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1/89. Persistent ST segment elevation: a new ECG finding in hypertrophic cardiomyopathy.

    Hypertrophic cardiomyopathy is a primary disease of myocardium resulting in myocardial hypertrophy without any inciting pressure or volume overload. The typical triad of symptoms includes exertional angina, syncope, and shortness of breath. Sudden cardiac death, the most dreadful complication of this disorder, can be the first manifestation of the disease and is more common in young patients. Elderly patients, on the other hand, may have a relatively benign course with normal or near-normal life span. The electrocardiogram (ECG) and echocardiography are the two most useful measures to diagnose hypertrophic cardiomyopathy. The electrocardiographic features of hypertrophic cardiomyopathy are numerous, including ST segment elevation that may simulate other ST segment elevation syndromes, including acute myocardial infarction, variant angina pectoria, acute pericarditis, bundle branch blocks, ventricular paced rhythm, dyskinetic ventricular segment, ventricular aneurysm, left ventricular hypertrophy, wolff-parkinson-white syndrome, and early repolarization syndrome. This report describes a case of an asymptomatic patient who presented with ST segment elevation of acute injury type and, therefore, was admitted to rule out silent myocardial infarction. myocardial infarction was ruled out by cardiac enzyme levels, but ST segment elevation remained persistent in all of the subsequent ECGs. echocardiography was performed, which clearly showed hypertrophic cardiomyopathy with left ventricular outflow tract obstruction and a high intracavity pressure gradient. Subsequently, retrieval of old ECGs showed a similar type of ST segment elevation in the patient's previous ECGs.
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2/89. Apical hypokinesis in a patient with hypertrophic cardiomyopathy and myocardial bridging: reversal with beta-blockade--a case report.

    A 42-year-old man presented with effort angina pectoris of 20 minutes' duration. Hypertrophic obstructive cardiomyopathy, severe myocardial bridging involving the midleft anterior descending coronary artery, and apical hypokinesis were identified. Regional wall motion normalized following the initiation of beta blockade.
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3/89. Electrophysiologic characteristics of accessory atrioventricular connections in an inherited form of wolff-parkinson-white syndrome.

    INTRODUCTION: A familial form of wolff-parkinson-white syndrome (WPW) occurs in association with hypertrophic cardiomyopathy and intraventricular conduction abnormalities. This syndrome, demonstrating autosomal dominant inheritance and segregating with a high degree of penetrance but variable expressivity, has been genetically linked to chromosome 7q3. The purpose of this study is to detail the electrophysiologic characteristics of accessory atrioventricular connections (AC) in four members of a kindred with this syndrome. methods AND RESULTS: We clinically evaluated 32 members of a single kindred and identified 20 individuals with ventricular preexcitation, abnormal intraventricular conduction including complete AV block and/or ventricular hypertrophy. genetic linkage analysis mapped the disease gene in this kindred to the chromosome 7q3 locus (maximum logarithm of the odds score = 6.88, theta = 0); recombination events in affected individuals reduced the genetic interval from 7 centimorgans (cM) to 5 cM. Electrophysiologic study of four individuals with preexcitation, identified seven AC (1 right sided, 3 septal, and 3 left sided). All four individuals had inducible orthodromic tachycardia; while three had multiple AC. Bidirectional conduction was demonstrated in 6 of 7 AC. Successful ablation was accomplished in 5 of 7 AC. CONCLUSION: The electrophysiologic characteristics and location of AC in family members having this complex cardiac phenotype are similar to those seen in individuals with isolated WPW. Identification of WPW in more than one family member should prompt clinical evaluation of relatives for additional findings of ventricular hypertrophy or conduction abnormalities.
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4/89. torsades de pointes in a case of hypertrophic cardiomyopathy with special reference to the pathologic findings of the heart including the conduction system.

    A clinicopathologic study was performed in a 77-year-old female with hypertrophic cardiomyopathy who had experienced recurrent syncopal attacks due to Torsades de Pointes (TdP) following QT prolongation and atrioventricular block. She died suddenly two years later while eating dinner. Pathologic findings of the heart showed a dilated and hypertrophied left ventricle. The heart weighed 550 g. There were two foci of localized endocardial fibroelastosis (EFE) beneath the aortic valve, one with a size of 3.5 x 3.5 cm, and the other (2 x 1 cm) located on the upper ventricular septum. Histologic findings showed hypertrophy and disarray in the left ventricular myocardium. The conduction system using serial sectioning revealed remarkable bilateral bundle branch fibrosis and hypertrophied purkinje fibers in the left bundle branch adjacent to the EFE on the ventricular septum. These findings were thought to be related to the occurrence of TdP.
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5/89. sirolimus in pediatric gastrointestinal transplantation: the use of sirolimus for pediatric transplant patients with tacrolimus-related cardiomyopathy.

