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Biomedical subjects

B Jegier

Publications and source records attributed to B Jegier.

6 recordsLinked to original sources
PubMed2000

Activation of blood platelets after percutaneous transluminal coronary angioplasty and coronary artery bypass graft surgery.

We have evaluated the activation of platelets in blood samples taken from patients with stable angina undergoing balloon angioplasty (percutaneous transluminal coronary angioplasty [PTCA]) (n=11) or coronary artery bypass grafting (CABG) under hypothermic (n=11) or normothermic conditions (n=11). We have found that surface expression of P-selectin on platelets in whole blood from PTCA patients upon thrombin treatment was significantly reduced, as compared with control platelets from healthy subjects. This effect was partially reversed when platelets washed from the same blood sample were used, but even then P-selectin expression was significantly lower in PTCA patients than it was in control subjects. There was a significant increase in basal expression of P-selectin in blood platelets taken from patients who underwent CABG under normothermic conditions (warm blood cardioplegia) as opposed to hypothermic patients (cold crystalloid cardioplegia). These platelets retain the ability to respond to agonists, although to a much lower extent than do those from healthy control donors. The surface exposure of P-selectin on resting and thrombin-treated platelets isolated from CABG surgery patients was not different from that of the control platelets. The adhesion to fibrinogen of resting and thrombin-treated platelets from patients who underwent balloon angioplasty as well as CABG surgery under normothermic and hypothermic conditions was significantly reduced when compared with the fibrinogen of the control platelets. These results suggest that the function of platelet fibrinogen receptor is impaired in patients with stable angina pectoris and that PTCA and CABG surgery activates platelets.

Adult↗
PubMed1997

[Myocardial revascularization for sudden cardiac death in patients after previous coronary angioplasty].

UNLABELLED: PTCA was introduced into our hospital in June 1991. Since then till the end of 1996 emergency CABG operations were performed in fourteen patients. They were indicated because of acute myocardial ischaemia and hemodynamic deterioration that was the result of the dissection and occlusion of a coronary artery during angioplasty. There were 11 male and 3 female patients in this group aged 34 to 65 average 50 years. Twenty-three grafts were performed in total (18 saphenous, 5 using internal mammary artery), that is 1.6 graft per patient. A female patient died of myocardial infarction on the first postoperative day. All other patients survived and are under outpatient clinic's care. Over the analysed 6 years' period of time 1079 PTCAs were performed. The low rate of the unsuccessful procedures (1.3%) that required the emergency CABG is noteworthy. Since 1995, when the implantation of stents was introduced into our hospital, there were only 2 such procedures (0.4% of all PTCAs). CONCLUSIONS: The CABG operation performed shortly after a dissection and occlusion of the coronary artery underwent angioplasty usually prevents myocardial infarction and saves the patient's live. The introduction of implantation of the stents significantly diminished a number of patients who required an emergency CABG operation.

Adult↗
PubMed1992

Beyond cold cardioplegia.

One hundred fifteen consecutive patients were operated on for myocardial revascularization or valvular disease or both with continuous antegrade and retrograde aerobic warm (37 degrees C) blood cardioplegia. Mean cross-clamp time was 56.3 +/- 21 minutes (+/- standard deviation). Mean reperfusion time was 18.4 +/- 11.8 minutes (range, 5 to 81 minutes). Five patients (4.3%) died, and 15 (13%) needed inotropic support. Two (1.7%) required intraaortic balloon support. Two patients (1.7%) had evidence of perioperative myocardial infarction, and 98 (85%) returned spontaneously to normal sinus rhythm. Sixteen patients had a cross-clamp time greater than 80 minutes. All 16 of them had an uneventful postoperative course except for 1 patient who required inotropic drugs. This method of myocardial protection is now used for all open heart procedures in our institution.

Adult↗
PubMed1990

[Surgical mitral valvuloplasty in the treatment of mitral valve diseases].

Mitral valve repair surgery, in presence of a pure mitral leakage or one associated to a stenosis, is not only possible but has been well codified for a decade. According to damage, there are two methods of operation: valvular mobilization surgery and valvular motion amplitude reduction surgery. They are usually associated to annuloplasty with a Carpentier prosthetic ring. The incidence of late mortality is of 0.6 p. 100 pt/yr, that is to say 91.7 p. 100 at 13 years. This late survival rate is about 20 p. 100 better than for a valvular replacement. Reoperations rate is 1.6 p. 100 pt/yr. The incidence of thromboembolic event occurrence is low: 0.5 p. 100 pt/yr. The ideal indications for mitral valve repair are represented by damage of prolapse from a degenerative origin for which results are better and more constant. For rheumatic damage, the valvular repair indication depend on the valvular tissue elasticity and area. The presence of calcification and extensive fibrosis remain on principle counter-indications.

Adult↗
PubMed1990

Mitral valve repair: results and the decision-making process in reconstruction. Report of 275 cases.

From January 1975 to June 1988, 275 patients underwent mitral valve repair for mitral regurgitation, pure (148 patients) or associated with mitral stenosis (127 patients). Patients with pure mitral stenosis were excluded from this study. The cause of mitral regurgitation was rheumatic in 180 patients (aged 28.6 +/- 1.2 years, mean +/- standard error of the mean) and degenerative in 84 patients (aged 54.7 +/- 1.5 years). Fifty-nine percent of the patients were in New York Heart Association classes III and IV before the operation. Intraoperative assessment of the mitral valve led us to identify four major mechanisms of mitral regurgitation: (1) restriction of leaflet motion by fibrosis (group I, 63 patients); (2) enhancement of leaflet motion by leaflet and chordal extension and prolapse (group II, 139 patients), (3) combination of both (group III, 64 patients); and (4) isolated dilatation of the anulus (group IV, 10 patients). One hundred sixty-one patients had isolated mitral disease and 114 had associated aortic or tricuspid valve disease, or both. The hospital mortality rate was 4.0%. Follow-up was 96% complete and totaled 1247.47 patient-years. At 13 years' follow-up, the survival rate was 93.0% +/- 6.8% in group I, 90.0% +/- 6.0% in group II, and 96.6% +/- 4.6% in group III. Freedom from reoperation was 78.1% +/- 21.0%, 83.2% +/- 18.9%, and 79.6% +/- 16.2%, respectively. Freedom from embolism was 94.7% for the whole series. In patients with isolated mitral valve repair, the cumulative morbidity was significantly higher in groups I (6.3 +/- 2.0%/pt-yr) and III 6.3% +/- 1.7%/pt-yr) than in group II (2.5% +/- 0.9%/pt-yr, p less than 0.05). Multivariate analysis identified age and associated tricuspid valve disease as significant predictors of reoperation (p less than 0.01 for both factors). These results suggest that conservative surgery should be used with caution in group I and III patients. In contrast, indications for mitral valve repair should be extended in group II patients. This observation has important clinical implications since, in Western countries, valve prolapse tends to be a major cause of mitral regurgitation.

Actuarial Analysis↗