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Transcript
Sinus Node Dysfunction in elderly patient with Pituitary Apoplexy and Rheumatic Heart Disease (A Case Report) Raymond Pranata1, Vito Damay2, Antonia Anna Lukito2, Wendy Wiharja1, Abraham Fatah1 1 Faculty of Medicine, University Pelita Harapan, Tangerang, Indonesia 2 Department of Cardiology and Vascular Medicine, Siloam Hospital Lippo Village, Tangerang, Indonesia INTRODUCTION Sinus node dysfunction (SND) refers to abnormalities in sinus node (SN) impulse formation and propagation and its clinical spectrum includes sinus bradycardia, sinus pause/arrest, sinoatrial exit block and chronotropic incompetence.1,2 CASE REPORT 68 y.o male presents with diplopia and frequent vomiting since 4 days before admission. Syncope (-), chest pain (-) and dyspnea (-). HR 50 b.p.m and diastolic murmur characteristic of mitral stenosis was found. Bitemporal hemianopsia (+). Laboratory findings reveal: panhypopituitarism. EKG: Sinus Bradycardia. Echocardiography: Left atrial dilatation, moderate mitral stenosis and mild regurgitation, moderate aortic stenosis and severe regurgitation with EF 46-48% suggestive of rheumatic heart disease. CTA and MRI reveals pituitary macroadenoma with feature of apoplexy. Patient was diagnosed with pituitary apoplexy and panhypopituitarism with stable bradycardia and rheumatic heart disease. Endoscopic transphenoidal surgery was performed. Patient was given hormone replacement. DISCUSSION This patient has sinus bradycardia; which is due to SND. There are few possible etiologies, in elderly patient, an age-related degeneration is a possibility, in which pathologically by fibrous replacement of the SA node or its connections to the atrium. Intrinsic heart rate decreases while sinoatrial conduction time increases with aging and senescent sinus node also exhibited increased action potential duration.3,4 Inflammatory processes may alter SA node function, ultimately producing replacement fibrosis hence, rheumatic heart disease is linked with SND.4,5 Increased intracranial pressure as the result of pituitary apoplexy may cause increased in parasympathetic tone, reducing probability of If channel opening, inhibiting depolarization.6,7 T3 hormone increases If pacemaker ion current in the sinoatrial node through hyperpolarization cyclic nucleotide (HCN) gene products. The L-type Ca channel ID, which also serves important pacemaker functions, is also increased by T3. Secondary hypothyroidism (due to pituitary apoplexy casuing pan-hypopituitarism) in this patient results in reversed physiology and hence slow heart rate.8 Stable bradycardia requires only observation without pacemaker be it temporary or permanent. Treatment of the lethal problem (pituitary apoplexy) is more urgent in this patient. CONCLUSION There are various etiologies of sinus node dysfunction and they may overlap. Keywords: Bradycardia, Sinus Node Dysfunction, Pituitary Apoplexy, Rheumatic heart disease References 1. Epstein AE, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008 May 27. 51(21):e1-62. 2. Epstein AE, et al. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013 Jan 22. 61(3):e6-75. 3. Zipes DP, Jalife J. Cardiac electrophysiology : From cell to bedside. 6th edition. Philadelphia: Elsevier; 2014.p.925931 4. Kasper DL, Fauci AS, Hauser SL et al. Harrison's Principles of Internal Medicine, 19 th edition. New York, NY: McGraw-Hill; 2015. 5. Murthy PRK. Heart in Fours: Cardiology for Residents and Practitioners. 3rd edition. Jaypee: New Delhi.2013 6. Agrawal A, Timothy J, Cincu R, Agarwal T, Waghmare LB. Bradycardia in neurosurgery. Clin Neurol Neurosurg. 2008;110:321–327 7. Lilly SL. Pathophysiology of heart disease: a collaborative project of medical students and faculty. 5 th edition. Philadelphia: LWW.2010 Kahaly GJ, Dillmann WH. Thyroid hormone action in the heart. Endocr Rev. 2005;26:704–728. doi: 10.1210/er.2003-0033. 8.