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Biomedical subjects

M I Turina

Publications and source records attributed to M I Turina.

At least 37 records · Page 2Linked to original sources
PubMed2001

Modification of surgical aortoatrial shunts for inaccessible bleeding in aortic surgery -- modification of the Cabrol-shunt technique.

Bleeding after complex ascending aortic, aortic root or transverse arch surgery which is inaccessible or difficult to control may present a major problem. Here, we describe a modified Cabrol-shunt technique using complete mediastinal coverage with decompression into the innominate vein where the classical technique is not suitable. The long-term fate of the classical aortoatrial and modified mediastinal to innominate shunts has been analyzed to assess their potential complications.

Aortic Aneurysm, Thoracic↗
PubMed2001

Technical considerations in the repair of combined aortic arch and diaphragm rupture after blunt trauma.

Rupture of the aortic arch and laceration of the diaphragm after blunt trauma are two serious lesions that are difficult to manage. (1,2) We repaired both lesions in a patient with an anterior approach (i.e., a median sternotomy and a superior median laparotomy). The repair, carried out during extracorporeal circulation, turned out to be relatively easy to perform. The potential dangers associated with the use of cardiopulmonary bypass after blunt trauma must be acknowledged. In selected cases, however, when no strong contraindications to the administration of anticoagulation exist, the anterior approach and the use of cardiopulmonary bypass offer an excellent exposure for the repair of both lesions.

Adult↗
PubMed2001

Combined resection and adjuvant therapy improves prognosis of sarcomas of the pulmonary trunk.

BACKGROUND: Diagnosis of pulmonary artery sarcoma is difficult and frequently delayed owing to the insidious, non-specific nature of the symptoms. We present our experience with surgery for this rare disease. METHODS: Between 1995 and 1998, four patients underwent surgery for pulmonary trunk sarcomas. They presented with similar symptoms and were initially treated for thromboembolic disease of the lung. Preoperative diagnosis was established using computer tomography and echocardiography. Postoperatively, two patients received radiotherapy and one combined radio-/chemotherapy. RESULTS: One patient underwent thrombendarteriectomy of the trunk with adjuvant radiotherapy and remains tumor-free after three years and one showed complete regression of metastases after chemotherapy and remains well after more than one year. The other two patients died within two months of surgery, one due to a tumor mass in the inferior caval vein and the other because of cerebral metastases. CONCLUSIONS: According to the literature, mean survival rate is 1.5 months without resection and 10 months with resection, with survival up to four years following combined resection and adjuvant therapy. Our findings are in agreement with this.

Adult↗
PubMed2000

HMG-CoA reductase inhibition improves endothelial cell function and inhibits smooth muscle cell proliferation in human saphenous veins.

OBJECTIVES: This study examined effects of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase inhibitor cerivastatin on human saphenous vein (SV), endothelial cells (EC) and smooth muscle cells (SMC). BACKGROUND: Venous bypass graft failure involves EC dysfunction and SMC proliferation. Substances that improve EC function and inhibit SMC proliferation would be of clinical relevance. METHODS: Both EC and SMC were isolated from SV. Endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production were analyzed by immunoblotting and porphyrinic microsensor. The SMC proliferation was assayed by 3H-thymidine incorporation. Protein kinases and cell cycle regulators were analyzed by immunoblotting. RESULTS: Cerivastatin (10(-9) to 10(-6) mol/liter) enhanced eNOS protein expression and NO release (about two-fold) in EC in response to Ca2+ ionophore (10(-6) mol/liter). This was fully abrogated by the HMG-CoA product mevanolate (2 x 10(-4) mol/liter). In SMC, platelet-derived growth factor (5 ng/ml) enhanced 3H-thymidine incorporation (298 +/- 23%, n = 4), activated cyclin-dependent kinase (Cdk2), phosphorylated Rb and down-regulated p27Kip1 (but not p21CiP1). Cerivastatin reduced the 3H-thymidine incorporation (164 +/- 11%, p < 0.01), inhibited Cdk2 activation and Rb phosphorylation, but did not prevent p27Kip1 down-regulation, nor p42mapk and p70S6K activation. Mevalonate abrogated the effects of cerivastatin on Cdk2 and Rb but only partially rescued the 3H-thymidine incorporation (from 164 +/- 11% to 211 +/- 13%, n = 4, p < 0.01). CONCLUSIONS: In humans, SVEC inhibition of HMG-CoA/mevalonate pathway contributes to the enhanced eNOS expression and NO release by cerivastatin, whereas in SMC, inhibition of this pathway only partially explains cerivastatin-induced cell growth arrest. Inhibition of mechanisms other than p42mapk and p70S6K or Cdk2 are also involved. These effects of cerivastatin could be important in treating venous bypass graft disease.

