Atrial Fibrillation in Hypothyroidism

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Atrial Fibrillation in Hypothyroidism

  1. 1. AN UNUSUAL PRESENTATION OF COMMON DISORDER Prof . Dr . G. Sundaramurthy’s unit, Dr. A.Prakash, PG,
  2. 2.  A 28 yr old female patient, Mrs.Neela, from vyasarpaadi, with  c/o episodic palpitations- 3 months  h/o associated chest pain- substernal,  Nonradiating, throbbing  h/o weight gain +  h/o constipation +  h/o menstrual disturbances +
  3. 3. No h/o  Sweating,  Dyspnoea  Giddiness  Syncope  Fever  Cough with expectoration  Abd pain, LOA  Bladder disturbances  Heat intolerance  Insomnia
  4. 4. Past & personal history  No h/o previous similar episode  Not a known DM, TB, HTN, BA, cardiac diseases, seizures  Taking mixed diet  Not an alcoholic & smoker
  5. 5. Menstrual history  Attained menarche at 14 yrs  Normal & regular – 3/30 moderate flow till 6 months back  Now, h/o menorrhagia -6 months  Increased flow --- 5 to 7 days  Not associated with abd pain & clots  Pt delivered 2 males, FTND  Last child birth -3 yrs back  No h/o any abortion
  6. 6. Family history & Rx history  Not relevant
  7. 7. Examination  Conscious, comfortable. oriented, afebrile  Well built & nourished  No pallor, no cyanosis, no clubbing, no significant lymphadenopathy  Hirsuitism +, no thyroid swelling  No pedal edema
  8. 8. vitals  HR- 140/min, irregularly irregular  PR- 126/min, irregularly irregular  Pulse deficit -14 BP- 120/70 mmHg  RR- 15/min  JVP –not raised  Temp- normal  Overweight (BMI 26)
  9. 9. Systemic examination  CVS- S1 S2 heard; tachycardia- irregularly irregular  RS- NVBS +, no added sounds  P/A soft not tender no organomegaly no free fluid  CNS- NFND
  10. 10. Provisional diagnosis  Palpitation for evaluation  ? AF
  11. 11. Investigation  ECG –  Rate 170/min.  Absent p wave.  RR irregularly irregular.  Rapid ventricular rate.  Imp ; AF with Rapid ventricular rate.
  12. 12. CXR normal
  13. 13. Investigations  Hb 12.8gm%  TC 8200  DC P60 L38 E2  ESR 6/12  PCV 37%  RBCs 5.2 million  Platelet count 2.3 lakhs
  14. 14.  Blood sugar 108 mg%  Urea 32mg%  Creatinine 0.9 mg%  Sr. Na 138meq/L  K 3.8 meq/L  Chloride 99 meq/L  HCO3 23 meq/L
  15. 15.  Cardiac enz- WNL  TFT- freeT4 0.4ng/dl (N- 0.58-1.64ng/dl)  Free T3 – 1.8 pg/ml (2.4-4.2pg/ml)  TSH 17mIU/ml (N-0.42-4.7 mIU/ml)  Sr. magnesium – 2.2 meq/L (1.5-2.5meq/L)  Sr.calcium – 9.2 mg% (9-11mg%)
  16. 16.  Cardiologist opinion- AF ?cause  Echo Normal LV function  No RWMA  EF 65%  Suggested  Inj. Diltiazem  T. verapamil  T. beta blocker
  17. 17. Diagnosis  AF  Hypothyroidism  AF –due to ? Hypothyroidism (?!!) or lone AF
  18. 18.  After initial one week treatment with verapamil and thyroxine ,AF converted to normal sinus rhythm.  After that patient continued thyroxine only, after one month, ECG taken ,it‘s normal SR.  So what could be the cause of AF ?
