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Table of Contents
CASE REPORT
Year : 2018  |  Volume : 7  |  Issue : 1  |  Page : 46-48

Ventricular Arrhythmia and Left Ventricular Dysfunction: A Rare Manifestation of Adrenal Adenoma


1 Cardiovascular Intervention Research Center, Rajaie Cardiovascular Medical and Research Center, University of Medical Sciences, Tehran, Iran
2 Cardiac Electrophysiology Research Center, Rajaie Cardiovascular Medical and Research Center, University of Medical Sciences, Tehran, Iran
3 Department of Radiology, Rajaie Cardiovascular Medical and Research Center, University of Medical Sciences, Tehran, Iran

Date of Web Publication26-Feb-2018

Correspondence Address:
Dr. Mohammad Javad Alemzadeh-Ansari
Cardiovascular Intervention Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/rcm.rcm_16_17

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  Abstract 


Primary aldosteronism is characterized by hypertension, suppressed plasma renin activity, increased aldosterone excretion, and hypokalemia with metabolic alkalosis. Ventricular arrhythmia is an uncommon finding. We report the case of a 46-year-old female who was referred to our center due to uncontrolled ventricular arrhythmia. The past medical history was positive for hypertension. On admission, echocardiography showed severe left ventricular (LV) dysfunction. Blood examination revealed severe hypokalemia. She had been diagnosed with acute coronary syndrome and decompensated heart failure elsewhere and was given diuretics. A diagnosis of primary aldosteronism due to adrenal adenoma was made according to laboratory findings and imaging modalities. The prompt management of bradycardia and correction of hypokalemia, along with surgical resection of adrenal adenoma, resulted in control of arrhythmias and improvement in LV function.

Keywords: Aldosteronism, heart failure, hypokalemia, torsades de pointes


How to cite this article:
Alemzadeh-Ansari MJ, Emkanjoo Z, Mohebbi B, Pouraliakbar HR. Ventricular Arrhythmia and Left Ventricular Dysfunction: A Rare Manifestation of Adrenal Adenoma. Res Cardiovasc Med 2018;7:46-8

How to cite this URL:
Alemzadeh-Ansari MJ, Emkanjoo Z, Mohebbi B, Pouraliakbar HR. Ventricular Arrhythmia and Left Ventricular Dysfunction: A Rare Manifestation of Adrenal Adenoma. Res Cardiovasc Med [serial online] 2018 [cited 2021 Mar 9];7:46-8. Available from: https://www.rcvmonline.com/text.asp?2018/7/1/46/226160




  Introduction Top


Primary aldosteronism is one of the common forms of secondary hypertension (about up to 5%–10% hypertensive patients) and is characterized by hypertension with suppressed plasma renin, and, less frequently, hypokalemia.[1] In this disorder, prolongation of the QT (U) interval secondary to hypokalemia and aldosterone excess may occur. Although in some patients development of life-threatening arrhythmias such as torsades de pointes or ventricular fibrillation [1],[2],[3],[4],[5] has been reported, malignant arrhythmias are extremely rare in primary aldosteronism because of other contributing factors such as maintained QT dispersion in this disorder.[6]


  Case Report Top


A 46-year-old woman was referred to our hospital because of frequent ventricular arrhythmias. Two days ago, the patient presented to another hospital with complaints of palpitation, dizziness, and atypical chest pain. The patient was admitted with diagnosis of acute coronary syndrome. The past medical history was positive for diabetes mellitus, hypertension, asthma, and hypothyroidism. The patient underwent coronary angiography 2 years ago that revealed mild coronary artery disease. The drug history included levothyroxine 0.1 mg/day, glibenclamide 5 mg/day, triamterene hydrochlorothiazide 1 tablet/day, and metoprolol 50 mg/day. After admission, because of low left ventricle systolic dysfunction (LVEF) (20%) and acute coronary syndrome, the triamterene hydrochlorothiazide and metoprolol were stopped and drugs including acetylsalicylic acid 80 mg/day, clopidogrel 75 mg/day, atorvastatin 40 mg/day, glyceryl trinitrate 2.6 mg BID, carvedilol 6.25 mg BID, losartan 12.5 mg BID, enoxaparin 60 mg subcutaneous BID, and furosemide 20 mg BID were prescribed. The laboratory data including cardiac biomarkers and electrolytes level were unremarkable, except the low serum potassium level (2.9 mEq/L). During the hospitalization, frequent premature ventricular contractions (PVCs) and some episodes of ventricular arrhythmia occurred, necessitating electrical cardioversion and intravenous infusion of amiodarone. In addition, furosemide was discontinued and intravenous infusion of potassium chloride was started. Due to uncontrolled arrhythmia, she was referred to our hospital.

On admission, her medical records in previous hospitalization were reviewed. The electrocardiogram (ECG) showed the prominent U wave and prolonged QT interval; in addition, episodes of polymorphic ventricular tachycardia compatible with torsades de pointes were recorded [Figure 1]. The physical examination showed elevated blood pressure (180/110 mmHg), and ECG revealed bradycardia accompanied with short-coupled polymorphic PVCs [Figure 2]. Laboratory findings including electrolyte, cardiac biomarkers, thyroid enzymes levels, and serum protein and albumin level were in normal ranges, except the low level of serum potassium (2.2 mEq/L) accompanied with metabolic alkalosis (pH: 7.55, PCO2:39, and HCO3:34). During ECG monitoring in emergency department, frequent short-coupled polymorphic PVCs were recorded. Her medications including carvedilol and amiodarone were stopped, and she put on intravenous infusion of isoproterenol 5 mcg/min for increasing resting heart rate and intravenous nitroglycerin for control of hypertension. In addition, intravenous magnesium sulfate, potassium chloride 15%, and spironolactone 50 mg/day were administrated. In addition, percutaneous temporary pacemaker was implanted and then the patient was transferred to coronary care unit. The transthoracic echocardiography revealed moderate left ventricle enlargement with severe LVEF of 15%–20%, global hypokinesia with preserved tissue, moderate tricuspid regurgitation with moderate pulmonary hypertension (systolic pulmonary artery pressure of 60 mmHg), and small pericardial and bilateral plural effusion. The cardiac magnetic resonance imaging also confirmed the echocardiography findings; however, no sign of late gadolinium enhancement was seen.
Figure 1: During monitoring in previous hospital, frequent short-coupled polymorphic premature ventricular contractions and some episodes of torsades de pointes were recorded

