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Catheter ablation of ventricular tachycardia in patients with post-infarction cardiomyopathy.

Nazer B, Gerstenfeld EP - Korean Circ J (2014)

Bottom Line: Monomorphic ventricular tachycardia (VT) in patients with post-infarction cardiomyopathy (CMP) is caused by reentry through slowly conducting tissue with in areas of myocardial scar.The use of implantable cardioverter-defibrillators (ICDs) has helped to decrease the risk of arrhythmic death in patients with post-infarction CMP, but the symptomatic and psychological burden of ICD shocks remains significant.In this review, we discuss the pathophysiology of VT in post-infarction CMP patients, and the contemporary practice of catheter ablation.

View Article: PubMed Central - PubMed

Affiliation: Electrophysiology Section, Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.

ABSTRACT
Monomorphic ventricular tachycardia (VT) in patients with post-infarction cardiomyopathy (CMP) is caused by reentry through slowly conducting tissue with in areas of myocardial scar. The use of implantable cardioverter-defibrillators (ICDs) has helped to decrease the risk of arrhythmic death in patients with post-infarction CMP, but the symptomatic and psychological burden of ICD shocks remains significant. Experience with catheter ablation has progressed substantially in the past 20 years, and is now routinely used to treat patients with post-infarction CMP who experience VT or receive ICD therapy. Depending on the hemodynamic tolerance of VT, a variety of mapping techniques may be used to identify sites for catheter ablation, including activation and entrainment mapping for mappable VTs, or substrate mapping for unmappable VTs. In this review, we discuss the pathophysiology of VT in post-infarction CMP patients, and the contemporary practice of catheter ablation.

No MeSH data available.


Related in: MedlinePlus

Mechanism of macro reentry in scar-based VT. A: three-dimensional electroanatomic voltage map of LV with areas of normal myocardium (purple), scar (red), and border zone (other colors). The yellow arrow demonstrates a potential "isthmus" area between areas of scar that may harbor the VT circuit. B: autopsy specimen of a heart with prior myocardial infarction with a septal scar (pale area). Note that the scar is heterogeneous with areas of surviving myocardium between areas of infarcted myocardium that may serve as a potential VT isthmus (black arrow). This specimen is from a different patient than that of the electroanatomic map, and is used as an example. VT: ventricular tachycardia, LV: left ventricle, RV: right ventricle.
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Figure 1: Mechanism of macro reentry in scar-based VT. A: three-dimensional electroanatomic voltage map of LV with areas of normal myocardium (purple), scar (red), and border zone (other colors). The yellow arrow demonstrates a potential "isthmus" area between areas of scar that may harbor the VT circuit. B: autopsy specimen of a heart with prior myocardial infarction with a septal scar (pale area). Note that the scar is heterogeneous with areas of surviving myocardium between areas of infarcted myocardium that may serve as a potential VT isthmus (black arrow). This specimen is from a different patient than that of the electroanatomic map, and is used as an example. VT: ventricular tachycardia, LV: left ventricle, RV: right ventricle.

Mentions: Post-infarction VT is caused by reentry through diseased myocardium due to prior myocardial infarction. These areas of scar are comprised of fibrotic, unexcitable tissue, interspersed with areas of surviving, partially depolarizable myocytes (often referred to as "isthmuses" or "channels"), and areas of functional block that lead to slow conduction and unidirectional block critical to initiating reentry (Fig. 1). Scar sustaining post-infarction VT can be quite large, comprising up to 50% of the left ventricular (LV) surface area,18) can contain several isthmuses and exit sites, and can lead to multiple VTs from the same scar area. Surface electrocardiogram (ECG) QRS morphology of a given monomorphic VT reflects only its exit site, and mapping with intracardiac electrograms (EGM) or three-dimensional (3D) electroanatomic systems is required to identify the extent of the scar and its associated isthmuses or channels. Early physiologic studies found that most macro reentrant VTs have protected, narrow isthmuses that are required for maintenance;19)20) in 1990 Morady et al.21) first described the successful treatment of VT using radiofrequency (RF) catheter ablation in three patients.


