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A B S T R A C T The roles of liver, kidney, and gut in maintaining fuel homeostasis were studied in 28 patients with severe hepatic cirrhosis, 25 of whom had alcohol-induced cirrhosis. Hepatic, portal, and renal blood flow rates were measured and combined with substrate concentration differences across liver, gut, and kidney to calculate the net flux of free fatty acids, ketone bodies, triglycerides, and glucose with selected glucose precursors, including glycerol, lactate, pyruvate, and amino acids. Data from the catheterization studies were related to hepatic histology, glycogen content, and activities of gluconeogenic enzymes and compared with data obtained from control patients. The effects of food deprivation on net flux of fuels across the liver, gut, and kidney were assessed after overnight and after 3 d of fasting.Activities of gluconeogenic enzymes were normal, but hepatic glycogen content was diminished in cirrhotic livers, probably as a consequence of extensive hepatic fibrosis. Extrahepatic splanchnic tissues (gut) had only a small influence on total splanchnic flux rates of carbohydrates, lipids and, amino acids. In cirrhotic patients, there was no mean renal glucose contribution to the bloodstream after an overnight or after a 3-d fast.After an overnight fast hepatic glucose production in patients with cirrhosis was diminished as a result of low-rate glycogenolysis. Hepatic gluconeogenesis and ketogenesis were increased. This pattern of hepatic metabolism mimics that seen in "normal" patients after more advanced stages of starvation. After 3 d of starvation, patients with hepatic cirrhosis have hepatic F. A. Reichle is presently chairman of surgery, Presbyterian-

SUMMARY The contractile capacity of the human ventricle when chronically pressure-overloaded by aortic stenosis remains a subject of major debate. The compensatory mechanisms used to maintain normal resting cardiac output and ejection fraction, and the relation of compensatory mechanisms to symptoms, have not been fully documented. In this report we examined ventricular performance and the relationship of compensatory mechanisms to symptoms in 11 patients with severe aortic stenosis and congestive heart failure symptoms (AS-CHF group), in 10 patients with significant aortic stenosis but no heart failure symptoms (AS-C group), and in 12 normal subjects. Alterations in afterload, preload and wall thickness in aortic stenosis may adversely affect the validity of indexes of contractile function, so we attempted to account for or avoid the effect of such alterations. The natural variations in ventricular volume were used to estimate group ventricular function relationships relating peak systolic wall stress to end-diastolic volume index (Frank-Starling), and to estimate group relationships of end-systolic pressure or stress to end-systolic volume (Sagawa). The slope of the linear regression lines that estimated the Frank-Starling index and the Sagawa index showed statistically significant depression (p < 0.01) of left ventricular contractile function in the AS-CHF patients, while ventricular contractile function was relatively normal in the AS-C patients. End-diastolic volume index and pressure were significantly increased (p < 0.01) only in the AS-CHF group. Peak systolic left ventricular wall stress, ejection fraction, resting cardiac index, and the ratio of ventricular mass to volume were not statistically different from normal in either group.ISOLATED cardiac muscle and intact animal hearts have shown decreased contractile function in the severely and acutely pressure-overloaded hypertrophied and failing heart.-.' When the pressure overload is less intense and less acute and when heart failure does not develop, ventricular performance is variable.6' 7 In experimental animals, it appears that depression of myocardial function is directly related to the severity of the overload, the presence of congestive failure and, possibly, the duration of the overload. 3,6,7 Despite these experimental studies, ventricular contractile function in patients with chronic pressure overload caused by aortic stenosis is still debated.8 17 From the limited patient studies available, it seems reasonable to postulate that ventricular contractile function is depressed when severe pressure overload has caused congestive failure, but normal when the overload is less severe and failure has not occurred.s9 11,16, 17 In this study, we tested this hypothesis by determining hemodynamic values and quantitative ventricular function measurements in three groups of patients. Patients with severe aortic stenosis and congestive heart failure symptoms were compared with

