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Transcript of Presented by: Fran Connolly. Prime Care Physicians Preceptor: Dr. Jose David Completed his residency...
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Case Study: Brugada’s Syndrome
Presented by: Fran Connolly
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Prime Care PhysiciansPreceptor: Dr. Jose David
• Completed his residency at Albany Medical College in 1991
• Started at Prime Care in 1997
• Board Certified in Family Practice in 2003
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Patient & Encounter
M.E. is a 28 year old white male who presents in his primary care office for his annual physical exam on March 27, 2014.
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History of Present Illness• Initial visit:
2/5/2013
• Pt c/o intermittent palpitations, felt his heart beating fast & irregular.
• Episodes last 3-4 hours and stop spontaneously, usually happened at night.
• Denied any C.P., syncope, SOB or dizziness.
• At that visit pt received Holter monitor for 24 hour period which showed a 4 hour episode of paroxysmal atrial fibrillation that was symptomatic.
• He stated most of the time events were triggered by large meals or alcohol.
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HPI (continued)
• Pt was started on Toprol XL 50 mg PO daily & Aspirin 325 mg PO daily
• Second visit: 3/8/2013
• Pt states he has been having several episodes of a-fib over the past two weeks, lasts a couple of hours.
• Changed medication to Rythmol 225 mg PO BID
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HPI (continued)Third visit: 4/29/2013• f/u pt had AICD pacemaker placed on
4/21/2013.
• Pt was jogging and had a syncopal episode, which he woke spontaneously from. Brought to the ER which his EKG revealed evidence of Brugada syndrome, pacer placed.
• D/C on Sotalol 160 mg PO BID, Toprol XL 50 mg PO BID & ASA 81 mg PO daily.
• Driving restriction placed for 6 months.
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HPI (continued)Fourth visit: 7/9/2013
• Pt continues with daily, intermittent episodes of a-fib
• f/u and plan for radio frequency ablasion therapy
• pt started on Coumadin
• Tests ordered prior to ablasion: TEE & CT chest
• Ablasion done on 9/12/2013 without incidence.
Visits up-to-date of 3/27/2014:
•Med changes: Currently on Toprol XL 50 mg PO BID & ASA 81 mg PO daily.
•Currently awaiting insurance approval for genetic testing regarding Brugada’s syndrome, denied the first time and there is an appeal in to the insurance company.
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Past Medical History
• Mononucleosis, hospitalized for 2 days 6/2007.
• Denies all other history including HTN, hyperlipidemia, stroke, lung disease, asthma, liver, kidney or gallbladder disease, cancer, diabetes, thyroid, hepatitis, TB or psychiatric disorders.
• Denies any allergies to drugs, food, latex or environment.
• Only medications are Toprol XL 50 mg PO BID & ASA 81 mg PO daily.
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Social History:• Married with a 6
year old son.
• Employed as an investment banker, financially secure.
• Denies smoking or illicit drug use, states he rarely drinks alcohol or caffeine.
• Exercises 5x week, 1 hr day.
Family History:• Mother- DMII
• Father- HTN
• PGF- deceased @ 52 from MI
• P (great) GF – deceased @ 60 from MI
• Denies any other family history of cardiac issues
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Review of Systems:• General: Denies any fever,
chills, fatigue, night sweats, appetite or weight changes.
• Head: Denies any headache, dizziness, syncope or head injuries
• Resp: Denies any pain, dyspnea, orthopnea, wheezing, asthma, bronchitis, hemoptysis or SOB.
• CV: Denies any C.P., murmurs, edema or palpitation @ this visit.
• Neuro: Denies any fainting, seizures, numbness, loss of sensation or tingling, tremors, speech difficulties or change in memory.
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Physical FindingsConstitutional: BP106/72, HR 68, RR 16,
98% Ht: 6’5” Wt: 212 lbs
BMI: 26General: Well nourished, well developed man. Alert & oriented x 3. Calm & cooperative. Appropriate mood & affect.Skin: Pink, warm & dry. No rashed or lesions. Scar over pacer placement on right chest wallResp: Pt sitting upright, resp resting 16/min, regular & even. Chest expansion symmetric. No tenderness to palpation. Lungs clear throughout lung fields anterior & posterior. No rales, rhonchi or wheezes heard.
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Physical FindingsCV: S1S2 present in APETM w/ bell & diaphragm. Regular apical rate. No heaves or thrills. No murmurs, rubs, gallops or clicks. RRR. Apical pulse not palpable in 5th ICS @ LMC. Carotids 2+ equal bilat, internal jugular veins pulsation not present. PV: Extremities pink, warm to touch. No edema. Pulses 2+ symmetric in radial & dorsalis pedals. No varicosities. Cap refill <3 seconds. No carotid bruit.
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Differential Diagnosis• Paroxysmal atrial fibrillation
(427.31)
• Cardiac dysrhythmia (427.9)
• Paroxysmal supraventricular tachycardia (427.0)
• Hyperthyroidism (242.9)
• Brugada’s syndrome (746.89)
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Diagnostic Tests• EKG (2/5/13)- sinus rhythm. Rate 67.
PR 188 QRS 118 QT 401. RSR Prime in lead V1 suggests right ventricular conduction delay. Poor R-wave progression.
• Holter (2/5/13)- SR w/ low grade atrial & ventricular ectopy & 4 hour episode of A-fib
• ECHO (2/15/13)- Mild left ventricular hypertrophy. Dilated left atrium.
• CT chest (8/21/13)- 4 pulmonary veins
• TEE (8/21/13)- left ventricle is mildly dilated w/ normal systolic function (EF 60%), mild left atrial enlargement.
