Arrhythmic Recurrence and Outcomes in Patients Hospitalized With First Episode of Electrical Storm

Abstract

Electrical storm (ES) is a life-threatening condition that may lead to recurrent arrhythmias, need for ventricular mechanical support, and death. The study aimed to assess the burden of arrhythmia recurrence and in-hospital outcomes of patients admitted for ES in a large urban hospital. We performed a retrospective analysis of patients admitted with ventricular arrhythmias from January 2018 to June 2021 and identified 61 patients with ES, defined as 3 or more episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF) within 24 hours. We reviewed the in-hospital outcomes and compared outcomes between patients who had no recurrence of VT/VF after the first 24 hours (34 [56%]), those with recurrence of 1 or 2 episodes of VT/VF within a 24-hour period (15 [24%]), and patients with 3 or more recurrent VT/VF events consistent with recurrent ES after the first 24 hours (12 [20%]). Patients with recurrent ES had significantly higher in-hospital mortality as compared with those with recurrent VT/VF not meeting criteria for ES or no recurrences of VT/VF (3 [25%] vs 0 [0%] vs 0 [0%]; p = 0.002). Moreover, patients with recurrent ES also had higher rates of the combined end points of ventricular mechanical support and death (7 [58%] vs 1 [6%] vs 1 [3%], p <0.001), invasive mechanical ventilation and death (10 [83%] vs 2 [13%] vs 2 [6%], p <0.001), catheter ablation or death (12 [100%] vs 7 [47%] vs 12 [35%], p <0.001) and heart transplantation and death (3 [25%] vs 2 [13%] vs 0 [0%], p = 0.018). In conclusion, patients admitted with ES have a high risk of in-hospital recurrence, associated with extremely poor outcomes.

Electrical storm (ES) is a state of cardiac electrical instability characterized by multiple episodes of ventricular arrhythmias occurring within a short period of time.¹ ES is often a marker of advanced cardiac disease, and ES may cause myocardial injury, inflammation, and fibrosis, thereby further contributing to cardiac damage and dysfunction. Up to 30% of patients with structural heart disease with an implantable cardioverter-defibrillator placed for primary prevention and 40% of those with an implantable cardioverter-defibrillator for secondary prevention experience ES in their lifetime.^2–4 Despite several available therapeutic strategies aimed at suppressing ES, it remains associated with a significant risk of recurrence, worsening heart failure, the need for mechanical support or heart transplantation, and death.^5–8 The incidence of recurrent arrhythmic events in patients admitted with ES has not been definitively established. The measures of outcomes vary based on the definition used, the methods to assess for recurrence and outcomes, and the treatment(s) received. The study aimed to assess the characteristics, arrhythmic burden, and outcomes of patients hospitalized with ES in a tertiary cardiovascular center serving a diverse urban population in Central Virginia in the United States.

Methods

Electronic health records were retrospectively reviewed to identify cases of ES between January 1, 2018, and May 31, 2021, at Virginia Commonwealth University (VCU) Health. The study was approved by the local Institutional Review Board. The initial search was based on the International Statistical Classification of Diseases and Related Health Problems, Tenth or Ninth Revision (ICD-10 or ICD-9). Since there are no codes for ES, ICD-10 codes for ventricular tachycardia (ICD-10 I47.2), ventricular fibrillation (ICD-10 I49.01), or ventricular flutter (ICD-10 I49.02), or the corresponding ICD-9 codes, were used for the initial subject identification. ES was defined as the occurrence of 3 or more sustained ventricular tachyarrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF]) or appropriate therapies for ventricular tachyarrhythmias, including anti-tachycardia pacing (ATP) or shocks, within 24 hours.^9,10 Patients with acute coronary syndrome (including coronary artery spasm), electrolyte imbalance, or drug toxicity were excluded for the purpose of this analysis. Structural heart disease was defined as a previous diagnosis of ischemic heart disease or nonischemic heart disease, including but not limited to idiopathic dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, valvular cardiomyopathy, myocarditis, hypertrophic cardiomyopathy, sarcoidosis, and left ventricular noncompaction cardiomyopathy.

Two cardiologists performed a chart review of electronic health records to complete a database including patients in whom the diagnosis of ES could be confirmed. Patients with a previous hospitalization of ES were excluded from the analysis.

