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.
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.
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
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
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.
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
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
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
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
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.
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
Repetitive complex PVCs, NSVT, and SMVT portend a worse arrhythmic outcome. 7
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
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
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.
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
Acute Therapy
Chronic Therapy
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
Dr Sakthivel R Consultant Cardiologist and Electrophysiologist Kauvery Hospital Chennai
