Jean-Noël Fabiani

Aortic cusp extension valvuloplasty for rheumatic aortic valve disease: midterm results

BACKGROUND The surgical management of rheumatic aortic insufficiency in the young remains problematic owing to the drawbacks of prosthetic valve replacement at this age. In young foreign patients, for whom long-term anticoagulation therapy is unavailable, we have used a glutaraldehyde preserved autologous pericardium cusp extension technique to repair rheumatic aortic valve insufficiencies resulting from cusp retractions. METHODS From September 1992 to December 2000, 89 consecutive patients with a mean age of 16 +/- 5 years underwent triple pericardial aortic cusp extension valvuloplasty. Eighty patients had pure aortic insufficiency, 9 had mixed aortic disease. Twenty-nine patients (33%) had isolated aortic valve disease and 60 patients (69%) had combined aortic and mitral valve disease with significant tricuspid valve disease in 21 (24%). Aortic repair consisted of free edge aortic cusp extension using three rectangular strips of glutaraldehyde stabilized autologous pericardium. Twenty-nine patients (33%) underwent an isolated aortic repair, 39 patients (44%) underwent combined aortic and mitral procedures (34 mitral repairs, 3 mitral homografts, and 2 prosthesis replacements), and 21 patients (23%) underwent a triple valve repair. RESULTS The hospital mortality was 2.2%. Primary failure of the aortic repair requiring immediate reoperation occurred in 2 patients. During follow-up (mean of 62 +/- 22 months) 1 patient died and 7 underwent redo valvular surgery. At 5 years the actuarial survival rate was 96.4%, and 92.1% of the patients were free from redo valvular surgery. At 7 years 90% of the patients were free from valve-related complications. Among the 76 patients free from redo valvular surgery at follow-up, 6 had deterioration of the repair resulting in grade II aortic and mitral insufficiencies. CONCLUSIONS Our midterm results of glutaraldehyde stabilized autologous pericardial aortic cusp extension are encouraging and suggest that this technique should be considered as a viable alternative palliative procedure in a young rheumatic population, allowing for growth of the annulus and delaying to a less critical period the need for the lifelong anticoagulation therapy required for a prosthetic mechanical valve.

Dynamic cardiomyoplasty: clinical follow-up at 12 years.

OBJECTIVE The purpose of this study is to evaluate the long-term outcome of dynamic cardiomyoplasty. This surgical technique was conceived to assist the failing heart. The many proposed mechanisms of action of cardiomyoplasty are: (1) systolic assist; (2) limitation of ventricular dilation; (3) reduction of ventricular wall stress (sparing effect); (4) ventricular remodeling with an active girdling effect; (5) angiogenesis; and (6) a neurohumoral effect. METHODS We investigated 95 patients in our hospital undergoing this procedure due to severe chronic heart failure, refractory to optimal medical treatment. Patients had a mean age of 51 +/- 12 years. The etiology of heart failure was ischemic 55%, idiopathic 34%, ventricular tumor 6%, and other 5%. The mean follow-up was 44 months. RESULTS The mean New York Heart Association (NYHA) functional class improved postoperatively from 3.2 to 1.8. Average radioisotopic left ventricular (LV) ejection fraction increased from 17 +/- 5 to 27 +/- 4% (P < 0.05). Stroke volume index increased from 32 +/- 7 to 43 +/- 8 ml/beat per m2 (P < 0.05). The heart size remained stable over the long term. Following cardiomyoplasty, the number of hospitalizations due to congestive heart failure was reduced to 0.4 hospitalizations/patient per year (preoperative: 2.5, P < 0.05). Computed tomography scans showed at long term a preserved latissimus dorsi muscle structure in 84% of patients. Survival probability at 7 years is 54%. Six patients underwent heart transplant after cardiomyoplasty (mean delay: 25 months), due to the natural evolution of their underlying heart disease. There were no specific technical difficulties. CONCLUSIONS Clinically, this procedure reverses heart failure, improves functional class and ameliorates quality of life. The latissimus dorsi muscle histological structure is maintained at long-term, when postoperative electrostimulation is performed, avoiding excessive stimulation. Cardiomyoplasty may delay or prevent the progression of heart failure and the indication of cardiac transplantation.

