Case
A 61-year-old male truck driver was admitted with acute systolic
decompensated congestive heart failure with AF/RVR. His exam was
remarkable for irregular tachycardia 130 – 150s, bilateral crackles,
and lower extremity edema with cold peripheries. His past medical
history is notable for hypertension, and paroxysmal atrial fibrillation
diagnosed five months prior. Transthoracic echocardiogram (TTE) showed
his LVEF to be 20% with severe LA dilatation. He was diagnosed with
tachycardia-induced cardiomyopathy after SPECT myocardial perfusion scan
ruled out ischemic cardiomyopathy. He was started on IV diuretic therapy
at admission. He underwent transesophageal echocardiography (TEE) and
direct current cardioversion (DCCV), receiving 150 J, and then 200 J.
Cardioversion was successful at 200 J, and EKG showed QTc of 532. He
reverted to AF/RVR in less than 24 hours. He was started on a loading
dose of amiodarone 150mg IV bolus and then 1mg/kg/min for 6 hours, and
apixaban 5 mg twice daily was started for anticoagulation based on a
CHADS VASC of 2. Amiodarone loading was ineffective in reducing
ventricular rate or maintaining sinus rhythm. Besides, he developed side
effects from the amiodarone, i.e., intense nausea and vomiting and
flushing. He could not tolerate both the oral and intravenous
formulations of amiodarone. Eventually, amiodarone had to discontinue
due to intolerance. Sotalol and Dofetilide were contraindicated due to
the prolonged QTc - 532, and Class 1c agents due to cardiomyopathy.
He rapidly decompensated and developed refractory cardiogenic shock with
SBPs 80 – 90s compounded by cardiorenal syndrome and ineffective
diuresis. AV nodal ablation with a biventricular pacemaker was
suggested, but the patient refused on the grounds of being a truck
driver. He wanted to get back to his job as a truck driver when he
recovered; therefore, having a device will prohibit that. AF ablation by
pulmonary vein isolation and posterior wall isolation (PVI/PWI) was an
acceptable treatment option for him despite the elevated risk of
hemodynamic decompensation and mortality.
A limited repeat echocardiogram showed his LVEF had worsened to 15%
with general hypokinesis and now moderate RV dysfunction.
Right heart catheterization showed he had PASP 53 mmHg, PADP 38 mmHg,
PCWP 37 mmHg, RA 28 mmHg. LVEDP 31 mmHg and LVEF was estimated to be
10%. Coronary angiogram showed normal coronary arteries.
An Impella CP was inserted via the left femoral artery under
fluoroscopic guidance (Figure 1), and support set to P6 with 3.4
liters/minute of cardiac output. A CT scan of the chest with a
reconstruction of the left atrium and pulmonary veins was utilized
during the ablation procedure to align the 3D electroanatomic map for
additional anatomic correlation. Artic front balloon cryoablation of the
right and left pulmonary veins (Figure 1). Entrance and exit blocks were
demonstrated more than 30 minutes after the ablation. Voltage mapping
post-ablation demonstrated successful radiofrequency ablation of the
posterior wall and successful radiofrequency ablation of the anterior
mitral isthmus line. Normal sinus rhythm was restored (Figure 2, Panel
A, and B).
Toward the end of the procedure, he required more impella support amidst
vasodilatory shock. The ECMO team assessed him for additional mechanical
circulatory support. However, he recovered reasonably quickly before the
ECMO cannulas were placed.
Due to complications of vasodilatory shock, the patient had shocked
liver and renal dysfunction requiring continuous renal replacement
therapy (CRRT) for several days.
Throughout the rest of his hospitalization, he maintained sinus rhythm.
Forty-eight hours later, repeat echocardiogram showed his LVEF had
improved to 40%. Impella support was weaned within 48 hours after the
PVI, and guideline-directed medical therapy for HFrEF was optimized.
There was renal function recovery. The patient was discharged to
rehabilitation.
Follow up six months later showed normalization of EF to 62%, moderate
to severely dilated left atrium, and was having NYHA I symptoms on
guideline-directed medical therapy for HFrEF.