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Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated
M Grogan1, H C Smith, B J Gersh
1Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905.
Insights
Atrial fibrillation (AF) with rapid ventricular response can cause severe left ventricular (LV) dysfunction, mimicking idiopathic dilated cardiomyopathy. Treating the arrhythmia can reverse LV dysfunction, improving heart failure symptoms.
Area of Science:
- Cardiology
- Electrophysiology
- Heart Failure Research
Background:
- Severe left ventricular (LV) dysfunction often presents with atrial fibrillation (AF).
- Patients with idiopathic dilated cardiomyopathy (IDCMP) and AF typically have unknown arrhythmia duration.
- Heart failure symptoms are common in patients with LV dysfunction and AF.
Purpose of the Study:
- To investigate whether AF with rapid ventricular response can be the primary cause of severe LV dysfunction.
- To evaluate the reversibility of LV dysfunction after controlling ventricular rate in patients with AF.
Main Methods:
- Evaluation of ten patients with severe LV dysfunction and AF.
- Ventricular rate control and sinus rhythm restoration.
- Assessment of LV ejection fraction and heart failure symptoms at baseline and follow-up.
Main Results:
- All patients achieved ventricular rate control; 5 restored sinus rhythm.
- At follow-up (median 30 months), all patients were asymptomatic.
- LV ejection fraction significantly improved from a median of 25% to 52%.
Conclusions:
- AF with rapid ventricular response can be the primary cause of severe LV dysfunction, not just a consequence.
- LV dysfunction in these cases may be completely reversible with effective ventricular rate control.
- This challenges the traditional view of IDCMP and suggests AF as a potential primary driver.
Abstract:
Ten patients aged 22 to 80 years (median 57) with severe left ventricular (LV) dysfunction and atrial fibrillation (AF) with rapid ventricular response were evaluated after therapy. Because most patients were unaware of their arrhythmia, duration was usually unknown. All patients had heart failure symptoms; 9 presented with New York Heart Association class III or IV disability, and 1 with class II disability. Initial LV ejection fraction ranged from 12 to 30% (median 25). No patient had symptomatic coronary artery disease (4 underwent angiography). Myocarditis and infiltrative processes were excluded by biopsy in 5 patients. All patients were considered initially to have idiopathic dilated cardiomyopathy with secondary AF. Ventricular rate was controlled in all patients, with sinus rhythm restored in 5. At follow-up (median 30 months, range 3 to 56), all patients were asymptomatic. LV ejection fraction after treatment ranged from 40 to 64% (median 52). It is concluded that in some patients initially considered to have idiopathic dilated cardiomyopathy, AF with rapid ventricular response may be the primary cause rather than the consequence of severe LV dysfunction. LV dysfunction may be completely reversible with ventricular rate control.