Biomedical subjects

K G Kolocassides

Publications and source records attributed to K G Kolocassides.

6 recordsLinked to original sources

PubMed2006

Increased C reactive protein and cardiac enzyme levels after coronary stent implantation. Is there protection by remote ischaemic preconditioning?

AIM: To investigate whether remote ischaemic preconditioning (RIPC) can attenuate the inflammatory response and enzyme leakage that can occur after uncomplicated routine percutaneous coronary intervention (PCI). METHODS: 41 consecutive normotensive patients with stable angina and single-vessel disease were assigned to be exposed to RIPC (n = 20) or not (control group; n = 21) before elective PCI with stent implantation. RIPC was induced by three cycles of 5-min ischaemia-reperfusion of both upper limbs (inflation/deflation of blood pressure cuff). C reactive protein (CRP), creatine phosphokinase (CK), CK cardiac isoenzyme (CK-MB) and troponin I (TNI) were serially measured for 48 h. RESULTS: No difference in baseline values was observed between the groups. The CRP rose significantly (p<0.001) and at 48 h was similarly increased (>fourfold) in both groups (15.7 (2.6) v 14.0 (3.3) mg/l, RIPC v control; p = NS). However, sub-group analysis on the basis of statin use showed that the highest rise was in the group of patients with RIPC not taking statins and was significantly greater than in patients with RIPC taking statins (23.8 (3.71) v 11.4 (3.0) mg/l, respectively, p<0.01). Both CK-MB and TNI leakage were raised (slightly but significantly) after PCI in controls at 24 h compared with baseline values. However, this small rise was significantly worse after RIPC (CK-MB, 1.33 (0.27) v 3.57 (0.97) ng/ml, p<0.01; TNI, 0.255 (0.059) v 0.804 (0.232) ng/ml, p<0.05, respectively at 24 h). The increase was more marked in the RIPC subgroup not taking statins. CONCLUSIONS: RIPC does not reduce, but exacerbates, the enzyme and TNI release from the heart after single-vessel angioplasty with stent. Furthermore, the increased circulating CRP remains raised. It seems that there is an enhanced inflammatory response after RIPC in the absence of statin treatment.

Angina Pectoris↗

PubMed1996

Dichotomy of ischemic preconditioning: improved postischemic contractile function despite intensification of ischemic contracture.

BACKGROUND: Acceleration of ischemic contracture is conventionally accepted as a predictor of poor postischemic function. Hence, protective interventions such as cardioplegia delay ischemic contracture and improve postischemic contractile recovery. We compared the effect of ischemic preconditioning and cardioplegia (alone and in combination) on ischemic contracture and postischemic contractile recovery. METHODS AND RESULTS: Isolated rat hearts were aerobically perfused with blood for 20 minutes before being subjected to zero-flow normothermic global ischemia for 35 minutes and reperfusion for 40 minutes. Hearts were perfused at a constant pressure for 60 mm Hg and were paced at 360 beats per minute. Left ventricular developed pressure and ischemic contracture were assessed with an intraventricular balloon. Four groups (n=8 hearts per group) were studied: control hearts with 35 minutes of unprotected ischemia, hearts preconditioned with one cycle of 3 minutes of ischemia plus 3 minutes of reperfusion before 35 minutes of ischemia, hearts subjected to cardioplegia with St Thomas' solution infused for 1 minute before 35 minutes of ischemia, and hearts subjected to preconditioning plus cardioplegia before 35 minutes of ischemia. After 40 minutes of reperfusion, each intervention produced a similar improvement in postischemic left ventricular development pressure (expressed as a percentage of its preischemic value: preconditioning, 44 +/- 2%; cardioplegia, 53 +/- 3%; preconditioning plus cardioplegia, 54 +/- 4% and control, 26 +/- 6%, P<.05). However, preconditioning accelerated whereas cardioplegia delayed ischemic contracture; preconditioning plus cardioplegia gave an intermediate result. Thus, times to 75% contracture were as follows: control, 14.3 +/- 0.4 minutes; preconditioning, 6.2 +/- 0.3 minutes; cardioplegia 23.9 +/- 0.8 minutes; and preconditioning plus cardioplegia 15.4 +/- 2.4 minutes (P<.05 preconditioning and cardioplegia versus control). In additional experiments, using blood- and crystalloid-perfused hearts, we describe the relationship between the number of preconditioning cycles and ischemic contracture. CONCLUSIONS: Although preconditioning accelerates, cardioplegia delays, and preconditioning plus cardioplegia has little effect on ischemic contracture, each affords similar protection of postischemic contractile function. These results question the utility of ischemic contracture as a predictor of the protective efficacy of anti-ischemic interventions. They also suggest that preconditioning and cardioplegia may act through very different mechanisms.

