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The cardiac profile of 38 patients readmitted to the hospital with the clinical and radiologic findings of pulmonary artery hypertension and right ventricular failure 2 months after ingestion of toxic rapeseed oil was determined with M-mode and two-dimensional echocardiography, pulsed Doppler flow studies and right and left heart catheterization and ventriculography. The echocardiogram and pulsed Doppler recordings revealed right ventricular enlargement in 84% of the patients, indirect evidence of pulmonary artery hypertension in 76% and tricuspid insufficiency in 13%. At cardiac catheterization (n = 11) the mean (+/- standard deviation) pulmonary artery pressure was 40 +/- 9 mm Hg, mean pulmonary systemic vascular resistance ratio was 0.45 +/- 0.12 and mean right ventricular end-diastolic pressure was 13 +/- 4 mm Hg. Pulmonary artery hypertension was sustained after the acute administration of 100% oxygen and persisted in six patients who were restudied within 6 months. Cardiac index and left heart pressures were normal in all but one patient. The contrast ventriculographic studies revealed right ventricular dilation in all patients, tricuspid regurgitation in three patients and a normal left ventricular contraction pattern in all but one patient. The data confirm that symptomatic pulmonary artery hypertension and associated right ventricular dysfunction can complicate toxic rapeseed oil ingestion and that these findings persist for at least 6 months.

To investigate the high-energy phosphate metabolic correlates of left ventricular (LV) dysfunction during the onset and recovery from severe, global myocardial ischemia in vivo, seven preinstrumented closed-chest dogs had ECG-gated phosphorus-31 (31P) NMR-spectroscopy (NMR-S) studies performed and LV micromanometer and sonomicrometer data measured before, during, and every 5 min following severe occlusive global myocardial ischemia. Ischemic LV + dP/dtmax fell from 2396 +/- 576 mm Hg/s at baseline to 2185 +/- 478 mm Hg/s (p less than 0.05) and did not normalize until after 30 min of reperfusion. LV ejection fraction (EF) decreased significantly (0.32 +/- 0.07 EF units to 0.12 +/- 0.13 EF units; p less than 0.05) and did not recover by 30 min of reperfusion (0.27 +/- 0.09 units; P less than 0.05 vs baseline). Simultaneous 31P NMR-S studies demonstrated excellent beta-ATP signal-to-noise (10 +/- 4:1). Myocardial acidosis occurred during global ischemia (delta pH = -0.22 +/- 0.23 units; p less than 0.05), with recovery at 30 min of reperfusion. Inorganic phosphate/phosphocreatine ratio (Pi/PCr) increased significantly during ischemia (0.46 +/- 0.07 to 0.61 +/- 0.07; P less than 0.05), with delayed normalization of this ratio at 30 min of reperfusion. beta-ATP peak area did not change during ischemia. Pi/PCr and LV contractility (+dP/dtmax) were significantly correlated at baseline (r = -0.70) and during global ischemia (r = -0.78; p less than 0.01), but not during recovery (r = 0.006; p = NS). Therefore, the simultaneous evaluation of high-fidelity hemodynamic data and topical 31P NMR-S can be performed in the intact state.

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