BACKGROUND AND OBJECTIVES: Chest pain is a complaint for which children are frequently evaluated. Cardiac causes are rarely found despite expenditure of considerable time and resources. We describe validation throughout New England of a clinical guideline for cost-effective evaluation of pediatric patients first seen by a cardiologist for chest pain using a unique methodology termed the Standardized Clinical Assessment and Management Plans (SCAMPs). METHODS: A total of 1016 ambulatory patients, ages 7 to 21 years initially seen for chest pain at Boston Children’s Hospital (BCH) or the New England Congenital Cardiology Association (NECCA) practices, were evaluated by using a SCAMPs chest pain guideline. Findings were analyzed for diagnostic elements, patterns of care, and compliance with the guideline. Results from the NECCA practices were compared with those of Boston Children’s Hospital, a regional core academic center. RESULTS: Two patients had chest pain due to a cardiac etiology, 1 with pericarditis and 1 with an anomalous coronary artery origin. Testing performed outside of guideline recommendations demonstrated only incidental findings. Patients returning for persistent symptoms did not have cardiac disease. The pattern of care for the NECCA practices and BCH differed minimally. CONCLUSIONS: By using SCAMPs methodology, we have demonstrated that chest pain in children is rarely caused by heart disease and can be evaluated in the ambulatory setting efficiently and effectively using minimal resources. The methodology can be implemented regionally across a wide range of clinical practice settings and its approach can overcome a number of barriers that often limit clinical practice guideline implementation.

The levels of streptococcal antibody titers in populations with or without rheumatic fever from an area with a relatively high incidence of rheumatic fever and an area with a low incidence of this disease were compared. Streptococcal antibody titers were determined for two populations, each of which included children without rheumatic fever (nonrheumatic children) and rheumatic fever patients. The two populations were derived from two separate geographic areas, one with a high incidence of rheumatic fever (Grenada) and another with a low incidence of this disease (central Florida). The results revealed an absence of consistent differences in the geometric mean antibody titers between the nonrheumatic subjects and the rheumatic fever patients from Grenada. In the population from Grenada, the mean anti-streptolysin O and anti-DNase B titers were higher in the nonrheumatic controls (P of 0.085 and 0.029, respectively). However, the mean titer of the antibody to the group A streptococcal cell wall carbohydrate was higher in the rheumatic fever patients than in the nonrheumatic controls (P ‫؍‬ 0.047). This finding contrasted with the finding that the means of all three streptococcal antibody titers in the patients with rheumatic fever were significantly higher than those in the nonrheumatic subjects from Florida (P ‫؍‬ 0.01-<0.001). The reason for this paradoxical finding became evident when the streptococcal antibody titers of the nonrheumatic subjects from Grenada and Florida were compared, revealing significantly higher levels of all three antibodies in the nonrheumatic subjects from Grenada than in the nonrheumatic subjects from Florida (P < 0.001). These results suggest that nonrheumatic individuals in an area with a high incidence of rheumatic fever have inordinately elevated levels of streptococcal antibodies in serum. The presence of elevated streptococcal antibody titers in such a population, which probably reflects a high background prevalence of streptococcal infections, should be taken into consideration when evaluating the role of the group A streptococcus in nonpurulent complications of infections.

Left ventricular function was evaluated in 34 patients with the echocardiogram, and an external mechanical cardiac stimulator was used to induce a ventricular premature contraction (VPC) noninvasively. Extent of post-extrasystolic potentiation (PESP) was determined by comparing systolic dimensional shortening and ejection fraction of the sinus beat preceding the VPC to that of the potentiated beat which followed it. Using this technique, a VPC could be introduced into the cardiac cycle of 30 of the 34 patients, six of whom were free of obvious cardiac disease and 24 of whom had valvular, coronary or myopathic heart disease. The only complication observed was mild breast ecchymosis in a female patient. Systolic dimensional shortening and ejection fraction increased from control values by an average of 21% and 17% respectively, with a range of 0-100%. The degree of PESP was very reproducible in repeat studies and when the same patients were subsequently evaluated during a spontaneously occurring or catheter-induced VPC. The technique can safely and reliably induce post-extrasystolic potentiation during echocardiography and is a potentially important adjunct to the noninvasive evaluation of left ventricular function.

SUMMARY Four hundred and ninety-nine surgically excised valves were examinedfor pathological evidence of myxomatous degeneration. Thirty-six valves (7%) had myxomatous degeneration as a major pathological finding. Fourteen valves (3%) had significant myxomatous degeneration of the pars fibrosa, a finding which we define as "primary myxomatous degeneration". Echocardiographic findings and catheterisation results were correlated with the clinical course, surgical results, and follow-up in these 14 patients. Echocardiograms in 10 of the 11 patients who had them (91%) showed abnormalities suggesting the presence of primary myxomatous degeneration. Echocardiography was more helpful than angiography in diagnosis. The histological pattern of primary mitral myxomatous degeneration appears to be identical to that seen in patients with mitral valve prolapse and five of six patients with mitral lesions had echocardiographic evidence of prolapse. None of the patients with primary myxomatous degeneration of the aortic valve had syphilis or Marfan's syndrome. While the aetiology of primary myxomatous degeneration of cardiac valves is not known, a link to a more generalised disorder is suggested.

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