eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
Current issue Archive Manuscripts accepted About the journal Special issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors
SCImago Journal & Country Rank
vol. 14
Clinical research

Risk factors and prognostic role of an electrical storm in patients after myocardial infarction with an implanted ICD for secondary prevention

Wojciech Kwaśniewski, Artur Filipecki, Michał Orszulak, Witold Orszulak, Dagmara Urbańczyk, Robert Roczniok, Maria Trusz-Gluza, Katarzyna Mizia-Stec

Arch Med Sci 2018; 14, 3: 500–509
Online publish date: 2016/05/05
Article file
- risk factors and.pdf  [0.10 MB]
Get citation
JabRef, Mendeley
Papers, Reference Manager, RefWorks, Zotero


The term electrical storm (ES) was used for the first time in the early 1990s and was defined as a state of high electrical instability of the heart, which is manifested by numerous episodes of ventricular tachycardia (VT)/ventricular fibrillation (VF) within a short period of time. Electrical storms are associated with a very high mortality (80–90%) both during the incident alone and during further observation [1, 2]. The use of an implantable cardioverter-defibrillator (ICD) changes the natural course of the disease. The main cause of death in this group is heart failure, and sudden cardiac death occurs in approximately 2–4% of cases. However, electrical storms are still an important problem, especially since the clinical presentation of an ES is often very dramatic with recurrent VT/VF that requires multiple defibrillator shocks. Eighty percent of patients with an ES are hospitalized [3, 4]. Most data about electrical storms come from patients with an implanted ICD for secondary prevention. By definition, an ES signifies the occurrence of three or more episodes of VT/VF that require ICD intervention within 24 h in which the interval between the distinct incidents is longer than 5 min [5].
Due to the increasing number of ICD recipients, electrical storms are observed more often and require adequate management that is specific for an ischemic and non-ischemic etiology of cardiac arrhythmia. However, pharmacological treatment is not always effective. In addition to pharmacological treatments, which are based on blockage of the sympathetic nervous system and the administration of class I agents, radio frequency ablation (RF ablation), neurosurgical sympathetic denervation and general anesthesia are used [6, 7]. On the other hand, ICD implantation for secondary prevention is the strongest predictor of ES [8, 9]. One of the major tasks is to select a group of patients who are at high risk of ES. There are limited data about ES, especially in high-risk patients who are homogeneous in terms of etiology and indications for ICD implantation. This encouraged us to investigate ES using our many years of experience in electrotherapy.
The aim of our study was to identify the risk factors for an ES in patients after myocardial infarction with an implanted ICD for the secondary prevention of SCD. We attempted to determine the influence of an ES and the type of therapy administered by an ICD, antitachycardia pacing (ATP) or shocks, on the long-term prognosis.

