Tachycardia-induced cardiomyopathy

Tachycardia-induced cardiomyopathy
Other names	Arrhythmia-induced cardiomyopathy, tachycardia-mediated cardiomyopathy, tachymyopathy, chronotropic cardiomyopathy, tachycardiomyopathy
Pronunciation	tak-i-kahr-dee-uh in-dyoos-duh kahr-dee-oh-mahy-op-uh-thee
Specialty	Cardiology
Symptoms	shortness of breath, ankle swelling, fatigue, weight gain, palpitations, chest discomfort [1] [2]
Duration	short or long term [1]
Causes	fast or irregular heart rhythm [1]
Risk factors	Prolonged tachycardia [3] [4]
Treatment	antiarrythmic agents, diuretics, catheter ablation, pacemaker [1]

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. ^{[1] [5]} People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). ^{[1] [2]} Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease. ^{[5] [1]}

Contents

• Signs and symptoms
• Causes
• Diagnosis
• Treatment
• Prognosis
• Epidemiology
• See also
• References
• External links

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. ^{[1] [5] [6]} Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. ^[1] TIC has a good prognosis with treatment, with most people recovering some to all of their heart function. ^[1]

The number of cases that occur is unclear. ^[5] TIC has been reported in all age groups. ^[6]

Signs and symptoms

People with TIC most often present with symptoms of congestive heart failure and/or symptoms related to their irregular heart rhythm. ^[1] Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. ^[2] Symptoms of an irregular heart rhythm can include palpitations and chest discomfort. ^[2]

The timecourse of TIC is most well-studied in experiments on animals. ^[1] 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). ^[1] As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. ^[1] The worsened heart function then persists at a stable state until the heart rate is returned to normal. ^[1] 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. ^[1]

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. ^[1]

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. ^[1] 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. ^[1] Atrial fibrillation is the most common and well-studied etiology of TIC. ^{[1] [5]}

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. ^[5] Additionally, it can occur in patients with or without underlying structural heart disease. ^[6] 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. ^[1] 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. ^{[1] [5] [6]}

Specific tests that can be used in the diagnosis and monitoring of TIC include:^{[ citation needed ]}

• 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. ^[1]

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. ^{[1] [5]} Radionuclide imaging can be used as a non-invasive test to detect myocardial ischemia. ^[6] 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. ^{[1] [5]} A decline in serial NT-pro BNP with control of tachyarrhythmia indicates reversibility of the cardiomyopathy, which would also suggest TIC. ^[5]

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. ^[8] Furthermore, patients with TIC display significant fibrosis due to collagen deposition. ^[8] The distribution of mitochondria has found to be altered as well, with an enrichment at the intercalated discs (EMID-sign). ^[8]

TIC is likely underdiagnosed due to attribution of the tachyarrhythmia to the cardiomyopathy. ^[1] Poor control of the tachyarrhythmia can result in worsening of heart failure symptoms and cardiomyopathy. ^[5] Therefore, it is important to aggressively treat the tachyarrhythmia and monitor patients for resolution of left ventricular systolic dysfunction in cases of suspected TIC.^{[ citation needed ]}

Treatment

Treatment of TIC involves treating both the tachyarrhythmia and the heart failure with the goal of adequate rate control or restoration of the normal heart rhythm (aka. normal sinus rhythm) to reverse the cardiomyopathy. ^{[5] [9]} The treatment of the tachyarrhythmia depends on the specific arrhythmia, but possible treatment modalities include rate control, rhythm control with antiarrhythmic agents and cardioversion, radiofrequency (RF) catheter ablation, or AV node ablation with permanent pacemaker implantation. ^[1]

For TIC due to atrial fibrillation, rate control, rhythm control, and RF catheter ablation can be effective to control the tachyarrhythmia and improve left ventricular systolic function. ^{[5] [9]} For TIC due to atrial flutter, rate control is often difficult to achieve, and RF catheter ablation has a relatively high success rate with a low risk of complications. ^[5] In patients with TIC due to other types of SVT, RF catheter ablation is recommended as a first-line treatment. ^[5] In patients with TIC due to VT or PVCs, both antiarrhythmics and RF catheter ablation can be used. ^{[5] [6]} However, the options for antiarrhythmic agents are limited because certain agents can be proarrhythmic in the setting of myocardial dysfunction in TIC. ^[6] Therefore, RF catheter ablation is often a safe and effective choice for treatment VT and PVCs causing TIC. ^{[1] [5]} In cases where other treatment strategies fail, AV node ablation with permanent pacemaker implantation can also be used to treat the tachyarrhythmia. ^{[6] [9]}