The database was populated with relevant demographic data, clinical characteristics, treatments received, in-hospital outcomes, and arrhythmic events. For the assessment of the arrhythmic events, available clinical notes, electrocardiogram, implantable cardioverter-defibrillator interrogations, telemetry strips were reviewed by at least 2 cardiologists before entry into the final database. Disagreements on findings or readings were resolved through discussion and consensus.

The study aimed to assess the burden of arrhythmic recurrence and in-hospital outcomes in patients admitted to the hospital with a first episode of ES. Recurrence of ventricular arrhythmias included sustained VT (lasting more than 30 seconds), ventricular fibrillation (VF) or appropriate therapies for VT or VF (including ATP or shocks), and recurrence of ES (occurring at least after 24 hours from the initial episode). The in-hospital outcomes of interest were need for sympathectomy (surgical sympathectomy or percutaneous stellate ganglion blockade), ventricular arrhythmia catheter ablation, invasive mechanical ventilation (defined as need for endotracheal tube placement), left ventricular mechanical support, heart transplantation, and death. Cardiogenic shock was defined as hypotension associated with either the use of left ventricular assist device, extracorporeal mechanical membrane oxygenation, or inotropic therapy.

Descriptive statistics were used to describe the characteristics of the study participants. Continuous data were reported as median and interquartile range, and data were compared with the Mann-Whitney U test or Kruskal-Wallis test, as appropriate. Categorical variables were expressed as numbers and percentages (%) and compared using chisquare test or Fisher’s exact test, as appropriate. Receiver-operating characteristic curve analysis was used to estimate the overall predictive accuracy of neutrophil:lymphocyte ratio (NLR) to define the optimal predictive cut-off value for in-hospital ES recurrence by evaluating the area under the curve and the respective 95% confidence interval (CI). Logistic regression analysis for the recurrence of in-hospital ES was performed, including clinically significant variables (age, gender, left ventricular ejection fraction [LVEF], structural heart disease, ischemic or nonischemic cardiomyopathy, presence of implantable cardioverter-defibrillator or cardiac resynchronization therapy [CRT], clinical presentation and laboratory data). Those meeting statistical significance in the univariable model (p <0.10, 2-tailed) were further evaluated in the multivariable logistic regression model to identify independent variables associated with the ES recurrence. For the univariable and multivariable analysis, the measure of association was expressed as an odds ratio (OR) and 95% CI. All the analyses were completed using SPSS Statistics for Windows Version 24.0 (Armonk, New York. IBM Corp.).

Results

A total of 257 adult patients were identified using the ICD-9/10 codes for VT (ICD-10 I47.2), VF (ICD-10 I49.01), or ventricular flutter (ICD-10 I49.02). After reviewing electronic health records for each of the patients, there were 61 patients in whom the diagnosis of ES could be confirmed. All cases had been previously identified as ES by the treating cardiac electrophysiologist.

Baseline characteristics of the patients are listed in Table 1. Of 61 eligible patients with ES, the median age was 61 (53–71) years, 45 patients (74%) were male, and 27 (44%) were self-referred as Black or African-American. A total of 54 patients (88%) had structural heart disease, 28 (52%) had ischemic heart disease, and 26 (48%) had nonischemic heart disease in etiology. The median (LVEF was 30% (20–40), (ranging from 10% to 65%).

Table 1.

Baseline characteristics of the patients admitted to the hospital for electric storm

