Abstract: Slide Presentations |


Ioannis Angomachalelis, *; Drosos Tsavlis; Alexander Hourzamanis, DSc; Chrysostomos Sofoudis, MD; Vassilios Tsaousis, MD; Evangelia Nena, MD; Alexander Sfikas; Nestor Angomachalelis, DSc
Author and Funding Information

Department of Internal Medicine, Pulmonary Diseases, Heart –Lung Section, “Geor, Thessaloniki, Greece


Chest. 2008;134(4_MeetingAbstracts):s42003. doi:10.1378/chest.134.4_MeetingAbstracts.s42003
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PURPOSE:Sarcoidosis is frequently complicated with myocardial or myo-pericardial involvement. The goal of this study was to investigate manifestations and discuss understanding and clarification of asymmetric septal hypertrophy (ASH) mimicking hypertrophic cardiomyopathy (HCM) which, when first clinically diagnosed, masks cardiac sarcoidosis by the suspected HCM.

METHODS:Eighty three consecutive patients (mean age 49±12 years) with biopsy-proven pulmonary and/or systemic sarcoidosis, free of other evident cardiovascular pathology or hepatitis C virus infection, underwent :1. Clinical and ECG examination 2. M-mode, Two-Dimensional and Doppler Echocardiography, 3. Tc-99m-pyp myocardial imaging, classified by computer analysis depending on the isotope activity and the percent bias of the isotope uptake between myocardial and right parasternal area.

RESULTS:1) ECG mainly non-specific abnormalities were found in less than 10% of the patients studied 2) 36% of patients showed signs of ASH = IVST / LVWT ≥ 1.3, occasionally followed by localized septal or apical hypertrophy and mitral valve systolic anterior motion. 3) Myocardial scintigrafy in 47/83 sarcoidosis patients manifested abnormal isotope uptake in 70%, while 40.6% of ASH patients had also abnormal uptake. 4) Diastolic abnormalities and pericardial effusion were found in 36% and 40% of ASH patients respectively.

CONCLUSION:36%–40% of sarcoidosis patients may present with echo signs of ASH mimicking HCM of unknown origin.However, about 40% of them or 14% of the totals, simultaneously develop abnormal Tc-99m-pyp myocardial scintigraphy, ventricular diastolic dysfunction and pericardial effusion, possibly compatible to and leading to sarcoidosis cause of ASH myocardial changes mimicking HCM, while the remaining group of 60% ASH patients (22% of the totals) seems to be a completely unknown entity also mimicking or representing real HCM. The present study suggests that further investigation should clarify origin and cause of both groups ASH and decide if this is a result of inflammatory process and consequently sarcoidosis may present as, or may cause, HCM.

CLINICAL IMPLICATIONS:Additional studies should clarify the original cause of ASH mimicking HCM and train doctors and patients to recognise and prevent the risk of sudden cardiac death if existed in fact.

DISCLOSURE:Ioannis Angomachalelis, None.

Tuesday, October 28, 2008

10:30 AM - 12:00 PM




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