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Immunocubes can detect very low HCMV IgG levels with at least the same sensitivity as the reference technique: ELISA. Samples containing bacteria showed no particular interference on the test, and results for non-infected material were in agreement with those of ELISA. The rapid test did not give any false positive reactions even with samples from patients with very high antiherpes immunoglobulins levels. Samples from transplant patients at the beginning of seroconversion or diluted to IgG titers corresponding to ELISA cut-off values were always detected as positive by immunocubes. In view of the rapidity of the test, its high specificity, its ability to detect levels corresponding to extremely low IgG signals in ELISA, and the possibility of conserving objective proof of the test, we conclude that this rapid immunocube technique is of great interest for current serologic screening in an emergency context, especially for transfusion and organ transplantation.

Cytomegalovirus (CMV) infection is a major cause of morbidity and death in heart transplant recipients. Cardiac graft involvement in CMV infection is a matter of controversy, considering its frequency and its relationship with acute or chronic rejection. Four heart transplant patients were selected because of a severe CMV infection (systemic, gastrointestinal, ophthalmic, and neurologic involvement). Immunoglobulin M and increased immunoglobulin G CMV antibodies developed. Twenty-two routine endomyocardial biopsies (EMB; mean: 5.5 EMB per patient; range, 3 to 9) from these patients were selected covering the period of CMV infection. Grading of rejection showed 12 biopsies with "no evidence of rejection (grade 0)," nine biopsies with "mild acute rejection (grade 1B)," and one biopsy with "moderate acute rejection (grade 3A)." One EMB exhibited a single CMV inclusion in an endothelial cell detectable by light microscopy. The EMB were assessed for CMV infection using in situ hybridization (ISH) for the detection of CMV genome with a biotinylated CMV probe and immunohistochemistry (IHC) for the detection of CMV immediate-early antigen with the monoclonal antibody E13. ISH and IHC detected a single CMV-infected cell, respectively, in one and two EMB from two patients. The patient with a CMV inclusion determined by light microscopy was also positive with both techniques. Positive ISH and IHC were always in enlarged inclusion-bearing cells, which were easily observable with routine staining. One EMB had mild acute rejection, and the other one had no rejection.(ABSTRACT TRUNCATED AT 250 WORDS)

This technique is original in that it involves a single site (the ascending aorta) easily accessible to cannulation. Following lateral clamping of the ascending aorta, a bifurcate Dacron prosthesis is anastomosed. The draining cannula is introduced through one of the branches of the prosthesis and manually guided through the aortic sigmoid leaflets down to the left ventricular ejection outlet. The perfusion cannula is introduced through the outer branch of the prosthesis. The end of this cannula is positioned at the origin of the prosthesis to avoid a possible bend in the fork. This technique is a simple and effective means of providing left ventricular support.

Cyclosporin is an immunosuppressive agent commonly used in transplant patients. It is actively metabolised by the cytochrome P450 system and interactions with drugs metabolised by the same system are predictable. This is particularly relevant since cyclosporin has a low therapeutic index and its renal toxicity is concentration-related. Roxithromycin, a new, well-tolerated macrolide with a weak interactive profile, uses the same isoenzyme of the P450 system as cyclosporin. To evaluate its interaction potential in clinical practice, 8 heart transplant recipients treated with cyclosporin for at least 1 month received roxithromycin for 11 days (150 mg twice daily). Bi-weekly controls of plasma cyclosporin concentrations and creatinine levels were carried out before, during and after roxithromycin treatment. A slight nonsignificant rise in cyclosporin concentrations was observed, but creatinine levels remained stable during roxithromycin treatment. Values of cyclosporin concentrations diminished after withdrawal of roxithromycin. Cyclosporin dosage adjustment was not necessary. There was a minor pharmacokinetic interaction, which can be considered safe for the usual therapeutic dosage of roxithromycin used.

