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.