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ATRIAL FIBRILLATION MAY BE “LIFE-SAVING” WHEN SEEN IN
NON-ISCHEMIC CARDIOMYOPATHY
Showkat Hamid, MBBS, Mrinalini Meesala, MD FACC, Salim Memon MBBS, Yuji
Saito, MD, PhD, FACC Khalid Rashid MBBS
Department of Medicine, Sisters of Charity Hospital/University at Buffalo, Buffalo, NY
INTRODUCTION:
Pause induced VT followed by V. Fib.
INTRODUCTION: QT prolongation and hence
susceptibility to VT is not unknown in
bradycardia which is thought to be due to
early after-depolarizations due to prolongation
of action potential duration. The cellular
mechanism responsible is depression of
electrogenic Na+ pumping and more complete
inactivation of IK . Moreover, in bradycardia the
plateau of action potential is shifted further
when the Ca2+ current availability is increased.
This happens due to sub-maximal activation of
the ITO in low ventricular rates.
Following case demonstrates how well the
physiologic concepts fit the clinical scenarios.
Amiodarone-induced QT prolongation was
initially suspected as a possible polymorphic
VT mechanism. However, her VT became even
worse after amiodarone was discontinued. Her
VT was always preceded by a pause or
bradycardia, suggesting early after
repolarization as a true VT mechanism. In this
case, our attempt to control AF rate was
eventually triggering polymorphic VT. If her
heart rate was not fast enough without the
presence of AF, polymorphic VT and sudden
cardiac death could have been the first
presentation of her non-ischemic
cardiomyopathy. In this regard, her AF was
considered “cardio-protective”, preventing
polymorphic VT by shortening QT interval.
Although AF is considered nuisance most of the
time, in rare occasions, AF may be a selfdefense cardio protective response when seen
in the patients with non-ischemic
cardiomyopathy.
CASE:
A 51 year-old previously healthy Caucasian
female presented to emergency room for 1week history of intermittent palpitations. She
was found to be in atrial fibrillation (AF) with
rapid ventricular response at 190 bpm. She was
started on diltiazem and amiodarone by iv
drip. Her heart rate was gradually better
controlled by the next morning when she
suddenly developed polymorphic ventricular
tachycardia (VT), which quickly degenerated
to ventricular fibrillation. She was defibrillated
and transferred to CCU. Amiodarone was
discontinued, but her polymorphic VT became
more frequent, requiring numerous
defibrillations. A pause or bradycardia was
noted to always precede polymorphic VT.
Pause-dependent triggered activity (early after
depolarization) was suspected and diltiazem
was discontinued. Right ventricular pacing at
80 bpm via a transvenous temporary pacing
lead eliminated further VT episodes. Echo
revealed global left ventricular hypokinesis
with EF 15%. Coronary angiogram showed no
flow-limiting stenosis. She underwent ICD
implant with the programmed pacing rate at
80 bpm. She was discharged home with stable
vital signs on ACE-inhibitor and beta-blocker
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DISCUSSION:
LEARNING OBJECTIVES:
Post AICD placement strips
1. QT segment is inversely related to HR by a
formula QTc = QT/(RR)1/2.
2. Prolonged QT serves as a substrate for
arrhythmogenesis.
3. Rapid HR as seen in A. Fib decreases the QT
interval.
4. Rate controlling medications in A.fib can
predispose to Ventricular dysrhythmias.
References
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5.
Harrisons principles of Internal Medicine 18/e
Braunwald’s Heart Disease 7t/e
Electrophysiology of Arrhythmias by Reginald T Ho
Basic Arrhythmias 7/e by Gail Walraven
Marriott's practical electrophysiology 10/e by Galen S
Wagner