Ventricular Tachycardia: Understanding the Causes
Ventricular tachycardia, often abbreviated as VT, is a type of rapid heart rhythm that originates in the ventricles. It is characterized by the spontaneous occurrence of three or more consecutive heartbeats at a rate exceeding 100 beats per minute. This condition is commonly associated with various forms of structural heart disease, especially in patients with widespread and severe myocardial damage. Individuals suffering from conditions such as coronary artery disease with a history of myocardial infarction, heart failure, or ventricular aneurysm are particularly at risk.
Underlying Mechanisms of Ventricular Tachycardia
Following a heart attack, several factors contribute to the development of ventricular tachycardia. These include abnormal electrical activity in the heart, irregularities in ventricular wall motion, impaired conduction through the bundle branches, and the presence of heart failure. These physiological disturbances create a favorable environment for the onset of VT.
Role of Scar Tissue and Reentry Circuits
In particular, the area of the heart affected by myocardial infarction or the surrounding viable myocardium often exhibits slow conduction properties. This tissue can form reentry circuits—either within the scarred region or between the scar and adjacent healthy tissue—which are a primary cause of ventricular tachycardia. These reentry pathways allow abnormal electrical signals to loop repeatedly, triggering rapid and irregular heartbeats.
Other Cardiac Conditions Linked to VT
Conditions such as dilated cardiomyopathy, arrhythmogenic right ventricular dysplasia, hypertrophic cardiomyopathy, and severe myocarditis can also lead to ventricular tachycardia. These diseases cause structural and functional changes in the heart muscle, including disorganized myocardial cell arrangement, myocardial ischemia, and reduced cardiac function. Such pathological alterations provide a substrate for the development of life-threatening arrhythmias like VT.