  19. 19. Case reports & journal evidence for AF due to hypothyroidism  the editorial by Forfar1 that both clinical and subclinical hyperthyroidism are associated with the subsequent development of atrial fibrillation. The association of hypothyroidism with atrial fibrillation is less recognised.2 3 For example, the Canadian Registry of Atrial Fibrillation Investigators4reported that 1.5% of 726 patients with atrial fibrillation had hypothyroidism over a period of 1.7 years. However, Tajiri et al reported that up to 8% of the 75 elderly patients with atrial fibrillation (mean age 75.6 years) studied were found to be hypothyroid -Heart 1997;78:623-624 doi:10.1136/hrt.78.6.623a
  20. 20.  There are also non-cardiac conditions that can lead to atrial fibrillation. Hyperthyroidism (high thyroid levels) is commonly accompanied by atrial fibrillation. On occasion, hypothyroidism (low thyroid levels) can also be accompanied by atrial fibrillation. -The Causes of Atrial Fibrillation By Richard N. Fogoros, M.D., About.com Guide Updated November 12, 2007
  21. 21.  Subclinical Hypothyroidism Might Increase the Risk of Transient Atrial Fibrillation -Ann Thorac Surg 2009;87:1846-1852. doi:10.1016/j.athoracsur.2009.03.032 © 2009 The Society of Thoracic Surgeons
  22. 22. C A S E R E P O R T JIACM 2009; 10(3): 140-2 * Fellow, Section of Cardiology, ** Associate Professor, Department of Medicine, Medical College of Georgia, 1120, 15th Street, Augusta, GA 30912, USA. Atrial Fibrillation in Hypothyroidism Dinesh Kumar Patel*, Jaspal S Gujral** Abstract A 27-year-old woman presented with palpitation, chest pain, and shortness of breath in the emergency room. Electrocardiogram revealed atrial fibrillation. Subsequent work-up was normal including oxygen saturation, chest X-ray, electrolytes, and echocardiogram, but showed clear evidence of primary hypothyroidism (sensitive thyroid stimulating hormone (TSH) of 14 mcIU/ ml and free T4 < 0.5 ng/dl). She was treated with appropriate thyroxin replacement without recurrence of atrial fibrillation. Key words: Atrial fibrillation, hypothyroidism, hyperthyroidism.
  23. 23. Conclusion This case is a reminder that hypothyroidism, as well as hyperthyroidism, can be associated with the development of atrial fibrillation, and careful vigilance is necessary
  24. 24. ATRIAL FIBRILLATION  Most common sustained arrhythmia  Characterized by disorganized rapid & irregular atrial activation  Ventricular response to rapid atrial activation is also irregular  Mechanism for AF initiation & maintenance also though debated appears to represent a complex interaction between drivers responsible for the initiation & complex anatomic Atrial substrate that promotes the maintenance of multiple wavelets of micro re entry  The drivers appear to originate predominantly from atrialized musculature that enters the pulmonary veins & either represent focal abnormal automaticity or triggered firing that is somewhat modulated by autonomic influence  Non pulmonary vein drivers has also been documented  The role of these drivers play in maintaining the tachycardias may also been significant & may explain the success of the pulmonary vein isolation procedure in eliminating more chronic & persistent form of AF
  25. 25.  AF is more common in adult population & children with structural heart disease  The incidence of AF increases with age such that 5 % of the adult population over 70 yrs will experience the arrhythmia  Because of more asymptomatic patients the overall incidence may be more than double of previously reported rates
  26. 26. Causes Cardiac causes Other causes •Structural heart diseases like MS, MR etc •Lung diseases such as pneumonia, lung ca, pulmonary embolism, sarcoidosis •Congenital heart diseases •CO poisoning •Coronary heart diseases •Low level of potassium, magnesium and calcium •Hypertension heart diseases •Pheochromocytoma •Cardiomyopathies •Hyper / hypothyroidism •hypothermia •Acute alcohol intoxication •Electrocution •Severe anaemia •Acute vagotonic episode •Acute or early recovery phase of major vascular abdominal & thoracic surgery (where autonomic fluxes and/or direct mechanical irritation potentiate the arrhythmia
  27. 27. Clinical features  Many patients are asymptomatic  Sometimes only minor palpitations or severe irregularities of the pulse  Or severe palpitation  Other features are hypotension, pulmonary congestion and anginal symptoms  Pt with Lv diastolic dysfunction (SHT, HOCM, AS) symptoms may be more dramatic especially if the ventricular rates doesn’t permit adequate ventricular filling  Exercise intolerance & easy fatigability are the hall marks of poor rate control with exertion  Occasionally the only manifestation of AF is severe dizziness or syncope ( associated with pause that occurs upon terminations of AF before sinus rhythm resumes)
