio greater than or equal to 1.3) was 11%. An abnormally increased septal-free wall ratio in these patients had two principal etiologies. First, it was a manifestation of genetically transmitted hypertrophic cardiomyopathy, as evidenced by disproportionate septal thickening in first degree relatives. Second, it was due to disproportionate septal thickening which did not appear to be a manifestation of genetically transmitted hypertrophic cardiomyopathy. This latter conclusion was suggested by negative echocardiographic studies in some families of patients with both coronary artery disease and disproportionate septal thickening. In addition, numerous disorganized cardiac muscle cells, characteristically present in patients with genetically transmitted hypertrophic cardiomyopathy, were absent from the septum of all patients with disproportionate septal thickening studied at necropsy. Although the mechanism responsible for this secondary type of disproportionate septal thickening is unknown, our results indicate that the presence of disproportionate septal thickening in a patient with coronary artery disease does not, per se, indicate the coexistence of genetically transmitted hypertrophic cardiomyopathy.

Coronary Disease↗
PubMed1978

Electrocardiographic findings in patients with obstructive and nonobstructive hypertrophic cardiomyopathy.

One hundred and thiry-four patients with hypertrophic cardiomyopathy were evaluated by standard 12-lead electrocardiography. Normal electrocardiograms were extremely uncommon, occurring in less than 7% of each subgroup of patients (i.e., those with or without either symptoms or obstruction to left ventricular outflow), with the exception of those who were both asymptomatic and had no left ventricular outflow obstruction. Even in this subgroup, however, normal electrocardiograms occurred in only 27% of patients. Repolarization abnormalities and left ventricular hypertrophy were the most common abnormalities, occurring in 81% and 62%, respectively, of the total population. A broad spectrum of other electrocardiographic abnormalities was found, but none was unique to hypertrophic cardiomyopathy. Patients with vs those without electrocardiographic left ventricular hypertrophy or left atrial abnormality had significantly (P less than 0.005) greater mean ventricular septal thickness (22 +/- 0.6 vs 19 +/- 0.6 mm) and left atrial dimension (48 +/- 1 vs 40 +/- 1 mm) measured by echocardiography, and signficantly (P less than 0.01) higher mean pulmonary capillary wedge pressure (16 +/- 1 vs 10 +/- 1 mm Hg) and left ventricular end-diastolic pressure (20 +/- 1 vs 15 +/- 1 mm Hg). The high prevalence and diverse nature of electrocardiographic abnormalities suggest that any patient with an unusual and unexplained electrocardiogram should be suspected of having hypertrophic cardiomyopathy even if the physical examination is normal, as is often the case in patients without obstruction.

Cardiomyopathy, Hypertrophic↗
PubMed1978

Cytogenetic abnormalities in orthopedic patients.

Patients with orthopedic problems may also have chromosomal abnormalities. Individuals who present with subtle clinical findings suggestive of a known syndrome resulting from a chromosomal abnormality, such as Klinefelter syndrome, Turner syndrome, or any of the known trisomiers, should be investigated further in order to confirm the diagnosis. In addition, those patients who have multiple congenital abnormalities in several systems should also have chromosome analysis. This should be done not only to gain new information in regard to chromosome abnormalities, but also to establish a diagnosis for the individual and thus provide proper genetic counseling for the family. If the clinical picture strongly suggests a chromosomal abnormality, and routine karyotyping does not demonstrate one, it is imperative that one or more banding techniques be utilized before a chromosomal abnormality can be ruled out.

Abnormalities, Multiple↗
PubMed1977

Sudden infant death syndrome (SIDS). Echocardiographic studies in relatives of infants with SIDS.

Echocardiographic studies were performed in 42 sets of parents who had at least one infant with Sudden Infant Death Syndrome (SIDS). Asymmetric septal hypertrophy (ASH) was detected by echocardiography in one member of only 5 percent of the 42 sets of parents. Echocardiograms were also obtained in three other sets of parents who had infants with SIDS (selected because their infants showed small foci of disorganized cardiac muscle cells in the ventricular septum, similar to those present in patients with typical ASH but less marked in severity). ASH was present in one member of each of these three sets of parents. Ventricular septal-to-posterobasal left ventricular wall thickness ratios in the five subjects in this study with echocardiographically determined ASH ranged from 1.3 to 1.7, although only one individual showed marked thickening of the ventricular septum (22 mm). Thus, SIDS and ASH do not appear to be commonly associated conditions.

Cardiomyopathy, Hypertrophic↗
PubMed1977

Prevalence and characteristics of disproportionate ventricular septal thickening in patients with acquired or congenital heart diseases: echocardiographic and morphologic findings.

