Na+/H+-exchange inhibition and aprotinin administration: promising tools for myocardial protection during minimally invasive CABG

Hendrikx, Marc; Rega, Filip; Jamaer, Luc; Valkenborgh, T; Gutermann, H.; Mees, Urbain

doi:10.1016/s1010-7940(01)00639-x

Cited by 13 publications

(7 citation statements)

References 25 publications

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“…11 Alternatively, sample-size limitations do not exclude the possibility of this benefit occurring by chance alone. A mechanism for this possible effect is unclear, although animal models show that aprotinin reduces myocardial ischemia-reperfusion injury, [24][25][26] and ischemia-reperfusion injury is associated with mitochondrial dysfunction and subsequent atrial fibrillation in patients undergoing cardiac surgery. 27 Concurrently, reduction in platelet transfusion may have a beneficial impact on this parameter in patients undergoing cardiac surgery.…”

Section: Discussionmentioning

confidence: 99%

Aprotinin use in thoracic aortic surgery: Safety and outcomes

Sedrakyan

Sedrakyan³

et al. 2006

The Journal of Thoracic and Cardiovascular Surgery

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Section: Discussionmentioning

confidence: 99%

Aprotinin use in thoracic aortic surgery: Safety and outcomes

Sedrakyan

Sedrakyan³

et al. 2006

The Journal of Thoracic and Cardiovascular Surgery

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“…25 In preclinical studies, aprotinin improved postischemic cardiac function in dogs 26 and sheep. 27 Clinically, aprotinin lowered perioperative requirements for cardiac inotropic support 28 and attenuated serum creatine kinase MB, troponin T and lactate dehydrogenase concentrations at one and three days postbypass. 29 Rahman et al tested aprotinin-mediated pulmonary protection in a prospective, randomized trial in 20 patients undergoing cardiopulmonary bypass.…”

Section: Synergistic Organ Protection By Aprotinin and Leukofiltrationmentioning

confidence: 97%

Leukocyte filtration and aprotinin: synergistic anti-inflammatory protection

et al. 2004

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Cardiopulmonary bypass activates an array of cellular and humoral inflammatory mechanisms that culminate in diverse or organ-specific injury. A manifestation of inflammatory injury to the heart, atrial fibrillation ranks among the most frequent and potentially life-threatening postsurgical complications. Pulmonary manifestations of the inflammatory response are also of major concern. Neutrophils activated by passage through the extracorporeal circuit inflict local injury and provoke the inflammatory cascade by producing oxyradicals and proinflammatory factors. This study tested if a combination of leukocyte depletion and aprotinin suppression of neutrophils could minimize postbypass atrial fibrillation and pulmonary dysfunction. In part one, two randomized groups of 90 patients undergoing primary coronary artery bypass grafting received full Hammersmith aprotinin alone (control group) or combined with leukofiltration (study group) and were prospectively examined. The dual treatment decreased the incidence of postoperative atrial fibrillation (7 of 90, 7.8%) by 67% versus aprotinin alone (21 of 90, 23.3%). Respiratory gas exchange in these patients was assessed from pulmonary shunt fraction. In the first two hours postbypass, pulmonary shunt fraction in the dual treatment group increased 40% less than in the group receiving aprotinin alone (p = 0.002), and subsided more quickly and completely over the next six hours. In part two, the cardiopulmonary bypass group receiving aprotinin + leukofiltration was retrospectively compared with 45 patients undergoing off-pump coronary revascularization. A strong, albeit not statistically significant trend (p = 0.08) toward a lower incidence of atrial fibrillation was found in the dual treatment group versus the off-pump group (8 of 45, 17.8%). These findings suggest that combining mechanical and pharmacologic suppression of the systemic inflammatory response could mitigate its deleterious arrhythmic and pulmonary complications.

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“…These results are in accordance with prior laboratory and clinical studies suggesting that aprotinin reduces the extent of myocardial damage caused by ischemia-reperfusion injury during CPB-supported surgery. [20][21][22][23][24] More recently, reduced myocardial damage during OPCAB surgery was reported in patients receiving aprotinin. 25,26 Considerable concern exists regarding graft patency and graft survival when antifibrinolytics are used during coronary bypass surgery.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, aprotinin has been reported to have cardioprotective properties during cardiac surgery with CPB by reducing ischemia-reperfusion injury, including reduced cardiac troponin I (cTnI) release in coronary artery bypass graft (CABG) patients. [20][21][22][23][24] Reducing inflammatory activation during surgical trauma and ischemia-reperfusion could lead to reduced myocardial tissue injury. If, in addition, activated PMN cells would become less resistant on apoptosis, their reduced lifespan could contribute to decreased tissue injury.…”

Section: B Oth Mechanical Injury During Cardiac Surgerymentioning

confidence: 99%

Aprotinin Reduces Cardiac Troponin I Release and Inhibits Apoptosis of Polymorphonuclear Cells During Off-Pump Coronary Artery Bypass Surgery

Bert

Buck

Sergeant³

et al. 2008

Journal of Cardiothoracic and Vascular Anesthesia

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Objectives: In addition to blood-sparing effects, aprotinin may have cardioprotective and anti-inflammatory effects during cardiopulmonary bypass-assisted cardiac surgery. In this study, the authors examined whether aprotinin had cardioprotective and/or anti-inflammatory effects in patients undergoing off-pump coronary artery bypass grafting.Design: A prospective randomized clinical trial. Setting: University hospital. Participants: Fifty patients were randomized to control (n ‫؍‬ 25) or aprotinin treatment (n ‫؍‬ 25) groups.Interventions: Aprotinin was given as a loading dose (2 ؋ 10 6 KIU) followed by a continuous infusion at 5 ؋ 10 5 KIU/h until skin closure.Measurements and Main Results: Blood samples for cardiac troponin I; interleukin-6, interleukin-8, and interleukin-10; tumor necrosis factor ␣; and elastase were taken after anesthesia induction, completion of revascularization, and 6 hours, 12 hours, and 24 hours after revascularization. Blood samples were taken to assess for apoptosis in polymorphonuclear cells. Baseline plasma levels for cardiac troponin I did not differ between groups but were significantly lower in aprotinin-treated patients at the time of revascularization (p ‫؍‬ 0.03) and 6 hours (p ‫؍‬ 0.004) and 24 hours (p ‫؍‬ 0.03) later. Aprotinin significantly reduced apoptosis in polymorphonuclear cells compared with control-treated patients (p ‫؍‬ 0.04). There were no differences in plasma cytokine or elastase levels between groups.Conclusions: The authors conclude that aprotinin reduces perioperative cardiac troponin I release and attenuates apoptosis in polymorphonuclear cells but has no significant effects on plasma cytokine levels in patients undergoing off-pump coronary artery bypass graft surgery.

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Na+/H+-exchange inhibition and aprotinin administration: promising tools for myocardial protection during minimally invasive CABG

Cited by 13 publications

References 25 publications

Aprotinin use in thoracic aortic surgery: Safety and outcomes

Aprotinin use in thoracic aortic surgery: Safety and outcomes

Leukocyte filtration and aprotinin: synergistic anti-inflammatory protection

Aprotinin Reduces Cardiac Troponin I Release and Inhibits Apoptosis of Polymorphonuclear Cells During Off-Pump Coronary Artery Bypass Surgery

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