The treatment of heart failure commonly involves neurohormonal blockade with beta-blockers and angiotensin convertase inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) along with symptomatic management with diuretics. ^[2] Beta-blockers and ACE inhibitors can inhibit and potentially reverse the negative cardiac remodeling, which refers to structural changes in the heart, that occurs in TIC. However, the need to continue these agents after treatment of the tacharrhythmia and resolution of left ventricular systolic dysfunction remains controversial. ^[5]

Prognosis

The prognosis for TIC after treatment of the underlying tachyarrhythmia is generally good. Studies show that left ventricular function often improves within 1 month of treatment of the tachyarrhythmia, and normalization of the left ventricular ejection fraction occurs in the majority of patients by 3 to 4 months. ^{[1] [5]} In some patients however, recovery of this function can take greater than 1 year or be incomplete. ^[5] In addition, despite improvement in the left ventricular ejection fraction, studies have demonstrated that patients with prior TIC continue to demonstrate signs of negative cardiac remodeling including increased left ventricular end-systolic dimension, end-systolic volume, and end-diastolic volume. ^{[1] [5] [6]} Additionally, recurrence of the tachyarrhythmia in patients with a history of TIC has been associated with a rapid decline in left ventricular ejection fraction and more severe cardiomyopathy that their prior presentation, which may be a result of the negative cardiac remodeling. ^[1] There have also been cases of sudden death in patients with a history of TIC, which may be associated with worse baseline left ventricular dysfunction. ^[5] Given these risks, routine monitoring with clinic visits, ECG, and echocardiography is recommended. ^[6]

Epidemiology

The true incidence of TIC is unclear. ^[5] Some studies have noted the incidence of TIC in adults with irregular heart rhythms to range from 8% to 34%. ^[5] Other studies of patients with atrial fibrillation and left ventricular dysfunction estimate that 25–50% of these study participants have some degree of TIC. ^[6] TIC has been reported in all age groups. ^[6]

See also

• Cardiomyopathy
• Congestive heart failure

Related Research Articles

Tachycardia, also called tachyarrhythmia, is a heart rate that exceeds the normal resting rate. In general, a resting heart rate over 100 beats per minute is accepted as tachycardia in adults. Heart rates above the resting rate may be normal or abnormal.

A premature ventricular contraction (PVC) is a common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt as palpitations in the chest. PVCs do not usually pose any danger.

Heart failure (HF), also known as congestive heart failure (CHF), is a syndrome caused by an impairment in the heart's ability to fill with and pump blood.

Sinus node dysfunction (SND), also known as sick sinus syndrome (SSS), is a group of abnormal heart rhythms (arrhythmias) usually caused by a malfunction of the sinus node, the heart's primary pacemaker. Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between fast and slow heart rates.

Palpitations are perceived abnormalities of the heartbeat characterized by awareness of cardiac muscle contractions in the chest, which is further characterized by the hard, fast and/or irregular beatings of the heart.

Arrhythmogenic cardiomyopathy (ACM) is an inherited heart disease.

Dilated cardiomyopathy (DCM) is a condition in which the heart becomes enlarged and cannot pump blood effectively. Symptoms vary from none to feeling tired, leg swelling, and shortness of breath. It may also result in chest pain or fainting. Complications can include heart failure, heart valve disease, or an irregular heartbeat.

Atrial flutter (AFL) is a common abnormal heart rhythm that starts in the atrial chambers of the heart. When it first occurs, it is usually associated with a fast heart rate and is classified as a type of supraventricular tachycardia. Atrial flutter is characterized by a sudden-onset (usually) regular abnormal heart rhythm on an electrocardiogram (ECG) in which the heart rate is fast. Symptoms may include a feeling of the heart beating too fast, too hard, or skipping beats, chest discomfort, difficulty breathing, a feeling as if one's stomach has dropped, a feeling of being light-headed, or loss of consciousness.

