Ziad Mansour

Risk factors for early mortality and morbidity after pneumonectomy: a reappraisal.

BACKGROUND Pneumonectomy remains a high-risk procedure. Comprehensive patient selection should be based on analysis of proven risk factors. METHODS The records of 323 pneumonectomy patients were retrospectively reviewed. Multiple demographic data were collected. End points were operative mortality at 30 and at 90 days, major procedurally related complications, and cardiovascular events. Univariate and multivariate statistical analyses were performed. RESULTS Smoking habits, chronic obstructive pulmonary disease (COPD) status, induction chemotherapy status, diabetes, and obesity had no statistical influence on short-term outcomes. After right pneumonectomy, 30-day mortality (p = 0.045) and the incidence of bronchopleural fistulas (p = 0.009) were increased. Multivariate analysis for postoperative bronchopleural fistulas discovered that right pneumonectomies are the sole risk factor (p = 0.015). Univariate analysis for postoperative atrial fibrillation showed that male gender, age 70 and older, hypertension, and dyslipidemia are risk factors. Multivariate analysis found no definite risk factor. Patients with coronary artery disease had more postoperative cardiovascular events (p = 0.003). Among patients free of coronary artery disease, COPD led to an increased 90-day mortality rate (p = 0.028). CONCLUSIONS Patients with right pneumonectomies are at increased risk. Postoperative cardiovascular events are more frequent in coronary artery disease patients. COPD is a risk factor in patients free of coronary disease.

Persistent N2 Disease After Induction Therapy Does Not Jeopardize Early and Medium Term Outcomes of Pneumonectomy

BACKGROUND Operative management of patients with persistent N2 disease after induction therapy is still debated. METHODS One hundred fifty-three consecutive patients underwent pneumonectomy from January 1999 until July 2005; 28 patients (18.3%) had persistent N2 disease after induction therapy (group 1), 32 patients (20.9%) had pathologic stage N0 or N1 after induction therapy (group 2), and 93 patients (60.8%) with pathologic N2 disease underwent immediate surgery (group 3). Short-term end points were operative mortality at 30 and 90 days and major complications. Long-term end points were 5-year survival and disease-free survival rates. RESULTS Demographics of the three groups were similar (age, sex, side of operation, type of chemotherapy, smoking status, and comorbidity such as coronary artery disease, diabetes, and chronic obstructive pulmonary disease). Thirty-day postoperative mortality was 10.7% in group 1, 3.1% in group 2 (p = 0.257), and 4.3% in group 3 (p = 0.201); 90-day postoperative mortality was 10.7% in group 1, 12.5% in group 2 (p = 0.577), and 9.7% in group 3 (p = 0.558). Incidence of major postoperative complications was similar. Five-year survival rate was 32.2% (median, 28 months; 95% confidence interval, 7 to 43) in group 1, 34.8% (median, 27 months; 95% confidence interval, 7 to 47) in group 2 (p = 0.685), and 12.4% (median, 15 months; 95% confidence interval, 11 to 19) in group 3 (p = 0.127). No statistical difference was found in terms of 5-year event-free survival, or regarding the side of pneumonectomy. CONCLUSIONS Our results suggest that pneumonectomy is justified in patients with persistent N2 disease after induction chemotherapy.

Remote and local ischemic postconditioning further impaired skeletal muscle mitochondrial function after ischemia-reperfusion