    Hypertrophic obstructive cardiomyopathy (HOCM) associated with the use of tacrolimus is a rare complication of liver and intestinal transplantation seen almost exclusively among pediatric patients. Reduction of tacrolimus dosage or conversion to cyclosporin A (CsA) has been used as an effective treatment in reviewed cases. We present three pediatric transplant recipients who developed hypertrophic obstructive cardiomyopathy while under tacrolimus immunosuppression and were treated with conversion to sirolimus (Rapamycin). The patients (ages 6 yr, 12 yr and 11 months) were transplant recipients (liver, n = 2; liver and intestine, n = 1) who developed significant cardiomyopathy 15 and 96 months post-transplant. One patient died of post-transplant lymphoproliferative disorder 21 days after starting sirolimus. One patient had received two liver transplants and had been on CsA for 12 yr before conversion to tacrolimus at 60 months post-transplant for acute and chronic rejection. The surviving patients were receiving mycophenolate mofetil, tacrolimus and steroids at the time of diagnosis. Dose reduction of tacrolimus and treatment with beta blockers failed to alleviate the hemodynamic changes. The patients were converted to sirolimus 1.6, 37 and 148 months post-transplant and maintained a whole-blood trough level of 15-20 ng/mL 21 days after starting sirolimus. Repeat echocardiograms in the surviving patients showed improvement in cardiomyopathy. One patient had one rejection episode (intestinal biopsy, mild acute cellular rejection) after starting sirolimus that responded to a transient increase in steroids. The early demise of the third patient after sirolimus conversion prevented an adequate assessment of cardiomyopathy. Conversion to sirolimus was associated with a reduction in the cardiomyopathy of the two surviving patients while still providing effective immunosuppression. To our knowledge this observation has not been previously reported.
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6/89. mitral valve repair and septal myectomy for hypertrophic obstructive cardiomyopathy.

    Combined mitral valve repair using the sliding leaflet technique and septal myectomy were employed to successfully treat left ventricular outflow tract (LVOT) obstruction and mitral regurgitation due to hypertrophic obstructive cardiomyopathy (HOCM). A 46-year-old man was diagnosed with HOCM along with congestive heart failure and was treated medically. These symptoms, however, were resistant to medical treatments with a beta-blocker, a Ca-antagonist, and disopyramide, and he was referred to our hospital for surgery. Doppler echocardiography demonstrated an LVOT obstruction at rest with a peak pressure gradient of 138 mmHg. The interventricular septum thickness was 14 mm. Mitral regurgitation of 3 with severe SAM was also observed. Temporary dual chamber pacing was tried without significant improvement. Following these examinations, the patient underwent surgery. A transaortic septal myotomy-myectomy was performed first, and the mitral valve was then approached through the left atrium. mitral valve repair was performed with the sliding leaflet technique to reduce the height of the posterior leaflet from 2 cm to 1 cm. Postpump transesophageal echocardiography revealed no MR and a peak LVOT gradient of 15 mmHg. The patient recovered well except for a residual mild SAM, and MR2 . We therefore concluded that this surgical approach might provide results which are superior to those of myectomy alone.
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7/89. Anteroapical stunning and left ventricular outflow tract obstruction.

    Dynamic left ventricular outflow tract (LVOT) obstruction is typically observed in the setting of hypertrophic cardiomyopathy. It has also been reported with concentric LV hypertrophy, excessive sympathetic stimulation, and acute myocardial infarction. We describe 3 patients with chest discomfort after emotional stress, who had pronounced abnormalities on electrocardiograms, insignificant obstructive coronary disease and hemodynamic instability with LVOT obstruction, and regional wall motion abnormalities. Suppression of contractility with beta-blockers resulted in resolution of the gradient and in clinical improvement. On follow-up, functional recovery was excellent, and ventricular function had normalized. The conditions and mechanisms that may produce this sequence of events are discussed. The most probable scenario is that an acute ischemic insult secondary to vasospasm, LV stunning, and acute geometric remodeling produced a substrate for LVOT obstruction that was exacerbated by basal LV hypercontractility. The importance of this observation is that routine treatment of cardiogenic shock cannot be used and that conservative management results in excellent prognosis.
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8/89. Biventricular hypertrophic cardiomyopathy with right ventricular outflow tract obstruction associated with noonan syndrome in an adult.

    This report describes an adult patient with noonan syndrome accompanied by biventricular hypertrophic cardiomyopathy causing isolated right ventricular outflow tract obstruction. Biventricular hypertrophic cardiomyopathy causing right- and/or left-side outflow tract obstruction, as well as valvular pulmonary stenosis, is relatively common in infants with noonan syndrome. However, this condition without a dysplastic pulmonary valve, or indeed any polyvalvular dysplasia, is rare in adults with noonan syndrome. Treatment with a beta-adrenergic receptor blocking agent improved the patient's symptoms. Because neither the etiologic and prognostic relationship nor the genetic linkage between hypertrophic cardiomyopathy associated with noonan syndrome and non-syndromic hypertrophic cardiomyopathy is clearly defined, clinicopathological findings and further follow-up may provide important evidence for the pathogenesis of hypertrophic cardiomyopathy.
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9/89. Rare association of hypertrophic cardiomyopathy and complete atrioventricular block with prompt disappearance of outflow gradient after DDD pacing.

    Although arrhythmias are common in hypertrophic cardiomyopathy (HCM), complete atrioventricular (AV) block is very unusual. A 27-year-old female presented with a recent history of syncope and exercise intolerance. ECG demonstrated complete AV block. Two-dimensional Doppler echocardiography revealed HCM with a 60 mmHg left ventricular outflow tract (LVOT) gradient. A temporary transvenous ventricular pacemaker was inserted urgently, and subsequently replaced by a permanent DDD pacemaker. All symptoms were eliminated. This symptomatic improvement was associated with complete disappearance of LVOT gradient at the time of implantation. No gradient was observed during early follow-up and at 6 months after DDD pacemaker implantation.
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10/89. The Mount Sinai Hospital clinicalpathological conference: a 45-year-old man with Pompe's disease and dilated cardiomyopathy.

    This is an unusual case of a 45-year-old man, born in ecuador, with evidence of profound left ventricular dysfunction, dilated cardiomyopathy and marked myocardial hypertrophy. Preceding events were advanced atrioventricular block (necessitating pacemaker implantation) and atrial flutter. The diagnosis of Pompe's disease was established by endomyocardial biopsy and appropriate staining, which indicated abnormal glycogen storage.
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