Postoperative visual loss due to complicated mediastinal dissection and haemorrhagic shock treatment during cardiac surgery.

We report the case of a patient who underwent third time revision of double heart valve replacement. Mediastinal dissection for right atrium cannulation was complicated by laceration of the superior vena cava; this required temporary rescue clamping of the vessel. The patient suffered complete visual loss related to bilateral retrobulbar haematoma. Acute elevation of superior vena cava pressure due to vascular clamping and administration of large amounts of fluid through the central venous jugular catheter could have caused the postoperative visual loss.

[Isolated carcinoid tumor of the ovary disclosed by tricuspid insufficiency]. / Une tumeur carcinoïde isolée de l'ovaire révélée par une insuffisance tricuspide.

A 68-year old woman was hospitalised because of isolated right heart failure. Doppler echocardiography revealed severe tricuspid regurgitation with thickened, shortened, hypomobile leaflets. Pulmonary valve was thickened with mild pulmonary regurgitation. Mitral and aortic valves were normal. The patient was finally diagnosed with carcinoid heart disease from an isolated ovarian carcinoid cancer without hepatic metastases. Ovarectomy was performed and the patient was considered cured of her cancer. Because of refractory right heart failure, she underwent tricuspid valve replacement with a bioprosthesis. Such cardiovascular manifestations are rarely the presenting symptoms of carcinoid disease. Carcinoid heart disease from ovarian primary cancer is exceptional. In this circumstance, carcinoid cardiac lesions may develop in the absence of hepatic metastases because the venous blood from the ovaries drains into the inferior vena cava without hepatic first past effect. Surgical resection of primary ovarian carcinoid tumor is often curative and the prognosis depends mainly on the cardiac condition. The diagnosis of carcinoid syndrome should be discussed in patients with organic tricuspid regurgitation without left valvular disease.

[Pneumococcal endocarditis in native valves. Three original observations in the adult]. / Endocardites à pneumocoque sur valves natives. Trois observations originales chez l'adulte.

The authors report three observations of acute pneumococcal endocarditis located in the aorta in one case, and mitral in the two other cases, admitted over a period of 4 years. Two of the three patients required surgical correction, with no surgical complications. Follow-up revealed a rare complication of infectious endocarditis linked to rupture of the head of the two anterior mitral pillars associated with an abscess. The severity of pneumococcal endocarditis is emphasised, concurring with the data from the literature. The role of echocardiography in pneumococcal septicaemia is clear; transthoracic examination is justified in every case of septicaemia, and transoesophageal echography complements this examination in case of diagnostic doubt or cardiovascular complication.

Contralateral lung transplantation: a left lung implanted in the right thorax.

Since the inception of lung transplantation in 1982, it has been standard practice to implant donor lungs on the ipsilateral side in the recipient. The development of the techniques of lobar and bilateral lobar transplantation has shown that lung morphology may adapt to the shape of the thorax. Thus, variations in implantation have become possible. We describe a case of a 30-year-old man with severe bronchiectasis due to ciliary dyskinesis which required a left lower lobectomy at the age of 11 years and a left completion pneumonectomy 10 years later. His disease progressed and he was listed for a right lung transplantation. At the time of transplantation, the donor right lung was noted to be edematous and unfit for transplantation. This required grafting the donor left lung in the right thorax of the recipient. Follow-up at 7 years shows good exercise capacity and excellent functional tests without evidence of rejection.

Quantitative analysis of inflammatory cells infiltrating the cystic fibrosis airway mucosa.

Airway inflammation represents a hallmark of the cystic fibrosis (CF) disease. However, the mucosal distribution of immune cells along the CF airways has not been clearly defined, particularly in intermediate bronchi and distal bronchioles. We analysed lung tissues collected at the time of transplantation from homozygous DeltaF508+/+CF patients versus non-CF donors. Using immunohistochemistry, the distribution of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin, polymorphonuclear neutrophils (PMN), mast cells, CD3+ T cells, including the CD4+ and CD8+ subsets, CD20+ B cells, CD38+ plasma cells and CD68+ macrophages, was analysed at lobar, segmental and distal levels of the bronchial tree. Using image cytometry, the number of cells per mm2 was assessed in the depth of the bronchial wall. In CF airways, alterations mainly consisted in lesions of the surface epithelium. Numerous immune cells were heterogeneously distributed all along the bronchial tree and mainly located in the mucosa, beneath the surface epithelium. Compared to non-CF donors, the lymphoid aggregates formed by B cells were significantly larger all along the CF airways (P = 0.001). The number of T lymphocytes was higher at the CF distal level (P = 0.035), where we observed an intense tissue damage. PMN preferentially accumulated (P = 0.033) in the CF surface epithelium, which overexpressed ICAM-1 but not VCAM-1 and E-selectin. These results highlight the nature of the inflammatory infiltrate in the CF airway mucosa and emphasize a prominent implication of PMN, B and T lymphocytes in the CF disease.

