A total of 177 M-mode echocardiography studies were done on three groups of fetuses at different gestational ages: group I, normally grown fetuses; group II, intrauterine growth-retarded fetuses (IUGR); and group III, fetuses of diabetic mothers. Adjusted for gestational age and for fetal weight, the hearts of fetuses with IUGR were found to have an increased minor axis dimension due to free wall hypertrophy. No ventricular dilation was found in this group. Furthermore, IUGR fetuses have a larger heart proportionally to their body weight, raising the possibility of a "sparing effect" in this particular group. The hearts of fetuses of diabetic mothers were also found to have a significantly larger cardiac size than that of a group of normally grown fetuses. The increase was secondary to free wall hypertrophy, interventricular septal hypertrophy, and right ventricular dilation. This study confirms previous reports about fetal diabetic cardiomegaly and documents the contribution of the different cardiac components to this increase in size. The free wall hypertrophy found in these two groups may occur by different processes, which needs to be further investigated.

A B S T R A C T Both the isolated perfused rabbit heart and kidney are capable of synthesizing prostaglandin (PG) I2. The evidence that supports this finding includes: (a) radiochemical identification of the stable end-product of PGI2, 6-keto-PGF,l, in the venous effluent after arachidonic acid administration; (b) biological identification of the labile product in the venous effluents which causes relaxation of the bovine coronary artery assay tissue and inhibition of platelet aggregation; and (c) confirmation that arachidonic acid and its endoperoxide PGH2, but not dihomo-y-linolenic acid and its endoperoxide PGH, serve as the precursor for the coronary vasodilator and the inhibitor of platelet aggregation. The rabbit heart and kidney are both capable of converting exogenous arachidonate into PGI2 but the normal perfused rabbit kidney apparently primarily converts endogenous arachidonate (e.g., generated by stimulation with bradykinin, angiotensin, ATP, or ischemia) into PGE2; while the heart converts endogenous arachidonate primarily into PGI2. Indomethacin inhibition of the cyclo-oxygenase unmasks the continuous basal synthesis of PGI2 by the heart, and of PGE2 by the kidney. Cardiac PGI2 administration causes a sharp transient reduction in coronary perfusion pressure, whereas the intracardiac injection of the PGH2 causes an increase in coronary resistance without apparent cardiac conversion to PGI1. The perfuLsed heart rapidly degrades most of the exogenous endoperoxide probably into PGE2, while exogenous PGI2 traverses the heart without being metabolized. The coronary vasoconstriction produced by PGH2 in the normal perfused rabbit heart suggests that the endoperoxide did not reach the PGI2 synthetase, whereas

Two-dimensional-directed M-mode echocardiography was done on 80 normal fetuses between the 17th to 42nd weeks of gestation. The M-mode beam transected the ventricles at the level of the chordae tendineae at the tip of atrioventricular valves. Right and left ventricular dimensions and free wall thicknesses correlated well with gestational age. Calculated measurements showed a good correlation of the stroke volume and cardiac output with gestational age. The right ventricular dimension, however, was significantly greater than the left ventricular one. Fractional shortening of the right and left ventricle did not change significantly with advancing gestational age. This study indicates that the human fetal right ventricle dimension, stroke volume, and cardiac output are slightly larger than that of the left ventricle. This study also suggests that the human fetus increases its cardiac output to match its growth and it does so by increasing ventricular size rather than fractional shortening or heart rate.

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A 14 month old boy with suprasystemic right ventricular pressure secondary to pulmonary valvular stenosis and anular size of 10 mm underwent percutaneous balloon valvuloplasty with a 12 mm balloon. Right ventricular pressure almost doubled after valvuloplasty and the electrocardiogram revealed development of severe right ventricular strain. Both findings persisted on the following day. A postvalvuloplasty right ventriculogram demonstrated a severe systolic infundibular obstruction not present before. The patient underwent surgical relief of infundibular obstruction; successful opening of the pulmonary valve by the balloon valvuloplasty was observed. It is concluded that a balloon size 20% larger than anular size can be safe in human subjects and that infundibular obstruction may appear or even worsen after balloon valvuloplasty. Such an obstruction may be related to the severity of pulmonary valvular obstruction and a hypercontractile infundibulum.