To evaluate the incidence, risk factors and effects of systemic hypertension on renal function and left ventricular hypertrophy after heart transplantation, 85 recipients under triple drug low low dosage immunosuppressive therapy were studied. After a mean follow-up of 12.5 +/- 8.7 months, high incidence of hypertension was observed in 67% of the patient and 71% had developed de novo hypertension. None of the pre-transplant nor post-transplant cardiovascular risk factors were significantly associated with post-transplant hypertension. Faster deterioration of renal function, as assessed by intraindividual variations of serum creatinine values, was demonstrated in hypertensive patients and appeared as an early indicator of cyclosporine nephrotoxicity in patients at risk for hypertension. [table: see text] Serial (early, intermediate, late) echocardiographic evaluations demonstrated early increase in left ventricular mass and in fractional shortening in both hypertensive and normotensive heart transplant recipients with sustained enhanced contractility in hypertensive patients. [table: see text] Further studies will help to determine the exact relationship between cyclosporine dosages and hypertension, and their respective roles in the development of renal insufficiency and left ventricular hypertrophy after heart transplantation.

To evaluate the incidence, risk factors and effects of systemic hypertension on renal function and left ventricular hypertrophy after cardiac transplantation, 85 transplant recipients on triple drug, low dosage, immunosuppressive therapy were studied. After a mean follow-up period of 12.5 +/- 8.7 months, a high incidence of hypertension was observed in 57 (67%) of the patients, and 42 (71%) of the 57 had developed new hypertension. None of the pretransplant and posttransplant cardiovascular risk factors were significantly associated with posttransplant hypertension. Faster deterioration of renal function, as assessed by intraindividual variations of serum creatinine values, was demonstrated in hypertensive patients and appeared as an early indicator of cyclosporine nephrotoxicity in patients at risk for hypertension. Serial echocardiographic evaluations demonstrated an early increase in left ventricular mass and fractional shortening in both hypertensive and normotensive heart transplant recipients. Fractional shortening further diminished significantly in normotensive patients but remained elevated in hypertensive patients, demonstrating sustained enhanced contractility in this group. Further studies will help to determine the exact relation between cyclosporine dosages and hypertension and their respective roles in the development of renal insufficiency and left ventricular hypertrophy after cardiac transplantation.

The aim of this study was to analyse variations in left ventricular mass (LVM) and systolic function after cardiac transplantation and to evaluate eventual changes induced by the onset of systemic hypertension (HT). In a retrospective study, we selected the echocardiographic examinations of 42 patients performed at the end of the first month (M1), sixth month (M6), and at the end of follow-up (ME) after cardiac transplantation. The patients were divided into two groups (NT: n = 14; HT: n = 28) depending on whether hypertension occurred during follow-up. The average duration of follow-up was 12.8 +/- 6 months; this was comparable in the two groups. Mild left ventricular hypertrophy was observed from the first postoperative examination: M1 = 193 +/- 50 g; M6 = 199 +/- 62 g; ME = 197 +/- 45 g (NS). The hypertrophy was constant with time and related to wall thickening; it was associated with an increased left ventricular fractional shortening (FS) which decreased with time especially in the NT group (average/42 patients: M1 = 0.38 +/- 0.09; M6 = 0.34 +/- 0.08; ME = 0.35 +/- 0.05; p = 0.03 between M1 and ME). The influence of hypertension on the development of LVH and wall thickening was negligible. The role of transplant rejection should be considered: the repetition of episodes of rejection was less marked than the histological severity of rejection. The role of other factors (ischaemia, persistent haemodynamic abnormalities) is a matter of discussion.

