Volume 4 - Issue 4
Deep Chandh Raja1,*, Sundar C2, Sakthivel R3, Selva Maheshwari4, Vishal5
1Cardiologist and Clinical Lead of Cardiac Electrophysiology, Kauvery Heart Rhythm Services, Kauvery Hospital, Chennai
2Senior Cardiologist, Kauvery Heart Rhythm Services, Kauvery Hospital, Chennai
3Cardiac Electrophysiologist, Kauvery Heart Rhythm Services, Kauvery Hospital, Chennai
4Physician Assistant, Kauvery Heart Rhythm Services, Kauvery Hospital, Chennai
5Cardiac Technician, Kauvery Heart Rhythm Services, Kauvery Hospital, Chennai
The most dreaded of the varied presentations of ventricular tachycardia (VT) is the VT storm. This is defined as more than 3 episodes of VT/ VF needing cardioversion in a 24 h period. Management of VT storm is even more daunting in the background of ST-elevation myocardial infarction (STEMI) and portends poor prognosis.1 Such a scenario poses special challenges to terminate the VT storm. The treatment involves medical as well as invasive procedures. We present a rare case of VT storm in the background of STEMI. This case presents a lot of learning opportunities to equip oneself while treating such patients.
A 55-year-old female presented to the emergency in cardiogenic shock. She had complaints of epigastric discomfort for 5 h. The ECG revealed sinus bradycardia and ST-T changes suggestive of inferior wall STE myocardial infarction with PVCs in bigeminy (Fig. 1). The patient was shifted to the catheterization laboratory. An emergency coronary angiogram showed normal left coronary arteries with thrombotic total occlusion of the right coronary artery. This was followed by an Intra-Aortic Balloon Pump (IABP) supported primary coronary angioplasty was performed with also, a temporary pacemaker insertion. The angioplasty was very eventful, as the patient had multiple runs of polymorphic ventricular tachycardia requiring direct current (DC) cardio-versions. Intravenous boluses of amiodarone were administered. After successful percutaneous coronary angioplasty (PTCA) to the occluded proximal right coronary artery, TIMI 3 flow was established. (Figure 1). The patient was shifted to the coronary care unit (CCU) with backup temporary pacing and on IABP support. The LV ejection fraction (EF) improved from 30% pre- PTCA to 40% post-PTCA.
Fig. 1. Panel A shows the 12-lead ECG with ST-segment elevation in the inferior leads and PVCs occurring in bigeminy; Panel B shows angiogram revealing the occluded proximal right coronary artery (RCA); Panel C shows the 12-lead ECG post angioplasty with substantial resolution of ST-segment elevation, however the PVCs of the same morphology persist in bigeminy; Panel D shows the patent RCA post angioplasty.
On day 1 the patient had satisfactory ST segment resolution on the ECG and no chest discomfort. (Fig. 1) However, the patient received 14 DC shocks over the next 48 h. Much of these shocks were thought to be secondary to polymorphic VT and ventricular fibrillation (VF) due to bradycardia-induced long QT. After failing medical management with intravenous amiodarone and lignocaine, the VT storm was successfully managed with ventricular overdrive pacing. Intravenous administration of magnesium and correction of hypokalemia were carried out. Beta-blockers could not be administered due to the underlying bradycardia causing long QT. As the ECG revealed long QT despite correction of electrolytes and no ongoing ischemia, further history was elicited from the patient. The patient recollected to have been diagnosed earlier with mild form of mitral valve prolapse with idiopathic PVCs. As the patient had never been symptomatic, she was not on any medical treatment for same.
A relook into the 12-lead ECG at presentation revealed outflow tract PVCs. (Fig. 1) These PVCs were then thought to be secondary to ischemia in the background of Inferior wall STEMI. However, PVCs of the same morphology persisted even after successful PTCA. (Fig. 1) Moreover, these PVCs were found to trigger the polymorphic runs of VT whenever the long QT became manifest due to bradycardia. (Fig. 2) The overdrive pacing was effective not only in preventing bradycardia but also in suppressing these PVCs. (Fig. 2) As the patient continued to have PVCs triggering VT and VF even on the 4th day, the patient was taken for invasive electro-anatomical mapping and Radio-Frequency Ablation (RFA) of the VT.