Material and methods

We retrospectively analyzed 416 patients with coronary artery disease after myocardial infarction who underwent ICD implantation for the secondary prevention of SCD in the years 1997–2004. Four hundred sixteen patients were included in the study. All were consecutive patients after MI implanted for secondary prevention in 1997–2004. Secondary prevention of SCD was defined as a history of cardiac arrest due to VF or hemodynamically not tolerated VT and also after recurrent sustained VT, without reversible causes. The observation was carried out until December 2006. The median length of the observation was 66 months.
Fifty (12%) patients in the study population had one or more incidents of ES: the ES (+) group. A representative control group was composed of 47 subjects who were matched with respect to age, sex and implantation date from the 366 patients without a history of ES.
An electrical storm was defined as the occurrence of three or more episodes of VT or VF that required the intervention of a device (ATP or defibrillation) within 24 h in which the intervals between distinct arrhythmias lasted more than 5 min [5].
Before an ICD implantation procedure, the following medical data were collected for all patients: age, sex, NYHA class, comorbidities (hypertension, hypercholesterolemia, diabetes mellitus, chronic renal disease), atrial fibrillation/atrial flutter, actual pharmacotherapy, indications for ICD implantation.
We evaluated the factors that might be of potential prognostic value for ventricular arrhythmia and an ES: the location of myocardial infarction (anterior/inferior/other), the extent of coronary artery disease (single or multi-vessel), any previous coronary revascularization and the type of revascularization (surgical/percutaneous), revascularization of the infarct-related artery, left ventricular ejection fraction and left ventricular end diastolic diameter (LVEDD) using echocardiography, the width of the QRS complex and heart rate in a resting electrocardiogram, the quantity of number of ventricular arrhythmic events and the average heart rate in 24-hour ECG Holter monitoring.
We analyzed all arrhythmic events that had been recorded in the ICD’s memory. Patients were followed up at 3- to 6-month intervals after the ICD implantation. Clinical evaluation and device testing were carried out at each follow-up visit. Information about arrhythmic events, the device’s current parameters and the current pharmacotherapy were noted during each visit.
Each case of ES was considered individually. All available methods, including changes in the pharmacological and non-pharmacological treatment, were used. Crucial decisions concerning coronary revascularization and ICD programming were made individually for each patient by the same team.
None of the patients died during an acute incident of ES. Two of the patients in the 50 ES (+) group had percutaneous coronary intervention (PCI) during follow-up. Among the 50 ES (+), 15 patients had RF ablation; 4 patients had more than one RF ablation. There was no correlation between RF ablation and survival. We did not analyze the impact of ablation on the recurrence of VT. During the follow-up none of the patients had an upgrade to cardiac resynchronization therapy (CRT).

Implantable cardioverter-defibrillator implantation and programming

Devices were implanted in the left subclavicular area. Device cans were placed on the surface of the pectoralis major muscle. Transvenous electrodes were equipped with one or two coils and had either an active or passive fixation. Electrodes were implanted at the right ventricular apex. Commercially available devices (Biotronik: Phylax AV Phylax XM AH, Phylax 06 AH, AH Mycrophylax, Tachos DR and Medtronic: Micro Jewel II, GEM II VR, GEM II DR) were implanted in the study population.
Devices were programmed for two detection zones (VT and VF):
– VT zone at a heart rate of 150/min or 10–20 bpm fewer than the previously documented ventricular arrhythmia, 25–30 intervals in the zone required for detection;
– VF zone at 200/min or more, 16–18 intervals in the zone required for detection.
Antitachycardia pacing in the VT zone was followed by shock therapy if pacing did not terminate the arrhythmia. In the VF zone, shocks of 30–40 J were programmed. In most cases atrial discriminators for supraventricular arrhythmias were turned on.
All of the devices were programmed in the same way (single center study, the same management in all patients). Each episode of arrhythmia was analyzed by experienced staff through the assessment of IEGM recordings. Each episode of arrhythmia was verified with regard to the adequacy of the therapy that was delivered. Inadequate interventions were not taken into account.

Statistical analysis

Statistical analysis was performed using Statistica 6 software. A p-value of less than 0.05 was considered statistically significant. The Shapiro-Wilk test was used to verify whether the variable had a normal distribution. The basic characteristics of the groups were analyzed using the ANOVA test, the Mann-Whitney U test and the 2 test. A logistic regression model was used to predict the outcome of dependent variables. The Hosmer-Lemeshow goodness-of-fit test for the logistic regression was performed. Survivals were estimated using the Kaplan-Meier method and compared with a log-rank test. A proportional hazard Cox model was performed to evaluate the effect of an independent variable on the risk of death.


Clinical characteristics from the period before the ICD implantation procedure

A comparison of the ES (+) and ES (–) groups did not show significant differences in age, NYHA class, concomitant diseases, the incidence of atrial fibrillation/flutter or the type of implanted device. VF in the history as an indication for ICD implantation was more frequent in the ES (–) than in the ES (+) group (27% vs. 6%, p = 0.003). An analysis of the pharmacotherapy showed significantly higher use of statins in the ES (–) group (53% vs. 32%, p = 0.034) (Table I).

