BACKGROUND Fibrosis or fatty infiltration of the human sinoatrial (SA) node is generally believed to represent replacement of the SA nodal cells by connective tissue. Quantitative analysis, however, has not been performed precisely to validate the interpretation of such histological changes. METHODS AND RESULTS The actual volume of the SA node and its components were calculated according to the sum of the pixel number representing the colors of SA nodal cells and connective tissue in serial sections using a digital color image analyzer. Average volume occupied by the total SA nodal cells in adolescents and adults (n = 7) was 3.55 +/- 0.45 mm3, which was 2.4 times greater than that in infants (n = 3). The rate of increase was smaller than that of the total SA node (4.2 times, 16.68 +/- 2.56 mm3 in adolescents and adults). The considerable discrepancy in the growth ratio between the SA nodal cells and the total SA node resulted from an increase in the volume of connective tissue (7.4 times). In the elderly (n = 9), the volume of total SA node and SA nodal cells actually decreased (13.10 +/- 1.85 mm3 and 2.18 +/- 0.44 mm3), whereas that of fibrous connective tissue remained unchanged. Constant DNA ploidy patterns of SA nodal cells determined by cytofluorometry indicated that SA nodal cells never synthesize DNA during growth. CONCLUSIONS Until adulthood, the actual volume of SA nodal cells does not decrease, although the increase in volume ratio of the interstitial tissue to the total SA node has merely given a false impression of involution of SA nodal cells. Atrophy of SA nodal cells, however, occurs during aging together with reduction of the SA node and/or infiltration of fatty tissue.

Clinical profiles were analysed of 18 children with congenital ventricular aneurysm (CVA) and diverticulum (CVD) (nine with CVA and nine with CVD). Of 18 children, only six had any symptoms, consisting of chest discomfort, palpitation, or convulsion. Heart murmurs were heard in nine of the 18 children, and a nonspecific systolic ejection murmur in one. A systolic click was heard in only four children. Dyskinesia of an abnormal protrusion of the cardiac silhouette on the chest x-ray film was detected in only three. The ECG revealed abnormal findings in all children. In those with CVA, signs of myocardial damage or left axis deviation (LAD) and left bundle branch block (LBBB) were the main findings. Among those with CVD, multiple premature ventricular contractions (PVCs) were present in four; some signs of myocardial damage were present in three. None of those with CVD had LAD or LBBB. Among the four children with right ventricular diverticulum, multiple PVCs were present in three. The lesions were detected by two-dimensional echocardiography (2DE) before angiography in 13 (72%) of 18 children. The wall kinetics of the lesions, as seen on 2DE, were in agreement with the subsequent angiographic findings.

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