Relationship between IkappaBalpha deficiency, NFkappaB activity and interleukin-8 production in CF human airway epithelial cells.

Several recent reports have suggested that airway inflammation may precede infection and relate to an endogenous dysregulation of pro-inflammatory cytokines in cystic fibrosis (CF) airways. Evidence suggests that activation of the nuclear factor kappa B (NFkappaB), which regulates the inflammatory gene transcription, depends on the degradation of the inhibitory factor IkappaBalpha. We show that, in in situ human DeltaF508 CF bronchial tissues, inhibitor factor IkappaBalpha is not present in gland cells, although endogenous levels of chemokine IL-8 are high. These data are confirmed by studying cultured CF human bronchial gland cells, in which a lack of cytosolic IkappaBalpha and high levels of activated NFkappaB, concomitant with IL-8 overproduction (a 13-fold increase) are found when compared to non-CF bronchial gland cells. Interestingly, treatment of CF gland cells with the isoflavone genistein, a well known CFTR mutant Cl(-) channel stimulator, results in a significant decrease ( P < 0.001) in IL-8 production down to levels released by non-CF gland cells. The addition of genistein also reverses the effects of lipopolysaccharide (LPS) Pseudomonas-aeruginosa-induced nuclear translocation of NFkappaB by increasing IkappaBalpha protein level (65%) in CF gland cells. Our data indicate that the induction of IkappaBalpha protein in CF airway glandular epithelial cells may be a novel mechanism by which IL-8-mediated lung inflammatory events are markedly reduced in CF patients, at least at the airway glandular level.

[Human valvular substitutes for the treatment of complex progressive endocarditis. Application to aortic, mitral and tricuspid valves]. / Substituts valvulaires humains dans le traitement des endocardites évolutives complexes. Application sur les orifices valvulaires aortiques, mitraux et tricuspides.

The aim of this study was to assess the immediate and long-term results of human valvular substitutes (homografts and autografts) in the treatment of complex progressive endocarditis in aortic, mitral and tricuspid valves. Since 1992, 80 patients (64 men, 16 women) aged 44 +/- 16 years (range 15 to 76 years), were treated. In 53 patients, the endocarditis involved native valves, 4 on previously plastified valves, or prosthetic valves in 27 patients. The endocarditis was recurrent 6 patients. The lesions were situated on the aortic valve (N = 59), mitral valve (N = 5), aortic and mitral valves (N = 12), aortic and tricuspid valves (N = 3), mitral and tricuspid valves (N = 1). The peroperative findings confirmed the lesions diagnosed at echocardiography: prosthetic valve dehiscence (27 patients), prosthetic cusp tear (N = 7), vegetations (N = 61), perforations (N = 48), periannular abscess (N = 47), aorto-ventricular discontinuity (N = 12), aorto-mitral discontinuity (N = 7), right ventricular aortic fistula (N = 1), aorto-pulmonary fistula (N = 1), pseudo-aneurysm (N = 1), ventricular septal defect (N = 1). Eighty-six human valvular substitutes were used (double homograft in 6 patients): aortic homograft (N = 63), pulmonary in the aortic position (N = 1), the mitral position (N = 12), of which 8 were in the mitral and 4 in the tricuspid position, pulmonary autograft (N = 10). Ten mitral valve repairs were performed on infected lesions. Associated procedures included mitral valve repair (N = 5), tricuspid valve repair (N = 1) for non-infarcted valve lesions, replacement of the ascending aorta (N = 2), the aortic arch (N = 1), coronary bypass surgery (N = 2) and one nephrectomy. The hospital mortality was 5% (4 patients). The causes of death were: infarction (N = 2), myocardial failure (N = 1) and multiorgan failure (N = 1). Four early reoperations were required for technical problems, none for endocarditis. Seventy-three of the 76 survivors were followed up for 43 +/- 24 months (range 1 to 84 months). Eight patients died during follow-up, but only 1 of cardiac causes (operation for recurrent endocarditis in a drug abuser). Seven operations were performed, 3 for technical problems or structural failure, 4 for recurrent endocarditis. At 5 years' follow-up, the survival was 81 +/- 5%; 88 +/- 6% of patients were free of endocarditis, 77 +/- 6% had no reoperation: no patient had thromboembolic complications. These results show that human valvular substitutes are adapted for the treatment of complex, progressive aortic, mitral and tricuspid valve endocarditis when techniques of valvular repair are no longer feasible.