Factors of potential prognostic value for an ES

Our analysis showed that patients in the ES (+) group had less frequent revascularization than subjects in the ES (–) group (36% vs. 56%, p = 0.049) as well as in relation to the infarct-related artery (patent or bypassed infarct-related artery) – 30% vs. 51%, relatively; p = 0.034. Moreover, in the ES (+) group, myocardial infarction was more frequently located at the inferior wall (46% vs. 21%, p = 0.007) (Table II).

Arrhythmic events during follow-up

We recorded and analyzed a total of 3,408 episodes of ventricular arrhythmias that required the intervention of an ICD. There were 3,148 episodes in the ES (+) group and 260 in the ES (–) group. ATP was successful in 2,302 (67%) episodes – 2,141 (68%) in the ES (+) group and 161 (62%) in the ES (–) group. Shock was required in 1,106 (33%) episodes – 1,007 (32%) in the ES (+) group and in 99 (38%) in the ES (–) group. Five patients in the ES (–) group had no intervention during follow-up. In the ES (+) group, there were 187 incidents of an ES – in 159 cases the therapy consisted of ATP and shocks and in 28 cases ATP alone was sufficient. In the ES (+) group the mean number of electrical storms was 3.74 ±3.27, the median 3, range: 1–15. The average number of arrhythmic events during a storm was 16.8 18.6, median: 6, range: 3–140. The average interval between MI and device implantation was 125 ±87 months. The average time from implantation to the first occurrence of an ES was 400 days, median 172 days.
The average cycle length of an arrhythmia in the entire study population was 347 ±59 ms (median: 347 ms). We found a statistically significant difference in the length of a cycle between the ES (+) and ES (–) groups (358 ±54 ms vs. 327 ±62 ms, p = 0.023; median 365 ms vs. 330 ms, respectively).
For the overall population, the average time until the first occurrence of intervention was 305 ±438 days (median: 140 days) and was longer in the ES (–) group than the ES (+) group (537 ±582 days, median: 314 days; and 166 ±238 days, median: 77 days, respectively). These differences were statistically significant (p = 0.0001) (Figure 1).

Logistic regression model

Multivariate logistic regression analysis showed that myocardial infarction of the inferior wall (RR = 3.98, 95% CI: 1.52–10.41) and the absence of coronary revascularization (RR = 2.92, 95% CI: 1.18–7.21) are independent predictors of an ES (p = 0.0014). In the Hosmer-Lemeshow goodness-of-fit test, p = 0.96.

Risk of death

During the long-term observation of 97 patients, there were 39 (40%) deaths. In the ES (+) group 25 subjects (50%) died and in the ES (–) group 14 (30%) subjects died. The Kaplan-Meier survival curves showed that patients in the ES (+) group had a higher cumulative mortality than patients in the ES (–) group; p = 0.036 (Figure 2). The multivariate proportional hazard model by Cox identified the following independent predictors of death (p < 0.001) – the occurrence of an ES (HR = 1.93), older age (HR = 1.06), and lower LVEF (HR = 0.95).

Type of therapy and risk of death in ES (+) group

In the ES (+) group, there was a correlation between the type of therapy administered (ATP vs. shocks) and survival. Among the patients who were treated with ATP alone, 2 of them (20%) died, and this number was significantly lower than in the patients who were treated with high-energy therapy – 23 (57%) subjects died; p = 0.033. In comparison to the ES (–) group, survival in the subpopulation of the ES (+) group treated with ATP alone was similar (Figure 3).


