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 Table of Contents  
REVIEW ARTICLE
Year : 2018  |  Volume : 3  |  Issue : 1  |  Page : 1-15

Prevention of sudden cardiac death after revascularization for coronary heart disease


The Cardiac Arrhythmia Center, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center For Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

Date of Web Publication23-Jul-2018

Correspondence Address:
Prof. Shu Zhang
The Cardiac Arrhythmia Center, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center For Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037
China
Prof. Yong Huo
The Cardiac Arrhythmia Center, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center For Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJHR.IJHR_19_16

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  Abstract 

Sudden cardiac death (SCD) is the leading cause of death in adults worldwide. Coronary heart disease is the underlying reason for most of the patients with SCD, including acute coronary syndrome and chronic ischemic heart disease. Revascularization is an important treatment technology for coronary heart disease, which includes percutaneous coronary intervention and surgical coronary artery bypass grafting. However, according to the recommended guidelines, even with the use of secondary prevention strategies such as medication treatment and a complete revascularization, there are still a great number of patients who have reduced left ventricular ejection fraction, heart failure, and ventricular arrhythmia at different stages in the course of disease. SCD remains to be a serious challenge in the long-term management of ischemic heart disease patients who have had revascularization. Here, we focus on broader issues of concerns to provide more insights by comprehensive recommendations for the clinical treatment of coronary artery disease after revascularization for SCD prevention.

Keywords: Coronary artery disease, guideline, prevention, sudden cardiac death


How to cite this article:
Huang D, Huo Y, Zhang S, Huang C, Han Y. Prevention of sudden cardiac death after revascularization for coronary heart disease. Int J Heart Rhythm 2018;3:1-15

How to cite this URL:
Huang D, Huo Y, Zhang S, Huang C, Han Y. Prevention of sudden cardiac death after revascularization for coronary heart disease. Int J Heart Rhythm [serial online] 2018 [cited 2018 Aug 20];3:1-15. Available from: http://www.ijhronline.org/text.asp?2018/3/1/1/237369


  Introduction Top


Sudden cardiac death (SCD),[1] according to the definition by the World Health Organization, is defined as the accidental death that occurred within 1 h after the onset of symptoms which was usually due to cardiac causes. SCD was the leading cause of death in adults worldwide, and the incidence is 41.8/100,000 in China, wherein 540,000 people die each year.[2] Sudden cardiac arrest (SCA) is a fatal event which occurs due to the circulatory failure by the sudden stopping of the heartbeat. There were over 320,000 people who suffered from SCA each year in America with a morbidity of 103/100,000, and the average age was 66, while the survival rate was 5.6%.[3] Coronary heart disease was the underlying reason for most of the patients with SCD, including acute coronary syndrome (ACS) and chronic ischemic heart disease.[4]

There has been a declining trend in the mortality rate of coronary artery disease due to the active promotion and implementation of the primary and secondary prevention strategies, as well as the modern treatment of coronary heart disease, especially extensive development of percutaneous coronary intervention (PCI) in the early stage of acute myocardial infarction (AMI).[3] However, the incidence of SCD does not decrease and inflicts 76/100,000 annually, which is still ranked first place in the fatality rate of US male patients when compared with the deaths caused by lung cancer, prostate cancer, colorectal cancer, cerebrovascular disease, diabetes, and lower respiratory tract infections.[5] SCD was also the leading cause of death in women, which was 1.7 times more (45/100,000) than the breast cancer mortality.[5] There was a significant drop in the ACS hospitalization and recent mortality rates due to the developments in treatment technology, but there were a total of 16%–25% of patients who were suffering from heart failure within 1 year.[6] This was an important reason for the rising prevalence of heart failure over the past 10 years.[7] Coronary artery disease was the cause of disease in two-third of patients with systolic heart failure.[8] The risk of SCD for the patients with heart failure was significantly higher than the patients with other heart diseases. A population-based study showed that the incidence of SCD with a history of myocardial failure was the highest compared with other patients with heart diseases, which was 3.65 times of the whole group of patients with heart disease.[9]