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Labs• Cholesterol 189, triglycerides
121, HDL 42, LDL 123
• WBC 5.9, H/H 49/15, PLT 304
• Glucose 110, K 4.0, Ca 8.7
• BUN 133333, Cr 1.2
• AST 18, ALT 21
• TSH 2.253, T4 7.7, T3 34, & free TI 2.6
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Diagnosis
• Atrial Fibrillation (427.31)
• Brugada’s Syndrome (746.89)
• However awaiting genetic testing to confirm 2nd dx.
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Brugada’s Syndrome• Potentially life-threatening heart rhythm
disorder (Mayo Clinic, 2011).
• This is a disorder characterized by an EKG pattern which has an incomplete right bundle branch block & ST-segment elevations in the anterior precordial leads (Dizon & Zanif, 2014)
• This EKG abnormality is known as the type -1 Brugada syndrome EKG & combined with an absence of heart abnormalities will give the diagnosis.
• This type of EKG is linked to increase risk for ventricular tachyarrhythmias, cardiac arrest & sudden death.
• Shows familial aggregation.(Postema, et al., 2009)
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Brugada’s Syndrome• It is recognized to cause sudden
cardiac death at a relatively young age and most patients are asymptomatic.
• The typical patient is a young, male, and otherwise healthy, with normal general medical and cardiovascular physical examinations.
• Genetic testing can be done for mutation in SCN5A.
(Dizon & Zanif, 2014)
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Signs & Symptoms• Syncope and cardiac arrest: in
many cases, cardiac arrest occurs during sleep or rest
• Nightmares or thrashing at night
• Asymptomatic, but routine ECG shows ST-segment elevation in leads V1-V3
• Associated atrial fibrillation (20%)
• Fever: Often reported to trigger or exacerbate clinical manifestations
(Dizon & Zanif, 2014)
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Pathophysiology• A disease caused by an alteration in
the transmembrane ion currents that together constitute the cardiac action potential.
• In 10-30% of cases a mutation of the SCN5A gene, which encodes the cardiac voltage-gated sodium channel have been found.
• This reduces the sodium current available during early repolarization & hence the ST elevations on EKG.
(Dizon & Zanif, 2014)
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Etiology• SCN5A gene mutation
• Many drugs can induce the type-1 EKG in Brugada syndrome & should be avoided:• Antiarrhythmics- Rythmol,
Procainamide
• Psychotropics- amitriptyline, lithium, nortriptyline
• Anesthesia- bupivacaine, propofol
• Tramadol, Benadryl, Reglan
(Postema, et al., 2009)
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Incidence• Most common in people from
Asia. In Asia it is the most common cause of natural death in men younger than 50. approximately 30:100,000.
• It is 8-10x more prevalent in men.
• Most commonly affects men between 30-50 who are other-wise healthy.
• The mean age of sudden death is 41 years old.
• An estimated 4% of sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts are due to the syndrome.
(Dizon & Zanif,2014)
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PlanInterventions:
• The only treatment proven effective presently is the implantation of an automatic implantable cardiac defibrillator (AICD).
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Review of Literature• described as a new clinical entity in
1992
• The syndrome may also be unmasked or precipitated by a febrile state, β-adrenergic blockers, tricyclic antidepressants, and hypokalemia, as well as by alcohol and cocaine toxicity.
• In the case of M.E. he first started noticing his symptoms after consuming alcohol & he did not have a syncopal episode until he was placed on Rythmol.
• Atrial fibrillation (AF) is reported in approximately 10%-20% of cases
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Review of Literature• The appearance of a right bundle
branch block (RBBB) morphology in Brugada patients may be due at least in part to early repolarization of RV epicardium.
• Sudden death usually occur at rest and at night,
• M.E. typically felt his heart racing with palpitations at night when lying down.
• The effectiveness of ICD preventing sudden cardiac death was 100% in a recent trial in which 258 patients dx with Brugada syndrome received an ICD.
(Antzelevitch & Fish, 2006)
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Education• Family should be educated on
CPR
• There should be s/p AICD insertion education
• The patient should be educated on medications that should be avoided
• They should also make any & all provider aware of their diagnosis
• They should be instructed to avoid alcohol, caffeine & cocaine
• They can also have their family members tested for the gene as well.
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Follow -up• Currently he is seen every 3
months by cardiology.
• He is seen in the PCP office every 6 months.
• Awaiting the authorization from insurance for genetic testing to be done.
• Was told to f/u sooner if having any s/s such as palpitations that do not subside after 2 hours.
• Was told to go straight to the ER for any syncopal/near-syncopal episodes or if AICD fires.
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ReferencesAntzelevitch, C. & Fish, J.M. (2006). Therapy for the
Brugada syndrome. Handb Exp Pharmacology (171). 305-330. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1474239/
Dizon, J.M. & Zanif, T.M. (2014) Brugada Syndrome. Retrieved from http://emedicine.medscape.com/article/163751-overview#aw2aab6b2b3aa
Mayo Clinic. (2011). Disease & conditions: Brugada syndrome. Retrieved from http://www.mayoclinic.org/diseases-conditions/brugada-syndrome/basics/definition/con-20034848
Postema, P.G., Wolpert, C., Amin, A.S., Probst, V., Borggrefe, M., Roden, D.M.,…Wilde, A.A. ( 2009). Drugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (www.brugadadrugs.org). Heart Rhythm 6(9). 1335-41. DIO: 10.1016/j.hrthm.2009.07.002