Yliopistologo Lääkäri Zhong-Kai Wun kirurgian alaan kuuluva väitöskirja

Ishaemic preconditioning in coronary artery bypass surgery. The protective effect of ischaemic preconditioning on myocardial ischaemia-reperfusion injury

tarkastetaan 12.1.2001 klo 12 Finn-Medin auditoriossa, osoitteessa Lenkkeilijäntie 6.

Vastaväittäjänä on professori Jarle Vaage  (Karolinska hospital). Kustoksena toimii professori Markku Järvinen.

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Wu on syntynyt Guangdongissa Kiinassa 13.4.1967. Wu on suorittanut lääkärin perustutkinnon Sun Yat-sen yliopiston lääketieteellisessä tiedekunnassa vuonna 1988 ja jatkaa opintojaan siellä edelleen.

Wun väitöskirja ilmestyy sarjassa Acta Universitatis Tamperensis; 787, Tampereen yliopisto, Tampere 2000. ISBN 951-44-4980-0 , ISSN 1455-1616. Ilmestyy myös sähköisenä sarjassa Acta Electronica Universitatis Tamperensis; 78, Tampereen yliopisto 2000. ISBN 951-44-4981-9 , ISSN 1456-954X, http://acta.uta.fi.

Väitöskirjan tilausosoite: Virtuaalinen kirjakauppa Granum, http://granum.uta.fi, tai Tampereen yliopiston julkaisujen myynti, PL 617, 33101 Tampere, puh. (03) 215 6055, e-mail: taju@uta.fi.

Lisätietoja: Zhong-Kai Wu, 050-327 3988, (03) 247 5756 (työ), e-mail wuzhongkai@hotmail.com

TIIVISTELMÄ

Ischaemic preconditioning (IP) has been proved to be the most effective mode of endogenous myocardial protection. However, studies of IP effects in cardiac surgery are rare and controversial. Myocardial protection in severely stenosed three-vessel disease is unsatisfactory in patients with RCA critical stenosis or occlusion. Thus consideration of strategies employing IP in myocardial protection against ischaemia-reperfusion injury appears necessary and useful.


Eighty consecutive patients with stable and unstable angina with 3 main coronary stenosis admitted for a CABG operation were randomised into IP and control groups, each with 20 cases. In the IP group two cycles of 2-minute ischaemia followed by 3-minute reperfusion were induced before cross-clamping. Left and right ventricular haemodynamic data were collected till the 1st POD. RVEF was measured by thermodilution technique using a fast-response volumetric thermister-tipped pulmonary artery catheter. Sinus and arterial samples were collected to measure CTnI, CK-MB, myoglobin and lactate. Sinus FR content was measured directly using PBN-spin spectroscopy in stable patients.


There was a larger amount of FR generated after the operation, which was associated with haemodynamic depression. IP improved haemodynamic functional recovery, manifested in better postoperative CI (p = 0.013) and RVEF (p = 0.012). IP did not protect against the myocyte necrosis and change the FR values in stable patients. The release of CTnI after the operation was significantly lower in unstable angina patients than in stable controls (p = 0.006). There was better recovery of CI (p = 0.005) and a tendency to better RVEF (p = 0.097) in the unstable patients experiencing antecedent angina within 48 hours than in stable controls. There was no difference in CI and RVEF between the unstable patients experiencing antecedent angina within 48-72 hours and stable controls. The haemodynamics and biochemical markers in the IP and control groups were similar in the unstable patients experienced antecedent angina within 48 hours. The RVEF recovery was significantly better in unstable IP patients experiencing antecedent angina within 48-72 hours (p = 0.030). CI after the operation was associated with myocardial FR generation during the IP protocol (p = 0.035), and negatively associated with age and lactate production during the protocol in IP patients (p = 0.002 and 0.026).


In patients with three-vessel coronary artery stenosis undergoing a CABG operation, IP has a protective effect on both left and right ventricular haemodynamic functional recovery. With recent unstable angina the myocardium has already been preconditioned before the operation. The IP protocol applied did not induce additional protection to the myocardium already preconditioned by antecedent unstable angina. However, the waned IP effect in unstable patients can be regained by the applied IP. The IP protective effects diminish in senescent patients. Lactate seems not to be involved in the IP triggering process. Whether FR acting as an IP trigger is an epiphenomenon or a real mechanism needs further studies.


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