Echocardiographic and necropsy studies were performed in 304 patients with various cardiac diseases. The overall prevalence of disproportionate ventricular septal thickening (septal to free wall ratio greater than or equal to 1.3) was 10%. However, it was related to the type of cardiac lesion. Prevalence was high (greater than 20%) in pulmonary stenosis or primary pulmonary hypertension, lower (less than 15%) in Eisenmenger syndrome or aortic or mitral valvular disease and was not present in atrial or ventricular septal defect. In right ventricular overload, prevalence of disproportionate septal thickening correlated with increasing ventricular systolic pressure. None of 16 patients with disproportionate septal thickening studied at necropsy showed marked disorientation of cardiac muscle cells in the ventricular septum, characteristic of genetically transmitted asymmetric septal hypertrophy (ASH). Furthermore, disproportionate septal thickening was demonstrated by echocardiography in only one of 59 first degree relatives of patients with disproportionate septal thickening and associated cardiac diseases. Thus, disproportionate ventricular septal thickening associated with other cardiac diseases usually is due to secondary hypertrophy and is not a manifestation of genetically transmitted ASH.

Adolescent↗
PubMed1976

Asymetric septal hypertrophy in childhood.

Although considerable information is available concerning the clinical features and natural history of asymmetric septal hypertrophy (ASH) in adults, little is known of this disease in children. The clinical characteristics and course of 46 children with ASH, who were evaluated at the National Heart and Lung Institute, have been analyzed. Twenty-four children had obstruction to ventricular outflow; 22 children had no obstruction to ventricular outflow, including 11 patients without overt manifestations of cardiac disease other than echocardiographic evidence of ASH. Thirty-five of the 46 children have been followed for one to 16 years (average 7.4 years). These latter children represent that subgroup of patients with ASH referred to the National Heart and Lung Institute and diagnosed prior to the general availability of echocardiography. The clinical course of these patients was variable. Fourteen (40%) of the 35 patients improved or remained stable, including four patients who received propranolol. Ten (29%) of the 35 patients deteriorated clinically and 11 (31%) of the 35 patients died suddenly (4% mortality per year). Two of the patients who died suddenly had previously undergone operation (six and 13 years previously) with resultant abolition of the outflow gradient; four others were taking propranolol. Neither symptomatology, electrocardiographic abnormalities, heart size, left ventricular ejection or upstroke time, magnitude of outflow gradient, or left ventricular end-diastolic pressure proved predictive of sudden death. Excluding patients who had previous operation, eight (40%) of 20 patients with obstruction who were followed long term and one (9%) of 11 patients without outflow obstruction died suddenly. Thus, the clinical and hemodynamic spectrum of ASH in childhood is broad. However, deterioration in clinical condition or sudden death has been relatively common in children with overt signs of cardiac disease.

Adolescent↗
PubMed1976

Relation between echocardiographically determined left atrial size and atrial fibrillation.

In an attempt to define quantitatively the relation between left atrial size and atrial fibrillation, echocardiography was used to study 85 patients with isolated mitral valve disease, 50 patients with isolated aortic valve disease, and 130 patients with asymmetric septal hypertrophy. In all three groups of patients, atrial fibrillation was rare when left atrial dimension was below 44 mm (3 of 117 or 3%) but common when this dimension exceeded 40 mm (80 of 148 or 54%). In addition, when left atrial dimension exceeds 45 mm, cardioversion, while initially successful, is unlikely to produce sinus rhythm that can be maintained at least six months. These data suggest that left atrial size is an important factor in the development of atrial fibrillation and in determining the long term result of cardioversion. The pathophysiologic mechansim most consistent with this is that a chronic hemodynamic burden initially produces left atrial enlargement which in turn predisposes to atrial fibrillation. Only prospective studies will determine definitively whether these observations will be useful in decisions concerning prophylactic anticoagulation and elective cardioversion.

Adolescent↗
PubMed1976

Determinants of ventricular septal motion. Influence of relative right and left ventricular size.

To test the hypothesis that the ventricular septum moves during systole toward the center of the ventricular mass (so that the end-diastolic position of the septum within the heart should determine both the direction and the magnitude of septal motion during systole), echocardiograms from patients with several different hemodynamic burdens were analyzed. A linear relation was noted between the end-diastolic intracardiac position of the ventricular septum and the direction and magnitude of systolic septal motion in 1) forty three patients with an atrial septal defect )regression coefficient r = 0.80), 2) fourteen patients with other causes of right ventricular volume overload (r = 0.82), 3) nineteen patients with left ventricular volume overload (r = 0.74), 4) ten patients with right ventricular pressure overload (r = 0.93), 5) ten patients with left ventricular pressure overload (r = 0.80), 6) twenty-eight normal subjects (r = 0.82). We conclude that, in the presence of normal ventricular activation and contraction, the direction and magnitude of sepatal motion during systole is determined by the intracardiac position of the septum at enddiastole.