[Cardiac fibroelastoma. Six operated cases and review of the literature]. / Fibroélastomes cardiaques. Six cas opérés et revue de la littérature.

The authors reviewed the cases of 6 patients operated between September 1994 and February 1999 for a rare benign tumour: papillary fibroelastoma of the heart. These patients, aged 51 +/- 14 years, all have single valvular involvement: mitral (N = 3), aortic (N = 2), tricuspid (N = 1). Five patients were symptomatic: transient ischaemic cerebral events (N = 3) associated with mesenteric infarction requiring ileal resection in 1 case; constituted cerebrovascular accident (N = 1); syncope (N = 1). In this last patient, the fibroelastoma was diagnosed fortuitously on the tricuspid valve. The features and location of the tumours were determined by transoesophageal echocardiography. Surgical treatment in all patients consisted in excising the tumour and preserving the valve. One aortic cusp was reconstructed after excising the tumour with a cryopreserved partial aortic homograft. Peroperative transoesophageal echocardiography confirmed the absence of regurgitation after the procedures in all patients. There were no postoperative complications in any of the cases. No cases of valvular regurgitation or of tumour recurrence were observed during follow-up. Despite the benign histology, cardiac fibroelastomas should be excised because of their embolic complications. Absence of recurrence justifies conservative reconstruction of the affected valve.

Inhibition by extracellular cAMP of phorbol 12-myristate 13-acetate-induced prostaglandin H synthase-2 expression in human pulmonary microvascular endothelial cells. Involvement of an ecto-protein kinase A activity.

Exposure of human pulmonary microvascular endothelial cells (HPMECs) to phorbol 12-myristate 13-acetate (PMA) leads to the increase of prostaglandin H synthase (PGHS)-2 protein levels. Under same conditions and according to its constitutive nature, no significant variation of PGHS-1 protein was noted. The elevation of the intracellular cAMP rate is known to enhance PGHS-2 levels through a protein kinase A pathway in various cells. To determine whether the extracellular cAMP also regulates the inducible expression of PGHS, cultured HPMECs were exposed to cAMP alone or in combination with PMA. The PMA-induced PGHS-2 protein was attenuated by the extracellular cAMP. In addition, PGHS-2 activity evaluated through 6-keto-PGF1alpha generation, which was enhanced by PMA was inhibited by extracellular cAMP. Furthermore, in HPMEC medium, PMA-induced PGHS-2 expression was accompanied by the generation of a transferable activity (TA) able to abolish platelet aggregation. This resulting TA was dependent from PGHS-2 pathway, because NS-398, a selective inhibitor of PGHS-2, suppressed its production. The inhibitory TA released by treated HPMECs was also prevented by extracellular cAMP. The specific protein kinase A (PKA) inhibitor blocked the extracellular cAMP effect on both PMA-induced 6-keto-PGF1alpha synthesis and inhibitory TA generation, suggesting the involvement of PKA signaling at the outer surface of HPMECs. Accordingly, we established, in phosphorylation experiments, the presence of an endothelial ecto-protein kinase activity, able to phosphorylate the synthetic substrate kemptide in a cAMP-dependent mode. Reverse transcription-polymerase chain reaction analysis showed that PMA-induced PGHS-2 mRNA was markedly reduced by extracellular cAMP. Together, these findings provide the first experimental evidence that extracellular cAMP is able to reduce HPMEC PGHS-2 expression in terms of mRNA, protein, and enzyme activity through an ecto-PKA pathway. In addition, they outline the potential role of endothelial PGHS-2 in the limitation of platelet activation during inflammatory processes.