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Stress-strain relations (σ-ε) were obtained in the form dσ/dε = kσ + c, where k is a stiffness constant. Utilizing the pressure-volume relation dP/dV = αP, the elastic stiffness (dσ/dε) and k were evaluated at end diastole in ten patients with normal ventricles (N), in 34 patients with coronary artery disease (CAD), and in 22 patients with primary myocardial disease. This latter group was classified into Type I (normal contraction patterns and elevated end-diastolic pressure), Type II (hypertrophy without obstruction), and Type III (hypokinetic and/or asynergic). The mean values and standard error of the means ( sem ) of k and elastic stiffness were 14.8 ± 0.7, 329 ± 54 gm/cm 2 (N); 17.8 ± 0.3, 684 ± 80 gm/cm 2 (CAD); 18.2 ± 0.5, 1133 ± 127 gm/cm 2 (Type I); 22.4 ± 1.2, 833 ± 150 gm/cm 2 (Type II); 18.7 ± 0.6, 1623 ± 348 gm/cm 2 (Type III). These studies indicate that 1) dP/dV, wall stress, and volume-mass ratio are the important determinants of stiffness, 2) normal stiffness levels can be recorded from hypertrophied ventricles, 3) CAD patients with end-diastolic pressure ≦ 12 mm Hg have normal stiffness levels, 4) normal contraction patterns and normal stiffness levels are not necessarily related.

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SUMMARY Fifteen patients have shown neovascularity in the left heart during selective coronary arteriography, with associated fistulous communication to a cardiac chamber in ten. In nine the abnormalities were adjacent to and within ventricular mural thrombi, associated with ventricular aneurysms in seven and congestive cardiomyopathy in two. In six patients with mitral stenosis and atrial fibrillation the angiographic changes related to left atrial thrombi.CORONARY NEOVASCULARITY and fistula formation are infrequent abnormalities usually attributed to neoplasm and congenital anomaly, respectively. Our experience with fifteen patients indicates that mural thrombus may stimulate both these abnormalities, and that they may be demonstrated by selective coronary arteriography and confirmed histologically. MaterialFifteen patients have shown neovascularity in the left heart during selective coronary arteriography, with associated fistulous communications to a cardiac chamber in ten. The clinical diagnosis and evidence for mural thrombus in each of these patients is summarized in table 1.Nine patients exhibited abnormal vascular blushing in the left ventricle during coronary arteriography. Ventriculography demonstrated filling defects, consistent with mural thrombus, in the same area as the blush in eight of these. Mural thrombus was not identified with certainty in the single plane right anterior oblique ventriculogram of the remaining patient whose vascular blush occurred in the region of a posterior aneurysm. Seven patients had ventricular aneurysms while two had congestive cardiomyopathy. In five patients a fistulous communication with the left ventricular cavity was associated with abnormal vascularization of portions of the filling defect. The key angiographic findings in these patients are listed in with the atrial chamber ( fig. 1) was associated in five, with sufficient contrast medium entering the chamber to outline filling defects in four patients; angiographic diagnosis of thrombus was inferential in the remaining two. The key angiographic findings in this group are summarized in table 3. Four of these six patients have come to surgery and the presence of thrombus was confirmed in each. Detailed histologic studies were made of the thrombus in two patients; the other specimens were not examined beyond confirming the thrombotic nature of the clot and excluding myxoma. Histologic sections through the left atrial appendage of one of these patients ( fig. 2) revealed fenestration of the lumen by interconnecting septa composed of mature collagenous fibrous tissue.These septa enclosed channels of varying size which were lined by distinct endothelium and were interpreted as representing complete organization and recanalization of a mural thrombus. The excised mural thrombus of another patient was grossly semi-gelatinous with an outer surface which was irregular, granular and variegated red and tan. The cut surface had a pitted appearance with irregular laminations (fig. 3). Microscopically, it consisted almost ent...