Heart failure is one of the commonest reasons for hospital admission. Its etiology, which may not always be apparent on initial assessment, has important prognostic implications. Tachycardia-induced cardiomyopathy (TIC) is rare in the adult population— only one case was encountered in two observational studies involving nearly 2,000 patients with unexplained dilated cardiomyopathy—but is potentially curable and should therefore be considered in all patients with heart failure and tachhyarrythmias.1,2 We describe a patient presenting with a broad complex tachycardia and severe heart failure in which significant restoration of cardiac function was obtained within six weeks of resolving her tachycardia.
A previously fit and well 50-year-old teacher presented with a two-week history of dyspnea on exertion. She denied any chest pain, palpitations, or recent flu-like illnesses. There was no family history of cardiac disease or sudden death and she was non-smoker with minimal alcohol intake.
On admission the patient had clinical and radiologic signs of severe heart failure. Her electrocardiogram (ECG) showed a regular broad complex tachycardia with left bundle branch block (LBBB) morphology and a ventricular rate of 215bpm (see Figure 1). She was given 6mg of intravenous adenosine which reverted her to sinus rhythm (SR). An ECG performed at this point (see Figure 2A) showed the presence of delta waves and a shortened PR interval, in keeping with a diagnosis of Wolff-Parkinson-White (WPW) syndrome. There was also T wave inversion (TWI) in the anterolateral leads.
The patient was treated with intravenous furosemide, ramipril, and bisoprolol for her heart failure. Anti-thrombotic therapy was initiated for presumed acute coronary syndrome but this was stopped when serial troponin I measurements reverted to normal. The ECG performed shortly after admission in SR revealed non-dilated ventricles but moderate-to-severe global biventricular dysfunction with an estimated left ventricular ejection fraction (LVEF) of around 15–20%. There was mild secondary mitral and tricuspid regurgitation.
The differential for her admission ECG in tachycardia includes ventricular tachycardia, pre-excited supraventricular tachycardia (SVT), or SVT with aberrant conduction. There were P waves identified with a 1:1 ventriculo–atrial association, suggesting SVT. The RP interval was >50% of the RR interval, making this a long RP tachycardia. The differential for a long RP tachycardia includes atrial tachycardia, atypical atrioventricular nodal re-entrant tachycardia (AVNRT—fast–slow variant), antidromic atrioventricular re-entrant tachycardia (AVRT—pre-excited SVT), or orthodromic AVRT with a slowly conducting accessory pathway.
Antidromic AVRT was unlikely as the morphology of the QRS complexes during tachycardia were different from those observed during sinus rhythm. The negative P waves in II, III, and avF during tachycardia suggest orthodromic AVRT with a slowly conducting pathway (also known as permanent junctional reciprocating tachycardia).
The patient was hospitalized for urgent electrophysiologic studies, confirming the clinical suspicion of orthodromic AVRT with functional LBBB and the location of a right-sided postero-septal accessory pathway (negative delta waves and QRS complexes in lead V1 and in leads II, III, and avF on ECG). Interestingly, the patient remained asymptomatic when the clinical tachycardia seen at presentation was induced during the electrophysiology study. Accessory pathway ablation was performed successfully, with no further evidence of pre-excitation (see Figure 2B).
Repeat ECG on the fifth day post-admission showed the LVEF had improved significantly. At eight weeks after initial presentation, the LVEF had improved from 17 to 34%, and at six months it was 50–55% with only minor septal hypokinesis.
TIC is an important cause of LV dysfunction that may result from persistent or frequent paroxysmal supraventricular or ventricular tachyarrhythmias.3 Orthodromic AVRT comprises 95% of the re-entrant tachycardias associated with WPW syndrome, and cases of TIC also have been described with AVRT.4,5 The incidence of TIC is poorly defined and is likely underestimated, as tachyarrhythmias are frequently the result of cardiomyopathy and yet are often overlooked as a cause. TIC is highly dependent on the ventricular rate: the higher the ventricular rate, the earlier the cardiomyopathy occurs, although the cut-off ventricular rate above which TIC occurs has not been determined.6
Time to onset of ventricular dysfunction is also dependent on the type and duration of the tachyarrhythmias, co-existing medical conditions, and any underlying structural heart disease.7 In this case, despite the profound tachycardia, the patient did not experience any palpitations, which may have allowed more time for TIC to develop and present with heart failure symptoms. Her ECG after restoration of sinus rhythm showed widespread, deep TWI, prompting her treatment for ischaemic cardiomyopathy.
However, the TWI was probably due to a ‘cardiac memory’ effect post-tachycardia, rather than coronary ischaemia per se.8 Additionally, minor STT repolarisation abnormalities are sometimes seen in ECGs with a WPW pattern. Recovery of LV function after restoration of a normal heart rate has been demonstrated for a range of different tachycardia mechanisms.4,9 Generally, about four weeks are needed for the recovery of systolic function after heart rate comes under control.3 The timescale for LV function recovery in this case is in keeping with TIC. Her LV chamber size was normal on admission despite the presence of significant LV dysfunction. A recent retrospective study comparing patients with TIC and matched patients with idiopathic dilated cardiomyopathy has shown that a LV diastolic dimension of ≤61mm predicted TIC with a sensitivity of 100% and specificity of 71.4%.10
TIC is an under-reported reversible form of dilated cardiomyopathy. Our case clearly demonstrates the huge beneficial effects on cardiac function of heart rate control in this condition and provides a reminder that TWI post-tachycardia can be due to a ‘cardiac memory’ effect and does not necessarily imply coronary ischaemia. Catheter ablation—a curative procedure—was carried out to prevent further recurrences of the SVT, but recovery of LV function was already in progress after SR was restored. TIC should be considered in all unexplained LV dysfunctions accompanied by a persistent tachyarrhythmia.