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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.

INTRODUCTION:

CASE:

Pause induced VT followed by V. Fib.

Post AICD placement strips

DISCUSSION:

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 self-defense cardio protective response when seen in the patients with non-ischemic cardiomyopathy.LEARNING OBJECTIVES:

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

1. Harrisons principles of Internal Medicine 18/e2. Braunwald’s Heart Disease 7t/e 3. Electrophysiology of Arrhythmias by Reginald T Ho4. Basic Arrhythmias 7/e by Gail Walraven5. Marriott's practical electrophysiology 10/e by Galen

S Wagner

A 51 year-old previously healthy Caucasian female presented to emergency room for 1-week 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

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

ATRIAL FIBRILLATION MAY BE “LIFE-SAVING” WHEN SEEN IN NON-ISCHEMIC CARDIOMYOPATHY