Variable	Electrical storm (n=61)
Male	45 (74%)
Age, (years) (median, IQR)	61 [53–71]
White	32 (52%)
Black	27 (44%)
Other	2 (4%)
Body mass index (Kg/m2) (median, IQR)	27.7 [24.4–35.2]
Structural heart disease	54 (89%)
Ischemic cardiomyopathy	28 (46%)
Non-Ischemic cardiomyopathy	26 (43%)
Hypertension	37 (61%)
Coronary artery disease	32 (52%)
Diabetes	20 (33%)
Dyslipidemia	37 (61%)
Atrial fibrillation	16 (26%)
Sarcoidosis	4 (7%)
Previous ventricular arrhythmia ablation	20 (33%)
Implantable defibrillator	52 (85%)
Primary prevention	27 (44%)
Secondary Prevention	25 (41%)
Cardiac resynchronization therapy	5 (8%)
Left ventricle ejection fraction % (median, IQR)	30 [20–40]
Home medications
Beta-blockers	52 (85%)
Metoprolol	44 (72%)
Sotalol	7 (12%)
Propranolol	1 (2%)
ACEI/ARNI/ARB	33 (54%)
Amiodarone	20 (32%)
MRA	19 (31%)
Mexiletine	2 (3%)
Trigger
Idiopathic	52 (85%)
Acute heart failure	9 (15%)
ICD shock at presentation	51 (84%)
Arrhythmia at presentation
VT	47 (77%)
VF	3 (5%)
VT/VF	11 (18%)
Number of events (median, IQR)	5 [3–7]
Symptoms/signs
Syncope/pre-syncope	36 (59%)
Palpitations	27 (44%)
Cardiogenic shock	9 (15%)
Cardiac arrest	3 (5%)
Laboratory at admission
Creatinine (mg/dL) (median, IQR)	1.17 [0.89–1.5]
Potassium (mmol/L) (median, IQR)	4.1 [3.7–4.4]
Sodium (mmol/L) (median, IQR)	138 [136–139]
Troponin I (ng/mL) (median, IQR)	0.08 [0.03–0.56]
BNP (pg/mL) (median, IQR)	311 [134–988]
Hemoglobin (g/dL) (median, IQR)	12.4 [11–13.9]
White blood cell (109/L) (median, IQR)	8.1 [6.4–9.3]
Neutrophils Absolut count (109/L) (median, IQR)	5.5 [3.8–7.17]
Lymphocyte Absolute count (109) (median, IQR)	1.3 [0.8–2.2]
Neutrophil : lymphocyte ratio* (median, IQR)	4.5 [1.9–7.0]
Treatment in-hospital
Device reprogramming	16 (26%)
Amiodarone	47 (77%)
Lidocaine	28 (46%)
Beta blockers	54 (89%)
Metoprolol	40 (66%)
Sotalol	8 (13%)
Nadolol	1 (2%)
Propranolol	5 (8%)
Procainamide	4 (7%)
Quinidine	5 (8%)
Potassium	32 (52%)
Magnesium	28 (46%)
Sedation and invasive ventilation	12 (20%)
Ventricular arrhythmia ablation	26 (43%)
Mechanical support	7 (12%)
Sympathectomy (surgical or SGB)	5 (8%)
Heart transplant	2 (3%)

^*Neutrophil: lymphocyte ratio, calculated as total neutrophil counts divided by total lymphocyte counts, was computed from the absolute values of neutrophils and lymphocyte.

ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blockers ARNI = angiotensin receptor neprilysin inhibitor; BMI = body mass index; ES = electrical storm; IQR = interquartile range; LVEF = left ventricle ejection fraction; MRA = mineralocorticoid receptor antagonists; SGB = stellate ganglion block; VT = ventricular tachycardia; VF = ventricular fibrillation.

A total of 51 patients (82% of all cases; 98% of those with an implantable cardioverter-defibrillator) had an ES associated with implantable cardioverter-defibrillator shocks. Heart failure exacerbation was present in 9 (15%) of patients, and 52 patients (85%) had no associated acute cardiac issues. The number of ventricular arrhythmias during the initial episode of ES was 5 (3–7) per patient. The highest number of ventricular arrhythmia episodes before admission ranged from 3 to 27. VT was the arrhythmia in 47 patients (77%), a combination of VT and VF episodes in 11 (18%), and isolated VF episodes in 3 patients (5%).

Hospital length of stay was 8 (5.5 to 14) days. The longest hospitalization was 81 days. The anti-arrhythmic drugs used during hospitalization and at discharge are listed in Table 1. Invasive mechanical ventilation with moderate or deep sedation was used in 12 patients (20%). Two patients (3%) underwent percutaneous stellate ganglion blockade, and 3 patients (5%) underwent both percutaneous stellate ganglion blockade and subsequent surgical sympathectomy. Twenty-six (43%) patients underwent ventricular arrhythmia ablation, of these, 4 (15%) were performed supported by a left ventricle assist device (Table 1). Percutaneous left ventricular mechanical support was required in 7 patients (12%), heart transplantation in 2 (3%), and 3 patients (5%) died. (Table 1).

Thirty-four (56%) patients had no recurrence of VT/VF during hospitalization. Twenty-seven (44%) patients had at least 1 recurrence of VT or VF after 24 hours from the first ES episode, of these 15 (corresponding to 24% of the entire population) had 1 or 2 episodes of VT/VF within a 24-hour period, and 12 (corresponding to 20% of the entire population) had 3 or more recurrent VT/VF events consistent with recurrent ES. ES storm recurrence occurred after a median of 6 (6–10) days. Three (5%) had more than 1 separate episode of recurrent ES (Table 1).