Our study presents the factors that predispose a patient to an ES and the clinical significance of an ES in patients after myocardial infarction with an implanted ICD for the secondary prevention of SCD. The study population comprised a relatively large, homogeneous (in terms of etiology and indications for ICD implantation) group of patients. During a few years of follow-up, an ES occurred in 12% of the patients, and this prevalence is similar to the results described in the literature [10–12]. During a few years of follow-up, an ES occurred in 12% of the patients. This prevalence is similar to the results described in the literature between 1997 and 2004 [10–12], when the study was carried out. Nowadays, widespread use of coronary interventional treatment is likely to reduce the incidence of ES in the population of patients with ICD.
We identified the factors which predispose a patient to the occurrence of an ES – a previous myocardial infarction other than at the anterior wall and the absence of coronary revascularization. On the other hand, the occurrence of an ES was a negative prognostic factor for death, especially in elderly patients and patients with impaired left ventricular systolic function.
In the study group, the most common indication for ICD implantation was a history of sustained ventricular tachycardia, and the presence of ventricular fibrillation was less frequent. In total, we analyzed more than 3,400 incidents of ventricular arrhythmia. The median heart rate during tachyarrhythmias was 170/min. What is important is that an ES was less frequent in patients with a history of VF as the indication for ICD implantation. Ventricular tachycardias were slower in the ES (+) group than in the ES (–) group (167/min and 183/min, respectively). Whether a history of VT alone (without VF) contributes to the occurrence of an ES at the same level as in patients with VF is still an unresolved problem. Some studies have presented results that are similar to ours [10, 13, 14].
It seems that the underlying etiology and transient factor are the main determinants of the nature of an arrhythmia. The above-mentioned factor, triggering VF, has a temporary effect, only under certain conditions. The re-entry loop for VF is unstable electrically. A post-infarct scar in ischemic cardiomyopathy predisposes a patient to a stable, re-entry VT. Therefore, the majority of ES include slow VT. The effect of antiarrhythmic drugs also plays an important role by modifying the electrophysiological substrate and the frequency of VT.
Half of the patients from the ES (+) group had an electrical storm in the first 6 months after ICD implantation. Some authors have reported the average time from implantation to the occurrence of an ES of between 133 and 270 days. In their studies, no relationship between ICD implantation and the severity of arrhythmia was found [10–12]. In our study we found that the time until the first adequate ICD intervention was significantly shorter in patients in the ES group (+) than in patients with single, isolated arrhythmias. A similar relationship was described by Villacastin et al. in one of the first studies about ES in patients with ICD, but those results were not confirmed by subsequent researchers [14]. Only in the subanalysis of the MADIT II study was it found that single, isolated episodes of VT/VF are predictors of an ES. It seems that a single VT/VF (especially VT) episode that requires an ICD intervention that occurs shortly after ICD implantation may be a risk factor for an ES [15].

Risk factors for an electrical storm

Our study demonstrated that myocardial infarction of the inferior wall and the absence of coronary revascularization are independent risk factors for an electrical storm. The number of patients who underwent CABG was significantly lower in the ES (+) group than in the ES (–) group. Similarly, patients who had either a patent or bypassed infarct-related artery were less frequent in the ES (+) group.
It seems that the location of infarct scar tissue within the inferior wall predisposes a patient to a re-entry ventricular tachycardia and is strongly influenced by the autonomic nervous system [16, 17]. A partial loss of innervation during MI leads to an imbalance between the sympathetic and parasympathetic tone of the autonomic nervous system [18, 19]. The Purkinje fibers system can also play a role in the creation of the VT re-entry circuit in patients after interior MI [20].
Pascale et al. [21] reported on a population of 252 patients with ischemic cardiomyopathy who were eligible for ICD implantation. They selected a group of post-MI patients with recurrent ventricular tachycardia which was dependent on the infarct scar. Patients with a history of MI of the inferior wall constituted 81% [21].
Myocardial ischemia is one of the factors that lead to malignant ventricular arrhythmias and cardiac arrest. Coronary revascularization, which is performed in acute coronary syndrome as well as in patients with stable angina and multi-vessel coronary artery disease, together with optimal medical therapy, is associated with a significant reduction in the risk for an SCD in short- and long-term follow-ups [22–24]. The patency of the infarct-related artery results in increased density of capillaries and delayed cardiomyocyte apoptosis in the infarct and periinfarct zones. These factors are responsible for the limitation of the infarct scar size and the reduction in left ventricular remodeling [25–27].
Heart failure and a reduced left ventricular ejection fraction (LVEF) are two of the most important risk factors for an SCD. Their significance has been proven in a number of clinical trials (MADIT, MADIT II, SCD-HeFT) [28–30].
In our study, there was no effect of HF and LVEF on the risk of occurrence of an ES. In the ES (+) group, there were more patients in the NYHA III class, but the difference was not statistically significant. However, some authors consider heart failure as a possible cause of an ES [31]. Among all of the cases of an ES, decompensation of heart failure was found in 10–20% of patients [13, 32]. There are conflicting literature data regarding a possible relation between LVEF and ES. Several studies have confirmed that a lower LVEF constitutes an independent factor for ES [9, 10, 32], while others have published opposite results [11–13]. Standard limitations of echocardiography in the assessment of LVEF as well as shock-related transient systolic dysfunction may influence these conflicting findings.
Atrial fibrillation (AF), especially permanent AF, is associated with higher rates of mortality and ICD discharge (appropriate and inappropriate) [33, 34]. In our study, we found no statistically significant difference in the number of AF patients in ES (+) and ES (–) groups.
The study groups did not differ in pharmacotherapy, except for the use of statins. Statins were recommended more often in the ES (–) group. The difference may be caused by the small number of people who were receiving statins in the entire study population. The low usage of statins is mainly due to economic reasons, but it is also due to the fact that hypolipidemic drugs were only becoming important in the treatment of coronary artery disease at the time of the study.

