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Updated: Aug 14, 2026

Tachycardia-Induced Cardiomyopathy As a Chronic Heart Failure Model in Swine
Published on: February 17, 2018
[Ventricular tachycardia of ischemic cardiomyopathies]
1Clinique cardiologique, hôpital Lariboisière, Saint-Cloud.
Insights
Ventricular tachycardia (VT) after myocardial infarction is linked to slow conduction zones. Left ventricular ejection fraction significantly impacts mortality risk, with beta-blockers showing reduced mortality in low ejection fraction patients.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Surgery
Context:
- Ventricular tachycardia (VT) frequently occurs in patients with ischemic heart disease post-myocardial infarction, particularly when border zones are not preserved.
- Monomorphic VT is associated with permanent electrophysiological substrates and slow conduction zones, often triggered by extrasystoles or sympathetic activation.
Purpose:
- To analyze the prognostic value of left ventricular ejection fraction (LVEF) and treatment strategies in patients with ischemic heart disease and ventricular tachycardia.
- To evaluate factors influencing mortality, including LVEF, syncopal episodes, inducible VT, and response to antiarrhythmic therapy.
Summary:
- Cardiac mortality, primarily sudden death, follows sustained monomorphic VT. LVEF is a critical prognostic indicator: 5-year mortality is 30% with LVEF > 0.3 versus 51% with LVEF < 0.3.
- While spontaneous or induced VT frequency doesn't alter prognosis, syncopal VT episodes increase mortality risk. Persistence of inducible VT despite therapy elevates mortality, highlighting the need for effective antiarrhythmic drugs.
- Treatment choice is crucial for patients with LVEF ≤ 0.30; Class I antiarrhythmics correlate with higher mortality, whereas beta-blockers demonstrate reduced mortality. Polymorphic VT with inducible VT/VF carries a very high mortality risk.
Impact:
- This study underscores the critical role of LVEF in stratifying mortality risk in ischemic VT patients.
- It emphasizes the importance of clinical history and effective antiarrhythmic therapy, particularly beta-blockers, in managing patients with reduced ejection fraction.
- Findings guide therapeutic decisions, aiming to reduce sudden cardiac death and improve survival rates in this vulnerable patient population.
Abstract:
Ventricular tachycardia in patients with ischemic heart disease are almost always observed after myocardial infarction without preservation of the border zone (thrombolysis or early angioplasty). Monomorphic tachycardias are related to permanent electrophysiological substrate with a zone of slow conduction. This may be affected by initiating factors such as extrasystoles, especially with alternating long and short cycles, and the sympathetic nervous system before the appearance of clinical tachycardia. Cardiac mortality is mainly due to sudden death after an initial episode of sustained monomorphic ventricular tachycardia. The prognostic value of left ventricular function as assessed by the ejection fraction is essential: the 5-year mortality is 30% if LVEF is > 0.3 compared with 51% if LVEF is < 0.3 (p < 0.01). On the other hand, the frequency of spontaneous VT and VT induced by programmed stimulation does not affect the prognosis. The mortality after an initial episode of syncopal tachycardia is greater than after a well tolerated tachycardia. This is why the clinical history of the patient is essential to guide management. The persistence of inducible VT despite antiarrhythmic therapy increases the mortality; it is therefore important to find a drug which prevents induction VT. The patient is then classified as "responder". The number of "responders" patients, however, is low when the ejection fraction is < or = 0.30. The choice of treatment seems important when the ejection fraction is < or = 0.30: in this case, patients receiving Class I antiarrhythmics have a higher mortality and those taking betablockers have a reduced mortality. After polymorphic VT, if VT or VF is inducible, the risk of mortality is very high.(ABSTRACT TRUNCATED AT 250 WORDS)
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