A Case of Coronary Artery Bypass Grafting in a Patient with Wolff-Parkinson-White Syndrome / 日本心臓血管外科学会雑誌

A 54-year-old man with unstable angina and Wolff-Parkinson-White (WPW) syndrome was admitted. Coronary angiography showed 90% stenosis of the left main trunk and 75% stenosis of the obtuse marginal branch. Coronary artery bypass grafting under cardioplegic arrest was done emergently. The left internal mammary artery graft was anastmosed to the left anterior descending artery, and a saphenous vein graft was used as a sequential bypass graft to the high lateral branch and obtuse marginal branch. Immediately after weaning from cardiopulmonary bypass, paroxysmal supraventricular tachycardia (PSVT) requiring electrical cardioversion was occurred, and catheter ablation was performed on the first postoperative day. There are controversus concerning the strategies of surgical treatment for unstable angina concomitant with WPW syndrome. Coronary bypass operation may trigger PSVT in patients with WPW syndrome. The optimal timing of perioperative catheter ablation needs further discussion.

Congenital Bicuspid Aortic Stenosis in Siblings / 日本心臓血管外科学会雑誌

The authors encountered 22 cases of congenital bicuspid aortic valve, some of which occurred in siblings. In this paper, a 58-year-old brother and a 56-year-old sister cardiac valve disease was diagnosed first at the age of 51 in the brother and at the age of 15 in the sister. Aortic valve replacement using a 21mm Medtronic-Hall prosthesis was done in both cases. Additionally, pacemaker implantation was carried out in the sister. Both cases showed favorable progress after operation. Hereditary factors are involved in congenital bicuspid aortic valve. Therefore if congenital bicuspid aortic valve are found in any patients, thorough investigations including cardiac auscultation, ECG and ultrasound cardiogram should be carried out routinely among immediate family members and relatives to reveal whether any of them is suffering from this congenital anomaly.

Evaluation of Antiplatelet Therapy with Aspirin and Trapidil in Patients with Prosthetic Heart Valve Replacement / 日本心臓血管外科学会雑誌

Twenty six adult patients who underwent prosthetic heart valve replacement and treated anti-thrombogenic therapy, were divided into 2 groups. One was administered Warfarin alone, another was administered Warfarin plus Aspirin (162mg/day) as antiplatelet therapy. Trapidil (300mg/day) was administered to all of the patients. Platelet aggregation, plasma level of TXB₂ (stable metabolite of thromboxane A₂), and 6-keto-PGF₁ (stable metabolite of PGI₂) were measured before and 1, 3, 6 months after Trapidil therapy. Platelet aggregability suppressed in both 2 groups. Plasma TXB₂ level, and TXB₂/6-keto-PGF₁ ratio showed a tendensy to decrease (<i>p</i><0.05) 6 months after administration. In the Aspirin plus Trapidil group, platelet aggregability, serum TXB₂ level, and TXB₂/6-keto-PGF₁ ratio are significantly lower than that in the Trapidil only. These results suggest that Trapidil is clinically useful for antiplatelet agent, but the combined Aspirin plus Trapidil therapy is more efficacious than the Aspirin or Trapidil single therapy.

Recording of Epicardial Monophasic Action Potentials Using Suction Electrode to Evaluate Myocardial Protection. As an Additive Effects of Diltiazem on Crystalloid Cardioplegic Solution / 日本心臓血管外科学会雑誌

This study was designed to evaluate the myocardial protection with observation of the monophasic action potential (MAP) which was recorded by suction electrode. Using the isolated working rabbit hearts, amplitude, duration of MAP at 50% repolarization level (MAPD₅₀), aortic flow and heart rate were measured after reperfusion. The comparative study obtained for all five groups under the following various conditions of the aortic cross clamping are stated as follows. Myocardial temperature were maintained at 20°C during aortic cross clamping. Group I was treated with St. Thomas' Hospital cardioplegic solution. The cardioplegic solution was infused every 20min during ischemia and kept at 20°C. The hearts of group I was divided into four sub-groups, all of which were infused with different concentration of diltiazem (D) in cardioplegia: group Ia D=0μg/ml (<i>n</i>=10), group Ib D=1μg/ml (<i>n</i>=5), group Ic D=5μg/ml (<i>n</i>=5). group Id D=10μg/ml (<i>n</i>=5), and in group II cardioplegic solution was not used. The amplitude of MAP following 30min working mode of reperfusion in group I showed a significantly higher recovery compared to those in group II. The MAPD₅₀ of MAP following 30min working mode of reperfusion in group I showed a significantly lower recovery compared to those in group II, and 10min Langendorff mode in group I a showed a significantly higher recovery compared to those in group Ib, group Ic and group Id. 20min working mode in group Ia and group Ib showed a significantly higher recovery compared to those in group Ic and group Id. The heart rate following 30min working mode of reperfusion in group Ia and group Ib showed a significantly higher recovery compared to those in group Ic and group Id. The aortic flow following 30min working mode of reperfusion in group Ia and group Ib showed a significantly higher recovery compared to those in group Ic, group Id and group II. We would like to conclude that the permeability of large amount of calcium across myocardial cell membrane seems to be depressed by diltiazem added to cardioplegia. But when the concentrations of diltiazem in cardioplegia was over 5μg/ml, it showed negative inotropic action and negative chronotropic action.

Pathophysiological Relevance of Oxygen to Reperfusion-Induced Arrhythmias / 日本心臓血管外科学会雑誌

We have examined the role of readmission of oxygen in the initiation of reperfusion-induced arrhythmias by separating readmission flow from readmission of oxygen on a temporal basis. Isolated rat hearts (<i>n</i>=12/group) were subjected to 10 minutes of global ischemia and reperfusion. In controls reperfused with aerobic perfusion medium, 100% of hearts developed ventricular tachycardia 1.48±0.78 seconds after reperfusion, and ventricular fibrillation occurred 13.47±2.91 seconds after reperfusion. Also in hearts reperfused with anoxic perfusion medium, 100% of hearts developed ventricular tachycardia 1.98±0.96 seconds after reperfusion, and ventricular fibrillation occurred 27.01±18.52 seconds after reperfusion. But the duration of the time from reperfusion to the onset of ventricular fibrillation were statistically differrent in these two groups (<i>p</i><0.05). In conclusion anoxic reperfusion delayed ventricular fibrillation but prevent neither ventricular fibrillation nor ventricular tachycardia. This implies that oxygen-derived free radicals may play an important role in the initiation of reperfusion-induced arrhythmias, but are unneccessary for arrhythmogenesis.