Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia (a fast heart rate) or arrhythmia (an irregular heart rhythm) causes an impairment of the myocardium (heart muscle), which can result in heart failure. People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease. There are no formal diagnostic criteria for TIC. Thus, TIC is typically diagnosed when (1) tests have excluded other causes of cardiomyopathy and (2) there is improvement in myocardial function after treatment of the tachycardia or arrhythmia. Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. TIC has a good prognosis with treatment, with most people recovering some to all of their heart function. The number of cases that occur is unclear. TIC has been reported in all age groups.
Signs and symptoms People with TIC most often present with symptoms of congestive heart failure or symptoms related to their irregular heart rhythm. Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. Symptoms of an irregular heart rhythm can include palpitations and chest discomfort. The timecourse of TIC is most well-studied in experiments on animals. Researchers have found that animals began to exhibit abnormal changes in blood flow after just one day of an artificially generated fast heart rate (designed to simulate a tachyarrythmia). As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month. Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years.
Causes TIC has been associated with supraventricular tachycardia (SVT), ventricular tachycardia (VT), frequent premature ventricular contractions (PVCs), rapid atrial and ventricular pacing, and left bundle branch block. The types of SVT associated with TIC include atrial fibrillation, atrial flutter, incessant atrial tachycardia, permanent junctional reciprocating tachycardia, atrioventricular reciprocating tachycardia, and atrioventricular nodal reentry tachycardia. Atrial fibrillation is the most common and well-studied etiology of TIC.
Diagnosis
There are no specific diagnostic criteria for TIC, and it can be difficult to diagnose for a number of reasons. First, in patients presenting with both tachycardia and cardiomyopathy, it can be difficult to distinguish which is the causative agent. Additionally, it can occur in patients with or without underlying structural heart disease. Previously normal left ventricular ejection fraction or left ventricular systolic dysfunction out of proportion to a patient’s underlying cardiac disease can be important clues to possible TIC. The diagnosis of TIC is made after excluding other causes of cardiomyopathy and observing resolution of the left ventricular systolic dysfunction with treatment of the tachycardia. Specific tests that can be used in the diagnosis and monitoring of TIC include:
electrocardiography (EKG) Continuous cardiac rhythm monitoring (e.g. Holter monitor) echocardiography Radionuclide imaging Endomyocardial biopsy Cardiac magnetic resonance imaging (CMR) N-terminal pro-B-type natriuretic peptide (NT-pro BNP) Cardiac rhythm monitors can be used to diagnose tachyarrhythmias. The most common modality used is an EKG. A continuous rhythm monitor such as a Holter monitor can be used to characterize the frequency of a tachyarrhythmia over a longer period of time. Additionally, some patients may not present to the clinical setting in an abnormal rhythm, and continuous rhythm monitor can be useful to determine if an arrhythmia is present over a longer duration of time. To assess cardiac structure and function, echocardiography is the most commonly available and utilized modality. In addition to decreased left ventricular ejection fraction, studies indicate that patients with TIC may have a smaller left ventricular end-diastolic dimension compared to patients with idiopathic dilated cardiomyopathy. Radionuclide imaging can be used as a non-invasive test to detect myocardial ischemia. Cardiac MRI has also been used to evaluate patients with possible TIC. Late-gadolinium enhancement on cardiac MRI indicates the presence of fibrosis and scarring, and may be evidence of cardiomyopathy not due to tachycardia. A decline in serial NT-pro BNP with control of tachyarrhythmia indicates reversibility of the cardiomyopathy, which would also suggest TIC. People with TIC display distinct changes in endomyocardial biopsies. TIC is associated with the infiltration of CD68+ macrophages into the myocardium while CD3+ T-cells are very rare. Furthermore, patients with TIC display significant fibrosis due to collagen deposition. The distribution of mitochondria has found to be altered as well, with an enrichment at the intercalated discs (EMID-sign). TIC is likely underdiagnosed due to attribution of the tachyarrhythmia to the cardiomyopathy. Poor control of the tachyarrhythmia can result in worsening of heart failure symptoms and cardiomyopathy. Therefore, it is important to aggressively treat the tachyarrhythmia and monitor patients for resolution of left ventricular systolic dysfunction in cases of suspected TIC.
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