Medical Archive

Introduction

Etiology

Rheumatic heart disease
Other forms of valvular heart disease
Dilated cardiomyopathy, ASD, hypertension, coronary artery disease
Thyrotoxicosis

Precipitation

Acute alcohol excess
Medications (eg, ?-adrenergic agents)
Pericarditis, chest trauma, thoracic surgery, or pulmonary disease

Pathophysiology

‘Absence of distinct P-waves and an irregularly irregular ventricular response’

Long-standing persistent AF is associated with greater structural remodeling with atrial fibrosis and electrophysiologic remodeling.

Cardioversion and anticoagulation

1. Conversion to sinus rhythm
   • DC cardioversion (200J) ?? ??
     • 120-200 joules (biphasic) or 200 joules (monophasic)
     • AIx: Hypotension, pulmonary edema, angina
     • CIx: embolic event ?????? ????? ? ??. ? ??? TEE? atrial thrombus ???? ??.
     • Synchronous cardioversion is used in acutely unstable patients (altered mental status, ongoing chest pain, hypotension or otehr signs of shock) with tachycardia and a pulse
     • Asynchronous cardioversion (defibrillation) is used in pulseless VT, ventricular fibrillation.
     • Chest compression if the patient develops PEA or asystole.
   • Anti-arrhythmics (“rate control”)
2. IV amiodarone
   • Structural heart disease(severe) ?? ?.
3. Anticoagulation ??? ??
   • >48hr ?? ?? cardioversion? ????.
   • target INR? 2.0~3.0; ?? ??? NOAC??.
4. The choice between rate control or rhythm control strategy
   • WPW with AF?? ??? ? ??…

Rate control

AV node? ??? ??, ?? ??.
Rapid ventricular response(RVR) control.

• LVEF <40% or signs of congestive heart failure
  1. Smallest dose of BB to achieve rate control
     • If severe, amiodarone is an option.
     • Initial resting HR target <110bpm
  2. Add digoxin
• LVEF >40%
  1. BB or diltiazem or verapmil
     • Initial resting HR target <110bpm
  2. Add digoxin

• BB
  • ??? ?? ? ?? ??.
• CCB
• Digoxin
  • HF ???.
  • Slows the ventricular rate during AF primarily by increasing parasympathetic tone, which leads to inhibition of AV nodal conduction.

Chronic rate control

In chronic AF (>7d) 

• ??? ???? ?? ?? flecainide (Ic) 200-300mg ?? propafenone (Ic) 450-600mg
• ???? ?? ?? amiodarone ?? ??.
• ??????? ?? ?? dofetilide (III), sotalol (III)

• Cox-Maze III Procedure

Stroke prevention in atrial fibrilllation

AF 2? ?? ?? ? ?? 3?? ??.
?? 2? ???? ????? ?? cardioversion ??.

?????? ??? ??? MS, or mechanical valve? ???.

Risk Factors	Points	CHA 2 DS 2 -VASc Score	Estimated Annual Stroke Rate
C—congestive heart failure	1	0	0
H—hypertension	1	1	1.3%
A—age ?75 y	2	2	2.2%
D—diabetes mellitus	1	3	3.2%
S—stroke or TIA, embolus	2	4	4.0%
V—vascular disease	1	5	6.7%
A—age 65–75 y	1	6–9	>9%
Sex—female	1

Anticoagulants	Mechanism	Excretion	Dosing Considerations	Risk/Benefit
Warfarin	Vitamin K antagonist	Liver	Adjusted to INR 2–3 Days to therapeutic ewect Multiple drug/food interactions (e.g., amiodarone)	Major hemorrhage: 1% per year Intracranial hemorrhage: 0.1– 0.6% per year Risk of bleeding increases with INR >3.5 Inexpensive
Dabigatran	Thrombin inhibitor	Kidney
		CCr >30 mL/min CCr 15–30 mL/min	150 mg bid 75 mg bid P-glycoprotein substrate (inducers— rifampin, reduce concentration) (inhibitors—amiodarone, verapamil, dronedarone, quinidine) Proton pump inhibitors may reduce absorption	Onset of action within hours No reversal agent for bleeding
Rivaroxaban	Xa inhibitor	Kidney	P-glycoprotein substrate	No reversal agent for bleeding
	CCr ?50 mL/min	20 mg daily
	CCr 15–50 mL/min	15 mg daily
Apixaban	Xa inhibitor	Kidney and liver	P-glycoprotein substrate	No reversal agent for bleeding
		Any 2 of: Cr >1.5 mg/dL, age >80 yrs, or wt <60 kg	5 mg bid 2.5 mg bid

Rhythm control

Indications
Those who have persistent symptoms despite rate-control therapy
certain patients with heart failure, or young patients

??? ???, HF ??? Ic, ??? III
AF? long term control?? amiodarone? m/i.

Catheter and surgical ablation for atrial fibrillation

Cut-&-sew
Cryolesion (-60?, 2 min)

?????? ?? ?? ????. Paroxysmal type?? ???? ?? (1? ??? ??? 80%)