Key result
Carvedilol pretreatment before CABG was associated with a significantly lower increase in creatine phosphokinase activity at the end of the procedure compared to no pretreatment (338 vs 644 U/L; p<0.05).
Why the study?
Does carvedilol pretreatment reduce biochemical damage (CPK levels) in male patients undergoing elective CABG?
Cohort (n=45)
Does carvedilol pretreatment reduce biochemical damage (CPK levels) in male patients undergoing elective CABG?
Absolute Event Rate: 338% vs 644%
p-value: p=<0.05
Carvedilol pretreatment before CABG may protect against reperfusion injury, potentially mediated by elevated serum uric acid levels.
Hypothesis-generating for carvedilol cardioprotection in elective CABG; prospective randomized trials needed before clinical adoption.
OBJECTIVES: Peroxynitrite is species claimed to propagate ischemia/reperfusion damage. In this report levels of serum uric acid (UA), a peroxynitrite scavenger, are compared with creatine phosphokinase (CPK) in male patients before and after open-heart surgery in order to asses if increased levels of UA may protect heart from biochemical damage induced by peroxynitrite during the coronary by-pass grafting (CABG) intervention. METHODS: 45 male patients (16 carvedilol pretreated (6.25 mg/ daily, during 6 weeks before surgery, mean age 55.3+/-1.7 years, range 50-71) and 29 patients without carvedilol pretreatment (mean age 58.3+/-1.4 years, range 47-73) underwent elective CABG were examined. Study inclusion criteria were CABG performed on two and more coronary-vessels with aortic cross-clamp during 30-40 minutes. For assessment of patients objective health status before operations EuroSCORE were used. Serum uric acid (UA) levels and creatine phosphokinase (CPK) were measured spectrophotometricaly by using a quantitative enzymatic assay. RESULTS: Carvedilol pretreated patients had higher amount of serum UA (p<0.05) comparing to non-treated patients. During the surgical procedure patients are subjected to temporary ischemia due to transfer from corporeal to extracorporeal circulation. In this period of time the amount of UA decreased in carvedilol pretreated group (406+/-46 (tl) vs. 300+/-22 mmol/L (t2)) to the level of non-treated patients (328+/-14 (t1) vs. 322+18 mmol/L. Carvedilol pretreated patients and non-treated patients had the same level of CPK at the beginning of the surgical procedure (tl) (78+/-6 vs. 83+13 U/L) but lower increase (p<0.05) in CPK activity in carvedilol pretreated patients in respect to non-treated patients (338+46 vs. 644+103 U/L) at the end of procedure (t2). Such results suggest that open heart surgery led to elevated CPK levels, but this effect was less pronounced in patients with higher level of UA. CONCLUSIONS: Our results suggest possible role of UA in the protection from reperfusion injury. Increase of UA before surgery may be beneficial factor during CABG procedure in patients treated with carvedilol by decreasing level of peroxynitrite as one of molecular causes of reperfusion injury. Our results showed influence of UA on CPK levels at the end of surgical procedure, indicating that increased levels of UA may protect heart from biochemical damage induced by peroxynitrite during the CABG intervention.
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Nikolić‐Kokić et al. (2006) conducted a cohort in Elective coronary artery bypass grafting (CABG) (n=45). Carvedilol pretreatment vs. No carvedilol pretreatment was evaluated on Creatine phosphokinase (CPK) activity at the end of procedure (p=<0.05). Carvedilol pretreatment before CABG was associated with a significantly lower increase in creatine phosphokinase activity at the end of the procedure compared to no pretreatment (338 vs 644 U/L; p<0.05).
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