Cell Division↗
PubMed2000

Tissue endothelin-converting enzyme activity correlates with cardiovascular risk factors in coronary artery disease.

BACKGROUND: Endothelin-converting enzymes (ECEs) are the key enzymes in endothelin-1 (ET-1) generation. However, their pathophysiological role in patients with cardiovascular disease remains elusive. METHODS AND RESULTS: Vascular reactivity to big endothelin-1 (bigET-1; 10(-9) to 10(-7) mol/L) and ET-1 (10(-9) to 10(-7) mol/L) were examined in the internal mammary artery (IMA, n=33) and saphenous vein (SV, n=27) of patients with coronary artery disease with identified cardiovascular risk factors. Vascular ECE activity was determined by conversion of exogenously added bigET-1 to ET-1. Tissue contents of bigET-1 and ET-1 were measured by radioimmunoassay. In addition, the effects of LDL and oxidized LDL on ECE-1 protein levels were determined by Western blot analysis in human IMA endothelial cells. In the IMA, vascular ECE activity showed an inverse correlation with serum LDL levels (r=-0.76; P<0.01) and systolic and diastolic blood pressure and a positive correlation with fibrinogen (r=0.58; P<0.05). In the SV, fibrinogen was the only parameter to be correlated with vascular ECE activity. Vascular tissue content of bigET-1 was attenuated in the IMA of patients with hyperfibrinogenemia but increased in patients with elevated systolic blood pressure and increased serum LDL levels (P<0.05). Most interestingly, LDL and oxidized LDL downregulated ECE-1 protein levels in human IMA endothelial cells (P<0.05). CONCLUSIONS: These data demonstrate, for the first time, that vascular ECE activity is (1) inversely correlated with serum LDL levels and blood pressure and (2) positively associated with fibrinogen in human vascular tissue. Hence, ECE-1 activity may modulate cardiovascular risk in patients with coronary artery disease.

Aspartic Acid Endopeptidases↗
PubMed2000

Experience with postinfarction left ventricular free wall rupture.

BACKGROUND: Postinfarction rupture of the left ventricle is a rare event in which approach is not clearly standardised and outcome after repair is unknown. Our experience with this pathology was reviewed to analyze methods of repair and assess outcome beyond the patient's hospitalisation. METHODS: Five patients underwent surgical repair of a postinfarction ventricular rupture between 1990 and 1998. Electromechanical dissociation (3 patients) and sudden hypotension and bradycardia (2 patients) were clinical indicators of rupture. Four patients underwent repair with cardiopulmonary bypass and 1 patient without. Repair consisted of epicardial patching (2 patients), direct suture (1 patient), infarct-exclusion (1 patient), and debridement and patch closure (1 patient) of the rupture. Myocardial revascularization was performed in 3 patients and mitral valve repair in 1 patient. RESULTS: A satisfactory hemodynamic state was restored and bleeding was controlled in all patients. Two patients died postoperatively and another patient died 4 months after hospital discharge as a result of cardiac failure and/or sepsis. The other 2 patients are alive and in excellent condition 6 and 30 months respectively after repair. CONCLUSIONS: Postinfarction rupture of the left ventricle bears a high mortality, but survival with an excellent quality of life is possible after surgical repair.

Aged↗
PubMed2000

Surgical treatment of acquired left ventricular pseudoaneurysms.

BACKGROUND: We present a review of our experience with acquired pseudoaneurysms of the left ventricle in order to establish the risk of surgical repair. METHODS: Ten patients operated upon for a left ventricular pseudoaneurysm in our clinic between 1984 and 1999 were reviewed. The pseudoaneurysm, a complication of myocardial infarction (four acute and three chronic) or previous cardiac surgery (three chronic), was resected in all patients and the ventricular wall defect closed with direct sutures (five cases) or a patch (five cases). Coronary artery bypass graft was performed in 6 patients. RESULTS: Three patients died (postoperative mortality 30%) after repair of an acute postinfarction (2 patients) or a chronic postsurgical (1 patient) pseudoaneurysm. Three patients died during follow-up (median 4 years) of a carcinological (2 patients) or cardiac (1 patient) cause. Two years after repair, 5 patients were in New York Heart Association class I or II, and 1 patient was in class III. CONCLUSIONS: Repair of left ventricular pseudoaneurysms can be performed with acceptable results, although mortality is significant in acute myocardial infarction and redo operations. Propensity for fatal rupture, however, is higher than the surgical risk in acute pseudoaneurysms or in large or expanding chronic ones and warrants surgical repair. The best approach to small asymptomatic chronic pseudoaneurysm is unsettled.

