The purpose of this study was to analyze potential "risk-factors" for late left ventricular dysfunction after surgical correction of Fallot's tetralogy (FT). As the ejection-phase indices cannot distinguish abnormalities of contractility from altered loading conditions, the slope values of the end-systolic pressure-length and stress-shortening relationships were analyzed by increasing afterload. Thirty-two patients were studied after surgical correction of FT in infancy. The age at investigation was 19.2 +/- 5.6 years, total correction had been performed at the age of 7.7 +/- 3.3 years. In 20 patients a one-stage operation was performed, and in 12 patients a two-stage correction. The control group consisted of 30 healthy volunteers, aged 18-30 years. The following potential risk factors for left ventricular dysfunction were evaluated: one-stage vs. two-stage correction, age at total correction, preoperative systemic oxygen saturation, preoperative hematocrit, occurrence of hypoxic spells, preoperative ratio of left-to-right ventricular peak systolic pressure, and preoperative ratio of left-to-right ventricular end-diastolic volume. In most patients the baseline data for end-systolic wall stress lay outside the normal range, indicating abnormal loading conditions. Thus, analysis of load-independent indices of the contractile state seems to be mandatory in these patients. Our data show that the severity of preoperative hypoxemia is an important risk factor for late dysfunction of the left ventricle (p less than 0.01). Additionally, the relation of left and right ventricular peak systolic pressures and end-diastolic volumes were related to the contractile state (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of persisting right ventricular myocardial sinusoids on left ventricular global and regional function were studied in 13 patients with pulmonary atresia and intact ventricular septum. Persisting myocardial sinusoids allow the inflow of undersaturated blood into the coronary circulation with subsequent myocardial ischaemia. 7 patients had myocardial sinusoids (group 1). 6 patients had normal coronary perfusion (group 2) The measures of global left ventricular function (ejection fraction, left ventricular enddiastolic volume, left ventricular enddiastolic pressure and shape index) showed no differences between the groups. All patients in group 1 showed disturbances of regional wall motion (P less than or equal to 0.005). There was a high degree of coincidence between the disturbances of regional wall motion and the topography of myocardial perfusion from persisting myocardial sinusoids. In group 1 apical hypokinesia was a regular finding, reflected by a significantly reduced shortening of the left ventricular long axis (P less than or equal to 0.01). As all of these patients had communications between the myocardial sinusoids and the left anterior descending coronary artery, this probably resulted from apical left ventricular ischaemia.
Changes in cardiac output, stroke volume, and systemic blood pressure have been correlated with changes in muscle blood flow during the periods of initial transient and subsequent sustamed vasodilatation during intravenous infusion of epinephrine. In the initial phase blood pressure decreased slightly; forearm blood flow increased by 308%, cardiac output by 50%, and stroke volume by 10%. During the sustained phase the systolic blood pressure increased; corresponding increases for the other measurements were 87, 47, and 25%, respectively. The lack of correlation between these changes in cardiac output and forearm blood flow suggests that in the transient phase vasodilatation does not occur simultaneously in all muscle groups. Stroke volume makes a greater contribution to the increased output during the sustained phase. Submitted on May 29, 1961
A 15-year-old girl with a congenital heart disease (pulmonary stenosis and aortic insufficiency), who had a ventriculoperitoneal shunt operation because of hydrocephalus internus at the age of two years, 12 years later underwent colectomy because of juvenile colonic polyposis. After this operation, enormous production of ascites began which, because of progressive development, finally required ventriculoatrial shunt operation. A total volume of 17 liters of fluid was removed in two ascites drainages before and during the latter operation. Postoperatively the ascites production stopped completely.
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