Revascularization is an important treatment technology for coronary heart disease, which also includes PCI and surgical coronary artery bypass grafting (CABG). Revascularization alleviates the symptom of myocardial ischemia, and also reduces the mortality and improve long-term prognosis. However, according to the recommended guidelines, even with the use of secondary prevention strategies such as medication treatment and a complete revascularization, there are still a great number of patients who have reduced left ventricular ejection fraction (LVEF), heart failure, and ventricular arrhythmia at different stages in the course of disease. SCD still becomes the main cause of death in such patients and constitutes for one-third of all other deaths in the patients who have received CABG complete revascularization. This is also supported by a clinical study (STICH trial) where patients with ischemic heart disease combined with heart failure underwent CABG treatment.[10] Therefore, SCD remains to be a serious challenge in the long-term management of ischemic heart disease patients who have had revascularization.

Hence, in this article, broader issues of concerns are focused, which provides more insights by comprehensive recommendations for the clinical treatment of coronary artery disease after revascularization for SCD prevention.


  Prevention Strategies of Sudden Cardiac Death Due to Ischemic Heart Disease Top


SCD prevention strategies:[11] According to the clinical guidelines, there are primary and secondary prevention strategies for treating SCD in people with ischemic heart disease based on their clinical features and laboratory indicators and based on a large number of published clinical trials.

The secondary prevention

Secondary prevention refers to the prevention of SCD in patients who have survived a prior SCA or sustained ventricular tachycardia (VT). There is a high risk of recurrence of SCA or VT for such patients. A long-term follow-up of SCA survivors and sustained VT patients showed that: the incidence of 1-year, 3-year, and 5-year VT or ventricular fibrillation (VF) was 19%, 33%, and 43%, respectively. Anti-arrhythmic drugs were essential for secondary prevention of SCD, besides medical therapy of coronary artery disease and revascularization in the ages before the application of the implantable cardioverter defibrillator (ICD). Amiodarone and β-blockers can reduce the occurrence of VT and VF but showed limited effectiveness.[12] ICD is currently the first-line therapy recommended in the secondary prevention of SCD.[13] Meta-analysis of three randomized trials of SCD secondary prevention (AVID, CASH, and CIDS) showed that the risk of arrhythmic death was reduced by 50% in the ICD group, and the risk of all-cause mortality was reduced by 28%.[14] Revascularization cannot effectively prevent the recurrence of VT for sustained monomorphic VT patients with a history of myocardial infarction. In addition, blood electrolyte abnormalities are common in SCA survivors. If there are no correctable risk factors in SCA survivors, ICD implant is recommended for these patients as the secondary prevention.[11]

The primary prevention

The main limitation of the secondary prevention strategy was that most of the SCA patients who never experience SCA before cannot survive and thereby lose the opportunity of prevention. According to the statistics released by AHA in 2015, there were 326,200 people suffering from SCA outside the hospital in America. It accounted for the survival rate of only 5.6% and finally discharged patients who received cardiopulmonary resuscitation and other rescue measures, even in a country like America which includes better SCA emergency systems outside the hospitals and a common artificial cardiopulmonary resuscitation. These data indicate that the secondary prevention is quite late for most of the patients who have a potential risk for SCA. The primary prevention is illustrated under this background. Primary prevention of SCD refers to the use of ICDs in individuals who are at risk but in those patients who do not yet have an episode of sustained VT, VF, or resuscitated cardiac arrest. ICD has been shown to decrease all-cause mortality of SCD and improve the long-term prognosis based on the optimal drug therapy and revascularization for coronary revascularization.[11]

The method of risk stratification for the primary prevention of sudden cardiac death