OBJECTIVE Muscular injuries contribute to perioperative and long-term morbidity after vascular surgery in humans. We determined whether local and remote ischemic postconditioning might similarly decrease muscle mitochondrial dysfunction through reduced oxidative stress. METHODS Eighteen male Black-6 mice were divided in three groups: (1) sham mice had no ischemia (sham), (2) ischemia-reperfusion (IR) mice underwent 2-hour tourniquet-induced ischemia on both hind limbs, followed by 2-hour reperfusion, and (3) postconditioning (PoC) mice underwent four bouts of 30-second reperfusion and 30-second ischemia at the onset of reperfusion on the right limb; thus, the right limb underwent local PoC and left limb underwent remote PoC (rPoC). Maximal oxidative capacity (V(max)) of the gastrocnemius muscle mitochondrial respiratory chain was measured. Oxidative stress was evaluated by dihydroethidium staining. Expressions of genes involved in antioxidant defense (superoxide dismutase [SOD1], SOD2, glutathione peroxidase [GPx]), apoptosis (Bax, BclII), and inflammation (interleukin-6) were determined by quantitative real-time polymerase chain reaction. Muscle inflammation was determined using immunohistochemistry. RESULTS IR reduced V(max) (8.5 ± 2.2 vs 10.2 ± 1.8 μmol O(2)/min/g dry weight; P = .034), and increased dihydroethidium staining (134.8%; P = .039). IR decreased GPx expression (-47.9%; P = .048) and increased the proapoptotic marker Bax (255.5%; P = .020). Local PoC and rPoC further increased these deleterious effects. PoC decreased V(max) to 4.4 ± 1.4 μmol O(2)/min/g dry weight (sham vs PoC, -56.9% [P < .001]; IR vs PoC, -48.2% [P < .001]). rPoC similarly reduced V(max) to 5.1 ± 1.9 μmol O(2)/min/g dry weight (sham vs PoC, -50.0% [P < .001]; IR vs PoC, -40.0% [P = .001]). Dihydroethidium staining was further increased by PoC (207.2%; P = .002) and rPoC (305.4%; P < .001) compared with sham and was associated with macrophage infiltration. Local PoC increased SOD1, SOD2, and the antiapoptotic Bcl-2, and rPoC increased Bax (391.6%; P < .001) and the Bax/BclII ratio (621.7%; P < .001). CONCLUSIONS Local and remote ischemic postconditioning further increased injury by enhancing mitochondrial dysfunction, oxidative stress production, and inflammation. Caution should be applied when considering ischemic postconditioning in vascular surgery.

Right Atrial Metastasis From Hepatocellular Carcinoma

Abstract  A 65‐year‐old patient with a past medical history of hypertension, alcoholism, micronodular cirrhosis, and coronary artery bypass grafting 10 years ago developed a hepatocellular carcinoma, treated by chemoembolization. One month after treatment, thoracoabdominal CT scan showed no residual hepatic tumor, but tumoral aspect in the right atrium with extension into the inferior vena cava. The patient being asymptomatic, cardiac ultrasound confirmed the presence of a free, mobile, pediculated tumor in the right atrium. Surgical exploration found a well‐circumscribed mass, attached to the atrial wall by a 1.5‐cm diameter pedicle implanted near the inferior vena cava ostium, moving freely in the right atrial cavity. The tumor was easily resected by section of the pedicle and its surrounding parietal implantation zone. No complications occurred postoperatively, and the patient was discharged on the 10th postoperative day. Three years after, the patient is in good health and is asymptomatic; cardiac ultrasound showed no tumor recurrence.

Exclusive Low-Molecular-Weight Heparin as Bridging Anticoagulant After Mechanical Valve Replacement

BACKGROUND Unfractionated heparin has been the standard anticoagulant used immediately after mechanical heart valve replacement (MHVR). The purpose of this study was to assess a postoperative anticoagulation protocol with low-molecular-weight heparin (LMWH) immediately after MHVR without the use of unfractionated heparin or anti-factor Xa monitoring. METHODS We performed a prospective, single-center, observational study of 1,063 consecutive patients undergoing elective MHVR with postoperative LMWH anticoagulation treatment. The exclusion criteria were as follows: renal failure, intraaortic balloon counterpulsation, critical perioperative state, or a recent neurologic event. The postoperative anticoagulation protocol used subcutaneous enoxaparin as a bridging anticoagulant treatment beginning on the first postoperative day and continuing until vitamin K antagonist treatment was fully effective. Patients were followed for 6 weeks. The primary endpoints were the incidence of thromboembolic or major bleeding events. RESULTS Eleven (1%) thromboembolic events occurred. Ten of these events were transient or permanent strokes. Major bleeding events occurred in 44 patients (4.1%), 7 of which were observed before the enoxaparin treatment period. At the time of discharge, 570 patients (53.6%) were no longer receiving LMWH treatment due to achieving the target international normalized ratio. The mean length of hospital stay was 8.5 ± 2.9 days. There were no deaths during the 6-week follow-up period. CONCLUSIONS In our highly selected population, after MHVR, postoperative anticoagulation using LMWH is associated with a low rate of thromboembolic and major bleeding events. This large observational study demonstrates that the use of LMWH as an anticoagulant is effective and safe after MHVR.