The centrilobular liver cell necrosis observed in hypoxic hepatitis is generally attributed to failure of hepatic blood perfusion. Accordingly, this injury of the liver is commonly recognized under the terms "shock liver" or "ischemic hepatitis." During a 10-year period, 142 episodes of hypoxic hepatitis were consecutively identified in the intensive care unit of a general hospital, and the clinical, biological, and hemodynamic parameters were prospectively collected on individual files. We conducted the current study to assess retrospectively the role of the hemodynamic mechanisms of tissue hypoxia: ischemia, passive venous congestion, and hypoxemia. Among the 142 episodes of hypoxic hepatitis, 138 were separated in 4 main groups based on clinical features: decompensated congestive heart failure (80 cases), acute cardiac failure (20 cases), exacerbated chronic respiratory failure (19 cases), and toxic/septic shock (19 cases). An elementary hemodynamic evaluation, including blood pressure, central venous pressure, and arterial blood gas analysis, was carried out in every episode and a more complete hemodynamic assessment through pulmonary artery catheterization was performed in 61 episodes. The hemodynamic mechanisms responsible for hypoxic hepatitis were different in the 4 groups. In congestive heart failure and acute heart failure, the hypoxia of the liver resulted from decreased hepatic blood flow (ischemia) due to left-sided heart failure and from venous congestion secondary to right-sided heart failure. In chronic respiratory failure, liver hypoxia was mainly due to profound hypoxemia. In toxic/septic shock, oxygen delivery to the liver was not decreased but oxygen needs were increased, while the liver was unable to use oxygen properly. In all conditions underlying hypoxic hepatitis, except toxic/septic shock, a shock state was observed in only about 50% of the cases. Therefore, the expressions "shock liver" or "ischemic hepatitis" are misleading and should be replaced by the more general term "hypoxic hepatitis."

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We report a case of coronary artery spasm induced by 5-fluorouracil. The symptoms occurred during continuous intravenous infusion of the drug, and a coronary spasm was visualized at angiography.

The value of exercise testing for the diagnosis of coronary artery disease is disputed but very few studies have taken advantage of all recent improvements, namely computer averaging of the ECG signals, multivariate analysis of the data, a compartmental diagnostic approach and probabilistic interpretation of the results. These methods were tested in a group of 387 men who had a computer-assisted multistage maximal exercise test; none had a history of myocardial infarction. In 284 symptomatic patients, the diagnosis was made by arteriography; 103 ostensibly healthy men were also included. The computer-averaged ECG signals (X, Y, Z) recorded at maximal exercise, maximal heart rate, blood pressure and workload, and the onset of angina pectoris during exercise were submitted to a multivariate stepwise discriminant analysis. The pretest likelihood for CAD was calculated from age and history; the post-test likelihood was calculated from Bayes' theorem and the average information content of several diagnostic methods was assessed in categorical and compartmental models. By multivariate analysis, 5 variables collected at maximal exercise were selected, namely the heart-rate, the ST60 segment level, the onset of angina during the test, the workload and the slope of the ST segment in lead X. The average information content of the analysis using 5 variables was 44% in a categorical model versus 55% in a compartmental model (P less than 0.001). For comparison, the information content of the analysis using the ST60 segment level alone was only 16% in the categorical model and 27% in the compartmental model. The clinical value of these diagnostic methods (categorical versus compartmental, univariate versus multivariate) was assessed by a probabilistic classification of the patients. The classification provided by the analysis of the ST60 segment changes was barely better than that one provided by the simple history. The probabilistic use of a multivariate and compartmental analysis of the data led to a significantly better and more accurate classification of the patients (83% of correct classification).

Among patients with severe hypercholesterolaemia and a family history of early cardiovascular disease, the presence of a genetically ascertained FH is associated with a higher prevalence of coronary artery calcifications and a positive exercise stress test. These results suggest that despite a similar phenotype, patients carrying mutations suggestive of FH may have a greater cardiovascular risk than patients without these mutations.

Twenty-three patients who had undergone aortic valve replacement with a mechanical aortic valve prosthesis (ball-valve: 17, tilting-disc: 6) were investigated by retrograde left ventricular catheterization using a 6 F pigtail catheter. Twelve of these 23 patients also had had combined aortic and mitral valve replacement. To assess the magnitude of the catheter-induced aortic regurgitation and its effect on left ventricular and mitral valve function, 10 patients (group 1) were simultaneously investigated by the transseptal route (8 patients) or direct left ventricular puncture. The 13 other patients (group 2) were studied only by the retrograde crossing of the aortic valve prosthesis. In group 1, placement of the catheter across the valve induced an increase in heart rate (+12%), in left ventricular end-diastolic pressure (from 17.2 +/- 9.6 to 33.3 +/- 12.0 mmHg), a decrease in aortic systolic (-19%) and diastolic (-25%) pressures, and left ventricular systolic pressure (-10%). Transvalvular aortic pressure gradient increased from 15.4 +/- 8.2 to 23 +/- 12.1 mmHg. Pre- and post-crossing pressure gradients were linearly correlated (r = 0.93). Left ventricular end-diastolic volume increased slightly but significantly (+9%), ejection fraction remained unchanged. Pre- and post-crossing regurgitation fractions were linearly related (r = 0.98). Hence, the magnitude of catheter-induced aortic regurgitation averaged 27% whether or not a pre-crossing regurgitation was noted. In group 2, retrograde crossing of the aortic valve prosthesis induced similar hemodynamic changes. There were no catheterization-related complications.(ABSTRACT TRUNCATED AT 250 WORDS)

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