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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
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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
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Murthy PRK. Heart in Fours: Cardiology for Residents and Practitioners. 3rd edition. Jaypee: New Delhi.2013
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Neurosurg. 2008;110:321–327
7.
Lilly SL. Pathophysiology of heart disease: a collaborative project of medical students and faculty. 5 th edition.
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Kahaly GJ, Dillmann WH. Thyroid hormone action in the heart. Endocr Rev. 2005;26:704–728. doi:
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