High susceptibility for cystic fibrosis human airway gland cells to produce IL-8 through the I kappa B kinase alpha pathway in response to extracellular NaCl content.

Increasing evidence suggests that in airways from cystic fibrosis (CF) patients, inflammation may precede bacterial infection and be related to an endogenous dysregulation of proinflammatory cytokines in airway epithelial cells. Several investigators have reported that, in CF airway fluids, elevated NaCl concentrations may also contribute to the diseased state by inhibiting the bactericidal properties of airway fluid. Because many proinflammatory cytokines are transcriptionally regulated by the NF-kappa B, we investigated whether an elevated extracellular NaCl content in airway fluids significantly impaired the regulation of the NF-kappa B/I kappa B alpha complex and the chemokine IL-8 production in primary non-CF and CF human bronchial gland epithelial cells. Exposure of non-CF gland cells to hypotonic (85 mM) NaCl solution, compared with isotonic (115 mM) NaCl and hypertonic (170 mM) NaCl solutions, resulted in a significant decrease in IL-8 production that was paralleled by a strong inhibition of activated NF-kappa B associated with an increased cytosolic expression of I kappa B alpha and a decrease in the I kappa B kinase alpha protein level. In CF gland cells, we demonstrated that, compared with the high IL-8 in an hypertonic solution, the release of IL-8 was significantly reduced 2-fold in an isotonic solution and 5-fold in a hypotonic solution. Strikingly, exposure of CF bronchial gland cells to either hypotonic or isotonic milieu did not result in a marked inhibition of the activated NF-kappa B/I kappa B alpha system. This is the first demonstration that primary human CF bronchial gland cells exhibit abnormally high IL-8 production through constitutively activated NF-kappa B and high I kappa B kinase alpha level, whatever the hypo-, iso-, and hypertonic NaCl milieu.

Coronary reoperations: indications, techniques and operative results. Retrospective study of 240 coronary reoperations.

BACKGROUND: We review twelve-year experience with coronary reoperations so as to better identify indications, techniques and results. METHODS: Between January 1986 and March 1998, 240 coronary reoperations (228 redux, 12 tridux) were performed. There were 223 male and 17 female patients, with a mean age of 63.6+/-7.9 years at the time of reoperation. Mean time interval between operations was 10+/-4.8 years. Symptomatology consisted of: stable recurrent angina (40%), unstable (57%), or congestive heart failure (3%). Pathological feature of the primary grafts was implicated in 95% of cases and atheroma sole progression over native network in 5% of cases. During reoperations 521 (2.2+/-0.8/patient) bypass [venous (40%), arterial (60%)] were performed as well as 15 associated procedures. RESULTS: Operative mortality represented 10% (n=24). Causes of death included infarct (7), left ventricular failure (12), rhythm disorders (2), mediastinitis (1) and multiorgan failure (2). Mortality risk factors were operation date (16.6% before 1992 and 7.4% after, p=0.03), age (13.1% after 60 years old, 2.7% before, p=0.01) time interval between intervention (12% after 8 years, 4% before, p=0.05) and anterograde cardioplegia only (11.8% versus 4.5% when a combined anterograde and retrograde access was used, p=0.06). Morbidity was 31% (71/240). Among the survivors 169 patients (78%) did not experience any complication. CONCLUSIONS: Thanks to a better medico-surgical management, the mortality rate of coronary reoperations is steadily decreasing.

Morphometric study of the pulmonary trunk: implications for a new approach of the Ross procedure.

