We present a case of a giant fenestration and a fibrous strand rupture of the aortic valve without massive regurgitation. A 56-year-old woman, was referred for coronary revascularization, had II-III degree aortic regurgitation without symptoms of heart failure. On the intraoperative direct view, the non coronary cusp (NCC) had the giant fenestration and the left coronary cusp (LCC) had the fibrous strand rupture. There was no severe inflammation, thrombi, or vegetation. Finally, she had coronary artery bypass surgery and aortic valve replacement.Although fenestration of the aortic valve is not rare, it is hard to determine its configuration preoperatively. When the echocardiographic findings indicate an eccentric regurgitation flow despite the absence of prolapse, we should perform examinations with the possibility of coexisting aortic valve fenestration in mind. Massive regurgitation does not necessarily correspond to a giant fenestration and a fibrous strand rupture.We report a rare case of the unusually large fenestration and the rupture of the fenestrated fibrous strand of the aortic valve without massive regurgitation.

Isolated noncompaction of the ventricular myocardium (INVM) is an unclassified cardiomyopathy [1]. Reported INVM cases were with severe clinical manifestations such as congestive heart failure (CHF), critical arrhythmia, or systemic to asymptomatic embolism [2-10]. We investigated the demographics and characteristics of echocardiographically diagnosed INVM.

A 41-year-old man with sudden onset of chest oppression and downslope ST depression was diagnosed as having type A aortic dissection with angina pectoris and aortic regurgitation. Intraoperative transesophageal echocardiogram (TEE) showed intimal flap inverting into the left ventricle through the aortic valve. This case was rare in that transient myocardial ischemia was induced not by dissection of the aortic root reaching the coronary ostia but by back-and-forth movement of the intimal flap, covering the coronary ostia and interrupting the coronary artery flow. TEE was important for correct diagnosis.

A 74-year-old man presented with palpitation and 12-lead ECG exhibited atrial premature contraction (APC) at general check-up. Holter ECG demonstrated narrow QRS tachycardia with a rate of 160/min and more than 31,000/day atrial premature beats. The P wave morphology of atrial premature beats showed negative in II, III, aVF and biphasic in V1. Venography was performed and disclosed persistent left superior vena cava (LSVC) draining into the right atrium via the markedly dilated coronary sinus (CS). Electrogram recordings from LSVC and CS were obtained with an electrode catheter via the left subclavian vein. At the level where a ventricular potential disappeared, the intra-LSVC potentials began to show a discrete second sharp potential after local left atrial signals. Double potentials were obtained within the LSVC from the lower left atrium (LA) to the higher LA. A proximal-to-distal activation sequence of the second components was observed. The interval between the 1st and 2nd component ranged from 8 to 22 msec between the proximal LSVC and distal LSVC. The double potentials resulted in fusion at the lower part of the LSVC, indicating the presence of an electrical connection between the LSVC and lower LA. The thoracic veins play an important role in the genesis and maintenance of atrial arrhythmias. 1)The left superior vena cava (LSVC) is the embryological precursor of the ligament of Marshall (LOM), which contains multiple electrical connections to the left atrium (LA). The electrical connection has also been implicated as an arrhythmogenic substrate of reentry in atrial tachy-arrhythmias. 2-4) Case ReportA 74-year-old man presented with palpitation and 12-lead ECG exhibited atrial premature contraction at general check-up. Holter ECG demonstrated narrow QRS tachycardia with a rate of 160/min and more than 31,000/day atrial premature beats. He was admitted for electrophysiologic study and radiofrequency ablation for the atrial tachycardia (AT).

A 74-year-old man presented with palpitation and 12-lead ECG exhibited atrial premature contraction (APC) at general check-up. Holter ECG demonstrated narrow QRS tachycardia with a rate of 160/min and more than 31,000/day atrial premature beats. The P wave morphology of atrial premature beats showed negative in II, III, aVF and biphasic in V1. Venography was performed and disclosed persistent left superior vena cava (LSVC) draining into the right atrium via the markedly dilated coronary sinus (CS). Electrogram recordings from LSVC and CS were obtained with an electrode catheter via the left subclavian vein. At the level where a ventricular potential disappeared, the intra-LSVC potentials began to show a discrete second sharp potential after local left atrial signals. Double potentials were obtained within the LSVC from the lower left atrium (LA) to the higher LA. A proximal-to-distal activation sequence of the second components was observed. The interval between the 1st and 2nd component ranged from 8 to 22 msec between the proximal LSVC and distal LSVC. The double potentials resulted in fusion at the lower part of the LSVC, indicating the presence of an electrical connection between the LSVC and lower LA. (J Arrhythmia 2008; 24: 38-44)