Patients with no arrhythmias recurrence after the initial treatment were more likely to present with syncope and less likely to present with shock than patients with arrhythmic recurrences (Table 2). Patients with recurrence of ES were significantly more likely to have a CRT device than patients with recurrent VT/VF not meeting ES criteria or no recurrent arrhythmias (3 [33%] vs 0 [0%] vs 2 [6%], respectively; p = 0.048) and more likely to receive treatment with lidocaine (11 [92%] vs 6 [40%] vs 11 [32%], respectively; p <0.002) (Table 2). There were no additional significant differences in terms of clinical (including the etiology of cardiomyopathy), laboratory or echocardiographic features between the 3 groups of patients.

Table 2.

Patient characteristics according to the recurrence of electrical storm, VT/VF or no arrhythmias recurrence

Variable	No recurrence (34)	VT/VF recurrence (15)	ES recurrence (12)	P Value
Male	23 (67%)	12 (80%)	10 (83%)	0.466
Age (years) (median, IQR)	61 [53–73]	60 [50–69]	67 [54–70]	0.605
White	16 (47%)	9 (60%)	7 (58%)	0.228
African American	18 (53%)	6 (40%)	3 (25%)	0.228
Other	0 (0%)	0 (0%)	2 (17%)	0.228
BMI (kg/m2) (median, IQR)	28.2 [24–36.1]	27.7 [24.3–31.7]	27.4 [25.2–34.3]	0.740
Structural heart disease	31 (91%)	12 (80%)	11 (92%)	0.490
Non-Ischemic cardiomyopathy	15 (44%)	7 (47%)	4 (33%)	0.574
Ischemic cardiomyopathy	16 (47%)	5 (33%)	7 (58%)	0.574
Hypertension	22 (65%)	8 (53%)	7 (58%)	0.742
Coronary artery disease	16 (47%)	5 (33%)	8 (67%)	0.226
Diabetes	12 (35%)	5 (33%)	3 (25%)	0.807
Atrial fibrillation	6 (18%)	5 (33%)	5 (42%)	0.206
Dyslipidemia	22 (65%)	6 (40%)	9 (75%)	0.139
Sarcoidosis	2 (6%)	1 (7%)	1 (8%)	0.957
VT ablation	10 (29%)	6 (40%)	4 (33%)	0.767
Implantable defibrillator	32 (94%)	11 (73%)	9 (75%)	0.090
Primary prevention	16 (47%)	6 (40%)	5 (42%)	0.939
Secondary Prevention	16 (47%)	5 (33%)	4 (33%)	0.939
Cardiac resynchronization therapy	2 (6%)	0 (0%)	3 (33%)	0.048
LVEF (%) (median, IQR)	27.5 [20–36]	35 [15–43]	27.5 [16–40]	0.921
Home medications
MRA	11 (32%)	6 (40%)	2 (17%)	0.418
ACEI/ARNI/ARB	18 (53%)	8 (53%)	7 (58%)	0.947
Beta-blockers	29 (85%)	11 (73%)	12 (100%)	0.152
Metoprolol	25 (73%)	8 (53%)	11 (92%)	0.084
Sotalol	4 (12%)	2 (14%)	1 (8%)	0.918
Propranolol	0 (0%)	1 (7%)	0 (0%)	0.210
Amiodarone	11 (32%)	4 (27%)	5 (42%)	0.709
Mexiletine	1 (3%)	0 (0%)	1 (8%)	0.475
Trigger
Idiopathic	32 (94%)	11 (73%)	9 (75%)	0.386
Acute heart failure	2 (6%)	4 (27%)	3 (25%)	0.386
Symptoms
Syncope/pre-syncope	25 (73%)	7 (47%)	4 (33%)	0.028
Palpitations	15 (44%)	8 (53%)	4 (33%)	0.582
Cardiogenic shock	2 (6%)	2 (13%)	5 (42%)	0.011
Cardiac arrest	2 (6%)	0 (0%)	1 (8%)	0.565
Laboratory at admission
Creatinine (mg/dL) (median, IQR)	1.14 [0.87–1.49]	1.28 [0.82–1.65]	1.18 [1–1.58]	0.724
Potassium (mmol/L) (median, IQR)	4.1 [3.6–4.4]	3.9 [3.5–4.3]	4.3 [3.8–4.9]	0.213
Sodium (mmol/L) (median, IQR)	137 [136–139]	139 [135–142]	138 [134–139]	0.650
Troponin I (ng/mL) (median, IQR)	0.05 [0.03–0.64]	0.1 [0.03–0.33]	0.19 [0.45–2.33]	0.572
BNP (pg/mL) (median, IQR)	266 [100–549]	241 [59–1089]	930 [374–3405]	0.062
Hemoglobin (g/dL) (median, IQR)	12.8 [11.7–14.5]	12.3 [11–13.6]	11.1 [10.4–13.1]	0.253
White blood cell (109/L) (median, IQR)	8 [6.5–9.1]	8.1 [6.4–9.1]	8.1 [5.5–11.8]	0.920
Neutrophils Absolut count (109/L) (median, IQR)	5.4 [3.9–7.0]	5.4 [2.5–7.0]	6.8 [4.3–8.3]	0.185
Lymphocyte Absolute count (109/L) (median, IQR)	1.4 [0.9–2.4]	1.6 [0.8–2.8]	0.9 [0.7–1.3]	0.200
Neutrophil : Llymphocyte ratio	4.3 [1.9–6.5]	2.6 [1.2–8.6]	6.8 [2.9–11.8]	0.185
Treatment in-hospital
Device reprogramming	8 (23%)	4 (27%)	4 (33%)	0.801
Amiodarone	25 (73%)	11 (73%)	11 (92%)	0.405
Lidocaine	11 (32%)	6 (40%)	11 (92%)	0.002
Beta-blockers	28 (82%)	15 (100%)	11 (92%)	0.189
Sotalol	3 (8%)	4 (27%)	1 (8%)	0.201
Nadolol	1 (3%)	0 (0%)	0 (0%)	0.668
Propranolol	2 (6%)	2 (13%)	1 (8%)	0.681
Procainamide	1 (3%)	1 (7%)	2 (17%)	0.256
Quinidine	3 (8%)	0 (0%)	2 (17%)	0.286
Potassium	20 (59%)	7 (47%)	5 (42%)	0.518
Magnesium	16 (47%)	6 (40%)	6 (50%)	0.856
Sedation and invasive ventilation	2 (6%)	2 (13%)	8 (67%)	<0.001
Ventricular catheter ablation	12 (35%)	7 (47%)	7 (58%)	0.357
Mechanical support	1 (3%)	1 (7%)	5 (42%)	0.001
Sympathectomy (surgical or SGB)	1 (3%)	2 (13%)	2 (17%)	0.232

ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blockers; ARNI = angiotensin receptor neprilysin inhibitor; BMI = body mass index; ES = electrical storm; IQR = interquartile range; LVEF = left ventricle ejection fraction; MRA = mineralocorticoid receptor antagonists; SGB = stellate ganglion block; VT = ventricular tachycardia; VF = ventricular fibrillation.

In-hospital outcomes were analyzed according to the occurrence of in-hospital recurrence of ventricular arrhythmias. We found that patients with recurrent ES had a significantly higher in-hospital mortality compared with patients with 1 or 2 VT/VF recurrence within a 24-hour period and not meeting criteria for recurrent ES, and patients with no arrhythmic recurrences (3 [25%] vs 0 [0%] vs 0 [0%]; p = 0.002) and higher rates of the combined end points of percutaneous ventricular mechanical support and death (7 [58%] vs 1 [6%] vs 1 [3%], p< 0.001), invasive mechanical ventilation and death (10 [83%] vs 2 [13%] vs 2 [6%], p<0.001), catheter ablation or death (12 [100%] vs 7 [47%] vs 12 [35%], p<0.001) and heart transplantation and death (3 [25%] vs 2 [13%] vs 0 [0%], p = 0.018) (Figure 1, Table 3).

Figure 1.

In-hospital outcomes of patients with recurrence of electrical storm compared with those with recurrence of VT/VF (not meeting the criteria for ES) and no recurrences.

Table 3.

In-hospital outcomes in patients with recurrence of electrical storm, recurrence of VT/VF or no recurrence

	No recurrence (n=34)	VT/VF recurrence (n=15)	Electrical storm recurrence (n=12)	P Value
Death	0 (0%)	0 (0%)	3 (25%)	0.002
Percutaneous ventricular mechanical support or death	1 (3%)	1 (6%)	7 (58%)	<0.001
Invasive mechanical ventilation or death	2 (6%)	2 (13%)	10 (83%)	<0.001
Sympathectomy or death	1 (3%)	2 (13%)	5 (42%)	0.003
Catheter ablation or death	12 (35%)	7 (47%)	12 (100%)	0.016
Heart transplantation or death	0 (0%)	2 (13%)	3 (25%)	0.018

VF = ventricular fibrillation; VT = ventricular tachycardia.