Does glutaraldehyde induce calcification of bioprosthetic tissues

BACKGROUND Glutaraldehyde has been said to be responsible in part for the calcification of glutaraldehyde-treated tissues after implantation in animals or humans. We investigated whether the origin of the tissue, autologous or heterologous, could have a more prominent role in the process of calcification. METHODS Three-month-old sheep received sheep pericardial samples (n = 133) and human pericardial samples (n = 123) implanted subcutaneously. Samples were treated with 0.6% glutaraldehyde for 5, 10, or 20 minutes or 7 days and then rinsed thoroughly before implantation. Samples were then retrieved after 3 months. Calcium content was assessed by spectrophometry. RESULTS The results show a low calcium content in the autologous group (mean 1.14+/-2.07) and a high calcium content in the heterologous group (mean 38.97+/-26). These results were the same regardless of the duration of the treatment. CONCLUSIONS Glutaraldehyde treatment (0.6%) does not play a significant role in the calcification of glutaraldehyde-treated tissue regardless of the origin, autologous or heterologous, of the tissue. Glutaraldehyde-treated autologous tissues are associated with an incidence of calcification lower than heterologous tissues.

A 10-year comparison of mitral valve replacement with Carpentier-Edwards and Hancock porcine bioprostheses

Two hundred fifty-three patients who underwent isolated mitral valve replacement with a porcine bioprosthesis had long-term evaluation. One hundred forty-seven patients received a Carpentier-Edwards porcine bioprosthesis and 106, a Hancock valve. There were no significant differences in preoperative clinical characteristics between the two groups. Cumulative follow-up was 1,375 patient-years. At 10 years, 93% +/- 2.5% of the patients in the Carpentier-Edwards group and 85% +/- 7.8% of those in the Hancock group were free from valve-related death (not significant), and 95% +/- 2% and 91% +/- 3.8%, respectively, were free from thromboembolism (not significant). At 10 years, 65% +/- 7.2% of the patients in the Carpentier-Edwards group and 66% +/- 7.2% of those in the Hancock group were free from structural valve deterioration (not significant), and 64% +/- 6% and 59% +/- 7.3%, respectively, were free from reoperation (not significant). We conclude that the first generation of Carpentier-Edwards and Hancock prostheses produce comparable long-term results in the mitral position.

Ventricular fibrillation during termination of pregnancy

In June, 2006, a 29-year-old woman underwent a termination of pregnancy at 35 weeks of gestation, because the fetus had been found to have porencephaly. She had had three previous pregnancies, of which two had proceeded to term; her medical history was otherwise unremarkable. The fetus was killed with sufentanil and lidocaine. Misoprostol was administered intravaginally to induce labour, and the membranes were artifi cially ruptured. 15 min later, the patient suddenly lost consciousness and began to gasp for breath. She entered ventricular fi brillation. She was immediately intubated and ventilated; cardiac massage was done; and she was given three DC shocks. The period between onset of cardiac arrest and the start of life support was estimated at around 3 min; life support was given for about 10 min. Immediate transthoracic echocardiography, using an obstetric ultrasound device, showed a massively dilated hypokinetic right ventricle, with fl oating echo-dense masses (fi gure). Blood test results indicated disseminated intravascular coagulation (platelet and fi brinogen concentrations very low at 20×109/L and 0·59 μmol/L respectively; activated partial thromboplastin time >120 s). Within 1 h of the onset of cardiac arrest, the fetus was delivered—with subsequent profuse vaginal bleeding. Manual exploration of the uterus, uterine massage, intravenous oxytocin, and uterine packing all failed to stem the bleeding, so a sulprostone infusion was started, and the patient was given several units of blood, which stabilised her condition. The combination of cardio vascular collapse, coagulopathy, and the echocardiographic fi ndings indicated that an amnioticfl uid embolism (AFE) was likely; a blood sample was immediately analysed by the pathologist, who observed amniotic and fetal cells after staining the sample with Wright’s stain and Nile blue stain. The patient was transferred to another hospital, where more intensive management was possible. She was given bilateral uterine embolisation, which caused the bleeding to cease. However, her haemodynamic stability deteriorated, despite increasing doses of epinephrine and dobutamine. Transoesophageal echo cardiography showed left ventricular failure (ejection fraction <15%). 8 h after cardiac arrest, extracorporeal life support (ECLS) was initiated, by use of a femoro-femoral bypass. The patient’s left ventricular function did not improve. She developed a fever and a raised white cell count that appeared to be caused not by an infection, but a systemic infl ammatory reaction. 12 days after cardiac arrest, the decision was made to give intravenous hydrocortisone (50 mg every 6 h). Left ventricular function began to recover within hours, and we were able to discontinue ECLS 20 days after cardiac arrest. The patient was extubated on day 26, and discharged on day 40. When last seen, in March, 2007, the patient was well, with no evidence of neurological damage; she had resumed work, and was preparing to run the Paris marathon. AFE is a rare complication of pregnancy, occurring in one in 20 000–50 000 deliveries. However, it is one of the leading causes of maternal mortality in developed countries; the proportion of patients surviving without neurological damage is only 15%. The presence of amniotic fl uid in the maternal bloodstream causes severe vasoconstriction and pulmonary hypertension. There follows a cascade of infl ammatory activation, similar to the systemic infl ammatory response caused by sepsis or burns. This process can cause multiple organ dysfunction, and typically depresses the myocardium. This scenario needs to be anticipated, so that alternative treatments—which can include ECLS—can be initiated or prepared. In this case, steroids appeared instrumental in reversing left ventricular dysfunction, perhaps because of their anti-infl ammatory activity. Had ventricular function not recovered, a heart transplant might have been necessary.