  28. 28. General classification AF category Defininig charecteristics Paroxysmal Episodes of Af that typically lasts <24hrs but can last upto 7 days; these terminate spontaneously persistent Episodes of AF that lasts > 7 days and recur either pharmacological or electrical intervention to terminate permanent Continuous AF that has failed cardioversion or where cardioversion has never been attempted Lone AF Has been used to describe AF in individual without structural or cardiac pulmonary diseases with low risk for thrombo embolism it has traditionally been applied to patient younger that 60 yrs
  29. 29. Classification of AF by the ACC / AHA & ESC AF category Defining characteristics First detected Only one diagnosed episode Paroxysmal Recurrent episode that self terminate in <7 days Persistent Recurrent episode that last > 7 days permanent Ongoing long term episode
  30. 30. ECG  Lack of organized atrial activity & irregularly irregular ventricular response  Lead V1 may frequently show the appearance of organized atrial activity that mimic atrial flutter. This occurs because the crista terminalis serves as an effective anatomic barrier to electrical conduction & the activations of the lateral right atrium may be represented by a more uniform activation wave front that originate over the roof of the right atrium  So, ECG assessment of the PR interval & chaotic P wave morphology in remaining ECG leads will confirm the presence of AF
  31. 31. Rx  Depends upon clinical situation, chronicity and risk factors of stroke , hemodynamic impact of AF & ventricular rate  Acute rate control: the initial goal of therapy –  1) to establish control of the ventricular rate 2) to address the anticoagulant status & begin IV heparin Rx, if the duration of AF is >12 hrs & risk factors for stroke with AF are present  Drugs are Beta blocker & CCBs  Digoxin may add to the rate controlling benefit of the other agents
  32. 32.  Risk factors of stroke in AF  h/o stroke or TIA, MS, SHT, DM, CCF, >75 yrs, LV dysfunction, marked left atrial enlargement (>5cm), Spontaneous echo contrast  Chronic anticoagulation with warfarin targeting an INR b/w 2-3 is recommended in patients with persistent or frequent and long lived paroxysmal AF & risk factors  Heparin is maintained routinely until the INR 1.8 with the administration of warfarin after TEE  For patients who don’t warrant early cardioversion of AF, anti coagulation should be maintained for at least 3 weeks with the INR confirmed to be >1.8 on at least 2 separate occasions prior to attempts at cardioversion.  Direct current transthoracic cardioversion during short acting anasthesia is a reliable way to terminate AF. Conversion rates using a 200 joule biphasic shock delivered synchronously with the QRS complex typically are >90%.  Oral and/or IV administrations of amiodarone or procainamide have only modest success  iV ibutilide somewhat more effective  A single episode of AF may not warrant any intervention or only a short course of beta blocker therapy.  The presence of any significant structural heart disease typically narrows RX to the use of sotalol, amiodarone or dofetilide.
  33. 33.  In patient without evidence of structural heart disease or hypertensive heart disease without evidence of severe hypertrophy ,the use of class 1C Anti arrhythmic agent flecainide or propofenone appears to be well tolerated and doesn’t have significant proarrhythmia risk.
  34. 34. Chronic rate control  With more persistent form of AF, rate control, with beta blocker, CCB and/or digoxine can frequently be achieved.  Heart rate >80/min at rest or 100/min with very modest physical activity are indications that rate control is inadequate in persistent AF.  For that -a hiss bundle /AV junction ablation can be performed.  The ablation must be coupled with the implantations of an activity sensor pacemaker with maintaining a physiological range of heart rates.  Occasionally biventricular pacing may be used to minimize the degree of dyssynchronization that can occur with RV apical pacing alone.
  35. 35. Catheter and surgical ablative therapy to prevent recurrent AF  Most ablation strategies incorporate techniques that isolate an atrial muscle sleeves entering the pulmonary veins.  Patient with recurrent symptomatic AF, because of by this procedure , elimination of AF is 50-80%.  Risk related to left atrial ablation procedure albeit low[over all 2-4 %], include pulmonary vein stenosis, atrio esophageal fistula, systemic embolic event & perforation/tamponade.  Surgical ablation usually performed at the time of other cardiac valve or coronary artery surgery & less commonly as a stand alone procedure.  The cox surgical maze procedure is designed to interrupt all macro re entrant circuits that might potentially develop in the atria thereby precluding the ability of the atria to fibrillate.  The multiple incisions of the traditional cox maze procedure have been replaced with linear lines of ablation, and pulmonary vein isolation using a variety of energy sources
  36. 36.  Thank you

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