Successful Prevention of Sudden Cardiac Death by Wearable Cardioverter-Defibrillator After STEMI With Late Gadolinium Enhancement Accompanied by Signs of Microvascular Obstruction in Cardiac MRI

Patients with reduced left ventricular ejection fraction (LVEF) after an acute myocardial infarction (MI) have an increased risk for sudden cardiac death within the first 30 days.^1,2 The VEST trial³ did not significantly reduce sudden death through the use of the wearable cardioverter-defibrillator (WCD) in these patients (patients with LV dysfunction after MI), in part because of the low rate of life-threatening ventricular arrhythmias (1.6% WCD group vs 2.4% control group), with the use of LVEF <35% as the only risk marker for sudden cardiac death. Recently, the extent of late gadolinium enhancement and microvascular obstruction assessed by cardiac magnetic resonance imaging (MRI) was reported to correlate with increased mortality in patients after an acute MI.⁴ Herein, we report a case where a WCD prevented sudden cardiac death due to ventricular fibrillation occurring during the gap in time between the index MI and the recommended timing for the decision making concerning an implantable cardioverter-defibrillator (ICD) indication.⁵

Case Report

A 49-year-old male patient was admitted to our university hospital via the emergency department (ED) due to syncope associated with chest pain. His colleagues reported that the patient exhibited convulsions, but recovered spontaneously. Because of the progressive chest pain associated with dyspnea and nausea, the ED physician was alerted. A significant ST-elevation in the precordial leads V1-V3 with a slow progression of the R wave, corresponding to an anterior ST-elevation MI (STEMI), was discovered in the 12-lead electrocardiogram (ECG). The patient was then transferred directly to our cath lab for an acute coronary revascularization.

Clinical Findings at Admission

Upon admission, the patient had a blood pressure of 120/85 mmHg without clinical signs of heart failure. He complained of persistent chest pain associated with nausea. The ST-elevation remained in the 12-lead ECG (Figure 1). Echocardiography performed while preparing the patient for coronary angiography showed a normal-sized left ventricle with an akinesia of the apex, the apical interventricular septum, and the apical part of the anterior wall. Preserved contractility was apparent in all other LV regions. A relevant valvular disorder could be excluded as far as pericardial effusion.

Coronary Angiography and Percutaneous Coronary Intervention (PCI)

The culprit lesion was located at the bifurcation (Medina 1-1-1) of the left anterior descending coronary artery (LAD) and the first diagonal branch (D1). There was TIMI-III flow in the first diagonal branch, but only TIMI-I flow in the LAD, caused by a thrombus at this bifurcation. The left circumflex artery originated atypically from the right coronary artery, but both vessels were without a relevant stenosis (Figure 2). Because of the occurrence of a hemodynamically relevant sinus bradycardia after the coronary angiography, temporary transvenous pacing was established and applied for some minutes. The LAD/D1-bifurcation was treated immediately, while the rhythm was stabilized by temporary transvenous pacing. Provisional T-stenting with a drug-eluting stent (Xience Alpine 3.0 mm x 23 mm, Abbott Vascular) was performed without intervention at the diagonal branch. Intracoronary administration of a glycoprotein (GP) IIb/IIIa-receptor antagonist resulted in TIMI-III flow in both branches. After the successful revascularization, non-sustained ventricular tachycardia (VT) occurred, although the ST-elevation disappeared within a few minutes. Dual antiplatelet therapy (DAPT) with aspirin and ticagrelor was started, accompanied by a continuous infusion of a GP IIb/IIIa receptor antagonist for 12 hours. The patient left the cath lab in a stable sinus rhythm, without need for pacing.

Further Therapy in the Hospital

After the successful coronary revascularization, the patient was admitted to the intensive care unit (ICU) for 48 hours. During his stay in the ICU, the patient remained in stable sinus rhythm, without additional arrhythmic events. Initial troponin was 7 ng/l at admission, peaking at 6760 ng/l after the coronary intervention.

Subsequent echocardiography confirmed persistent impairment of the contractility (strain analysis) in the infarcted myocardium involving the apex, the apical septum, and the apical lateral wall (Figure 3), resulting in a reduced LVEF of 35-40%.

Three days after the STEMI, cardiac MRI revealed a left ventricle with slight hypertrophic myocardium. The cine loops confirmed hypokinesia in the anteroseptal, apical, and apical lateral LV wall. The perfusion study revealed an area with delayed perfusion in the apical septum, including the apical parts of the anterior and posterior wall. Late gadolinium enhancement at 50% of myocardial wall thickness was found in the septal, apical, and inferior parts of the left ventricle (segments 2, 8, 9, 14,15, 16, 17). Additionally, signs of microvascular obstruction could be detected in the LV apex.

The patient left the hospital in good clinical condition. DAPT with aspirin and ticagrelor was accompanied by secondary prophylaxis for coronary artery disease with a statin and ß-blocker. Additionally, an ACE inhibitor and eplerenone were prescribed for the reduced LVEF.

The patient was supplied with a wearable cardioverter-defibrillator (WCD), since an ICD was not indicated according to the current guidelines for prevention of sudden cardiac death within the first 40 days after an acute MI and 90 days after revascularization.^1,5

Follow-Up

Although the patient left our hospital in good clinical condition without any signs of heart failure, he experienced an episode of sustained ventricular fibrillation (VF) 2 weeks after discharge that was successfully treated by the WCD. The patient continued wearing the WCD for at least 3 months after the STEMI. In accordance with current guidelines, LVEF was re-assessed by echocardiography. Despite a good recovery (an LVEF at approximately 50%), another cardiac MRI revealed a persistent area of late gadolinium enhancement in the interventricular septum. An ICD for secondary prophylaxis (i.e., the WCD-treated VF) was inserted in accordance with the guidelines for prevention of SCD.¹ At a later follow-up (6 months), only one non-sustained VT (recorded, but not treated) was documented by the ICD.

