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1/22. Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy.

    The 12-lead electrocardiogram (EKG), a powerful tool used in evaluating the chest pain patient, has its shortcomings. One such failing is encountered in a patient with one of the following electrocardiographic patterns: left bundle branch block (LBBB), ventricular paced rhythm (VPR), and left ventricular hypertrophy (LVH). These patterns reduce the ability of the EKG to detect acute coronary ischemic change and acute myocardial infarction (AMI). Several strategies are available to assist in the correct interpretation of these complicated electrocardiographic patterns, including a knowledge of the ST segment-T wave changes associated with these confounding patterns, performance of serial EKGs, and comparison with previous EKGs if available. This article suggests guidelines and interpretive tools for diagnosing AMI on EKG in patients with these confounding patterns.
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2/22. Transient left ventricular aneurysm and hypertrophy accompanied by polymorphic ventricular tachycardia in a patient suspected of acute myocarditis.

    A 75-year-old woman presented with recurrent ventricular tachycardia (VT) compatible with torsades de pointes (TdP) based on sinus bradycardia and QT prolongation. Previously she had received pirmenol, at a serum concentration within therapeutic range, for her paroxysmal atrial fibrillation. Emergent cardiac catheterization identified a ventricular aneurysm of the anteroapical and inferior wall along with angiographically normal coronary arteries. A right ventricular endomyocardial biopsy revealed postmyocarditic change. The left ventricular contraction improved after 5 weeks of conservative treatment. A follow-up echocardiogram revealed transient thickening of partial left ventricular wall consistent with the segment of the aneurysm. Several months later, almost all abnormal findings had improved except for sustained deep negative T waves in precordial leads. Acute myocarditis was primarily suspected as the cause of her clinical presentation.
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3/22. Pseudo ventricular hypertrophy and pseudo myocardial infarction in wolff-parkinson-white syndrome.

    In wolff-parkinson-white syndrome, the sequence of ventricular activation is altered and depending on the anatomic site of the accessory conduction pathway may result in pseudo ventricular hypertrophy and pseudo myocardial infarction patterns on electrocardiogram. The right-sided accessory pathway may direct the depolarization vector towards left amplifying R-wave amplitude in left-sided limb-leads simulating left ventricular hypertrophy. The left-sided accessory pathways may give rise to prominent R-waves in right precordial leads simulating right ventricular hypertrophy. The right lateral accessory pathways may simulate anterior infarction because of prominent Q-waves in right precordial leads. The left lateral accessory pathways directing depolarization vector towards right may cause Q-waves in lateral limb-leads simulating high lateral myocardial infarction. In posteroseptal accessory pathway, the ventricular depolarization vector is directed superiorily giving rise to prominent Q-waves in inferior limb leads simulating inferior myocardial infarction. Therefore, ventricular hypertrophy and myocardial infarction should not be diagnosed from the electrocardiograms of wolff-parkinson-white syndrome.
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4/22. Giant negative T waves during interferon therapy in a patient with chronic hepatitis c.

    interferon-alpha (IFN-alpha) has been widely used for treatment of chronic hepatitis c in japan. In general, cardiovascular adverse reactions are rare in association with IFN-alpha therapy. Here, a 64-year-old man with chronic active hepatitis c complained of fatigue, palpitation and depression, and developed atrial fibrillation with prominent negative T waves during IFN-alpha therapy. Echocardiogram showed septal and apical hypertrophy. Three days after discontinuation of IFN-alpha, subjective symptoms and atrial fibrillation subsided. It is unclear whether or not IFN-alpha induced the giant negative T waves with apical hypertrophy. We might observe the developing course of hepatitis c virus (HCV)-related myocardial hypertrophy by chance. Cardiovascular toxicity should be carefully monitored during IFN-alpha therapy even in patients with minor cardiac disease, such as premature ventricular contracture (PVC) and mild hypertension.
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5/22. Two case reports on incessant left ventricular tachycardia: curative therapy with radiofrequency ablation.

