Ventricular Arrhythmias in Ischemic Heart Disease

Coronary heart disease is the most frequent cause of clinically documented ventricular tachycardia (VT) and ventricular fibrillation (VF) (76% to 82% of patients). With the use of timely revascularisation, the incidence of ventricular arrhythmias both in short and long-term post-myocardial infarction (MI) has reduced significantly with the 1 year mortality rate reduced to less than 5%. (Ref) However sustained VT and VF tend to cause more death events in the first 30 days of MI, in almost 6% of patients, particularly in patients with left ventricular dysfunction and heart failure.^1,2

Whereas patients with ST elevation MI are more likely to have VT/VF occurrence, more confined to the first 1-2 days of MI, patients with non-ST elevation MI tend to have fewer arrhythmic events not confined to the early phase alone.

Premature Ventricular Contractions (PVCs)

Early PVCs (within the first 48 hours) do not appear to affect the prognosis. However, repetitive complex PVCs (ventricular bigeminy, couplets, or multiform PVCs) occurring beyond 48 hours after acute MI can be associated with increased arrhythmic risk, particularly in patients with larger infarctions and impaired LV function.

Accelerated Idioventricular rhythm (AIVR)

It is neither a sensitive nor a specific marker for successful reperfusion. Abnormal automaticity secondary to intracellular calcium overload and catecholamine excess is the likely mechanism. The rhythm when timed with the successful restoration of flow, may indicate the larger infarct size and reflect my-cellular reperfusion injury.³

Non sustained VT (NSVT)

The importance of NSVT is similar to that of PVCs in the period after MI. Early occurrence before 24-48 hours of MI is considered to be benign and occurrence later in the course of acute MI portends a bad prognosis.³

Polymorphic VT (PMVT)

It is a marker of ongoing ischemia and is due to abnormal automaticity or triggered activity. It is very rare in the healed MI in the absence of ischemia.

Ventricular Fibrillation (VF)

Primary VF occurring in the first 48 hours of MI, in the absence of recurrent ischemia or heart failure, is an important cause of in-hospital mortality but has little impact on long term mortality. However, non-primary VF occurring after 48 hours, in the presence ofrecurrent ischemia or heart failure, is associatedwith marked increases in both 30-day mortality and 6-month mortality.⁴

Sudden Cardiac Death

Cardiac arrest is the initial manifestation of heart disease in approximately 50% of cases. Acute MI is a common precipitant of out-of-hospital cardiac arrest, especially in older patients. The risk of arrhythmic mortality tends to peak in the first 1 and 6 months of MI and later have a second peak again, after a period of quiescence, in 4-10 years after acute MI, likely due to delayed ventricular remodelling.⁴

Sustained monomorphic VT (SMVT)

The occurrence of SMVT after MI indicates an established permanent substrate (developing necrosis or pre existing scar) and signifies high long term mortality. Late SMVT often reflects significant LV dysfunction and the presence of a ventricular aneurysm or scarring. ⁵

Initial Evaluation of patients with post-MI VT

12-lead ECG and ambulatory cardiac monitoring (Holter or Event monitoring) may be required to document the type, burden, and clinical impact of the arrhythmia. In patients with ICDs, stored device data such as electrogram morphology and TCL can be used to identify the clinical VT.

In patients with post-MI VT, reversible causes should be ruled out first, such as electrolyte imbalances, acute ischemia, heart failure, hypoxia, hypotension, drug effects, and anemia.

SMVT is rarely due to myocardial ischemia. If coronary artery evaluation was not done in the past or is unknown, and myocardial viability is certain, cardiac catheterisation should be considered. Revascularisation should potentially improve long term arrhythmic outcomes. However, if the severity of the coronary disease has been recently defined and symptoms and hemodynamic tolerance of VT do not suggest significant ischemia, further evaluation with cath may not be required.

An invasive electrophysiological study should be considered in post-MI patients in the following situations ⁶

• Unexplained syncope
• Sustained palpitations,
• Wide complex tachycardia of uncertain mechanisms.
• Risk stratification – Ischemic cardiomyopathy, NSVT (see later)

Although the rate and QRS morphology of the induced VT can differ from that observed during spontaneous tachycardia, the induction of VT signifies the presence of a fixed anatomical substrate associated with an increased likelihood of future spontaneous events.

