Tachycardia-Induced Cardiomyopathy: How Can Arrhythmia Affect Your Heart Muscle?

About 5.7 million people in the US have heart failure, one of the three cardiovascular epidemics of the third millennium. This emphasizes how important it is to recognize conditions that lead to heart failure but can be reversed once the cause is treated. One such cause is tachycardia-induced cardiomyopathy, a rare disorder that happens as a consequence of prolonged elevated heart rate. 

What is cardiomyopathy?

There are four main types of CM (dilated, arrhythmic, hypertrophic and restrictive). They can have a variety of causes, from genetic to ones acquired later in life. Unlike the genetic cardiomyopathies, acquired CMs can usually be reversed once the cause is no longer present. One of the causes leading to acquired CM is tachycardia, a common condition in which the heart beats too fast.

What is tachycardia-induced cardiomyopathy?

The normal human heart beats between 55 and 95 times per minute. While it’s normal to have elevated heart rate in situations of high stress or physical activity, anything over 100 beats per minute while you are resting is considered a disorder of the heart rhythm, called tachycardia. Tachycardia is a common type of arrhythmia (irregular heart rhythm). If your heart beats too fast for a prolonged period, it can cause structural and functional changes of the heart muscle, a disorder termed tachycardia-induced cardiomyopathy (TIC) or tachycardiomyopathy.

Your heart is a muscular pump with four chambers — the two upper chambers are called atria, while the two lower chambers are the ventricles. "Natural pacemaker cells" grouped into nodes and bundles regulate the way in which the heart contracts. These nodes are positioned elegantly so the movement of the different parts of the heart are tightly coordinated to allow its function: the contraction of the atria that pushes the blood to the ventricles, followed by a strong contraction that pumps blood from the ventricles to the blood vessels (leading either to the lungs or the rest of the body).

The electrical signal starts at the sinus node located in the right atrium which contracts the right atrium and continues to the AV node. The AV node delays this signal, giving the right ventricle enough time to completely fill with blood. This is a simplified version of the heart’s electrical network ttasked with ensuring a regular and controllable fashion.

Types of tachycardia that can cause TIC include supraventricular tachycardias — which originate above the ventricles; the atria or the AV node. This includes:

• Atrial fibrillation. the heartbeats are rapid and irregular (common).
• Atrial flutter. The heartbeats are rapid but regular (common).
• Rare types of tachycardia such as persistent fast atrial pacing and permanent junctional reciprocating tachycardi

​Ventricular tachycardias originate in the ventricles, and include:

• Ventricular tachycardia (V-tach). The ventricles contract fast but regularly; this form is particularly dangerous and can be life-threatening.
• Premature ventricular contractions, in which there is an extra beat between normal heartbeats.

How does tachycardia cause cardiomyopathy?

People with cardiomyopathy often present with different arrhythmias, which is why it took some time to recognize tachycardia as a cause rather than just a symptom.

The first experimental confirmation came from a group of scientists who experimented on animal models by inducing tachycardia with pacemakers and observing their consequences on the heart’s structure and function. They’ve confirmed that only 13 days of induced tachycardia can lead to symptoms of congestive heart failure, observing several structural and functional changes of the heart muscle.

Heart failure means that the heart is unable to meet the body's demands. Its function is often estimated in terms of systolic and diastolic function. The heart works through cycles, each consisting of the muscle relaxation and filling with blood, called diastole, followed by a contraction that pumps the blood out of the chamber, called systole.

The observed changes in animal models were consistent with a type of CM called dilated cardiomyopathy (DCM), in which the ventricles (one or both) become enlarged. Their walls stretch (dilate) and become thinner, making it harder for them to pump blood. Other structural changes include fibrosis (formation of excessive connective tissue) and reduced blood flow. Other changes they’ve noticed were typical manifestations of heart failure, described in greater detail in the section about the symptoms of CIM. 

While this group gave a valuable confirmation that tachycardia can indeed cause cardiomyopathy, the answer to how it happens is a much more complicated one, and to this day still incomplete. There are several suggested mechanisms to various changes that happen. These changes can be observed on the level of the cell and the muscle structure while the change in function is a consequence.

Changes on the cellular level

• Metabolical changes and oxidative stress. Heart muscle cells or myocytes are the building block of the heart muscle. For a cell to contract, it needs energy and it consumes this energy in the form of a molecule called ATP. The need for ATP regulates virtually every other pathway, overstimulating some and shutting down others. Chronic tachycardia depletes energy reservoirs in the cell and the way that the energy is utilized. Some biochemical pathways that take place in the mitochondria produce reactive oxygen species (ROS) as byproducts.  ROS are molecules that can react with anything that crosses their path, including very important molecules in the cells like the DNA. While they would normally be neutralized by antioxidants, when the pathway is overstimulated too many reactive oxygen species are produced. This damages mitochondrial DNA and has been linked with a higher degree of cell death.
• Abnormal calcium channel activity. There’s been a lot of talk about electrical signaling in the heart, but have you ever wondered how we have an electrical current in our cells and how it’s transported? The answer lies in the movement of ions, charged particles. One of the most important ions for the contraction of the muscle cells is calcium.  
• Disruption of the extracellular matrix. We call the meshwork of proteins between the heart cells the cardiac extracellular matrix. This web of proteins is very important for the contractions because it positions the cells in the right way and coordinates them. Disruption of the protein meshwork observed in animal models explains, at least to a certain degree, why tachycardia leads to decreased pumping ability. The heart can’t contract as well as it’s supposed to because the material that glues and coordinates contractions of cells is disrupted.

What are the symptoms of tachycardia-induced cardiomyopathy?

TIC presents with a combination of symptoms of tachycardia and symptoms of heart failure.

Symptoms of arrhythmia include:

• Palpitations
• Chest pain 
• Symptoms of heart failure include:
• Shortness of breath
• Fatigue
• Swelling of the ankles and legs
• Unexplained weight gain

Prognosis and treatment