ENOXIMONE AS ALTERNATIVE TO MECHANICAL SUPPORT WHILE AWAITING CARDIAC TRANSPLANTATION

ENOXIMONE AS ALTERNATIVE TO MECHANICAL SUPPORT WHILE AWAITING CARDIAC TRANSPLANTATION

153 ENOXIMONE AS ALTERNATIVE TO MECHANICAL SUPPORT WHILE AWAITING CARDIAC TRANSPLANTATION in cardiac transplantation have led to widening of the indi...

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ENOXIMONE AS ALTERNATIVE TO MECHANICAL SUPPORT WHILE AWAITING CARDIAC TRANSPLANTATION in cardiac transplantation have led to widening of the indications for the operation and to an increase in the number of candidates who cannot wait for a suitable donor. Despite intensive inotropic support from vasodilators some patients still get worse and when the cardiac index drops below 18 1/min perm2, mechanical support is mandatory. But mechanical support is dangerous and expensive. From January, 1985, to December, 1988, we did 125 heart transplantations. 9 patients were bridged with heterotopic biventricular devices (3 with the Pierce ’Thoratec’, 6 with an Abiomed ’BVS 5000’). 7 were later transplanted successfully but 5 died of complications probably related to the mechanical devices (2 strokes, 2 pancreatitis). Following the work ofDubois-Rande et all we have recently used enoximone as an alternative to mechanical support. Enoximone is a type III phosphodiesterase inhibitor, which both enhances ventricular contractility and is a powerful vasodilator.2 A 59-year-old man was admitted to intensive care for urgent medical support. He had had dilated cardiomyopathy for 7 years. Deterioration in his condition had led, in the previous month, to increasing oral therapy (enalapril 50 mg daily, frusemide 40 mg per day, nitrates, and procainamide). 5 days before transfer to our unit he had entered class IV of the New York Heart Association classification. On admission he had a low cardiac index (2-05 1/min per m2. Pulmonary vascular resistance (PVR) was 35Wood units (table). Echocardiography revealed a dilated hypokinetic heart with an end-diastolic left-ventricular diameter of 78 mm. Under dobutamine infusion (15 up to 35 ug/kg per min) the patient continued to deteriorate, and mechanical support seemed indicated. Haemodynamic data at admission and after enoximone infusion are shown in the table. The patient had severe dyspnoea (35/min) and cold extremities. His heart rate was 100/min, with an S3 gallop. His blood pressure, while on 35 g/kg per min of dobutamine, was

SiR,—Improvements

88159 mm Hg (mean 69), capillary pulmonary wedge was 35 mm Hg, and urinary output was less than 10 ml/h. Oxygen saturation in the pulmonary artery was 26% with cardiac index at 1-38 1!min was given at a dose of 1 mg/kg in 10 min, immediately followed by a continuous infusion at 12 ug/kg per min. The dobutamine dose was tapered to 20 ug/kg per min since the two agents seem to be synergistic.2,3 2 h later the patient was much better and the orthopnoea had disappeared. Pulmonary artery oxygen saturation had risen to 56%. On the next day haemodynamic assessment (table) confirmed the improvement; in contrast there was no change in mean arterial blood pressure or in heart rate. Pulmonary and capillary pressures fell; the cardiac index rose to 4’161/min per m2; and urinary output rose to 70 ml/h. Pulmonary vascular resistance was 1 73 Wood

per m2. Enoximone

units. 30 h later a 25-year-old donor became available. Transplantation was successful and the patient was extubated on day 3 and back to the ward by day 6. Without enoximone this patient would have been a candidate for mechanical biventricular support on the day of admission.In this setting enoximone has been more effective than dobutamine in restoring an acceptable cardiac index. Reduction of contractility,

The blood pressure did not increase but cardiac output was doubled and filling pressures, left and right, became normal. Enoximone did not increase heart rate, while increasing cardiac

output. 2,4 G. DREYFUS R. GUILLEMAIN C. ACAR V. JEBARA J. P. COUETIL C. AMREIN C. VULSER A. CARPENTIER B. ABRY Department of Cardiovascular Surgery, Hôpital Broussais, 75014 Paris, France

1. Dubois-Rande

2.