Aged↗
PubMed2000

Temporary one-and-a-half ventricular repair to relieve lymphomatous obstruction of the pulmonary artery.

Mediastinal lymphoma may infiltrate the conoarterial junction of the heart and cause life-threatening compression of the pulmonary artery. Partial debulking of the tumor along the left pulmonary artery and creation of a cavopulmonary anastomosis on the right pulmonary artery restored satisfactory perfusion of the lungs and unloading of the right ventricle in a 19-year-old woman. Remission of the tumor after chemotherapy allowed subsequent takedown of the cavopulmonary anastomosis.

Adult↗
PubMed2000

Role of myocardial revascularization in postinfarction ventricular septal rupture.

BACKGROUND: Postinfarction ventricular septal rupture requires urgent closure. The role of systematic coronarography and coronary revascularization needs clarification. METHODS: Fifty-four patients who underwent patch closure of postinfarction ventricular septal defect were reviewed. A coronarography had been systematically and myocardial revascularization selectively (when significant coronary artery stenosis existed) performed. RESULTS: No patient died or deteriorated during coronarography. Twenty-six patients showed no coronary artery disease besides the infarct-related artery, and 28 had associated disease. Threatened myocardial territories were revascularized usually with venous grafts (mean number of distal anastomosis, 2.5). Operative mortality was 19% and 32% (p = 0.36) and late mortality 43% and 53% (p = 0.75) in patients without and in patients with associated coronary artery disease, respectively. Survival curve in both group was similar, at least up to 8 years after operation. CONCLUSIONS: Myocardial revascularization controlled the added risk of associated coronary artery disease in the postoperative period and in median term. A coronarography should be performed in all patients who can be stabilized hemodynamically and myocardial revascularization performed in case of significant stenosis.

Aged↗
PubMed2000

Reoperative surgery for degenerated aortic bioprostheses: predictors for emergency surgery and reoperative mortality.

OBJECTIVE: The long-term outcome of patients with aortic bioprosthetic valves could be improved by decreasing the reoperative mortality rate. METHODS: Predictors of emergency reoperation and reoperative mortality were identified retrospectively in 172 patients who had the first bioprosthetic aortic valve replacement between 1975 and 1988 (mean age 46+/-13 years) and were subjected to replacement of the degenerated bioprostheses between 1978 and 1997 (mean age 56+/-14 years). Emergency reoperation had to be performed in 31 patients (18%). RESULTS: The operative mortality was 5.2% (9/172), 22.6% for emergency (odds ratio 11.17; 95%-confidence limit 4.33-28.85) and 1.4% for elective replacement of the degenerated aortic bioprosthesis (P<0.0001; OR=20.3). Patients who died at reoperation had higher transvalvular gradients before the primary aortic valve replacement (P=0.007), received smaller bioprostheses at the first operation (P=0.03), had later recurrence of symptoms after the first aortic valve replacement (P=0.04), a higher pre-reoperative New York Heart Association (NYHA) class (P=0.02), and a higher incidence of coronary artery disease (P=0.001) and pulmonary artery hypertension (P=0.009). Endocarditis before the primary aortic valve replacement (P=0.004), postoperative pneumonia at the first operation (P=0.005), pulmonary hypertension (P=0.0004) acquired during the interval, later recurrence of symptoms (P=0.04) after the first operation, a lower ejection fraction at the time of reoperation (P=0.03) and acute onset of bioprosthetic regurgitation (P=0.00002) were predictors for emergency surgery. Higher transvalvular gradients at the primary aortic valve replacement (P=0. 006), coronary artery disease (P=0.003) acquired during the interval, the need for concomitant coronary artery revascularization (P=0. 001), sex (P=0.02) and size (P=0.05) and type of the bioprostheses used (P=0.007) were incremental predictors for reoperative mortality which were independent of emergency surgery. CONCLUSIONS: Elective replacement of failed aortic bioprostheses is safe. Patients undergoing emergency reoperation have a considerably higher mortality. They can be identified by a history of native aortic valve endocarditis, higher transvalvular gradients at primary aortic valve replacement, smaller bioprostheses, and pulmonary hypertension or coronary artery disease acquired during the interval. A failing bioprosthesis must be replaced at its first sign of dysfunction.

Aortic Valve↗