SCD is mainly caused by life-threatening ventricular arrhythmias (VF or VT). These serious arrhythmias are considered to change the ion channels of the myocardial cell and intercellular electrical conduction features that are caused by the scar of ischemic myocardium and myocardial infarction, cardiac remodeling, and heart failure. These ventricular arrhythmias result in the SCD by triggering factors such as increased sympathetic tone, hemodynamic deterioration, blood electrolyte concentration, and PH changes.[15],[16],[17],[18],[19] Factors such as environment and time period also affect SCD, which is a very complex and dynamic process.[20] It is hard to accurately predict when SCD occurs or as to how a particular patient could suffer from SCD, but risk stratification has been performed according to the existing clinical results, thereby determining the level of risk for SCD. Prevention of SCD requires immediate action according to the level of risk. Currently, the following four methods and indicators for SCD risk stratification for the patients with ischemia heart disease were present: (1) the method of anatomy matrix to detect the presence of ventricular arrhythmia, (2) the indicators of changes of ventricular electrophysiological properties, (3) the indicators of autonomic nervous system dysfunction, and (4) other methods and indicators [Table 1].
Table 1: The methods and indicators of sudden cardiac death risk stratification of coronary artery disease

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The method of anatomy matrix to detect ventricular arrhythmias

Myocardial scarring and the alteration of anatomical structures are the prerequisites for the generation of ventricular arrhythmias. Myocardial scar and its surrounding areas may have slow electrical conduction and increase conductive characteristics, which forms the basis of VT/VF generation.[21] The degree of reduced LVEF can roughly reflect the size and scar burden of the left ventricle in patients with coronary artery disease after myocardial infarction, which is currently the most crucial indicator in predicting the SCD risk.[22],[23] Cardiac imaging examination can be used to evaluate the size and anatomical features of myocardial scar, including echocardiography, ultrasonic tissue Doppler imaging, single photon emission computed tomography (SPECT), and positron emission tomography (PET).[24],[25] Cardiac magnetic resonance imaging (MRI) helps in examining myocardial fibrosis and scars through delayed imaging enhancement, and the spatial resolution is better than that of SPECT and PET, as this is not affected by blood perfusion. Myocardial scar burden was measured by MRI which showed good predictive value for SCD and is widely used in the current clinical studies.[26],[27] Further clinical studies are required to verify the imaging techniques that mediate the detection of myocardial scars to determine the predictive value of SCD. Due to these limitations, such as resolution, reproducibility, and other factors such as high cost and time consumption, the measurements of myocardial scar burden are not used as common methods for determining risk stratification of SCD in the current clinical practice. DETERMINE trial was aimed to evaluate the predictive value of MRI on SCD by observing the appropriate therapy rate of ICD in patients whose left ventricular scar was >10%, but due to the difficulty in the patient selection, the trial was stopped prematurely.[27]

The indicators of the state of alteration of electrophysiological properties and the autonomic nervous function

The alteration of electrophysiological properties is also the basis of the formation of ventricular arrhythmia. The indicators that reflect abnormal depolarization include (1) the increase of QRS wave width, (2) the fragmentation waves in QRS wave, and (3) the occurrence of ventricular late potentials (using ECG averaging technique). The indicators that reflect abnormal repolarization include (1) prolonged QT interval, (2) increased dispersion of QT, (3) T-wave alternans, and (4) spatial angle deviations between QRS-T vectors. The measurement of the status of the autonomic nervous system usually includes (1) heart rate variability, (2) heart rate turbulence, and (3) baroreceptor sensitivity. These indicators have been extensively studied, but the predictive value and repeatability of SCD remain uncertain. Thus, they are not utilized in the risk stratification of SCD in the clinical guidelines for patients with coronary artery disease and heart failure.[8],[13],[28],[29],[30],[31],[32],[33]

Other methods used in risk stratification

Nonsustained VT (NSVT) and frequent premature ventricular contractions had a certain predictive value for SCD.[13],[34],[35] Programmed stimulation used in the invasive electrophysiological study showed a high positive predictive value, but a low negative predictive value. Electrophysiological examination should be recommended for the patients with chronic myocardial infarction if symptoms such as syncope, presyncope, or palpitation occur, which were speculated to be related to the ventricular arrhythmias. If the sustained and monomorphic VT was induced, there is a high risk for SCD and then ICD should be implanted to perform active prevention.[13],[35],[36]

Left ventricular ejection fraction is currently the most important and widely used indicator for risk stratification