Animals↗

PubMed1996

Ischemic preconditioning, cardioplegia or both? Differing approaches to myocardial and vascular protection.

We compared the anti-ischemic efficacy of cardioplegia and ischemic preconditioning and whether their effects are additive for both myocyte and vascular protection. Isolated blood-perfused rat hearts were subjected to zero flow global ischemia (37 degrees C) for 30 min and reperfusion for 40 min. Left ventricular developed pressure (LVDP) was assessed with an intraventricular balloon. Coronary flow and vascular reactivity (percentage change in coronary vascular resistance, CVR) to 5-hydroxytryptamine (5HT; 0.0215 mmol/l) and sodium nitroprusside (SNP; 0.0160 mmol/l) were measured. Study 1; "dose" effect of preconditioning in four groups (n = 6/group): (i) controls (unprotected ischemia) and (ii, iii and iv) 1, 2, or 3 cycles of preconditioning (3 min ischemia + 3 min reperfusion) prior to ischemia. LVDP recovery in controls was 31 +/- 9%; preconditioning by 1, 2 or 3 cycles afforded significant (P < 0.05) improvements (58 +/- 6%, 54 +/- 3% and 54 +/- 5%, respectively). Overall, the pre-ischemic change of CVR to SNP was -28 +/- 1%. The post-ischemic response in controls was -4 +/- 7% (P < 0.05); with 1, 2, or 3 cycles of preconditioning the values were -23 +/- 4%, -24 +/- 5%, and -26 +/- 3%, respectively (P < 0.05 v controls). With 5HT the overall pre-ischemic change in CVR was -18 +/- 2%; after ischemia a vasoconstrictor response was seen in all groups. Study 2: the effect of preconditioning added to cardioplegia with four groups subjected to 35 min ischemia (n = 8/group): (i) controls, (ii) one cycle of preconditioning (3 min ischemia + 3 min reperfusion), (iii) cardioplegia with St Thomas' solution immediately prior to ischemia, and (iv) preconditioning followed by cardioplegia prior to ischemia. The recoveries of LVDP were 26 +/- 6%, 44 +/- 2%, 53 +/- 3% and 54 +/- 4%, respectively (P < 0.05 all interventions v controls). Post-ischemic CVR increased greatly in controls (+ 167 +/- 60% of its pre-ischemic value) but was little changed in groups (ii), (iii), and (iv) (+ 11 +/- 7%, + 27 +/- 10% and -2 +/- 6% respectively; P < 0.05 v controls). The post-ischemic change in CVR to SNP was protected by all interventions (-21 +/- 1%, -21 +/- 1% and -22 +/- 1% v -14 +/- 2% in controls; P < 0.05). Again, the post-ischemic response to 5HT was vasoconstriction in all groups. In conclusion, preconditioning and cardioplegia alone afford similar and substantial protection of post-ischemic contractile and vascular functions. In general, the combination of the two techniques afforded no significant additional protection.

Animals↗

PubMed1996

Paradoxical effect of ischemic preconditioning on ischemic contracture? NMR studies of energy metabolism and intracellular pH in the rat heart.

