Thromboembolic events after cardiac surgery, including ischemic strokes, can be devastating complications, however only a few studies manifest the platelet activation and coagulation state after off-pump coronary artery bypass (OPCAB). Platelet-derived microparticles (PMP) are observed as released vesicles from platelets following platelet activation, and are believed to play a role in some clinical diseases because of their procoagulant activity. The aim of the present study was to evaluate the hypercoagulant state after OPCAB using PMP and other indices. Data were obtained from 15 patients (aged 69±7 years; only men) undergoing elective OPCAB surgery. One hundred milligrams of aspirin were used as postoperative antiplatelet drugs. Preoperative risk factors, operation time, postoperative hospital stay, transfusion and blood samples of CBC, PMP, βTG, PF 4, platelet aggregation, FDP, D-dimer and TAT of pre- and postoperative days (POD) 3 and 7 were studied. There was no difference between the PMP level with or without risk factor. The PMP levels of POD 3 and 7 were significantly higher compared to the preoperative levels (pre-op, POD 3, 7:9.1±5.1, 15.2±10.3, 28.4±24.5/10⁴plt respectively, p<0.05). The levels of FDP, D-dimer and TAT rose significantly on POD 3 and 7 and significantly correlated with the PMP levels. Beta TG, PF 4 and platelet aggregation did not change after OPCAB surgery, and no correlation was found with the PMP levels. Elevated levels of PMP, TAT, FDP and D-dimer persisted until POD 7 and suggested not only platelet activation, but also activation of the coagulation and fibrinolytic system. The findings suggest that 100mg of aspirin may not be adequate for the inhibition of platelet activation after OPCAB surgery.

A 52 year-old man was admitted to our institution with sudden onset of severe chest and back pain. The electrocardiogram showed ST segment depression in leads I, II, aVL, aVF, V3-6. Emergent coronary angiogram was performed, but the catheter did not reach to the coronary ostia, and it only performed false lumen aortogram. Computed tomography showed acute Stanford A aortic dissection. Ultrasound echocardiography also showed aortic regurgitation 3/4 degree. We decided to perform an emergency operation. During anesthesia induction, systemic blood pressure fell below 80 mmHg during systolic period, and pulmonary pressure raised to 60 mmHg. Transesophageal echography showed the movements of dissection flap intermittently obstructed the coronary blood flow and aortic valve annuls. Those flap movements, so called ‘flap suffocation’ was thought to be the cause of cardiac failure. Intra-operative findings of the ascending aorta showed an entry of dissection just above the left coronary ostia, and the entire detachment of intima to aortic wall. We performed ascending aorta replacement with aortic valve resuspension and fixation of coronary ostia. The postoperative course was uneventful, and he was discharged on the 25th postoperative day. For the precise treatment of acute Stanford A aortic dissection with such coronary ischemia, quick diagnosis and operative correction is essential.

A 64-year-old woman who had been followed for complete right bundle branch block at another hospital was found to have heart failure due to cardiac sarcoidosis. She was admitted because of progressive thinning of the ventricular septum and septal aneurysm which protruded into the right ventricle. On echocardiogram, her left ventricular ejection fraction had decreased to 40%. We decided to perform an operation because the patients's heart failure was thought to be due to dyskinesia of the ventricular septum with bulging of the septum into the right ventricle during systole, which consequently decreased cardiac output. The scarred ventricular septum, which was observed through right atrial, right ventricular and aortic incisions, was incised along the marginal normal interventricular myocardium. A tailored 4×3 cm oval Dacron patch was secured over this opening. A DDD pacemaker was implanted for complete atrio-ventricular block and, to synchronize both ventricles, ventricular leads were fixed on the right and left ventricular epicardium. Her postoperative course was uneventful. A postoperative pathologic study revealed a noncaseating granuloma on the border of the normal myocardium. We report a rare surgically treated case of cardiac sarcoidosis.

The purpose of this study was to compare the effect between cyclists and noncyclists of pedal rates on ankle, knee, and hip joint torque during pedaling exercises. Six male cyclists (CY) and seven male noncyclists (NC) pedaled at 40, 60, 90 and 120 rpm with a power output of 200 W. The lower limb was modeled as three rigid segment links constrained to plane motion. Based on the Newton-Euler method, the equation for each segment was constructed and solved on a computer using pedal force, pedal, crank, and lower limb position data to calculate torque at the ankle, knee, and hip joints. The average planter flexor torque decreased with increasing pedal rates in both groups. The average knee extensor torque for CY decreased up to 90 rpm, and then leveled off at 120 rpm. These results were similar to NC. The average knee flexor torque in both groups remained steady over all pedal rates. The average hip extensor torque for CY decreased significantly up to 90 rpm where it showed the lowest value, but increased at 120 rpm. For NC, the average hip extensor torque did not decrease at 90 rpm compared with 60 rpm, and was significantly higher than CY at 120 rpm (CY : 28.1 ± 9.0 Nm, NC : 38.6 ± 6.7 Nm, p<0.05) . The average hip flexsor torque for NC at 120 rpm increased significanly from 90 rpm, and was significantly higher than CY (CY : 11.6±2.9 Nm, NC : 22.6±11.8 Nm, p<0.05) . These results suggest that it would be better for cyclists to select a pedal rate of between 90 to 110 rpm to minimize joint torque, and, as a result, reduce peripheral muscle fatigue.