LVEF has been known to predict the risk of SCD, though has limitations,[37] but so far, significant reduction of LVEF (<30%–40%) acts as the main indicator for selected patients in the clinical trials who used ICD as the primary prevention of SCD. The results of these clinical trials confirmed that ICD can effectively prevent SCD in patients with ischemic or nonischemic heart disease and significant left ventricular dysfunction (reduced LVEF).[38],[39] Moreover, it has been further illustrated that LVEF can predict the risk of SCD; therefore, it acts as an important indicator of risk stratification. However, other factors of risk stratification are listed in [Table 1], but these factors were not similar to LVEF which was confirmed in the clinical trials of SCD primary prevention.[28],[30],[33] Therefore, LVEF still remains as an important indicator of risk stratification for SCD when the current clinical guidelines involve the primary prevention of SCD, for both ischemic heart disease and nonischemic heart disease. The direction of future efforts should include research by combining other indicators, including the indicators listed in [Table 1] and some biochemical indicators (such as B-type natriuretic peptide and C-reactive protein)[40] and genetic detection,[41],[42] to compose a risk stratification system based on LVEF to overcome the limitations of LVEF as the only indicator.

The importance of implantable cardioverter defibrillator in the primary prevention

There were a total of almost 6000 cases enrolled in the randomized clinical trials of ICD for the primary prevention of SCD in patients with ischemic heart disease. MADIT trial was the first randomized controlled trial for the primary prevention, in which 196 cases of ischemic heart disease patients were enrolled. LVEF ≤35% and the electrophysiological study can induce VT by combining with NSVT. The results found that the risk of death of ICD group was reduced by 54% when compared with the conventional therapy group (amiodarone was used in 75% cases). Based on this, the FDA approved that ICD could be used in the primary prevention of SCD in 1996. Subsequently, 704 cases of patients with myocardial infarction were enrolled in the MUSTT trial, with the LVEF ≤40%, accompanying NSVT. ICD significantly reduced the risk of SCD after 5 years of follow-up.[43] The MADIT and MUSTT trials found that ischemic heart disease combined with left ventricular dysfunction accompanying NSVT as well as the VT introduction by electrophysiological tests, showed the high risk of SCD, while ICD could significantly reduce the risk of SCD.[43],[44] There were 1232 cases with a history of myocardial infarction enrolled in MADIT II trials to easily screen the SCD high-risk patients to perform the primary prevention (the time of myocardial infarction was >30 days). In this study, LVEF ≤30% or its combination with NSVT or electrophysiological test induced VT was not included in the inclusion criteria, whereas the significant reduction of LVEF was the only inclusion criterion. The trial was terminated in 20 months because the risk of all-cause death in the ICD group reduced by 28% compared with the control group.[39] The LVEF of enrolled patients in the following SCD-HeFT trial was ≤35% and cardiac function was NYHA II or NYHA III. The risk of all-cause death in the ICD group was reduced to 23% compared with the control group based on optimal drug therapy after 3.8 years of follow-up.[38] The evidence provided by these clinical trials showed that the ischemic heart disease patients whose cardiac function was either NYHA II or III had a cardiac and LVEFs ≤35%, or whose cardiac function had NYHA I and LVEFs were ≤30%, met the Class I indications of ICD implantation which were recommended by the guidelines.[11] It should be emphasized that most of the coronary artery disease patients had received revascularization (PCI or CABG) in MUSTT, MADIT, and MADIT II trials, suggesting that as long as LVEF was significantly reduced, ICD was also essential for the prevention of SCD no matter the patients accepted revascularization or not.[43],[44],[45]