Using the blood-perfused rat heart, we have previously shown that although ischemic preconditioning (PC) and cardioplegia (CP) afforded similar protection against post-ischemic contractile dysfunction this effect was not additive even though PC accelerated whereas CP delayed ischemic contracture. Using NMR we examined the effects of these interventions on pHi and ATP metabolism during global ischemia. Isolated rat hearts (n = 6/group) with an intraventricular balloon were aerobically perfused with buffer, subjected to zero flow ischemia (37 degrees C) for 35 min and reperfused for 40 min. The groups were: (1) controls without protection, (2) PC (2 cycles), and (3) St Thomas' cardioplegia, prior to test ischemia. PC accelerated whereas CP delayed ischemic contracture (P < 0.05 v controls). Yet, after 40 min reperfusion, both interventions produced substantial improvements in the recovery of LVDP (P < 0.05 v controls). During 35 min ischemia, the decline of ATP was delayed by CP but accelerated by PC (P < 0.05 v controls). The pHi fell steeply in controls to a plateau of 5.9 after 14 min ischemia. PC had no effect on the rate of fall of pHi but reduced its extent (P < 0.05). CP delayed the onset of the decline in pHi (P < 0.05) but, once initiated, there was no effect on the rate of decline to a plateau. Thus, despite protecting post-ischemic contractile function, PC accelerated ischemic contracture and the depletion of ATP, but substantially reduced intracellular acidosis. In contrast, CP slowed ischemic contracture and the depletion of ATP; it also delayed the onset of acidosis.

Animals↗

PubMed1995

Preconditioning accelerates contracture and ATP depletion in blood-perfused rat hearts.

We investigated the effect of preconditioning on the ischemia-induced depletion of ATP in the blood-perfused rat heart. Isolated hearts (n = 5/group) were aerobically perfused with whole blood from a support rat and subjected to zero-flow global ischemia (37 degrees C) for periods up to 35 min. Frozen hearts were taken for metabolic analysis. Ischemic contracture was assessed with an isovolumic intraventricular balloon. The study groups were 1) control (C) with unprotected ischemia, 2) preconditioning (PC; 2 cycles of 3-min ischemia/3-min reperfusion), and 3) cardioplegia (CP; St. Thomas') before ischemia. Preconditioning accelerated, whereas cardioplegia delayed, ischemic contracture (time to peak contracture: PC = 8.1 +/- 0.3 and CP = 25.1 +/- 0.2 min vs. C = 15.6 +/- 0.3 min, P < 0.05). The ischemia-induced decline in ATP was delayed by cardioplegia but accelerated by preconditioning (P < 0.05). In a parallel study, preconditioning and cardioplegia protected postischemic contractile function to a similar extent. Thus, in the blood-perfused rat heart, preconditioning accelerated ischemic contracture and depletion of ATP. In contrast, cardioplegia slowed ischemic contracture and ATP depletion.

Adenosine Triphosphate↗

PubMed1994

Ischemic preconditioning, cardioplegia or both?

UNLABELLED: With the continuing search for superior methods of myocardial protection, we compared the protective efficacy of ischemic preconditioning with that of St Thomas' cardioplegia, alone and in combination, against vascular and myocyte injury during ischemia and reperfusion. Rat hearts were perfused with blood for 20 min, subjected to zero flow global ischemia for 35 min (37 degrees C) and reperfused for 40 min. Left ventricular developed pressure (LVDP) was assessed with an intraventricular balloon. Coronary flow was measured at a constant perfusion pressure. Study groups (n = 8 hearts/group) were: (i) controls (unprotected ischemia), (ii) preconditioning (PC, 3 min ischemia + 3 min reperfusion), (iii) cardioplegia (CP, infused for 1 min before ischemia) and (iv) PC + CP. The post-ischemic recoveries of LVDP were 26 +/- 6, 44 +/- 2, 53 +/- 3 and 54 +/- 4% respectively (P < 0.05 all others v control). Post-ischemic coronary vascular resistance increased in controls by 167 +/- 60% from its pre-ischemic baseline value but was well protected with PC, CP and PC + CP (changing by only + 11 +/- 7, + 27 +/- 10 and -2 +/- 6% respectively). CONCLUSIONS: Preconditioning and cardioplegia alone afford similar and substantial protection of post-ischemic contractile and vascular function. The combination of the two affords no significant additional protection.

Animals↗