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Patients with apical hypertrophic cardiomyopathy (APH) associated with paradoxic jet flow (ie, diastolic flow away from the apex) may gradually develop an apical aneurysm, which often leads to arrhythmia and mural thrombus formation. We observed systolic outward motion of the left ventricular apical myocardium in patients with APH using a magnetic resonance tagging procedure and examined the relationship of the outward motion to echocardiographic and scintigraphic findings and to cardiac events. Systolic displacement of the myocardial tags of the apical region perpendicular to the long axis in the 4-chamber view was recorded in 31 patients with APH. Of these patients, 14 showed no outward movement of tags (group A), and 17 showed outward movement (group B). In group B, apical hypertrophy was more severe (35 +/- 7 mm vs. 29 +/- 6 mm, p < 0.05), paradoxic jet flow was more frequent (64% vs. 14%, p < 0.05) and the defect score in I-123-beta-methyliodophenylpentadecanoic acid scintigraphy was higher (2.1 +/- 0.7 vs. 1.3 +/- 0.7, p < 0.01). During a mean follow-up period of 55 months, only 1 patient experienced paroxysmal atrial fibrillation in group A. In group B, 1 patient died suddenly, 1 was admitted to hospital because of congestive heart failure, 2 developed angina pectoris, 2 exhibited non-sustained ventricular tachycardia, and 1 showed multifocal premature ventricular contraction; in these 7 patients the outward movement was greater than in the 10 patients in Group B who had no cardiac events (1.00 +/- 0.59 vs. 0.52 +/- 0.40, p < 0.05). Hence, our results show that outward tag displacement is frequently associated with severe apical hypertrophy, paradoxic jet flow, apical ischemia, and cardiac events. The tagging method may be useful in assessing the severity of APH and predicting the occurrence of cardiac events at an early stage.

The present case showed gradual increase of QRS duration from 100 ms up to 180 msec during an ergometer exercise test along with the heart rate increase. After exercise, QRS duration shortened and normalized. Laboratory test showed hyperkalemia (K = 8.0 mEq/l). T1 myocardial scintigraphy revealed exercise-induced transient ischemia in posterolateral region of left ventricle. Coronary angiography showed significant stenosis in the distal portion of left circumflex coronary artery. The increase of QRS duration was possibly due to the combination of hyperkalemia and the effect of mexiletine. The rate dependent blocking effect on sodium channel of mexiletine might be intensified under hyperkalemia.

A patient with idiopathic long QT syndrome had repeated syncopal episodes. The QTc interval on the electrocardiogram at rest was 530 ms and was prolonged by exercise up to 740 ms with T wave alternation. Intravenous epinephrine (0.1 microg/kg weight per min), but not isoproterenol (0.7 microg/min), produced early after depolarization of the monophasic action potential recorded at the right ventricular apex. Epinephrine prolonged the QTc interval to 710 ms. After the addition of propranolol to the epinephrine, the QTc (580 ms) was longer than at baseline. Methoxamine also prolonged the QTc to 580 ms. The QT interval in long QT syndrome is generally considered to be prolonged by a beta-adrenergic effect, but in the present case alpha-adrenergic stimulation had an additional effect on the prolongation of the QT interval.

Subepicardial aneurysm is a rare complication of acute myocardial infarction and the present case was associated with ventricular septal perforation. Echocardiography showed the subepicardial aneurysm adjoining the true apico-anteroseptal aneurysm, with the former being discontinuous with the myocardium at its neck, which was narrower than the diameter of the aneurysm. In addition, color Doppler imaging showed shunt flow from the aneurysm to the right ventricle. Coronary angiography revealed extension only of the anterior descending artery without any discernible stenosis. The apical aneurysm was excised and the defect closed with an epicardial patch. The myocardial infarction was probably caused by coronary spasm. Echocardiography was useful for diagnosing the anatomy and hemodynamic condition of the subepicardial aneurysm.

Tachycardia-induced cardiomyopathy is a well-known and reversible condition, but the left ventricular dysfunction caused by frequent isolated premature ventricular complexes (PVCs) has been rarely reported. Apparent dilated cardiomyopathy was resolved in a patient after the focal source of PVCs was eliminated by radiofrequency catheter ablation. Echocardiography showed progressive improvement of the abnormal wall motion. Frequent PVCs could be the cause of left ventricular dysfunction in a subset of patients with dilated cardiomyopathy and radiofrequency ablation should be the choice of therapy in those patients.

Verapamil is widely used for the termination of paroxysmal supraventricular tachycardia (PSVT) with little proarrhythmic effect. We describe two cases of PSVT that changed to non-sustained polymorphic ventricular tachycardia after administration of verapamil. Electrophysiological study revealed atrioventricular nodal reentrant tachycardia in the first case, and atrioventricular reentrant tachycardia due to a concealed left lateral accessory pathway in the second case. Catecholamine-induced automaticity was one of the possible mechanisms of VT in the first case, but the mechanism is unknown in the second case.