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Figure 2: At presentation to our hospital, electrocardiogram showed sinus bradycardia, prominent U wave, reduced P- and T-wave amplitude, prolonged QT (U) interval, and short-coupled polymorphic premature ventricular contractions

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Regarding the high suspicion of hyperaldosteronism, specific laboratory examinations including the level of plasma aldosterone and renin, 24 h urine collection for the evaluation of metanephrine, vanillylmandelic acid, norepinephrine, and epinephrine were requested and confirmed the diagnosis. Abdominal magnetic resonance imaging was performed that revealed a 23.8 mm mass in the left adrenal [Figure 3]. Surgical resection of tumor was scheduled and left adrenalectomy was performed using laparoscopic approach. The pathology study showed the adrenal neoplastic mass composed of proliferation of compact polygonal cells characterized by increased variation in nuclear size and abundant eosinophilic cytoplasm arranged in nests and cords pattern, without any sign of mitosis. These findings confirmed the diagnosis of adrenocortical adenoma. After 3-month follow-up, the symptoms were improved, blood pressure was controlled, and serum potassium level was in the normal range. Interestingly, the LVEF was increased (55%), and other abnormal echocardiography findings were improved.
Figure 3: Abdominal magnetic resonance imaging showed a mass in the left adrenal

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  Discussion Top


Our patient had a history of uncontrolled hypertension and been treated as decompensated heart failure. Another contributing factor to raising potassium level, along with adrenal adenoma, may be the prescription of furosemide. Although after measurement of serum potassium level, the furosemide was discontinued and infusion of potassium chloride was initiated, it was not sufficient to normalize the potassium level. In addition, the misdiagnosis of arrhythmia as a ventricular tachycardia in the context of acute coronary event and then the administration of carvedilol with amiodarone accelerated the course of arrhythmia with even more decrease in heart rate and prolongation of QT (U) interval.[7] In addition, β-blockers are known to decrease the outward potassium current. After referring the patient to our hospital, controlling the heart rate and treatment of hypokalemia with potassium chloride and spironolactone led to control of the ventricular arrhythmia. Regarding the presence of hypertension, hypokalemia, and metabolic alkalosis, the diagnosis of hyperaldosteronism was suggested. After adrenalectomy, the arrhythmia was stopped and LVEF was improved. Improvement of ventricular arrhythmia and LVEF was also described after surgery in the case of pheochromocytoma.[8] Increase in serum aldosterone level is correlated with heart failure,[9] so reduction in serum aldosterone level by drugs or in the case of adrenal adenoma by surgical removing could improve the systolic function.

We report an unusual case of adrenal adenoma, presenting with malignant ventricular tachycardia and severe left ventricular dysfunction. This case highlighted the risk of hypokalemia-induced malignant ventricular tachycardia, in particular when diuretic treatment for hypertension is associated.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Rossi GP, Pessina AC, Heagerty AM. Primary aldosteronism: An update on screening, diagnosis and treatment. J Hypertens 2008;26:613-21.  Back to cited text no. 1
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2.
Abdo A, Bebb RA, Wilkins GE. Ventricular fibrillation: An extreme presentation of primary hyperaldosteronism. Can J Cardiol 1999;15:347-8.  Back to cited text no. 2
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3.
Curry P, Fitchett D, Stubbs W, Krikler D. Ventricular arrhythmias and hypokalaemia. Lancet 1976;2:231-3.  Back to cited text no. 3
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4.
Sade E, Oto A, Oto A, Oner Z, Daver A, Onalan O, et al. Adrenal adenoma presenting with torsade de pointes – A case report. Angiology 2002;53:471-4.  Back to cited text no. 4
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5.
Zelinka T, Holaj R, Petrák O, Strauch B, Kasalický M, Hanus T, et al. Life-threatening arrhythmia caused by primary aldosteronism. Med Sci Monit 2009;15:CS174-7.  Back to cited text no. 5
    
6.
Yang TY, Cheng NJ, Ko YS, Kuo CT. QT interval is prolonged but QT dispersion is maintained in patients with primary aldosteronism. Int J Clin Pract 2007;61:392-6.  Back to cited text no. 6
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7.
Schrickel JW, Schwab JO, Yang A, Bitzen A, Lüderitz B, Lewalter T, et al. “Torsade de pointes” in patients with structural heart disease and atrial fibrillation treated with amiodarone, beta-blockers, and digitalis. Pacing Clin Electrophysiol 2006;29:363-6.  Back to cited text no. 7
    
8.
Roshan J, George OK, Vineet S, George PV, Jose VJ. Torsade de pointes in a case of pheochromocytoma – An unusual presentation of an uncommon disease. Indian Heart J 2004;56:248-9.  Back to cited text no. 8
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9.
Weber KT. Aldosterone in congestive heart failure. N Engl J Med 2001;345:1689-97.  Back to cited text no. 9
[PUBMED]    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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