Limitation of thrombin generation, platelet activation, and inflammation by elimination of cardiotomy suction in patients undergoing coronary artery bypass grafting treated with heparin-bonded circuits.

OBJECTIVE: Reports evaluating the efficacy of heparin-bonded circuits to blunt inflammation, platelet dysfunction, and thrombin generation in response to cardiopulmonary bypass have varied. We hypothesized that this variability may in part be related to the use of cardiotomy suction, which has been demonstrated to reintroduce procoagulant and proinflammatory factors into the systemic circulation during cardiopulmonary bypass. A prospective, randomized study was undertaken to evaluate the specific effects of cardiotomy suction. METHODS: Thirty-six patients undergoing first-time, nonemergency coronary artery bypass grafting with cardiopulmonary bypass were randomly assigned to one of three treatment groups: group I, non-heparin-bonded circuits with the use of cardiotomy suction (n = 12); group II, Duraflo II (BCR-3500; Jostra Bentley Corp, Irvine, Calif) heparin-bonded circuits with cardiotomy suction (n = 12); and group III, Duraflo II heparin-bonded circuits without cardiotomy suction (n = 12). Thrombin generation, neutrophil activation (polymorphonuclear elastase), platelet activation (beta-thromboglobulin), and neuronal injury (neuron-specific enolase) were analyzed by enzyme-linked immunosorbent assays after cardiopulmonary bypass and compared with prebypass levels. Results are presented as mean +/- SEM. RESULTS: Prebypass levels of all markers were similar among treatment groups. However, postbypass levels were significantly and consistently highest in group I relative to groups II and III. Thrombin generation levels were 5.0 +/- 0.9 nmol/L in group I, 3.0 +/- 0.6 nmol/L in group II, and 1.5 +/- 0.1 nmol/L in group III (P <.05 vs group II and P <.001 vs group I). Polymorphonuclear elastase levels were 307 +/- 64 microg/L in group I, 128 +/- 24 microg/L in group II (P <.05 vs group I), and 75 +/- 14 microg/L in group III (P <.001 vs group I). beta-Thromboglobulin levels were 2692 +/- 401 IU/mL in group I, 912 +/- 99 IU/mL in group II (P =.001 vs group I), and 646 +/- 133 IU/mL in group III (P =.001 vs group I). Neuron-specific enolase levels were 9.8 +/- 0.9 ng/mL in group I, 10.5 +/- 1.6 ng/mL in group II, and 4.2 +/- 0.5 ng/mL in group III (P =.001 vs groups I and II). CONCLUSIONS: Use of cardiotomy suction resulted in significant increases in thrombin, neutrophil, and platelet activation, as well as the release of neuron-specific enolase, after cardiopulmonary bypass. Limiting increases in these markers would be best accomplished by eliminating cardiotomy suction and routinely using heparin-bonded circuits whenever possible.

Simultaneous papillary muscle avulsion and free wall rupture during acute myocardial infarction. Intra-aortic balloon pump: a bridge to survival.

Mechanical complications of acute myocardial infarction (AMI) are rare, but often fatal. Medical therapy does not provide adequate risk reduction, and surgical correction is recommended when feasible. Supplemental hemodynamic support utilizing intra-aortic counterpulsation with a balloon pump provides an improvement in morbidity and mortality when combined with a corrective surgical approach. We report a case of an elderly male with a progressive 2-week history of ischemic symptoms presenting with acute pulmonary edema, hypotension and an inferior wall ST-elevation MI. His hospital course was complicated by ischemic mitral regurgitation (MR) and cardiogenic shock, which resulted in a papillary muscle rupture/avulsion from the inferolateral myocardial wall, and a communication for blood from ventricle to pericardial space. Initial management included mechanical ventilation, pharmacologic inotropic support, percutaneous revascularization of the culprit lesion and intra-aortic balloon counterpulsation. The patient underwent further successful cardiovascular surgical correction of his incompetent mitral valve, free wall rupture and other obstructive coronary arteries, leading to discharge and survival. Mechanical complications from AMI and the role of intra-aortic balloon support are discussed.

Triple valve repair for rheumatic heart disease.

The onset of the clinical expression of rheumatic heart disease (RHD) is variable. Exercise or other states that necessitate increased cardiac output often precipitate symptoms. Mitral stenosis (MS) is present in 25% of patients with RHD, and 40% of patients have concomitant MS and mitral regurgitation. About two third of patients with MS have concurrent aortic insufficiency. Pulmonary and tricuspid insufficiency may occur from rheumatic involvement of these valves, or secondary to dilatation of valve annuli from pulmonary hypertension secondary to mitral and/or aortic valve disease. Pregnancy is associated with many hemodynamic changes including expanded intravascular volume, tachycardia, increased intracardiac dimensions, and valvular regurgitation. We report a case of a young female who developed flash pulmonary edema during parturition and was found to have abnormal rheumatic involvement of her aortic, mitral, and tricuspid valves. Successful triple valve repair was performed in a single operation. A review of rheumatic valvular abnormalities, and literature supporting multivalvular repair for rheumatic heart disease is provided.