Triple valve repair for young rheumatic patients.

BACKGROUND Facing young foreign polyvalvular rheumatic patients, for which long-term anticoagulation is not available, we have chosen to attempt triple valve repair procedures in order to avoid prosthetic implantation in this particular population suffering from triple valve disease. METHODS Twenty-one young rheumatic patients (mean age:11+/-4 years) underwent triple valve repair procedures including cusp extension on the aortic valve aortic between September, 1992 and December, 2000. Valvular pathology characteristics according to Carpentiers classification included mitral insufficiency type III post+II ant (n=10), type III post (n=4), type II ant (n=2), mitral stenosis (n=5), type III aortic insufficiency (n=21), type I (n=13) and type III (n=8) tricuspid insufficiency. RESULTS Firstly, the mitral valve disease were corrected using Carpentiers techniques of repair: prosthetic ring annuloplasty (n=16), commissurotomy (n=12), chord transposition (n=11) or shortening (n=4), papillary muscle sliding plasty (n=4) and pericardial patch leaflet enlargement (n=6). Secondly, aortic lesions were corrected using glutaraldehyde stabilized autologous pericardium triple cusps extension technique (n=21). Lastly, tricuspid repairs were always performed on beating hearts using commissurotomy (n=8), prosthetic ring (n=12) or other techniques (n=9) of annuloplasty. The operative mortality was 4.7% (one patient died). Echocardiograms before discharge showed grade I mitral insufficiency in seven patients and grade I aortic insufficiency in five patients. There was no late death during a mean follow-up of 51+/-31 months. Two patients underwent valvular redo surgery because of aortic and mitral plasty deterioration due to rheumatic disease progress. After 5 years, 90% of the patients were free from redo valvular surgery. CONCLUSIONS In rheumatic patients, autologous pericardial patch extension of the aortic valve permitted widespread use of reconstructive surgery even in patients suffering from triple valve disease. Triple valve repair, in this particular challenging setting of patients, has provided satisfactory initial and mid-term results and could be considered as an interesting palliative surgical approach.

Intracardiac renal cell carcinoma metastasis.

Cardiac involvement by intravascular protruding renal cell carcinoma is a well-recognised phenomenon. It most commonly occurs through inferior vena cava extension. Here, we report a case of a lower lobar lung metastasis from renal cell carcinoma involving the left atrium via the inferior pulmonary vein in a patient presenting with von Hippel-Lindau disease. Complete surgical resection was achieved under cardiopulmonary bypass.

Cardiac epicardial tumor with coronary artery compression

An asymptomatic 58-year-old male was incidentally found to have an epicardial mass on CTscanwith compression of left anterior descending coronary artery (Fig. 1). Coronary angiogram confirmed compression (Video 1). Tumor was resected along with left coronary bifurcation (Fig. 2). Histopathology showed inflammatory pseudotumor consistent with localized Castleman’s disease. Six-month follow-up CT was normal.

Clastogenic Factor in Ischemia-Reperfusion Injury: Protective Effect of Allopurinol

Many studies have established a major role for toxic metabolites of oxygen as mediators of tissue injury following ischemia-reperfusion in a wide variety of species and organs.1–3 The source of the oxygen free radicals is still the subject of debate. Tissue damage may be due in part to direct radical attack, in part to longer-lived secondary compounds derived from lipid peroxidation of membranes.

Malignancy with Cavoatrial Extension

Surgical treatment of retroperitoneal tumors with cavoatrial involvement can be challenging. Completeness of resection of the cava tumor extension is crucial for the patient’s survival. Our experience with the use of cardiopulmonary bypass and deep hypothermic low flow for the surgical resection of malignancy with cavoatrial extension allows us to obtain a nearly bloodless field. Reconstruction of the atriohepatic confluent can then be carried out with a pericardium patch without inferior vena cava reconstruction. Cardiopulmonary bypass with deep hypothermic low flow facilitates tumor resection and reconstruction of the atriohepatic confluent. It provides satisfactory postoperative results and should be considered as an option in the management of malignancies with cavoatrial extension.