Prognostic role of an electrical storm

During the more than five years of follow-up, we found a significant difference in mortality between the ES (+) and ES (–) groups. In a multivariate Cox analysis, an ES was shown to be related to a lower survival rate. An ES increases the risk of death 1.9-fold. This observation is in accordance with the literature data [11–13, 35]. In the first meta-analysis on this topic, an ES is associated with a three-fold increased risk of death [9] in whole populations of patients with both ischemic and non-ischemic etiology of cardiac arrhythmia.
Apart from ES, older age and reduced LVEF were related to higher mortality in our population.
A possible contribution to the higher mortality could come from the shocks themselves, and we attempted to determine the influence of the type of therapy administered by an ICD (ATP or shocks) on the long-term prognosis.
Sixty-seven percent of all ventricular arrhythmias were successfully treated with ATP, but only 14% of electrical storms did not require high-voltage therapy. We found that there is a better prognosis for patients in the ES (+) group if ATP is successful. The survival curve for this subpopulation of patients is similar to the ES (–) group. The vast majority of ventricular incidents disappeared after the first therapy. Recently, some studies have shown a better prognosis if arrhythmias are resolved using ATP, and therefore the number of high-voltage therapies is reduced [36, 37]. In some cases, the ineffectiveness of ATP may be due to the focal nature of the arrhythmia [38].
We did not evaluate the impact of inappropriate shocks on the risk of death in patients with an implanted ICD. However, a subanalysis of MADIT II and SCD-HeFT showed that inadequate therapy is also associated with a higher risk of death [39, 40]. The mechanism of the harmful effect of numerous discharges on the myocardium still remains unclear and requires further investigations. Increased troponin levels reflect damage to the myocardium. Moreover, ventricular arrhythmia alone has a negative influence on the myocardium [41, 42]. The total number of VT/VF episodes was much greater in the ES (+) group. Recurrent ventricular arrhythmia affects the metabolism of cellular calcium, which leads to the accumulation of calcium within the myocyte and apoptosis. An ES causes Ca2+/calmodulin-dependent protein kinase II activation and phospholamban dephosphorylation, which can explain the vicious cycle of arrhythmia promotion and mechanical dysfunction that characterizes ES [43, 44].
This mechanism impairs the left ventricle and increases the risk of recurrence of a ventricular arrhythmia. Death is most often not sudden, but results from the aggravation of heart failure [45].
The study is a retrospective analysis of data collected over a very long period. Due to the lack of data regarding the direct causes of death, the study only analyzed total mortality. The history of arrhythmic events was carried out only after ICD implantation, and was primarily based on the memory in the ICDs. The results of all of the examinations (echocardiography, 24-hour Holter recording and coronary angiograms) were interpreted by different researchers. Moreover, different machines were used to perform particular examinations. We did not analyze any inadequate therapies that were delivered by an ICD. The long period between the observation and the manuscript preparation limited the interpretation of our results. However, the limited number of reports on this topic and the final results prompted us to write it. In our opinion, changes in guidelines of treatment of coronary artery disease influenced the incidence of ES in the general population. The impact on prevalence in ES (+) and ES (–) remains the same, due to the fact that both groups were treated in the same way. Pharmacological treatment when the study was performed (1997–2004) and pharmacological treatment currently being administered do not differ significantly. In recent years, no new antiarrhythmic drugs have been introduced to the treatment of ventricular arrhythmias. In the cardiology center where the follow-up was performed, each patient with an ES was evaluated for eligibility of RF ablation of ventricular arrhythmias. During an incident of ES, each patient was evaluated for ACS, and in most of them control coronary angiography was performed. Therefore, it seems that treatment applied during the study (1997–2004) does not differ significantly from the current one.
In conclusion, an electrical storm was found in 12% of the patients after myocardial infarction with an ICD for the secondary prevention of SCD.
Our study showed that myocardial infarction of the inferior wall and the absence of coronary revascularization are independent risk factors for the occurrence of an ES. A patent or infarct-related artery and coronary revascularization reduce the risk of occurrence of an ES.
An electrical storm, especially one that results in a large number of shocks, together with older age and a reduced LVEF, is an independent predictor of death in patients after myocardial infarction with an implanted ICD for secondary prevention. Effective ATP therapy may reduce the risk of death among ES patients.


