Tachycardia-Mediated Cardiomyopathy

You are sitting in the Critical Care area of your ED and the walk-in triage nurse approaches you with an ECG and a patient. She tells you he is a 60 year-old male with a PMH of cardiac stents presenting with 5 days of shortness of breath. At triage his vitals were BP 159/102, HR 134, RR 22, SpO2 100% on RA, 98.2F, FSG 357. You have eyeballed the patient enough to notice he doesn’t have signs of respiratory distress and have looked at the ECG while she is presenting to you.

What is the rhythm?

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.

What is your differential and what do you want to do with him?

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

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.

Beyond ED Treatment

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).

The Case Revisited

Let’s return to our patient. Throughout this entire work-up, his heart rate never varied more than 132-134. Sitting up, lying down, talking, urinating, it was 133+/-1. This supports the diagnosis of atrial tachycardia. The P waves are best seen in lead II. It is not likely atrial flutter given the rate but likely an ectopic atrial tachycardia at a rate of 266 with a 2:1 AV block. We attempted to control his rate with a diltiazem bolus and drip, and it did not budge from 133. For diagnostic or possible therapeutic effect, we next tried adenosine 6mg and 12mg, but again there was no response and no movement of the HR from 133. Next up we tried esmolol, again his heart rate held firm at 133. He was transferred to the CCU on continued esmolol infusion, and carvedilol was started. His “SVT” then terminated spontaneously, and he was discharged 2 days later. As this was a recent case, we will have to wait to see what his long-term management will be.



Question for discussion: Same patient, but you are in a rural ED without a cardiologist. Given the QTc of 516, what would have been your next step after beta-blockers in this seemingly stable patient?

Take Home Points

  1. For tachycardia-mediated cardiomyopathy (TMC) due to ectopic atrial tachycardia -> need rate control to slow the HR
  2. Short-Term in the ED –> Depending on rhythm or underlying mechanism, there may or may not be a response to typical AV nodal blocking agents
    1. Calcium-Channel Blocker or Beta Blocker (except for aFib, perhaps CCB preferred) + consider digoxin
    2. Class III antidysrhythmics (i.e. ibutilide)
    3. Cardioversion -> may be short-lasting and then need post-conversion antidysrrhythmic infusion
  3. Long-Term –> Catheter Ablation
    1. Follow-up to determine significance of damage and whether mediated vs. induced
    2. CHF medication for undetermined period of time


  1. Gopinathannair R, Etheridge SP, Marchlinski FE, Spinale FG, Lakkireddy D, Olshansky B. Arrhythmia-Induced Cardiomyopathies: Mechanisms, Recognition, and Management. J Am Coll Cardiol. 2015 Oct 13;66(15):1714-28. doi:10.1016/j.jacc.2015.08.038. Review. PubMed PMID: 26449143; PubMed Central PMCID: PMC4733572.
  2. Fromm C, Suau SJ, Cohen V, et al. Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. The Journal of emergency medicine. 2015;49(2):175-182. PMID: 25913166
  3. Martindale JL, deSouza IS, Silverberg M, Freedman J, Sinert R. beta-Blockers versus calcium channel blockers for acute rate control of atrial fibrillation with rapid ventricular response: a systematic review. European journal of emergency medicine : official journal of the European Society for Emergency Medicine. 2015;22(3):150-154.
  4. Gopinathannair R, Olshansky B. Management of tachycardia. F1000Prime Rep. 2015 May 12;7:60. doi: 10.12703/P7-60. eCollection 2015. Review. PubMed PMID: 26097733; PubMed Central PMCID: MC4447058
  5. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016;67(13):e27-e115.

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Andrea Ferrari

Emergency Medicine, PGY 4  Raised in Berkeley • Schooled in Detroit • Training in Brooklyn

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