Journal of cardiology
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Journal of cardiology · Jan 1993
[Retained intracardiac air in coronary artery bypass grafting detected by intraoperative transesophageal echocardiography].
The incidence and location of retained air in 35 patients who underwent coronary artery bypass grafting (CABG) were examined using B mode transesophageal echocardiography. The origin of air detected in the left atrium or left ventricle on weaning from a cardiopulmonary bypass was sought as far as the 4 pulmonary veins. Air appeared as: highly echogenic dots with high mobility, buoyancy and no disappearance in the blood flow. ⋯ In one patient, the air at the LV apex was suddenly flushed into the ascending aorta when the heart was manipulated. Air retention is not uncommon in CABG and is mainly located in the RUPV. Retained air at the LV apex may remain indefinitely, and suddenly flow into the aorta with manipulation of the heart or a change of posture.(ABSTRACT TRUNCATED AT 250 WORDS)
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Journal of cardiology · Jan 1993
Comparative Study[A newly-devised nine-lead Holter system for diagnosing myocardial ischemia evaluated using Tl-201 exercise scintigraphy].
A 9-lead Holter monitoring apparatus was devised using a commercially-available 3-lead Holter recorder. The CM5 lead was monitored continuously on channel 1, and our apparatus was applied to channels 2 and 3. Channel 2 was switched serially to V1-like (CM1), V4-like (CM4), V2-like (CM2) and V3-like (CM3) leads every 20 sec. ⋯ Both the percent extent score and percent severity score in the latter group were significantly higher than those in the former group (p < 0.001, p < 0.01, respectively), suggesting that the degree of ST depression in the LB lead reflects the degree of myocardial ischemia. The HL and LL leads had high sensitivity and specificity for detecting lateral ischemia. It was concluded that the CM5 lead is necessary for screening global myocardial ischemia and that leads LB and HL (or LL) are mainly useful for detecting inferior and lateral ischemia.
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Journal of cardiology · Jan 1993
[Serial changes in hemostatic and fibrinolytic states induced by coronary thrombolytic therapy].
The effects of coronary thrombolytic therapy with urokinase on the intrinsic hemostatic and fibrinolytic states were investigated by determining several markers for hemostatic and fibrinolytic activities in 6 patients with acute myocardial infarction who underwent coronary thrombolysis with urokinase. The markers for hemostasis and fibrinolysis were: markers for plasmin generation [alpha 2-plasmin inhibitor (alpha 2-PI), plasminogen, plasmin alpha 2-PI complex (PIC)]; markers for fibrinolysis [fibrin/fibrinogen degradation products-E fragment (FDP-E), FDP D-D dimer (D dimer), fibrinogen]; markers for hemostatic activity (prothrombin time (PT), antithrombin III (AT-III), protein C); markers for thrombin generation [thrombin antithrombin III complex (TAT)]; markers for intrinsic fibrinolytic activity [tissue plasminogen activator plasminogen activator inhibitor complex (TPA PAI complex)]. These markers were measured before, at 1 to 2 hours intervals during first 6 hours, daily during the next 3 days, and subsequently on the 7th and the 14th day after urokinase therapy. ⋯ TAT increased from 13.1 +/- 15.4 to 70.8 +/- 65.8 ng/ml soon after fibrinolysis occurred, indicating that thrombin generation occurred at the same time as fibrinolysis. The TPA PAI complex level before urokinase administration (26.4 +/- 6.4 ng/ml) was greater than the normal upper limit, indicating increased intrinsic fibrinolytic activity, then decreased after urokinase administration. These findings suggested that urokinase administration might affect the intrinsic fibrinolytic activity.(ABSTRACT TRUNCATED AT 250 WORDS)