Study data have been accepted and presented at the Congress of Heart Rhythm Society in 2009 in Boston, USA and the Congress of European Heart Rhythm Association EUROPACE in 2011 in Madrid, Spain.

Conflict of interest

The authors declare no conflict interest.


1. Kowey PR. An overview of antiarrhythmic drug management of electrical storm. Can J Cardiol 1996; 12 suppl B: 3B-8B.
2. Nademanee K, Taylor R, Bailey WE, Rieders DE, Kosar EM. Treating electrical storm: sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation 2000; 102: 742-7.
3. Haverkamp W. Electrical storm: still a cryptogenic phenomenon? Eur Heart J 2006; 27: 2921-2.
4. Pires LA, Lehmann MH, Steinman RT, Baga JJ, Schuger CD. Sudden death in implantable cardioverter-defibrillator recipients: clinical context, arrhythmic events and device responses. J Am Coll Cardiol 1999; 33: 24-32.
5. Israel C, Barold S. Electrical storm in patients with an implanted defibrillator: a matter of definition. Ann Nonninvasive Electrocardiol 2007; 12: 375-82.
6. Mitsunori M. Management of electrical storm: the mechanism matters. J Arrhythmia 2014; 30: 242-9.
7. Vaseghi M, Gima J, Kannan C, et al. Cardiac sympathetic denervation in patients with refractory ventricular arrhythmias or electrical storm: intermediate and long-term follow-up. Heart Rhythm 2014; 11: 360-6.
8. Stuber T, Eigenmann C, Delacretaz E. Characteristics and relevance of clustering ventricular arrhytmias in defibrillator recipients. Pacing Clin Electrophysiol 2005; 28: 702-7.
9. Guerra F, Shkoza M, Scappini L, Flori M, Capucci A. Role of electrical storm as a mortality and morbidity risk factor and its clinical predictors: a meta-analysis. Europace 2014; 16: 347-53.
10. Exner DV, Pinski SL, Wyse DG, et al. Electrical storm presages nonsudden death. The antiarrhythmics versus implantable defibrillators (AVID) trial. Circulation 2001; 103: 2066-71.
11. Credner SC, Klingenheben T, Mauss O, Sticherling C, Hohnloser SH. Electrical storm in patients with transvenous implantable cardioverter-defibrillators: incidence, management and prognostic implications. J Am Coll Cardiol 1998; 32: 1909-5.
12. Greene M, Newman D, Geist M, Paquette M, Heng D, Dorian P. Is electrical storm in ICD patients the sign of a dying heart? Outcome of patients with clusters of ventricular tachyarrhythmias. Europace 2000; 2: 263-9.
13. Verma A, Kilicaslan F, Marrouche NF, et al. Prevalence, predictors and mortality significance of the causative arrhythmia in patients with electrical storm. J Cardiovasc Electrophysiol 2004; 15: 1265-70.
14. Villacastin J, Almendral J, Arenal A, et al. Incidence and clinical significance of multiple consecutive, appropriate, high-energy discharges in patients with implanted cardioverter-defibrillators. Circulation 1996; 93: 753-62.
15. Sesselberg HW, Moss AJ, McNitt S, et al. Ventricular arrhythmia storms in postinfarction patients with implantable defibrillators for primary prevention indications: a MADIT-II substudy. Heart Rhythm 2007; 4: 1395-402.
