Antiphospholipid syndrome in cardiac surgery-an underestimated coagulation disorder?

OBJECTIVE: Antiphospholipid syndrome (APS) is a rare coagulation disorder associated with recurrent arterial and venous thrombotic events. We analysed our experience with five APS patients who underwent cardiac surgery. In three of them the diagnosis of APS had been established before surgery, two patients were diagnosed after surgery. METHODS: From March 1999 to March 2004 five patients with APS underwent cardiac surgery using cardiopulmonary bypass (CPB). We retrospectively reviewed their clinical data, operative and postoperative courses, and the long-term results. RESULTS: Procedures performed were heart and lung transplantation (patient 1), endoventriculoplasty and CABG (patient 2), biventricular resection of endoventricular fibrosis and thrombus (patient 3), mitral valve repair repair and coronary artery bypass grafting (CABG, patient 4), and mitral valve replacement with closure of a patent foramen ovale (patient 5). There were three perioperative deaths (patients 1, 2 and 3), two of three patients in whom the diagnosis was known before surgery, survived (patients 4 and 5). In these patients, only half the dose of protamin (patient 4) and no protamin at all (patient 5) was applied to reduce the probability of postoperative thromboembolic complications. At 1 year follow up, only patient 4 had survived, patient 5 had died of the complications of intestinal thromboembolism. CONCLUSIONS: Patients with APS undergoing cardiac surgery belong to a high risk subgroup. Thus, though rare, APS can be a critical issue in cardiac surgery. Some of the cardiac patients with unexplained perioperative thromboembolic complications, such as graft occlusion, may turn out to have an undiagnosed APS.     

Reactive oxygen species and nitric oxide in myocardial ischemia and reperfusion

Summary Oxygen radicals and reactive oxygen species (ROS) are known to be generated in large amounts under inflammatory conditions and in the first few minutes of postischemic organ reperfusion. Due to the interaction of ROS with nitric oxide (NO), formed constitutively by endothelial cells, two alternatives are feasible. On the one hand, reaction with superoxide radicals may induce toxification (formation of peroxynitrite), and, on the other hand, by reacting with superoxide and hydroxyl radicals, NO can serve as a radical scavenger (formation of the innocuous anions, nitrate and nitrite, respectively). However, NO is considered to play a pivotal role in numerous physiological and pathophysiological processes, with effects arising from both lack and surfeit of this easily diffusible and chemically very reactive molecule. Physiologic contributions to vascular dilatation and inhibition of platelet and leukocyte activation, e. g., are infringed by enhanced inactivation of NO. Such inactivation occurs readily due to spontaneous reaction of NO with the superoxide radical, formed, e. g., by stressed endothelial cells and activated leukocytes. Conversely, overproduction of NO by induced NO synthase (iNOS) may lead to circulatory shock, cell apoptosis or even cell necrosis. Caution would, thus, seem to be warranted when attempting to interfere with homeostasis of NO. We have investigated the ability of NO to act as a radical scavenger during myocardial reperfusion in experimental and clinical settings. In the former, inhibition of angiotensin converting enzyme was employed to generate more endogenous NO (via bradykinin), in the latter, low-dose sodium nitroprusside was used as the donor of exogenous NO in patients undergoing coronary bypass grafting. Inhibition of leukocyte adhesion, attenuation of platelet activation and mitigation of redox-stress and inflammation were observed in both instances. Accordingly, modest enhancement of NO levels should afford cardioprotection during reperfusion.     

Diagnostic discrimination between graft-related and non-graft-related perioperative myocardial infarction with cardiac troponin I after coronary artery bypass surgery.

AIMS: The rise of markers for myocardial injury indicates early graft-related or non-graft-related perioperative myocardial infarction (PMI) after coronary artery bypass grafting (CABG). A diagnostic discrimination between these two situations may enable adequate therapeutic measures, limiting myocardial damage, and improving outcome. METHODS AND RESULTS: In a prospective study, 94 among 3308 consecutive CABG patients underwent acute reangiography because of evidence of PMI. Of these 94 patients, 56 had graft-related PMI (group 1), 38 patients had non-graft-related PMI (group 2), and 95 patients without evidence of PMI and angiographically patent grafts served as control (group 3). Cardiac troponin I (cTnI), creatine kinase (CK), and its MB fraction were determined. CTnI, but not CK/CK-MB levels were significantly higher in group 1 than in groups 2 and 3 at 12 and 24 h after aortic unclamping (P<0.0001). Receiver operating characteristic and multivariable logistic regression analyses indicated cTnI as the best discriminator between PMI 'in general' and 'inherent' release of cTnI after CABG with a cut-off value of 10.5 ng/mL and between graft-related and non-graft-related PMI with a cut-off value of 35.5 ng/mL. CONCLUSION: Perioperative cTnI elevation after CABG separates among patients with graft-related, non-graft-related, and without PMI, however, not earlier than 12 h after surgery.     

Amyloid of heart and lungs in a patient with low output syndrome after coronary artery bypass grafting

A 70-year-old patient with two-vessel disease and moderately reduced left ventricular function after a recent myocardial infarction was admitted for a routine coronary artery bypass grafting (CABG) procedure. During anesthetic induction, he became unstable and cardiopulmonary bypass had to be instituted urgently. Despite good bypass flows, the patient died in myocardial failure shortly after surgery. At autopsy, besides severe atherosclerotic coronary artery disease, cardiac and pulmonary amyloidosis were found.