JL, Loisance D, Deleuze P, et al. Enoximone: a pharmacological bridge to transplantation Eighth International Symposium on Intensive Care and Emergency Medicine (Brussels, March 21, 1988); abstr. Lellouche D, Delorme G, Merlet P, et al. Etude de la relation dose-réponse de l’enoximone inravemeux dans l’insuffisance cardiaque congestive. Arch Mal Coeur 1988, 81: 1107-13.

3. Vincent JL, Carlier E, Berré J, et al. Adminstratation of enoximone in cardiogenic shock. Am J Cordiol 1988; 62: 419-23. 4. Weber KT, Janicki JS, Jain MC. Enoximone (MDL 17,043), a phosphodiesterase inhibitor, in the treatment of advanced, unstable chronic heart failure. J Heart

Trampl 1986; 5: 105-12.

DUODENAL ULCER "EPIDEMIC" IN A PATHOLOGY DEPARTMENT

S)R,—Our

pathology department has four staff pathologists and four residents. A 41-year-old staff pathologist has a 20-year history of duodenal ulcer; at his latest gastroscopy, 6 months ago, there was chronic atrophic gastritis and a small duodenal ulcer; Campylobacter pylori was abundant in the gastric crypts. In October, 1988, four other members of the department experienced epigastric burning, nausea, flatulence, and epigastric pain, relieved by food. Gastroscopy on three of the other four revealed, in a 36-year-old woman and a 24-year-old man, a chronic duodenal ulcer; a 24-year-old woman had chronic superficial gastritis; and all three had C pylori in the gastric crypts, demonstrated by Giemsa. A 32-year-old man refused gastroscopy and radiographic study. In the department the three pathologists with duodenal ulcer are the only smokers (20, 20, and 6 cigarettes per day, respectively). There is no common factor that could explain this "epidemic" of duodenal ulcer. Of other factors known to have a role in the formation of duodenal ulcer only stress was relevant, and that in only one pathologist. C pylori is now established as a cause of most cases of active chronic gastritis and duodenal ulcer; I;J. and almost all duodenal ulcer patients have C pylori positive antral gastritis. Little is known about the source and method of spread of this microorganism. An exogenous source seems unlikely since Cpylori has not been isolated from a material animal host. Transmission of infection has not been reported, other than via a gastroscope;3 however, transmission within families seems possible.4 Antibody studies strongly suggest person-to-person transmission,sby respiratory droplets or the faecal/oral route. We suggest that transmission of C pylori via respiratory droplets may be the cause of this outbreak; once more it seems that it is cigarette smokers who are especially prone to duodenal ulcer. We do not think that simply being a pathologist is a risk factor for the gastralgia of the undersigned-until it is proved that microscopes are a source of C pylori.

unresponsive to endogenous and exogenous catecholamines, may be explained by the down-regulation of myocardial receptors.3o4 HAEMODYNAMIC DATA BEFORE AND WITH ENOXIMONE

Department of Pathology, Clinica Universitaria, University of Navarra, 31080 Pamplona, Spain

F. J. PARDO-MINDAN M. JOLY C. ROBLEDO

J. SOLA S. VALERDIZ

1. McNulty CAM. The treatment of campylobacter-associated gastritis. Am J Gastroenterol 1987; 82: 245-47. 2. Rathbone BI, Wyatt JI, Heatley RV. Campylobacter pyloridis a new factor in peptic ulcer disease? Gut 1986; 27: 635-41. 3 Ramsey EJ, Carey AV, Peterson WL, et al. Epidemic gastritis with hypochlorhydria. Gastroenterology 1979; 76: 1449-57. 4. Mitchell HM, Bohane TD, Berkowicz J, et al. Antibody to Campylobacter pylon in families of index children with gastrointestinal illness due to C pylori Lancet 1987; i: HR = heart rate; PAP = pulmonary artery pressure; PWP pulmonary wedge pressure; CO = cardiac output; PVR = pulmonary vascular resistance; SV02 oxygen saturation in =

pulmonary artery.

681-82. 5. Berkowicz J, Lee A. 1987, ii: 680-81.

Person-to-person transmission of Campylobacter pylori. Lancet