Case Based for June

A 62-year-old male presenting to the emergency department with a 2-week history of progressive dyspnea and generalized weakness.  He had not noticed any palpitations, but cardiac monitoring showed atrial fibrillation with a ventricular rate of 170.  EKG did not show any signs of acute ischemia or infarction.  CT angio of the chest showed no PE but moderate bilateral pleural effusions, worse on the right, with mild pulmonary edema.  The patient had no previous history of CHF (EF unknown).  Patient’s heart rate was controlled with IV Cardizem.  BNP was 21,000 and troponin 3,600. The patient was suspected of having a tachycardia-induced cardiomyopathy.  The patient was transferred to VM for further evaluation.

Echo showed moderate global LV hypokinesia with EF 38%.  There was an LV apical clot measuring 1.26 cm.  The patient was diuresed and rate was controlled with digoxin and metoprolol.  Heart cath showed no significant coronary artery disease.  He was placed on GDMT for HFrEF with the 4 pillars of HFrEF medications.  His history was not compatible with alcohol or methamphetamine induced cardiomyopathy, and viral cardiomyopathy also seemed unlikely.  It was felt that he most likely had tachycardia-induced cardiomyopathy.  He was anticoagulated on Eliquis and discharged on sacubitril/valsartan (entresto), metoprolol, spironolactone, empagliflozin (jardiance), lasix and digoxin.  Repeat echo 2 months later showed resolution of the global LV hypokinesis, and the EF returned to normal at 55-60%.  He remained in atrial fibrillation.  Six months after his initial presentation he underwent electrical cardioversion resulting in sinus rhythm but had recurrent atrial fibrillation.  He was started on amiodarone and there is a pending plan for ablation therapy.

Tachyarrhythmia-induced cardiomyopathy is a relatively rare cause of dilated cardiomyopathy and can result from virtually all types of tachyarrhythmias, as well as from high PVC burden (higher risk if greater than 15% of total beats on ziopatch).  CM can occur as soon as a few days after the onset of the tachycardia.  If patients present after the cardiomyopathy has developed, they commonly present with symptoms of heart failure (dyspnea, edema, orthopnea).  Initial rate control with beta-blockers is recommended.  If there is a suspicion for another etiology for cardiomyopathy, further cardiology workup is indicated such as cardiac MRI or coronary angiography.  The prognosis is relatively good for tachycardia-induced cardiomyopathy with most patients improving significantly or completely resolving over a few months after rate control.  If EF normalizes within a few months, the diagnosis is consistent with tachyarrhythmia-induced cardiomyopathy, and no further workup is indicated.

An interesting aspect of this case is the medication for rate control; it is recommended to avoid Cardizem if EF is unknown or low, but b-blockers are recommended for rate control in such circumstances.  On the other hand, b-blockers should generally not be initiated while a patient is volume overloaded with pulmonary edema.  Meta-analysis has shown that diltiazem has better efficacy, works faster, and carries less risk of bradycardia than metoprolol for a-fib with RVR.  This is consistent with my experience; I find that diltiazem bolus + infusion works better than metoprolol 5mg X 3.  Unfortunately, diltiazem has been given a class 3 (harm) designation with HFrEF (EF<40%) by the ACC and AHA based on retrospective analysis.  Can someone please perform a prospective multicenter double-blind placebo-controlled RCT of diltiazem versus metoprolol for rate control and A-fib with reduced EF??

Digoxin takes 30 minutes to start slowing the rate with maximal effect taking up to 3-6 hours.  A standard digoxin loading protocol would be digoxin 0.5 mg IV initially, then 0.5 mg IV Q 6 hours for two more doses for a total of 1.0 mg.  ACC guidelines describe giving 0.25 mg IV Q 2hours up to a total of 1.5 mg.

Amiodarone has multiple mechanisms of action and can slow rates (due to B-blockade and calcium channel blockade effects), as well as being antiarrhythmic.   It can be given as an infusion, starting with a bolus 300 mg over one hour, but may take many hours to achieve rate control.  I obtain cardiology consultation when using this drug, and thromboembolic risk must be considered if using it as an antiarrhythmic.

Of note, this patient was started on the 4 pillars of guideline-directed medical therapy (GDMT) for HFrEF (EF<40%) while hospitalized.  This includes an ARNI (angiotensin receptor–neprilysin inhibitor) or ACEi/ARB, a beta-blocker, an MRA (mineralocorticoid receptor antagonist), and an SGLT 2 (sodium-glucose cotransporter 2 inhibitor).  This combination of medications can frequently be started during a single admission and has been shown to reduce hospitalizations and reduce mortality.

An example of the regimen:

Sacubitril/valsartan (Entresto $$$) or lisinopril or losartan

Carvedilol or metoprolol

Spironolactone

Empagliflozin (Jardiance)

Written by Mark Scott, D.O.

ERx Clinical Partners Medical Director

This is for informational purposes only. For medical advice or diagnosis, consult a physician