Tachycardia-Mediated Cardiomyopathy

Sinus tachycardia? Atrial flutter? Atrial fibrillation? Atrial tachycardia?

We’ll answer this question more thoroughly later. (end text of drop down)

Before deciding to clear him to the main ED or keep him in the critical care area, you put down the EKG and talk to the patient. He denies other medical problems and his only medication is baby aspirin. The EMR shows ICD 9 codes for HTN, DM and HLD. When asked, he denies these but also reports he hasn’t been to a doctor since he got his stents 4 years ago. The shortness of breath he noticed 5 days ago and has just been getting worse. Sometimes he has chest pain with it but not now. The dyspnea is worse with exertion but still present at rest. He has also noticed swelling in his legs bilaterally and denies recent travel or calf pain. On physical exam you note that he is speaking in full sentences, there are no retractions, his lungs are clear to auscultation bilaterally with possible crackles at the base, and there is bilateral mild peripheral edema. The exam is otherwise unremarkable.

CHF exacerbation, ACS leading to CHF, PE less likely. (end text of drop down)

You decide he looks good but given your suspicion for a CHF exacerbation with this tachycardia, you treat him in the critical care area. You place him in the room and reach for your handy US. The US shows poor EF, minimal B lines at the bases bilaterally– not really enough to diagnose interstitial syndrome/pulmonary edema, no pericardial effusion, and a plethoric IVC. In short, his heart is failing, but he doesn’t really look like a typical CHF patient. The answer is in the ECG. This is likely tachycardia-mediated cardiomyopathy from an ectopic atrial tachycardia.

Tachycardia-Mediated Cardiomyopathy (TMC) is defined by structural heart changes secondary to a tachydysrhythmia that often lead to heart failure. It is also referred to as Arrhythmia-Induced Cardiomyopathy (AIC). Rarely does sinus tachycardia lead to this condition. Thus, it is usually some type of SVT (in the most inclusive use of the term), and the rhythm is generally pathologic, as opposed to compensatory, like sinus tachycardia in sepsis. In people with ectopic atrial tachycardias, TMC is found in 8.3-34% of patients (1).

In TMC there are physiologic changes that take place to cause the cardiomyopathy.

1. Compensatory Phase: <7 Days – normal function: During this phase there is minimal dilatation and the EF is minimally decreased.
   
2. Extracellular Remodeling->Cellular Remodeling; 7-21 days – LV dysfunction: During this phase, remodeling begins to occur with loss of extracellular structure leading to further dilatation resulting in decreased LVEF. Neurohormonal activation is triggered leading to leakage of BNP. In addition, there is an increase in norepinephrine levels and the RAAS system is activated leading to increased peripheral vascular resistance that puts added stress on cardiac function. Lastly, inflammatory markers are released (endothelin, TNF-alpha and other cytokines). This is when the patient will start to look like your typical CHF patient.
   
3. Defects in Ca⁺⁺ handling and severe Contractile Dysfunction: >21 days – Heart Failure (decreased contractility): At this stage, intracellular changes occur that alter Ca⁺⁺ handling and result in a decrease in contractility; this is in addition to the dilatation that is already occurring. Likewise, the changes that have already started to take place extracellularly continue to worsen (dilatation, decreased EF, more neurohormonal/RAAS activation, pulmonary/systemic edema).
   

As people with structural abnormalities are more prone to tachydysrhythmias, such as aFib, aFlutter, SVT, or PVCs, there can also be a mixed picture where someone with pre-existing cardiomyopathy has an exacerbation or worsening of their symptoms due to a tachydysrhythmia. This is called Arrhythmia-Mediated Cardiomyopathy (AMC). AFib is found in 10-50% of people with heart failure; thus, AMC can be all too common (1). Distinguishing AMC from TMC in the acute setting is difficult, and at best, speculated based on the patient’s history. It is generally differentiated months later based on response to treatment. Despite the physiologic changes that occur, the cardiomyopathy that occurs with TMC is reversible and the heart will remodel to its previous, normal function. In contrast, with AMC, the person will return to their baseline HF status. For the purpose of treatment in the ED, it doesn’t really matter if it is TMC or AMC, the initial treatment is the same.

In an unstable patient, ACLS is the guiding principle. You need to terminate the rhythm emergently, so cardioversion is in order. In the stable patient with adequate end-organ perfusion, like ours, the question becomes rate versus rhythm control. If rate control works, than by all means do it. It is more likely to work in a person with aFib than any other rhythm. Guidelines state that for aFib, first-line agent should be either calcium-channel (CCB) or beta-blocker (BB) although there is some recent evidence suggesting that CCB may be more effective in the acute setting (2, 3). For ectopic atrial tachycardia, CCB or BB are also equally recommended as first-line agents (5). If they don’t work, you can consider adding digoxin to help slow conduction through the AV node (although the onset of effect may take hours) (4). Adenosine can be administered and may terminate tachycardias that are triggered (5). For all other rhythms, rate control is first-line but often unsuccessful. The next choice is rhythm control with Class III antiarrhythmics (amiodarone, dofetilide, ibutilide) (5). If that still doesn’t work, reach for the paddles and try sedation and cardioversion; if successful, this is then often followed by antidysrrhythmic infusion. The last line in the acute setting is catheter ablation.

Patients should be discharged from the hospital on a heart failure regimen of beta-blocker, ACE inhibitors, and aldosterone. There is no good data to support how long this treatment should continue once all signs/symptoms of cardiomyopathy resolve. For patients who are not controlled on beta-blockers, catheter ablation is the preferred long-term management over antidysrhythmic therapy. It is more effective at preventing recurrence with a 70-90% success rate and considered lower-risk in comparison to the side effect profiles of antidysrhythmics (1).