The univariable analysis showed the presence of CRT (OR 7.8, CI [1.14 to 53.7], p = 0.036), cardiogenic shock at admission (OR 8.0, CI [1.7 to 37.3], p = 0.008) and NLR (OR 1.05, [0.99 to 1.11], p = 0.075) were the only variables that predicted ES recurrence during hospitalization. At multivariable logistic regression analysis, CRT (OR 30.3 [2.1 to 432.8], p = 0.012), cardiogenic shock at admission (OR 13.8 [2.1 to 88.4], p = 0.006) and NLR (OR 1.1 [1.0 to 1.5], p = 0.028) remained predictors of in-hospital ES recurrence (Table 4).

Table 4.

Variables associated with electrical storm recurrence by univariate and multivariate logistic regression analysis

	Univariable analysis		Multivariable analysis
Variables	OR (95% C.I.)	p		p
Age	1.01 [0.96–1.1]	0.595
Male	2 [0.38–10.3]	0.407
LVEF (%)	0.99 [0.94–1.04]	0.749
Structural heart disease	1.53 [0.16–14.1]	0.705
Ischemic cardiomyopathy	1.83 [0.46–7.1]	0.385
Presence of ICD	0.41 [0.08–1.99]	0.274
Syncope at admission	0.226 [0.70–1.01]	0.052
Presence of CRT	7.83 [1.14–53.7]	0.036	30.3 [2.1–432.8]	0.012
Cardiogenic shock at admission	8.0 [1.7–37.3]	0.008	13.8 [2.1–88.4]	0.006
Neutrophil : lymphocyte ratio	1.05 [0.99–1.11]	0.075	1.1 [1.0–1.5]	0.028

CI = confidence interval; CRT = cardiac resynchronization therapy; ICD = implantable cardiac defibrillator; LVEF = left ventricle ejection fraction; OR = odds ratio.

NLR was available for 56 patients (92%) (45 [80%] in those without ES recurrence and 11 [20%] in those with ES recurrence). Receiver-operating characteristic curve was constructed to assess the ability of NLR to predict recurrence of ES. The area under the curve for NLR to predict in-hospital recurrence of ES was 0.677 (p = 0.071), with a sensitivity and specificity of 73% and 71% using an NLR cut-off value of 5.9. In-hospital recurrence of ES occurred in 3 [9%] patients with NLR levels below 5.9 and 8 [38%] patients in those with NLR above the cut-off of 5.9 (p = 0.013).

A sensitivity analysis was done excluding patients that presented with cardiac arrest with prolonged cardiopulmonary resuscitation and intubation during the first 24 hours: 58 patients were included; patients with recurrence of ES during hospitalization had a higher rate of the different combined end points when compared with patients with 1 or 2 VT/VF recurrence within 24-hour period and not meeting criteria for recurrent ES, and patients with no arrhythmic recurrences (Supplementary Table 1).

Discussion

We herein report the clinical characteristics, arrhythmic burden, and in-hospital outcomes of a diverse patient population with hospitalization for first ES in a large urban hospital in the United States. The main findings of our study are the following: (1) patients admitted for ES are at high risk of in-hospital arrhythmia recurrence occurring in 44% of these patients; (2) despite the relatively low in-hospital mortality (5%), patients admitted for ES have a complicated clinical course often requiring invasive mechanical ventilation, mechanical ventricular support, ablation, sympathectomy or heart transplantation; (3) patients with in-hospital ES recurrence have a worse prognosis compared with those having a recurrence of only 1 or 2 episodes of VT/VF within a 24-hour period after initial treatment or no arrhythmic recurrence; (4) patients with recurrent ES have a higher prevalence of CRT devices and higher use of lidocaine, although this may not reflect causality; (5) the presence of CRT, cardiogenic shock and NLR at admission were the only predictors of in-hospital ES recurrence.