16. Wilber DJ, Kopp DE, Glascock DN, Kinder CA, Kall JG. Catheter ablation of the mitral isthmus for ventricular tachycardia associated with inferior infarction. Circulation 1995; 92: 3481-9.
17. Lacroix D, Klug D, Grandmougin D, Jarwe M, Kouakam C, Kacet S. Ventricular tachycardia originating from the posteroseptal process of the left ventricle with inferior wall healed myocardial infarction. Am J Cardiol 1999; 84: 181-6.
18. Cao JM, Fishbein MC, Han JB, et al. Relationship between regional cardiac hyperinnervation and ventricular arrhythmia. Circulation 2000; 101: 1960-9.
19. Komaru T, Ashikawa K, Kanatsuka H, Sekiquchi N, Suzuki T, Takishima T. Neuropeptide Y vasoconstriction in coronary microvessels in the beating canine heart. Circ Res 1990; 67: 1142-51.
20. Okada T, Yamada T, Murakami Y, Yoshida N, Ninomiya Y, Toyama J. Mapping and ablation of trigger premature ventricular contractions in a case of electrical storm associated with ischemic cardiomyopathy. Pacing Clin Electrophysiol 2007; 30: 440-3.
21. Pascale P, Schlaepfer J, Oddo M, Schaller MD, Vogt P, Fromer M. Ventricular arrhythmia in coronary artery disease: limits of a risk stratification strategy based on the ejection fraction alone and impact of infarct localization. Europace 2009; 11: 1639-46.
22. Mäkikallio TH, Barthel P, Schneider R, et al. Frequency of sudden cardiac death among acute myocardial infarction survivors with optimized medical and revascularization therapy. Am J Cardiol 2006; 15: 480-4.
23. O’Rourke RA. Role of myocardial revascularization in sudden cardiac death. Circulation 1992; 85 (Suppl I): 112-7.
24. Holmes DR, Davis KB, Mock MB, et al. The effect of medical and surgical treatment on subsequent sudden cardiac death in patients with coronary artery disease: a report from the Coronary Artery Surgery Study. Circulation 1986; 73: 1254-63.
25. Prech M, Grajek S, Marszalek A, et al. Chronic infarct-related artery occlusion is associated with a reduction in capillary density. Effects on infarct healing. Eur J Heart Fail 2006; 8: 373-80.
26. Abbate A, Bussani R, Biondi-Zoccai GL, et al. Persistent infarct-related artery occlusion is associated with an increased myocardial apoptosis at postmortem examination in humans late after an acute myocardial infarction. Circulation 2002; 106: 1051-4.
27. Abbate A, Bussani R, Biondi-Zoccai GL, et al. Infarct-related artery occlusion, tissue markers of ischaemia, and increased apoptosis in the peri-infarct viable myocardium. Eur Heart J 2005; 26: 2039-45.
28. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med 1996; 335: 1933-40.
29. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002; 346: 877-83.
30. Bardy GH, Lee KL, Mark DB, et al. Sudden Cardiac Death in Heart Failure Trial (SCD-HEFT) Investigators. Amiodaron or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005; 352: 225-37.
31. Guerra F, Flori M, Bonelli P, Patani F, Capucci A. Electrical storm and heart failure worsening in implantable cardiac defibrillator patients. Europace 2015; 17: 247-54.
