Cardiographic Assessment of Pulmonary Vascular Disease in Ventricular Septal Defect.

The electrocardiogram in ventricular septal defect has long been recognized as affording some ndication of the size of the defect and of the hmodynamic disturbance. In 1954, Wood, Magidson, nd Wilson reported that small defects and some defects of medium size had normal cardiograms, but that in larger defects evidence of both right and left ventricular enlargement was common. Dther workers have confirmed these findings, and since the introduction of effective methods of surgical closure, much attention has also been paid to the relation of the cardiographic changes to the degree of associated pulmonary vascular disorder. Char, Adams, and Anderson (1959) noted some association between right ventricular hypertrophy and pulmonary vascular disease, but did not find strong correlations between cardiographic patterns and physiological data: their series is notable for having lung biopsies from 54 patients at operation. Fyler et al. (1958) found the cardiogram useful in selecting patients for operation and considered that pure right ventricular hypertrophy in those without pulmonary stenosis "almost excludes the possibility of surgery". Toscano-Barboza and DuShane (1959) found that the pattern of right ventricular diastolic overload was produced by defects that were situated in the inflow portion of the ventricle or were associated with tricuspid regurgitation. They concluded that "Precise quantitative correlation could not be established between the electrocardiographic criteria and the data for pulmonary arterial pressure or for pulmonary vascular resistance." DuShane et al. (1960) reported on 100 surgically treated patients with pulmonary hypertension: after closure of the defect the pulmonary arterial systolic pressure decreased to 70 per cent or less of the systemic pressure in 88 out of 90 with the electrocardiogram of "left ventricular overwork" but in only 2 out of 10 without this pattern. Blount and Woodwark (1960), however, found that lone left ventricular hypertrophy might be associated with considerable elevation of pulmonary vascular resistance. They noted, as did Dack (1960) and Vince and Keith (1961), that lone right ventricular hypertrophy was always associated with severe pulmonary vascular disease. It has long been realized that pulmonary vascular disease is a serious hazard to successful surgical treatment, and it has been shown (Cleland et al., 1958; Goodwin, 1961) that the single most important factor in determining the operative risks and results is the degree ofpulmonary vascular disorder before operation, as judged by the length of the systolic murmur, the pulmonary vascular resistance, and the fall of pulmonary arterial pressure immediately after closure. If such disorder is present, the patient will have substantial pulmonary hypertension after the defect is closed, and the operative risk is high. Furthermore, the level of the pulmonary arterial pressure immediately after closure of the defect usually agrees well with the pressure measured at catheterization months or years later, indicating that the immediate fall in pressure is a good index of the degree of pulmonary vascular disease (Hollman, 1961).