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1/55. Anaesthetic considerations in a patient with lepromatous leprosy.

    PURPOSE: To consider the anaesthetic problems in a patient with lepromatous leprosy undergoing general anaesthesia. CLINICAL FEATURES: A 52 yr old man with lepromatous leprosy for five years was booked for elective radical nephrectomy. He received 100 mg dapsone per day po. The patient was asymptomatic for cardiovascular disease but his electrocardiogram showed complete left bundle branch block, inferior wall ischaemia with echocardiogram findings of 58% ejection fraction and left ventricular diastolic dysfunction. Other preoperative investigations (haemogram, serum urea and creatinine, liver function tests and chest X-ray) were normal. After premedication with diazepam, meperidine and promethazine, the patient received glycopyrrolate and anaesthesia was induced with thiopentone. atracurium was given to facilitate tracheal intubation. Anaesthesia was maintained with intermittent positive pressure ventilation using N2O in oxygen with halothane. Anaesthesia and surgery were uneventful except that the patient had a fixed heart rate that remained unchanged in response to administration of anticholinergic, laryngoscopy, intubation and extubation. CONCLUSION: patients with lepromatous leprosy may have cardiovascular dysautonomia even when they are asymptomatic for cardiovascular disease.
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2/55. myocardial stunning in hyperthyroidism.

    The cases of two patients with hyperthyroidism and acute left ventricular (LV) dysfunction with segmental wall motion abnormalities resulting in heart failure are reported. Both had electrocardiographic changes mimicking ischemic coronary artery disease. Treatment with antithyroid medications, beta blockers, and angiotensin-converting enzyme inhibitors rapidly restored LV function. The rapid reversibility suggests a role for myocardial stunning, an important entity to recognize in hyperthyroidism since this form of LV dysfunction can be reversed with appropriate treatment.
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3/55. Diffuse and severe left ventricular dysfunction induced by epicardial coronary artery spasm.

    Endothelial dysfunction and effectiveness of treatment of calcium antagonists are suggestive of coronary artery spasm as an underlying disorder in dilated cardiomyopathy (DCM). The aim of this study is to determine whether or not the epicardial coronary artery spasm can induce severe cardiac dysfunction like DCM. Thirty-four consecutive patients with angiographically normal coronary arteries and diffuse left ventricular hypokinesis whose causes had been unknown underwent acetylcholine provocation test and left ventricular biopsy. Eight patients were excluded according to the clinical and laboratory data and biopsy findings suggesting myocarditis or other systemic diseases. According to the results of the acetylcholine provocation test, 17 patients were finally diagnosed as having DCM, and nine patients (35% of the study patients), who had acetylcholine-induced diffuse and multivessel coronary spasm, were diagnosed as having DCM-like vasospastic angina pectoris (VSA). Clinical and cardiac catheterization data including hemodynamics and biopsy findings were similar between the two groups except that left ventricular end-systolic volume was significantly greater in DCM than in DCM-like VSA. After the acetylcholine provocation test, DCM patients received both a beta blocker and an angiotensin-converting enzyme inhibitor, and DCM-like VSA patients received antianginal drugs. In echocardiographic findings at predischarge and those after 6-month drug treatment, both DCM-lke VSA and DCM showed significant reduction in end-diastolic and end-systolic diameters and significant increase in fractional shortening and ejection fraction, whereas changes in ejection fraction and fractional shortening were significantly greater in DCM-like VSA than those in DCM. Epicardial coronary artery spasm can induce diffuse and severe left ventricular dysfunction like DCM in VSA. Although antianginal drugs markedly improve left ventricular function of these patients, only the acetylcholine provocation test can identify DCM-like VSA.
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4/55. Reduction of symptoms from LVOT tachycardia following inadvertent fast pathway ablation.

    VT was mapped to above the aortic valve in a young patient with troublesome palpitations. A single 15-second RF application was inadvertently delivered to a reference His catheter producing permanent first-degree heart block. The patient has been completely asymptomatic since.
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5/55. 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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6/55. Pacing-induced left ventricular dysfunction. Relationship with coronary perfusion.