Accelerated coronary atherosclerosis is a major risk limiting long-term survival after heart transplantation and is commonly associated with dyslipoproteinemia even in subjects who were not dyslipoproteinemic before intervention. The purpose of this study was to analyse the abnormalities in the lipid profiles of 2 different groups of heart-transplanted males: 18 subjects with underlying ischemic heart disease (IHD) and 19 subjects with non-obstructive cardiomyopathy of unknown aetiology (CM). Both groups were compared to 33 healthy males. All patients were under immunosuppressive therapy including prednisone, cyclosporin A and azathioprine. A moderate hyperlipidemia was found in all transplant recipients, associated with high HDL-cholesterol concentrations in the CM group (1.80 +/- 0.37 vs. 1.29 +/- 0.23 mmol/l) and normal HDL-cholesterol levels in the IHD group (1.40 +/- 0.23 mmol/l). HDL subfractionation showed a marked increase in HDL2-cholesterol (CM: 1.12 +/- 0.32; IHD: 0.69 +/- 0.28; control: 0.40 +/- 0.17 mmol/l) while HDL3-cholesterol was significantly lower than in the control group. Analysis of HDL particle sizes showed in all transplant subjects an increase of an intermediate size particle HDL2a (diameter 9.0 +/- 0.10 nm) which is a minor form in control subjects. In the CM group, both the common HDL2b (10.2 +/- 0.13 nm) and HDL2a were abundant in 13 of 17 patients. The pattern was more heterogeneous in the IHD group but witnessed to a high frequency of HDL2a particles either alone (5/14) or associated with larger HDL2b (4/14) or with small HDL3 (4/14).(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial hypertension is frequent after cardiac transplantation. Since cyclosporin was introduced its incidence has risen up to 40 to 100 per cent of the patients. Its date of onset and severity are variable. Arterial hypertension acts on the heart by increasing left ventricular hypertrophy and transplant dysfunction and on the kidney by aggravating the cyclosporin-induced renal impairment which is often present. Several mechanisms have been suggested to account for the occurrence of hypertension in these patients, including poor neurological control of blood pressure, a hypothetical haemodynamic effect and the influence of corticosteroids and cyclosporin. Cyclosporin seems to play the main role. The treatment of this iatrogenic arterial hypertension remains to be precisely determined.

The number of patients who survive heart transplantation has considerably increased in recent years, but mortality during the first 3 months still reaches 10 to 20 p. 100 depending on the authors. Among the various causes of death, acute graft deficiency due to pulmonary arterial hypertension plays an important role. In most cases, pulmonary vascular resistance has been misevaluated or its progress has not been foreseen. Between January 1985 and June 1988, 96 heart transplantations were performed at the Broussais Hospital, Paris. We thought that pulmonary vascular resistance could be better evaluated by using dobutamine to mimick transplantation and to assess pulmonary pressure and resistance variations associated with the increase in cardiac output. High doses of dobutamine ranging from 10 to 30 mcg/kg/min were administered to bring the basal cardiac output level up to the theoretical output level or to increase it by 50 p. 100. The 96 patients who had heart transplantation during the aforementioned period were divided into two groups: group I comprised 35 patients who were transplanted before dobutamine was used, while group II comprised 61 patients for whom the dobutamine test was always considered. The mortality rate was 11.75 p. 100 (4/35) in group I and nil in group II as regards death from pulmonary arterial hypertension (p = 0.04). We demonstrate that a single resistance value is not reliable, even when it is normal, when the cardiac output is low. Furthermore, there is no threshold value for contraindication, and indexing resistance alters the scale of values but does not enable normality to be defined. By using the dobutamine test we were able to reduce considerably the mortality due to pulmonary arterial hypertension and also to exclude orthotopic transplantation in some patients.

Right ventricular failure is relatively frequent and constitutes one of the causes of post-operative heart failure. Few drugs are available to treat right ventricular failure. We present a simple and effective means of mechanical support available in all cardiovascular units: counterpulsation in the pulmonary artery. Our experience and a review of the literature have enabled us to determine the indications for this method to support a failing heart.

In patients with heart transplant, the combined determination of serum beta 2-microglobulin and urinary neopterin, as rejection marker, prevented the interference by renal function and cyclosporin therapy. Unfortunately, the simultaneous measurement of these two parameters cannot distinguish between a rejection episode and the early stage of viral infection.