Atrial Fibrillation in Hypothyroidism

AN UNUSUAL PRESENTATION OF COMMON DISORDER

Prof . Dr . G. Sundaramurthy’s unit,Dr. A.Prakash, PG,

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 +

No h/o

Sweating, Dyspnoea Giddiness Syncope Fever Cough with expectoration Abd pain, LOA Bladder disturbances Heat intolerance Insomnia

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

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

Family history & Rx history

Not relevant

Examination

Conscious, comfortable. oriented, afebrile

Well built & nourished No pallor, no cyanosis, no clubbing, no

significant lymphadenopathy Hirsuitism +, no thyroid swelling No pedal edema

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)

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

Provisional diagnosis

Palpitation for evaluation ? AF

Investigation

ECG – Rate 170/min. Absent p wave. RR irregularly irregular. Rapid ventricular rate. Imp ; AF with Rapid ventricular rate.

CXR normal

Investigations

Hb 12.8gm% TC 8200 DC P60 L38 E2 ESR 6/12 PCV 37% RBCs 5.2 million Platelet count 2.3 lakhs

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

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%)

Cardiologist opinion- AF ?cause Echo Normal LV function No RWMA EF 65% Suggested Inj. Diltiazem T. verapamil T. beta blocker

Diagnosis

AF Hypothyroidism

AF –due to ? Hypothyroidism (?!!) or lone AF

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 ?

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

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 FibrillationBy Richard N. Fogoros, M.D., About.com Guide

Updated November 12, 2007

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

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 HypothyroidismDinesh Kumar Patel*, Jaspal S Gujral**AbstractA 27-year-old woman presented with palpitation, chest pain, and

shortness of breath in the emergency room. Electrocardiogramrevealed atrial fibrillation. Subsequent work-up was normal

including oxygen saturation, chest X-ray, electrolytes, andechocardiogram, 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.

ConclusionThis case is a reminder that

hypothyroidism, as well ashyperthyroidism, can be associated with

the developmentof atrial fibrillation, and careful vigilance is

necessary

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

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

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

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)

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

Classification of AFby 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

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

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

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.

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.

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.

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

Thank you