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1/5. Atrial epicardial pacing with long stimulus to P wave interval in a patient with arrhythmogenic right ventricular dysplasia complicated by right atrial thrombosis.

    Atrial epicardial pacing with a long stimulus to P wave interval in a patient with arrhythmogenic right ventricular dysplasia complicated by right atrial thrombosis is discussed. arrhythmogenic right ventricular dysplasia (ARVD) is associated with a high incidence of malignant ventricular arrhythmias. Most patients with ARVD need antiarrhythmic drugs, catheter ablation, or an implantable cardioverter defibrillator. We report a patient with ARVD in whom effective treatment with sotalol caused severe, symptomatic sinus bradycardia requiring permanent pacing. Due to leftward displacement of the right ventricle and the presence of two thrombi in the right atrium, an epicardial atrial lead and AAI pacemaker were implanted. A long stimulus to P wave interval caused by severe dilatation of the right atrium was recorded. During a 6 months of follow-up on sotalol treatment there were neither ventricular tachycardia (VT) attacks nor pacing problems.
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2/5. Twenty-seven-year follow-up of arrhythmogenic right ventricular dysplasia.

    This case report describes clinical features, especially of surface ECG changes, observed for 27 years in a patient with arrhythmogenic right ventricular dysplasia (ARVD). The course of this patient was characterized by progressive deterioration of right ventricular function and progression of delayed potentials (so-called epsilon waves) following QRS complexes. However, the relation between ventricular arrhythmias and ECG changes or the degree of right ventricular abnormality was difficult to discern.
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3/5. Postoperative death in a patient with unrecognized arrhythmogenic right ventricular dysplasia syndrome.

    arrhythmogenic right ventricular dysplasia is an inherited disease causing fatty replacement of heart tissue. This disease often presents as T-wave inversion in the anterior leads of the electrocardiogram (ECG) with life-threatening ventricular arrhythmias. In older patients, progressive right and left ventricular failure can develop. This is a case report of postoperative death occurring in a 59-yr-old woman with undiagnosed arrhythmogenic right ventricular dysplasia after hepatic cystectomy. The patient had T-wave inversion in the inferior ECG leads and no history of arrhythmias. During general anesthesia, cardiovascular collapse occurred in the absence of arrhythmias that was unresponsive to resuscitation.
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4/5. The presence of epsilon waves in a patient with acute right ventricular infarction.

    Epsilon wave is an unusual electrocardiographical finding, which may appear in other pathological conditions besides the arrhythmogenic right ventricular dysplasia, particularly in the acute myocardial infarction of the right ventricle, the inferior, or the posterior wall of the left ventricle. Its real incidence in these acute coronary syndromes remains unknown and will be probably difficult to assert, since it may be unnoticed by inexperienced physicians because of its little voltage. The outstanding interest of this case lies in the clear electrocardiographical images and in the step-by-step differential diagnosis discussed by the authors.
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5/5. Novel mutation in desmoplakin causes arrhythmogenic left ventricular cardiomyopathy.

    BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a familial heart muscle disease characterized by structural, electrical, and pathological abnormalities of the right ventricle (RV). Several disease loci have been identified. Mutations in desmoplakin have recently been isolated in both autosomal-dominant and autosomal-recessive forms of ARVC. Primary left ventricular (LV) variants of the disease are increasingly recognized. We report on a large family with autosomal-dominant left-sided ARVC. methods AND RESULTS: The proband presented with sudden cardiac death and fibrofatty replacement of the LV myocardium. The family was evaluated. diagnosis was based on modified diagnostic criteria for ARVC. Seven had inferior and/or lateral T-wave inversion on ECG, LV dilatation, and ventricular arrhythmia, predominantly extrasystoles of LV origin. Three had sustained ventricular tachycardia; 7 had late potentials on signal-averaged ECG. Cardiovascular magnetic resonance imaging in 4 patients revealed wall-motion abnormalities of the RV and patchy, late gadolinium enhancement in the LV, suggestive of fibrosis. Linkage confirmed cosegregation to the desmoplakin intragenic marker D6S2975. A heterozygous, single adenine insertion (2034insA) in the desmoplakin gene was identified in affected individuals only. A frameshift introducing a premature stop codon with truncation of the rod and carboxy terminus of desmoplakin was confirmed by Western blot analysis. CONCLUSIONS: We have described a new dominant mutation in desmoplakin that causes left-sided ARVC, with arrhythmias of LV origin, lateral T-wave inversion, and late gadolinium enhancement in the LV on magnetic resonance images. Truncation of the carboxy terminus of desmoplakin and consequent disruption of intermediate filament binding may account for the predominant LV phenotype.
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