Ventricular tachycardia (VT) occurs most often in the context of structural heart disease, with a small group of patients presenting idiopathic VT without any structural abnormalities. The most common underlying heart disease is coronary artery disease, often in the context of previous myocardial infarction leaving a substrate for re-entry VTs. Other structural heart diseases leading to VT are cardiomyopathies and inflammatory heart disease. VT is an important cause of hemodynamic compromise and in some cases, causing deterioration, ventricular fibrillation, and even sudden cardiac death. Pharmacological therapy often fails, necessitating catheter ablation with or without the implantation of a cardioverter-defibrillator.
There are many remaining questions arising around VT involving mechanisms of development, anatomic characterization of the substrate as well as identification of optimal treatment strategies. VT mechanisms have consequences for optimal ablation or pharmacological therapy. Imaging modalities have gained interest to aid ablation but also for risk stratification. Biomarkers such as blood values, electrocardiographic parameters, echocardiography, and advanced imaging including computed tomography and magnetic resonance imaging can improve mechanistic understanding and planning of treatment strategies. Last but not least, genetic testing can aid risk stratification but also in understanding the underlying pathophysiology.
The main topics of this Research Topic focus on:
1) Mechanistic studies of VT origin en perpetuation.
2) Risk stratification.
3) Optimal therapy of VT.
4) Ablation strategies.
5) Substrate imaging.
Ventricular tachycardia (VT) occurs most often in the context of structural heart disease, with a small group of patients presenting idiopathic VT without any structural abnormalities. The most common underlying heart disease is coronary artery disease, often in the context of previous myocardial infarction leaving a substrate for re-entry VTs. Other structural heart diseases leading to VT are cardiomyopathies and inflammatory heart disease. VT is an important cause of hemodynamic compromise and in some cases, causing deterioration, ventricular fibrillation, and even sudden cardiac death. Pharmacological therapy often fails, necessitating catheter ablation with or without the implantation of a cardioverter-defibrillator.
There are many remaining questions arising around VT involving mechanisms of development, anatomic characterization of the substrate as well as identification of optimal treatment strategies. VT mechanisms have consequences for optimal ablation or pharmacological therapy. Imaging modalities have gained interest to aid ablation but also for risk stratification. Biomarkers such as blood values, electrocardiographic parameters, echocardiography, and advanced imaging including computed tomography and magnetic resonance imaging can improve mechanistic understanding and planning of treatment strategies. Last but not least, genetic testing can aid risk stratification but also in understanding the underlying pathophysiology.
The main topics of this Research Topic focus on:
1) Mechanistic studies of VT origin en perpetuation.
2) Risk stratification.
3) Optimal therapy of VT.
4) Ablation strategies.
5) Substrate imaging.