Ventricular tachycardia is a cardiovascular disorder in which fast heart rate occurs in the ventricles of the heart. Although a few seconds of VT may not result in permanent problems, longer periods are dangerous; and multiple episodes over a short period of time are referred to as an electrical storm. Short periods may occur without symptoms, or present with lightheadedness, palpitations, shortness of breath, chest pain, and decreased level of consciousness. Ventricular tachycardia may lead to coma and persistent vegetative state due to lack of blood and oxygen to the brain. Ventricular tachycardia may result in ventricular fibrillation (VF) and turn into cardiac arrest. This conversion of the VT into VF is called the degeneration of the VT. It is found initially in about 7% of people in cardiac arrest.

Flecainide is a medication used to prevent and treat abnormally fast heart rates. This includes ventricular and supraventricular tachycardias. Its use is only recommended in those with dangerous arrhythmias or when significant symptoms cannot be managed with other treatments. Its use does not decrease a person's risk of death. It is taken by mouth or injection into a vein.

Mitral regurgitation (MR), also known as mitral insufficiency or mitral incompetence, is a form of valvular heart disease in which the mitral valve is insufficient and does not close properly when the heart pumps out blood. It is the abnormal leaking of blood backwards – regurgitation from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts. Mitral regurgitation is the most common form of valvular heart disease.

Catheter ablation is a procedure that uses radio-frequency energy or other sources to terminate or modify a faulty electrical pathway from sections of the heart of those who are prone to developing cardiac arrhythmias such as atrial fibrillation, atrial flutter and Wolff-Parkinson-White syndrome. If not controlled, such arrhythmias increase the risk of ventricular fibrillation and sudden cardiac arrest. The ablation procedure can be classified by energy source: radiofrequency ablation and cryoablation.

Disopyramide is an antiarrhythmic medication used in the treatment of ventricular tachycardia. It is a sodium channel blocker and is classified as a Class 1a anti-arrhythmic agent. Disopyramide has a negative inotropic effect on the ventricular myocardium, significantly decreasing the contractility. Disopyramide also has general anticholinergic effects which contribute to unwanted adverse effects. Disopyramide is available in both oral and intravenous forms. In 1972, when it was one of the only alternatives to quinidine, it was praised for being more potent and somewhat less toxic. However, a 2012 review of antiarrhythmic drugs noted that disopyramide is among the most toxic agents, with a high burden of side effects and increased mortality when used to treat atrial fibrillation.

Clinical cardiac electrophysiology, is a branch of the medical specialty of cardiology concerned with the study and treatment of rhythm disorders of the heart. Cardiologists with expertise in this area are usually referred to as electrophysiologists. Electrophysiologists are trained in the mechanism, function, and performance of the electrical activities of the heart. Electrophysiologists work closely with other cardiologists and cardiac surgeons to assist or guide therapy for heart rhythm disturbances (arrhythmias). They are trained to perform interventional and surgical procedures to treat cardiac arrhythmia.

The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

Atrial fibrillation is an abnormal heart rhythm (arrhythmia) characterized by rapid and irregular beating of the atrial chambers of the heart. It often begins as short periods of abnormal beating, which become longer or continuous over time. It may also start as other forms of arrhythmia such as atrial flutter that then transform into AF.

Boxer cardiomyopathy is a disease of the myocardium primarily affecting Boxer dogs. It is characterized by the development of ventricular tachyarrhythmias, resulting in syncope and sudden cardiac death. Myocardial failure and congestive heart failure are uncommon manifestations of the disease.

Arrhythmias, also known as cardiac arrhythmias, are irregularities in the heartbeat, including when it is too fast or too slow. A resting heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a resting heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms, when present, may include palpitations or feeling a pause between heartbeats. In more serious cases, there may be lightheadedness, passing out, shortness of breath, chest pain, or decreased level of consciousness. While most cases of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure. Others may result in sudden death.

Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; this may be measured by echocardiography or cardiac catheterization. Approximately half of people with heart failure have preserved ejection fraction, while the other half have a reduction in ejection fraction, called heart failure with reduced ejection fraction (HFrEF).

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

External links