A pulmonary valve autograft may be proposed to replace diseased aortic valves. The explanted pulmonary valve is replaced with a pulmonary homograft with the inherent risk of calcified degeneration. A monocusp valve using the anterior pulmonary trunk has been proposed to reconstruct the right ventricular outflow tract. The aim of this study was to determine the feasibility of this technique. In hearts from 17 adult cadavers, we measured: pulmonary trunk diameter at the leaflet tops (D1). H1 and H2 were respectively from leaflet top to lower and upper levels of the pulmonary trunk bifurcation. D2 = 1.4 D1 was calculated as the monocusp size allowing a 45 degrees opening of the valve and thus permitting good valvular efficacy. G = H1 - D2 determined the feasibility of the technique: G greater than 10 mm, appeared the most favorable, G between 0 and 10 mm, appeared possible, and G less than 0, appeared to be impossible. Mean values of D1, H1 and H2 were respectively: 20.19 mm, 37 mm and 57 mm. The technique was possible in 16 cases (94%) and impossible in 1 case (6%). Preoperative determination of these parameters, by echocardiography or magnetic resonance imaging, appears necessary before applying this new surgical technique.

Single breath exhaled nitric oxide in lung transplant patients: a preliminary clinical study.

Exhaled nitric oxide is considered as a marker of airway inflammation. We report here our preliminary experience with single-breath exhaled nitric oxide measured in lung transplant patients with and without bronchiolitis obliterans syndrome and in cardiac transplant patients. Peak and end-expiratory nitric oxide concentrations did not differ between groups, but single-breath exhaled nitric oxide recordings were strikingly different in patients suffering from bronchiolitis obliterans syndrome, with a slower decrease from peak to end-expiratory nitric oxide concentration. Further studies are required in order to determine whether theses abnormalities reflect the inflammatory process of bronchiolitis obliterans syndrome.

Genistein inhibits constitutive and inducible NFkappaB activation and decreases IL-8 production by human cystic fibrosis bronchial gland cells.

The inflammatory pathogenesis in airways of patients with cystic fibrosis (CF) is still unresolved. We demonstrate here that in in situ human DeltaF508 homozygous CF bronchial tissues, submucosal gland cells exhibit an absence of inhibitor factor kappaBalpha (IkappaBalpha) and high levels of chemokine interleukin-8 (IL-8) expression. These results were confirmed by cultured human CF bronchial gland cells in which a lack of cytosolic IkappaBalpha and high levels of constitutively activated nuclear factor kappaB (NFkappaB) associated with an up-regulation of IL-8 production (13-fold increase) were found when compared to non-CF (control) disease bronchial gland cells. We also demonstrated that the isoflavone genistein, a well known CFTR mutant Cl(-) channel stimulator, significantly reduces the endogenous and Pseudomonas aeruginosa lipopolysaccharide-induced IL-8 production in cultured CF bronchial gland cells by increasing cytosolic IkappaBalpha protein levels. Overall, results show that genistein is a potent inhibitor of the activated NFkappaB identified in CF gland cells. This strong inhibition of constitutively activated NFkappaB and the resulting down-regulation of IL-8 production by genistein in the CF gland cells highlights the key role played by cytosolic IkappaBalpha in the regulation of inflammatory processes in CF human airway cells.

Cardiac valve papillary fibroelastoma: surgical excision for revealed or potential embolization.

OBJECTIVE: We have reviewed the case histories of 4 patients who underwent operations between September 1994 and November 1997 at Broussais Hospital for cardiac valvular papillary fibroelastoma. METHODS: Diagnosis was strongly suggested by echocardiography. Tumor locations were mitral (1), tricuspid (1), and aortic (2). Indications for operation were previous stroke for the mitral tumor, prophylaxis for the tricuspid tumor, syncopal episodes for the first aortic tumor, and transient ischemic attack and mesenteric ischemia for the second aortic tumor. RESULTS: Surgical excision with a conservative, valve-sparing approach was performed in all cases. For the first aortic tumor, aortic valve reconstruction was achieved with part of a cryopreserved aortic homograft cusp. Intraoperative transesophageal echocardiography showed no evidence of valvular regurgitation after excision in all cases. All patients had uneventful postoperative recoveries. No evidence of regurgitation or recurrence was seen on echocardiography at follow-up. CONCLUSIONS: Despite their histologically benign aspect, cardiac papillary fibroelastomas should be excised because of potential embolic complications. A conservative, valve-sparing approach is recommended, however, because of the absence of recurrence after total excision.

Decreasing occupational risk related to blood-borne viruses in cardiovascular surgery in Paris, France.