Adolescent↗
PubMed1976

Potential role of QT interval prolongation in sudden infant death syndrome.

To investigate the possibility that a genetically transmitted cardiac abnormality is involved in the genesis of the sudden infant death syndrome (SIDS), 42 sets of parents who had at least one infant with SIDS were studied by electrocardiography. Prolongation of the QT interval was present in at least one member of 11 (26%) sets of parents. In families in which QT interval prolongation was found in a parent, prolonged QT interval was also present in 39% of the siblings of infants with SIDS, suggesting an autosomal dominant pattern of inheritance. In addition, an infant with "near-miss" SIDS showed marked prolongation of the QT interval. Thus, our data suggest that prolonged QT interval may play a role in a considerable proportion of sudden and unexpected infant deaths. However, definitive confirmation of the relation between QT interval prolongation and SIDS will require large prospective investigations.

Adolescent↗
PubMed1976

The effects of ascorbic acid on diphtheria toxin and intoxicated HeLa cells.

Ascorbic acid (vitamin C) prevented diphtheria toxin from inhibiting the incorporation of [U-14C]-alanine into trichloroacetic acid precipitable material in HeLa cells. Ascorbic acid did not exhibit an effect on the adenosine diphosphate-ribosylation of amino acyl transferase II nor did it separate fragment A from fragment B in "nicked" toxin. A non-specific reducing agent, para-methylaminophenol sulfate, exhibited an effect on HeLa cells very similar to the results of ascorbic acid. Citric acid, a tricarboxylic acid, had no effect on HeLa cells.

Alanine↗
PubMed1975

Mechanism of left ventricular outlfow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis).

Left ventricular outflow obstruction in patients with idiopathic hypertrophic subaortic stenosis or obstructive asymmetric septal hypertrophy is due to abnormal forward motion during systole of the anterior mitral leaflet. To determine why some patients with this disease hav left ventricular outflow obstruction whereas others do not, we studied a large number of patiens with assymetric septal hypertrophy using both one- and two-dimensional echocardiography. In 100 patients with asymmetric septal hypertrophy and 22 normal subjects, mitral valve position at the onset of systole was quantitated by measuring the distance from the ventricular septum to the mitral valve and the distance from the mitral valve to the posterior left ventricular wall. None of the normal subjects and only 3 (6 percent) of 51 patients with nonobstructive asymmetric septal hypertrophy had a septal-mitral valve distance of less than 20 mm compared with 23 (66 percent) of 35 patients with obstructive asymmetric septal hypertrophy. Moreover, the mitral valve at the onset of systole was actually positioned forward in the left ventricular activity. Two-dimensional studies in 11 patients with obstructive asymmetric septal hypertrophy revealed that contraction of the malaligned papillary muscles did not cause the abnormal forward mitral valve motion. We propose that the left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy occurs as a result of two factors: (1) narrowing of the left ventricular outflow tract at the onset of systole, and (2) hydrodynamic forces generated by contraction on the left ventricle.

Aortic Stenosis, Subvalvular↗
PubMed1975

Congenital heart malformations associated with disproportionate ventricular septal thickening.

Asymmetric septal hypertrophy, or ASH, is a genetically determined myocardial disorder that is transmitted as an autosomal dominant trait. ASH is characterized by a disproportionately thickened ventricular septum that contains numerous hypertrophied, bizarrely-shaped and disorganized cardiac muscle cells. Disproportionate hypertrophy of the ventricular septum has also been observed in association with certain congenital cardiac malformations. To determine whether such congenital cardiac malformations are part of the disease spectrum of genetically determined ASH, cardiac pathologic observations were made in eight patients with disproportionate septal thickening (ventricular septal to posterobasal left ventricular free wall thickness ratios of 1.5 to 2.5) and the following three categories of associated lesions: 1) parachute deformity of the mitral valve (occurring either as an isolated lesion or with ventricular septal defect, coarctation of the aorta, supravalvular ring of the left atrium, or double outlet right ventricle); 2) complete interruption of the aortic arch; and 3) ventricular septal defect. The arrangement of cardiac muscle cells in the disproportionately thickened ventricular septum was normal in six of the eight patients; in the other two patients (one with parachute deformity of the mitral valve and one with ventricular septal defect) numerous bundles of hypertrophied cardiac muscle cells were interlaced in a disorganized fashion among more normally arranged bundles of cells. First degree relatives of six of the eight patients were studied by echocardiography and found to have normal ventricular wall thicknesses and septal-free wall ratios. It is concluded that disproportionate ventricular septal thickening may occur in patients with a variety of congenital heart malformations, but that such a finding is not necessarily a manifestation of the disease spectrum of genetically determined ASH.

Adult↗