32. Brigadeau F, Kouakam C, Klug D, et al. Clinical predictors and prognostic significance of electrical storm in patients with implantable cardioverter defibrillators. Eur Heart J 2006; 27: 700-7.
33. van Boven N, Theuns D, Bogaard K, et al. Atrial fibrillation in cardiac resynchronization therapy with a defibrillator: a risk factor for mortality, appropriate and inappropriate shocks. J Cardiovasc Electrophysiol 2013; 24: 1116-22.
34. Kleemann T, Hochadel M, Strauss M, Skarlos A, Seidl K, Zahn R. Comparison between atrial fibrillation-triggered implantable cerdioverter-defibrillator (ICD) shocks and shocks caused by lead failure: different impact on prognosis in clinical practice. J Cardiovasc Electrophysiol 2012; 23: 735-40.
35. Gatzoulis KA, Andrikopoulos GK, Apostolopoulos T, et al. Electrical storm an independent predictor of adverse long-term outcome in the era of implantable defibrillator therapy. Europace 2005; 7: 184-92.
36. Sweeney MO, Sherfesee L, DeGroot PJ, Wathen MS, Wilkoff BL. Differences in effects of electrical therapy type for ventricular arrhythmias on mortality in implantable cardioverter-defibrillator patients. Heart Rhytm 2010; 7: 353-60.
37. Powell BD, Saxon LA, Boehmer JP, et al. Survival after shock therapy in implantable cardioverter-defibrillator and cardiac resynchronization therapy – defibrillator recipients according to rhythm shocked. J Am Coll Cardiol 2013; 62: 1674-9.
38. Fiek M, Remp T, Fleckenstein M, Pohl T, Deiss M, Reithmann C. Incidence and relevance of nonreentrant monomorphic ventricular tachycardia in patients with frequent implantable cardioverter defibrillator interventions. J Interv Cardiac Electrophysiol 2015; 42: 151-60.
39. Daubert JP, Zareba W, Cannom DS, et al. Inappriopriate implantable cardioverter-defibrillator shocks in MADIT II: frequency, mechanisms, predictors, and survival impact. J Am Coll Cardiol 2008; 51: 1357-65.
40. Poole JE, Johnson GW, Hellkamp AS, et al. Prognostic importance of defibrillator shocks in patients with heart failure. N Engl J Med 2008; 359: 1009-17.
41. Joglar JA, Kessler DJ, Welch PJ, et al. Effects of repeated electrical defibrillations on cardiac troponin I levels. Am J Cardiol 1999; 83: 270-2.
42. Epstein AE, Kay GN, Plumb VJ, Dailey SM, Anderson PG. Gross and microscopic pathological changes associated with nonthoracotomy implantable defibrillator leads. Circulation 1998; 98: 1517-24.
43. Tsuji Y, Hojo M, Voigt N, et al. Ca(2+)-related signaling and protein phosphorylation abnormalities play central roles in a new experimental model of electrical storm. Circulation 2011; 123: 2192-203.
44. Stöckigt F, Peche V S, Linhart M, et al. Deficiency of cyclase-associated protein 2 promotes arrhythmias associated with connexin43 maldistribution and fibrosis. Arch Med Sci 2016; 12: 188-98.
45. Bogun F, Good E, Reich S, et al. Role of Purkinje fibers in post-infarction ventricular tachycardia. J Am Coll Cardiol 2006; 48: 2500-7.
Copyright: © 2016 Termedia & Banach. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Quick links
© 2019 Termedia Sp. z o.o. All rights reserved.
Developed by Bentus.
PayU - płatności internetowe