Discussion

We present the case of a patient admitted to our hospital with STEMI. Despite an immediate and successful revascularization, the patient suffered LV dysfunction (LVEF between 35-40%). A cardiac MRI revealed a large area of late gadolinium enhancement in the infarcted myocardium with signs of microvascular obstruction. The patient was discharged on guideline-compliant medical treatment and a WCD (since an ICD was not indicated by current guidelines for the prevention of sudden cardiac death). Two weeks after discharge from hospital, the patient was successfully treated by the WCD for ventricular fibrillation. In this case, the WCD was life-saving in the gap of time between the STEMI and the recommended timing for an ICD implantation decision (48-hour and 40-day rule).⁵ Documented ventricular arrhythmias within the first 48 hours of an acute MI are supposed to be related to the myocardial ischemia, whereas arrhythmic events occurring later than this time period, in the absence of further myocardial ischemia, are currently an indication for ICD implantation as a secondary prevention of sudden cardiac death.

Sudden Cardiac Death After MI

Sudden cardiac death caused by a ventricular tachyarrhythmia still contributes to the increased mortality in patients with acute MI and a reduced LVEF.^6-9 The highest risk seems to be within the first month after an acute MI (per the VALIANT trial) with an event rate of 1.4% in the first month, decreasing to 0.5%/month between the first and the sixth months.² However, two large randomized trials, DINAMIT^10,11 and BEST-ICD^12,13, did not show any survival benefit from an ICD implanted for primary prevention within the first 40 days after MI. In DINAMIT, impaired heart rate variability in addition to LVEF ≤35% was required for inclusion. Patients with VT/VF >48 hours after the acute MI, representing a high-risk group, were excluded. The BEST-ICD trial compared conventional medical treatment, including at least 25 mg/d metoprolol, vs an early ICD implantation guided by electrophysiological testing. BEST-ICD enrolled patients with an LVEF ≤35% and further evaluated the presence of >10/premature ventricular contractions (PVCs)/h, reduced heart rate variability, and an abnormal signal-averaged ECG as potential risk factors for sudden cardiac death. Even though both trials have substantial limitations concerning patient inclusion criteria, patient recruitment, and a low revascularization proportion, the current guidelines clearly exclude early implantation of a defibrillator (within 40 days after MI) and do not mention the use of an additional non-invasive risk marker for decision making beyond LVEF ≤35%.

The WCD is a promising therapy to protect patients with temporary risk of SCD, and current evidence has resulted in a class IIb recommendation for patients with a reduced LVEF after a myocardial infarction.¹ The WCD has been shown to be a reliable device for detection and effective treatment of ventricular tachyarrhythmias^7,14,15, avoiding the potential risks associated with ICD implantation, especially while the patient is on DAPT¹⁶ after PCI.

The VEST trial³ used LVEF below 35% after AMI as the main inclusion criterion, and compared the use of a WCD added to an optimal guideline-compliant medical treatment with medical treatment only. Unfortunately, the VEST trial, while demonstrating a total mortality benefit, did not meet its primary goal of significantly reducing sudden cardiac death, in part because of the low event rate of life-threatening ventricular arrhythmias (1.6% WCD group vs 2.4% control group) through the use of LVEF ≤35% as the only risk marker for sudden cardiac death.

With this background, cardiac MRI may contribute to a better identification of patients at risk after acute MI. Recently, the extent of late gadolinium enhancement and microvascular obstruction assessed by cardiac MRI was reported to correlate with an increased mortality in patients after AMI.⁴ In a cohort of 1688 patients from seven randomized primary PCI trials with assessment of late gadolinium enhancement and microvascular obstruction after reperfusion, the extent of microvascular obstruction was associated with increased mortality and heart failure hospitalization. The multivariable analysis further identified the infarct size, the symptom-to-device-time and the baseline TIMI flow grade 0 or I as significant predictors for all-cause mortality. All these parameters may have a negative influence on ventricular remodeling, thus leading to a larger substrate for tachyarrhythmias. A cardiac MRI-based risk score for patients with STEMI has recently been proposed¹⁷ to improve the identification of high-risk patients.

Our specific patient met some of the risk factors mentioned above: he had a prolonged symptom-to-device time and a baseline TIMI flow grade I in the angiography caused by the presence of a thrombus at the culprit lesion, predictive for the development of microvascular obstruction.^18-20 The large acute MI led to impaired LV function as evaluated by echocardiography (LVEF 35-40%). Disturbance of the regional contractility in the strain analysis corresponded to the areas of late gadolinium enhancement in the cardiac MRI with signs of microvascular obstruction. Furthermore, a non-sustained VT was documented after reperfusion. In our patient, the individual decision to provide a WCD after the myocardial infarction was life saving.

In light of these findings, further study of patients with reduced LVEF after a MI may be warranted. Combining an LVEF <35% with a reduced initial TIMI flow and cardiac MRI-based parameters to evaluate the risk of sudden cardiac death in these patients may prove to be a beneficial strategy. As evidenced by this case report, the WCD can be a useful tool²¹, as it provides not only continuous rhythm monitoring, but also an effective treatment of life-threatening tachyarrhythmias. 

Disclosure: The authors report no conflicts of interest regarding the content herein.

The authors can be contacted via Konstantin M. Heinroth, MD, at konstantin.heinroth@uk-halle.de.

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