    In a patient admitted with symptomatic complete heart block, a DDD pacemaker was implanted. Prior to implantation, echocardiography showed normal left ventricular function. Shortly after implantation, acute congestive heart failure developed with extensive regional hypo- and akinetic segments in the anteroseptal, anterolateral and apical region. Subsequent perfusion imaging with methoxyisobuticeisonitrite (MIBI) at rest demonstrated hypoperfusion in the same regions while coronary angiography showed normal epicardial coronary vessels. Thus, impaired regional coronary flow can be associated with cardiac stimulation, inducing marked deterioration of left ventricular function.
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7/55. Diagnostic superiority of continuous-loop electrocardiographic recording over other testing in a patient with recurrent syncope and underlying coronary artery disease with severe left ventricular dysfunction.

    Dysrhythmic causes of syncope may elude diagnosis in postinfarction patients despite elaborate testing, including electrophysiologic study. For a correct diagnosis, capture of cardiac rhythm during patient's typical symptoms is crucial. This report describes a patient with coronary artery disease and decreased left ventricular ejection fraction who experienced recurrent syncopal episodes without obvious precipitating factors. The 12-lead electrocardiogram showed left bundle-branch block indicating a possible conduction abnormality as the underlying cause of syncope. Twenty-four-h Holter monitoring exhibited no sinus rhythm or conduction disturbances but revealed a nonsustained run of ventricular tachycardia. Findings at electrophysiologic testing led to a presumptive diagnosis of tachyarrhythmic cause of syncope; however, the correct diagnosis was only made with use of a loop monitor which documented a 15-s sinus pause during a syncopal episode.
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8/55. 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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9/55. hypotension and functional left ventricular obstruction during dobutamine stress echocardiography--two case reports.

    Although hypotension during dobutamine stress echocardiography has been reported, the mechanism of this response is still controversial. In two patients, a 72-year-old woman and 64-year-old man, with exercise-induced ST-T change, continuous-wave Doppler examination of the left ventricular cavity was performed at baseline and peak dobutamine infusion. No echocardiographic abnormalities at rest or angiographic coronary lesions were observed in either patient. The intracavitary pressure gradient at peak dosage of dobutamine for both patients was 121 mm Hg and 100 mm Hg, and was reproducibly confirmed by cardiac catheterization. During dobutamine infusion, echocardiography or left ventriculography revealed that papillary muscle motion was dramatically augmented by dobutamine and mid-left ventricular obstruction was produced at the systolic phase. Although blood pressure response improved following beta-blocker treatment, intracavitary pressure gradient during dobutamine infusion remained the same. A hypotensive response during dobutamine stress echocardiography may be produced by the development of dynamic intraventricular obstruction and a vasodepression reflex. The exercise-induced electrocardiographic changes may have been related to the systolic pressure augmentation in the mid-to-apical left ventricular cavity.
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10/55. Electroanatomic substrate of idiopathic left ventricular tachycardia: unidirectional block and macroreentry within the purkinje network.

    BACKGROUND: An abnormal potential (retroPP) from the left posterior Purkinje network has been demonstrated during sinus rhythm (SR) in some patients with idiopathic left ventricular tachycardia (ILVT). We hypothesized that this potential can specifically be identified and be a critical substrate for ILVT. methods AND RESULTS: In 9 patients with ILVT and 6 control patients who underwent mapping of the left ventricle during SR using 3-dimensional electroanatomic mapping, an area with retroPP was found within the posterior Purkinje fiber network only in patients with ILVT. The earliest and latest retroPP was 185.4 /-57.4 and 465.2 /-37.3 ms after Purkinje potential; in the other patient with ILVT, an entire left ventricle mapping demonstrated a slow conduction area and passive retrograde activation along the posterior fascicle during ILVT. ILVT was noninducible in 3 patients after SR mapping. Diastolic potentials critical for ILVT during ILVT coincided with the earliest retroPP during SR in 7 patients. Mechanical termination of ILVT occurred in 5 patients. A single radiofrequency pulse was applied at the site with mechanical translation in 5 patients and the site with diastolic potential in 2 patients, and 3 radiofrequency pulses were delivered to the site with the earliest retroPP in the other 3 patients without inducible ILVT after SR mapping. No ILVT was inducible during control stimulation, and none recurred during follow-up of 9.1 /-5.1 months. CONCLUSION: In patients with ILVT, abnormal retroPP within the posterior Purkinje fiber network is a common finding. The earliest retroPP critical for ILVT substrate can be used for guiding successful ablation.
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