Risk stratification

Various tests have been proposed to identify patients at high risk of SCD who are likely to benefit from prophylactic ICD therapy. To date, only two approaches have been proven useful in guiding prophylactic ICD therapy in post-MI patients; the presence of significant LV dysfunction alone or in combination with the inducibility of sustained VT/VF during programmed electrical stimulation beyond the early phase after MI. ⁵

Following events/tools are useful in long term arrhythmic risk stratification in post-MI patients

1. Ventricular arrhythmias

Repetitive complex PVCs, NSVT, and SMVT portend a worse arrhythmic outcome. ⁷

2. Syncope (in the setting of structural heart disease)

If sustained VT is detected on cardiac monitoring or is inducible at EP study, an arrhythmic cause of syncope should be considered, and ICD implantation isrecommended ⁷

3. LV Ejection Fraction

Although LVEF is a good marker of risk for total mortality, it does not provide insight into how patients are likely to die (sudden vs. non-sudden). Furthermore, patients with low LVEF are not uniform with regard to other prognostic markers, and not all are at high risk for SCD. Obviously, these criteria are not used in the guidelines for secondary prevention of sudden cardiac death. ⁸

4. Invasive EP study

VT inducibility as a criterion is not helpful in risk stratification in patients with severely depressed EF of less than 30-35%, as observed in both MUSTT and MADIT II trials. These patients can still have arrhythmic risk even with non-inducibility. Current guidelines recommend prophylactic ICD therapy in post-MI patients with nonsustained VT and LVEF less than 40% if sustained VT/VF is inducible at EP study.

5. Miscellaneous

Measures of cardiac repolarisation (T wave alternans), autonomic imbalance, and myocardial conduction disorders (Increased QRS duration, fragmented QRS) may indicate increased arrhythmic risk, but are not very clinically useful.

Non-transmural hyper-enhancement in cardiac MRI suggests arrhythmogenicity.⁵

Principles of management

Acute Therapy

• Immediate reperfusion is critical when there is acute ischemia. Polymorphic VT or VF is the type of arrhythmia usually seen with acute ischemia. ²
• Besides ischemia, correction of electrolyte abnormalities (hypomagnesemia and hypokalemia), discontinuation of proarrhythmic drugs, and treatment of heart failure are other treatable causes, especially in PMVT/VF.
• Beta-blockers (BB) play the main role in the management of post-MI VT.
• Antiarrhythmics are not to be routinely used in PVCs and NSVT unless the burden is very large despite BB use and/or is associated with refractory angina/HF. Amiodarone may be useful in such situations. ⁵
• Similarly, prophylactic antiarrhythmics in the absence of arrhythmia are not recommended.
• Treatment of pulseless VT and VF should follow ACLS protocol. Electrical cardioversion is recommended in unstable patients.
• In case of stable sustained VT, IV Amiodarone is the drug of choice.
• Treatment of drug-refractory electrical storm, failing BB and Amiodarone.
  • Neuraxial modulation (Thoracic epidural anaesthesia, left or bilateral cardiac sympathetic denervation) ^9,10
  • Deep sedation and mechanical ventilation
  • Mechanical circulatory support for hemodynamic stabilisation.

Chronic Therapy

Implantable Cardioverter-Defibrillator

• ICD implantation is recommended for secondary prevention of SCD in patients with prior cardiac arrest or documented ventricular arrhythmias, even when LV systolic function is normal, and even in patients undergoing successful catheter ablation of VT or responding to antiarrhythmic therapy, because of residual SCD risk.¹¹
• AICD is recommended in patients with syncope and inducible SMVT even if they do not otherwise meet the criteria for primary prevention.¹¹
• Post AICD implantation, care must be exercised to reduce inappropriate as well as appropriate shocks, which are associated with increased mortality and reduced quality of life.
  • To reduce the risk of these events, ICD detection criteria and therapies should be programmed to minimise inappropriate shocks, prevent shocks for potentially self-terminating VTs, and favor anti-tachycardia pacing therapies when feasible.¹²
  • Management of HF, optimal BB use, antiarrhythmics, and catheter ablation can reduce the appropriate shock.