    INTRODUCTION: Incessant ventricular tachycardia is a rare arrhythmia which can be life threatening. Treatment with anti-arrhythmic agents may occasionally fail. CLINICAL PICTURE: We report 2 cases of incessant ventricular tachycardia. The first case was a young man with idiopathic left ventricular tachycardia who was in incessant ventricular tachycardia despite treatment with multiple anti-arrhythmic drugs and developed dilated cardiomyopathy. The second case was an asymptomatic girl with the incidental finding of an incessant ventricular tachycardia which originated from the left ventricular outflow tract. TREATMENT AND OUTCOME: Both patients underwent electrophysiologic study and radiofrequency ablation with complete termination of the tachycardia. CONCLUSION: Radiofrequency catheter ablation in experienced centres should be the first-line therapy for incessant ventricular tachycardia.
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6/22. The prominant T wave: electrocardiographic differential diagnosis.

    The prominent T wave is an abnormal T-wave morphology encountered in the earliest phase of ST-segment elevation acute myocardial infarction (AMI). Prominent T waves, however, are associated with other diagnoses, including hyperkalemia, early repolarization, and left ventricular hypertrophy (LVH). This article focuses on the electrocardiographic differential diagnosis of the prominent T wave with the presentation of 4 illustrative cases. We also recommend that the designation hyperacute should refer exclusively to the prominent T waves of ST-segment elevation AMI.
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7/22. Left ventricular dysfunction resulting from frequent unifocal ventricular ectopics with resolution following radiofrequency ablation.

    A case is presented, in which asymptomatic but persistent right ventricular outflow tract (RVOT) ectopics resulted in left ventricular (LV) dilatation and systolic dysfunction. The patient underwent extensive investigation with no other cause for the cardiomyopathy being found. Successful ablation of the RVOT ectopic focus resulted in normalization of LV size and function. This case suggests that frequent ventricular ectopy should be considered as a potentially remediable cause of LV dysfunction.
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8/22. Multiple coronary artery-left ventricular microfistulae in a patient with apical hypertrophic cardiomyopathy: a demonstration by transthoracic color Doppler echocardiography.

    Among the congenital coronary artery fistulae, multiple coronary artery microfistulae arising from the left and right coronary artery and emptying into the left ventricle are very rare and little is known of their anatomic and clinical features, especially in apical hypertrophic cardiomyopathy. A 67-year- old woman was referred for the evaluation of chest pain at exertion, and shortness of breath. Electrocardiographic and echocardiographic findings were typical of apical hypertrophic cardiomyopathy. Coronary arteriography showed normal epicardial coronary arteries, but multiple coronary artery-left ventricular microfistulae arising from the left and right coronary arteries. Transthoracic color Doppler echocardiography, using a high frequency transducer with a low Nyquist limit, demonstrated multiple coronary artery-left ventricular microfistulae just beneath the apical impulse window.
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9/22. ventricular fibrillation during anesthesia in association with J waves in the left precordial leads in a child with coarctation of the aorta.

    A 14-year-old boy with coarctation of the aorta who showed repeat ventricular fibrillation during anesthesia, and ultimately sudden cardiac death in school, is presented. electrocardiography showed J waves in the left precordial leads, which became prominent after an episode of ventricular fibrillation. While some of the clinical features and electrophysiological findings were similar to those seen in brugada syndrome, others were inconsistent. J waves in the left precordial leads should be recognized as a possible waveform change inducing ventricular fibrillation predominantly at rest.
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10/22. Improvement of ventricular arrhythmia by octreotide treatment in acromegalic cardiomyopathy.

    We report a case of acromegalic cardiomyopathy in a 46-year-old Japanese man with pituitary adenoma. Increased secretion of growth hormone and insulin-like growth factor I were detected. He had left ventricular hypertrophy, impaired cardiac function, and frequent ventricular premature complexes. After 2-month treatment with octreotide, a long-acting somatostatin analogue, levels of both hormones were decreased. At the same time, left ventricular hypertrophy (intraventricular septal thickness: 22.5 to 17.8 mm), cardiac function (ejection fraction: 38 to 50%), and frequency of ventricular premature complexes (17,249 to 2,882 beats a day) were improved. Transsphenoidal surgery was then safely performed. Treatment with octreotide is thought to have some effect on improvement of ventricular arrhythmia in acromegalic heart.
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