BACKGROUND: Surgeons face the risk of patient-to-physician transmission of blood-borne viruses. This risk is related to the seroprevalence of the viruses in the patient population. METHODS: The seroprevalence of the human immunodeficiency virus, hepatitis B virus, and hepatitis C virus were determined in cardiovascular patients at Hôpital Broussais in Paris, France, over a 5-year period (1994 to 1998). RESULTS: Hepatitis C virus is the most prevalent virus in the patient population, whereas human immunodeficiency virus is the least frequent. The seroprevalence of hepatitis C virus and human immunodeficiency virus has decreased over time, whereas hepatitis B virus has remained constant. We apply the seroprevalence data to a mathematical model to estimate the occupational risk of seroconversion faced by surgeons over the length of their career. Our results show that the principal risk faced by the surgeon arises from hepatitis B virus and hepatitis C virus. The decreasing seroprevalence of the hepatitis C virus has resulted in a decrease in the occupational risk. CONCLUSIONS: The probability of becoming infected with a blood-borne virus over the career of the surgeon is notable. The greatest occupational risk to the surgeon is from the hepatitis viruses and not HIV.

New approach for reconstruction of the pulmonary outflow tract during the Ross procedure.

BACKGROUND: This study describes and evaluates the early results of a new surgical technique to reconstruct the right ventricular outflow tract and fit it with a new valve after the Ross procedure. METHODS AND RESULTS: Between March 1996 and November 1997, 20 patients underwent a Ross operation with a new approach consisting of a direct anastomosis between the remaining pulmonary artery trunk and the infundibulum and of the creation of a monocusp tailored from the anterior pulmonary artery wall as a means of reconstructing the valve. The 20 patients (12 males and 8 females) had a mean age of 27.4 years (range, 17 to 42 years). Ten of them had predominant aortic regurgitation, 8 had aortic stenosis, and 2 had mixed disease. There were no deaths during the follow-up period of up to 20 months, no early or late repeat operations, and no specific complications secondary to the surgical technique. During the follow-up, at the aortic autograft site, 19 patients had no or trivial regurgitation, and a mild regurgitation was found in only 1 patient. Across the pulmonary monocusp, color flow Doppler demonstrated no or trivial incompetence in 10 patients, mild incompetence in 7, and moderate incompetence in 3. No significant pressure gradient was shown. CONCLUSIONS: Our experience supports the use of this new surgical procedure and allows extension of the Ross operation to where there are no facilities for homografts. It may be an alternative for right ventricular outflow tract reconstruction with a homograft should the results be confirmed at long-term follow-up.

[Coronary reoperation: indications, methods and immediate postoperative prognosis. Retrospective study of 184 reoperations]. / Réinterventions coronaires: indications techniques et pronostic post-opératoire immédiat. Etude rétrospective sur 184 réinterventions.

The authors performed 184 coronary reoperations (172 redux, 12 tridux) between January 1986 and december 1995 in 177 patients (165 men, 12 women) with an average age at surgery of 62.9 +/- 7.6 years. The average interval between the surgical procedures was 9.5 +/- 4.5 years. The symptoms were recurrent angina, stable in 44%, unstable in 51%, and cardiac failure, 7%. Graft dysfunction was the cause in 94.5% of cases with progression of atheroma of the native coronary vessels in only 5.6% of cases. At reoperation 389 bypass procedures were performed (venous 39.5%, arterial 60.5%) (2.1 +/- 0.6 per patient) with 10 associated procedures (3 mitral valvuloplasties, 2 left ventricular aneurysmectomy, 3 aortic valve replacements, 1 replacement of the ascending aorta, 1 carotid endarteriectomy). The operative mortality was 10.9%. The causes of the 20 deaths were myocardial infarction (7), left ventricular failure (8), arrhythmias (2), mediastinitis (1) and multi-organ failure (2). The risk factors for death were: the date of surgery (19% before 1991 and 8% after: p = 0.03), age (18% after 60 years, 2% before: p = 0.015), the interval between the surgical procedures (33% after 15 years, p = 0.02), anterograde cardioplegic injection alone (15% versus 4.5% when mixed antero and retrograde perfusion was used: p = 0.02). The morbidity was 28% (52/184 patients); 132 patients (72%) had uncomplicated postoperative courses. The incidence of repeat coronary artery surgery is in constant progression. Improved medico-surgical management should continue to reduce the mortality which is still high.