The survivors of ES represent a group of patients at very high risk of morbidity and mortality.⁷ Recently, Gadula-Gacek et al. showed that in 101 patients admitted for a first episode of ES, one-third were suspected of having myocardial ischemia as a trigger, in-hospital mortality was 3%, ES recurrence at 12-month follow-up was 15.8%, and 12-month mortality was 21.8%.⁴ In another study including 667 patients with ES who underwent catheter ablation, in-hospital mortality was 5%, with a 1-year follow-up mortality of 32%.¹¹ In a meta-analysis including 471 ES patients treated with VT ablation, a mortality of 17% and a rate of recurrence of 6% at 15 months follow-up was reported.¹² The clinical characteristics of our population are similar to other studies previously published in terms of age, preponderance of male gender, presence of structural heart disease, and prevalence of anti-arrhythmic medications present at the time admission.^7,12–14

Agreeing with the previous findings, we found that in-hospital mortality was relatively low in this high-risk population, despite a complicated clinical course that included 2 patients (3%) requiring urgent heart transplantation and 7 patients (12%) who required hemodynamic support with ventricular assist devices. None of these studies have, however, described the short-term in-hospital risk of arrhythmia recurrence in patients hospitalized for an initial episode of ES. Indeed, despite pharmacologic and nonpharmacologic strategies to suppress the arrhythmic burden, including multiple medications, sympathetic blockade, and radiofrequency or cryo-ablation, there is a persistent risk of early ventricular arrhythmias recurrence. This has important implications because we found that patients with recurrence of ES during the initial hospitalization have a significantly higher risk of in-hospital death (25% vs 0%), highlighting the need for future studies to identify novel potential therapeutic targets in patients with ES.

In the plethora of clinical variables associated with a higher incidence of ES in the literature, implantable cardioverter-defibrillator for secondary prevention, lower LVEF, VT as triggering arrhythmia, and the use of class I anti-arrhythmic drugs therapy were more commonly found in patients who experienced a first ES event.⁷ In our population of patients surviving a first episode of ES, we found that the presence of CRT, cardiogenic shock, and elevated NLR at admission were associated with a higher risk of in-hospital ES recurrence. This may simply reflect more underlying conduction abnormalities and myocardial disease in patients with CRT. CRT, however, has been proposed to potentially change myocardial repolarization and precipitate an arrhythmic event in patients with prolonged QT.^15–17 Moreover, patients with cardiogenic shock usually have more advanced cardiomyopathy with higher susceptibility to further arrhythmic deterioration and are more aggressively treated with inotropes and vasopressors that may further exacerbate ventricular arrhythmias. Finally, NLR, easily calculated as a ratio between the neutrophil and lymphocyte counts, is a biomarker reflecting the balance between innate and adaptive immunity.^18,19 Elevated NLR has been associated with worse outcomes in patients with cardiovascular diseases and with an increased arrhythmic burden and risk of ventricular arrhythmias.^20–24 Treatment with interleukin-1 blockade in patients with ST-elevation acute myocardial infarction showed to normalize NLR.^25–27 Whether or no therapeutic options targeted at blunting the inflammatory response, including IL-1 blockade, can be useful in patients admitted with ES remains, however, to be determined.

We acknowledge the limitations of our study. This is a single-center study with a small sample size that may not have sufficient power to detect potential statistical differences between the comparison groups. The small number of patients with CRT and the wide CI values may suggest that multivariable modeling is of limited value given the few events. Unfortunately, we did not explore the predictive role of C-reactive-protein in predicting ES recurrence because of the elevated number of missing values. Further, the results generated from a single-center may not fully generalizable to all settings and practices. Moreover, data about the morphology of the VT episodes before admission and during hospitalization were not available because it was not systematically collected during the hospitalization. Our study has, however, also several strengths. We excluded patients with an acute coronary syndrome or electrolyte imbalance as a trigger for ES to focus on a more homogenous population, as these patients often have a treatable and reversible cause of arrhythmia and may benefit from percutaneous coronary intervention and electrolyte supplementation. Furthermore, we meticulously reviewed each case to confirm the diagnosis of ES using very strict criteria and only included those subjects with more than 3 episodes of VT/VF within 24 hours. This aspect is particularly important considering that ICD-10 and ICD-9 codes may be unreliable for ES diagnosis. Finally, we studied a diverse urban population, including a significant number of Black or African-American patients, who often are underrepresented in clinical studies.

In conclusion, we found that patients admitted with a first episode electrical storm have high morbidity and mortality despite existing treatment options, and in these, patients with a recurrent electrical storm have extremely poor outcomes. Larger, prospective studies are needed to better characterize to further strengthen our findings.