Catheter ablation of ventricular tachycardia in patients with post-infarction cardiomyopathy.

Nazer B, Gerstenfeld EP - Korean Circ J (2014)

Mechanism of macro reentry in scar-based VT. A: three-dimensional electroanatomic voltage map of LV with areas of normal myocardium (purple), scar (red), and border zone (other colors). The yellow arrow demonstrates a potential "isthmus" area between areas of scar that may harbor the VT circuit. B: autopsy specimen of a heart with prior myocardial infarction with a septal scar (pale area). Note that the scar is heterogeneous with areas of surviving myocardium between areas of infarcted myocardium that may serve as a potential VT isthmus (black arrow). This specimen is from a different patient than that of the electroanatomic map, and is used as an example. VT: ventricular tachycardia, LV: left ventricle, RV: right ventricle.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4117840&req=5

Figure 1: Mechanism of macro reentry in scar-based VT. A: three-dimensional electroanatomic voltage map of LV with areas of normal myocardium (purple), scar (red), and border zone (other colors). The yellow arrow demonstrates a potential "isthmus" area between areas of scar that may harbor the VT circuit. B: autopsy specimen of a heart with prior myocardial infarction with a septal scar (pale area). Note that the scar is heterogeneous with areas of surviving myocardium between areas of infarcted myocardium that may serve as a potential VT isthmus (black arrow). This specimen is from a different patient than that of the electroanatomic map, and is used as an example. VT: ventricular tachycardia, LV: left ventricle, RV: right ventricle.
Mentions: Post-infarction VT is caused by reentry through diseased myocardium due to prior myocardial infarction. These areas of scar are comprised of fibrotic, unexcitable tissue, interspersed with areas of surviving, partially depolarizable myocytes (often referred to as "isthmuses" or "channels"), and areas of functional block that lead to slow conduction and unidirectional block critical to initiating reentry (Fig. 1). Scar sustaining post-infarction VT can be quite large, comprising up to 50% of the left ventricular (LV) surface area,18) can contain several isthmuses and exit sites, and can lead to multiple VTs from the same scar area. Surface electrocardiogram (ECG) QRS morphology of a given monomorphic VT reflects only its exit site, and mapping with intracardiac electrograms (EGM) or three-dimensional (3D) electroanatomic systems is required to identify the extent of the scar and its associated isthmuses or channels. Early physiologic studies found that most macro reentrant VTs have protected, narrow isthmuses that are required for maintenance;19)20) in 1990 Morady et al.21) first described the successful treatment of VT using radiofrequency (RF) catheter ablation in three patients.

Bottom Line: Monomorphic ventricular tachycardia (VT) in patients with post-infarction cardiomyopathy (CMP) is caused by reentry through slowly conducting tissue with in areas of myocardial scar.The use of implantable cardioverter-defibrillators (ICDs) has helped to decrease the risk of arrhythmic death in patients with post-infarction CMP, but the symptomatic and psychological burden of ICD shocks remains significant.In this review, we discuss the pathophysiology of VT in post-infarction CMP patients, and the contemporary practice of catheter ablation.

View Article: PubMed Central - PubMed

Affiliation: Electrophysiology Section, Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.

ABSTRACT
Monomorphic ventricular tachycardia (VT) in patients with post-infarction cardiomyopathy (CMP) is caused by reentry through slowly conducting tissue with in areas of myocardial scar. The use of implantable cardioverter-defibrillators (ICDs) has helped to decrease the risk of arrhythmic death in patients with post-infarction CMP, but the symptomatic and psychological burden of ICD shocks remains significant. Experience with catheter ablation has progressed substantially in the past 20 years, and is now routinely used to treat patients with post-infarction CMP who experience VT or receive ICD therapy. Depending on the hemodynamic tolerance of VT, a variety of mapping techniques may be used to identify sites for catheter ablation, including activation and entrainment mapping for mappable VTs, or substrate mapping for unmappable VTs. In this review, we discuss the pathophysiology of VT in post-infarction CMP patients, and the contemporary practice of catheter ablation.

No MeSH data available.


Related in: MedlinePlus