Fig. 2. Panel A shows a run of polymorphic VT triggered by PVCs of monomorphic QRS morphology in a background of markedly prolonged QT interval; Panel B shows a similar run of polymorphic VT triggered by PVCs; Panel C shows the trace from the monitor showing overdrive pacing successfully suppressing these PVCs.
The electrophysiology study revealed frequent monomorphic PVCs triggering runs of VT and VF. With aid of 3-dimensional electro-anatomical mapping (NavX PrecisionR), these monomorphic PVCs were localized to the right ventricular outflow tract septum beneath the pulmonary valve. Also, the sinus voltage map revealed very low fractionated signals in the RVOT suggesting substrate that was harboring electrical abnormalities (Fig. 3). Substrate modification was performed in the RVOT by RFA at powers of 30-40 watts using irrigated contact force catheters (Fig. 4). The PVCs terminated and no VT was inducible at the end of the procedure. The patient was free of any VT for the next 48 h. Following successful RFA of the VT, the patient also received a dual chamber defibrillator (ICD) implant for prevention of sudden cardiac death due to the underlying electrical abnormalities detected during the EP study (Fig. 4). The recovery was uneventful and the patient was discharged on the 14th day with stable hemodynamics and heart failure medications.
Fig. 3. Panel A shows the intracardiac traces from the mapping catheter. Please note the late potentials during sinus rhythm (red arrows), which precede the QRS during the PVC (vertical red line); Panel B shows the low voltage zone (colors other than purple) in the outflow tract of the right ventricle (RVOT); Panel C shows the earliest activation site of the PVCs (white-red color) at the RVOT.
Fig. 4. Panel A shows the radio-frequency burns (red spheres) delivered at the substrate in the RVOT; Panel B shows the dual chamber defibrillator implant (ICD).
The salient learning points from the above case presentation are: 1). Preexisting arrhythmogenic substrate should be sought for when the VT storm post STEMI successful revascularization is not explainable 2). Invasive treatment strategies like RFA have excellent outcomes to terminate the VT storm arising due to electrical abnormalities 3). Strategies like overdrive ventricular pacing should be considered while addressing a VT storm in addition to administration of anti-arrhythmic medications and correction of electrolyte abnormalities.
VT storm post MI is known to occur in three settings- delayed presentation, partial revascularization and underlying arrhythmogenic substrate . In this era of thrombolysis and primary PTCA, coronary reperfusion is achieved early in patients with STEMI. Reperfusion of myocardium subjected to prolonged ischemia can set-up an electrophysiological substrate conducive to spontaneous after-depolarizations and unidirectional blocks causing reentry circuits . Ongoing ischemia due to partially revascularized or revascularized myocardial territories can also trigger VT. In the above discussed case, there seems to have been an underlying arrhythmogenic substrate with preexisting triggers in form of PVCs. These PVCs which were incapable of triggering VT/ VF pre-STEMI, seem to have found the right milieu in the context of MI, for reentry, thus leading to sustained VT. These short runs of monomorphic VT were degenerating to polymorphic VT and VF due the long QT induced by bradycardia.
Management of such VT storms is again very challenging, and this case is a good example to highlight why such strategies must be individualized to each clinical scenario . While Class 1A, 1C and III anti-arrhythmic drugs must be avoided in a structurally abnormal heart and particularly in the setting of long QT due high risk of arrhythmias, amiodarone and lignocaine have found to have the reasonable efficacy-safety profile. Stop-gap strategies like overdrive ventricular pacing is very helpful to suppress the PVCs/VT provided the hemodynamics are tolerable. One or more of the sympathetic suppression modalities like betablockade, stellate ganglion block, deep sedation and general anesthesia have also been found to be helpful to suppress the VT storm .
Invasive treatment modalities like RFA are being increasingly explored as options to treat the underlying electrical abnormalities, as demonstrated in this case . This strategy works best when there are preexisting triggers for polymorphic VT/ VF like PVCs and monomorphic runs of VT. These triggers could be pre-existing as shown in this case or could be triggers from the ischemic Purkinje fibers. Substrate homogenization by RFA can homogenize the electrical scar and thereby eliminate regions of unidirectional block. RFA can thus abolish the substrate responsible for VT/ VF.
We have presented a case of VT storm in the background of MI despite successful primary angioplasty to the occluded vessel. RFA was effective in eliminating the trigger for the VT storm.
Consultant Cardiologist and Clinical Lead - Cardiac Electrophysiology