Catheter Ablation

• Catheter ablation can be used as a palliative and adjunctive therapy in post MI patients with frequent ICD discharges.
  • If device programming or antiarrhythmics fail to suppress frequent ICD therapies, catheter ablation is recommended.
• This can be used as a life saving therapy in patients withelectrical storms.
• It is not recommended in polymorphic VT or VF in post MI patients unless it is triggered by a PVC of consistent QRS morphology, where ablation targets the trigger, not the substrate.
• Catheter ablation also should be considered for patients with frequent PVCs or nonsustained or sustained VT that is presumed to cause ventricular dysfunction.
• Catheter ablation is offered as a curative option in select types of VT in post MI patients, such as bundle branch reentry and interfascicular VTs.
• Recent studies suggest that catheter ablation should generally be considered early in the course of treatment of post-MI VT, before escalating medication therapy, or even before initiating antiarrhythmic drug therapy in select patients.
• Catheter ablation is contraindicated in the presence of mobile LV thrombus, wherein epicardial ablation may be considered.
• Percutaneous catheter ablation via a surgically created subxiphoid epicardial window is an option in the case of pericardial adhesions ^{5, 13}

 Alternative Interventional Treatment

Transcoronary ethanol ablationis used as a last resort in case of intramural circuits with failed epicardial and endocardial attempts. Surgical methods like LV aneurysm resection and reconstruction are promising in select cases. ¹⁴

References

1. Liang JJ, Prasad A, Cha Y-M. Temporal evolution and implications of ventricular arrhythmias associated with acute myocardial infarction. Cardiol Rev. 2013;21:289–294.
2. Gorenek B, et al. Cardiac arrhythmias in acute coronary syndromes:position paper from the joint EHRA, ACCA, and EAPCI Task Force. 2015;10:1095–1108.
3. van der Weg K, et al. Prospective evaluation of where reperfusion ventricular arrhythmia “bursts” fit into optimal reperfusion in STEMI. Int J Cardiol. 2015;195:136–142.
4. Fordyce CB, et al. Long-term post-discharge risks in older survivors of myocardial infarction with and without out-of-hospital cardiac arrest. J Am Coll Cardiol. 2016;67:1981–1990.
5. Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald’s Heart Disease. Third edition. Ziad F.Issa, John M. Miller, Douglas P. Zipes. Elsevier Publications.
6. Peachey H, et al. EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Heart Rhythm. 2014;11:e166–e196.
7. Kusumoto FM, et al. HRS/ACC/AHA expert consensus statement on theuse of implantable cardioverter-defibrillator therapy in patients who are not included or not well represented in clinical trials. J Am Coll Cardiol. 2014;64:1143–1177.
8. Dagres N, Hindricks G. Risk stratification after myocardial infarction: is left ventricular ejection fraction enough to prevent sudden cardiac death? Eur Heart J. 2013;34:1964–1971.
9. Vaseghi M, et al. Cardiac sympathetic denervation in patients with refractory ventricular arrhythmias or electrical storm: intermediate and long-term follow-up. Heart Rhythm. 2014;11:360–366
10. Al-Ahmad A, Shenasa M, Shenasa H, et al. Incessant ventricular tachycardia and fibrillation: electrical storms. Card Electrophysiol Clin. 2014;6:613–621.
11. Al-Khatib SM, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Heart Rhythm. 2017 Oct 26. [Epub ahead of print].
12. Guerra F, et al. Implantable cardioverter-defibrillator programming and electrical storm: results of the OBSERVational registry On long-term outcome of ICD patients (OBSERVO-ICD). Heart Rhythm. 2016;13:1987–1992.
13. Priori SG, Blomström-Lundqvist C, Mazzanti A. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2015;8:746–837.
14. Kumar S, et al. Role of alternative interventional procedures when endo- and epicardial catheter ablation attempts for ventricular arrhythmias fail. Circ ArrhythmElectrophysiol. 2015;8:606–615.

 

Dr Sakthivel R
Consultant Cardiologist and Electrophysiologist
Kauvery Hospital Chennai