Situation of the clinical application of implantable cardioverter defibrillator

According to the ICD registration material from the National Cardiovascular Disease Data Registration (NCDR), there were 139,991 cases of patients with ICD implantation in 1435 hospitals of America in 2011, and the primary prevention of SCD was conducted for 106,131 cases, accounting for 75.8%.[45] PCI registration materials (Cath PCI Registry) from NCDR showed that there were 632,557 cases performed with PCI in 1337 hospitals of America in 2011, with the proportion of PCI cases to ICD cases of 4.5:1.[45] According to the data published by the European Heart Rhythm Society in 2014, there were 36,100 cases with ICD implantation and cardiac resynchronization therapy pacemaker with defibrillator (CRTD) in Germany, and the implantation population ratio was 445/million. Furthermore, the implantation population ratio was 369/million, 118/million, and 17.6/million in Italy, Spain, and Russia, respectively.[46]

In 1992, the first epicardial ICD was implanted by surgical operation in China and the first operation of ICD was implanted transvenously in 1996. There was a greater increase each year after 2001. However, up to 2013, there were only 3068 cases of annual ICD and CRTD implantations in China, with the implantation population ratio of 2.3 per million, which was significantly less than that in Russia. In 2013, a total of 404,505 cases of PCI were performed in China, with the ratio of PCI cases to ICD and CRTD cases of 148:1, which was 32.9 times higher than the ratio in America. Taken together, it indicates that China has a big gap with foreign countries for the prevention of SCD using ICD and also receives much less attention toward the prevention of SCD post-PCI operation for the coronary heart disease patients. To change this situation, the national health insurance reimbursement for ICD should be improved, while the common knowledge of the prevention of SCD among doctors and patients should be widespread. The risk of SCD is still high for some patients with coronary heart disease after revascularization (for instance, LVEF ≤35%), but the prevention of SCD is neglected for the patients who have received revascularization therapy that is considered for the cause of disease.

Cost-effectiveness analysis of ICD in the primary prevention of SCD abroad showed that the consumed resources increased 1-year survival which was similar to the renal dialysis (renal dialysis was $30000–50000 and ICD was $25300–50700).[47],[48] The cost-effectiveness can be improved if patients with severe ventricular arrhythmias and high risk of SCAs were selected, but with low risk of death due to other causes. The increase of other risk factors in the risk stratification of SCD may achieve this goal besides significant LV dysfunction.[49]


  The Risk of Sudden Cardiac Death After Revascularization Top


Revascularization is the most important therapeutic measure for ischemia associated with ventricular arrhythmias. From this perspective, revascularization has a great significance in the prevention of ischemic heart disease of SCD.[50] Ischemia-associated severe ventricular arrhythmias and SCA are the most common in ST-segment elevation myocardial infarction (STEMI) in 48 h after the onset. It is also common in the non-ST-segment elevation with ACS (NST-ACS) as well as in chronic ischemic heart disease. For patients with chronic stable ischemic heart disease combined with heart failure and patients with chronic myocardial infarction, the occurrence of arrhythmias is mainly due to the alteration of cardiac electrophysiological properties, which forms the substrate for generating and maintenance of the ventricular arrhythmias based on cardiac scar and fibrosis and occurrence of severe ventricular arrhythmias and SCA under the action of trigger factors.[16],[17] Therefore, revascularization alone cannot effectively prevent SCA caused by arrhythmias.[10],[11],[51] After revascularization, according to the different status of patients, the risk of SCD should be evaluated and comprehensive treatment measures including ICD implantation should be adopted to prevent SCD in the indicated patients.

The risk of sudden cardiac death after primary percutaneous coronary intervention

Direct percutaneous coronary intervention can reduce the risk of ventricular arrhythmias

VT/VF within 48 h of onset of STEMI is terminated by acute electric events, which is related to the onset of myocardial ischemia.[52] To prevent VT/VF at the early stage of STEMI, it is important to carry out PCI as early as possible, optimize reperfusion therapy of myocardial ischemia, correct electrolyte imbalances, prescribe β-blockers, and take measures to prevent ischemic stress and the resulted heart failure and cardiogenic shock. PCI is the most critical element in the series of treatments. Moreover, direct PCI can reduce the risk of ventricular arrhythmias and SCD in STEMI patients. A registered research led by two centers of Germany and Finland showed that the incidence of SCD was quite low if the patients with AMI had received revascularization (direct PCI or CABG), combined with the treatment of β-blockers, aspirin, statins, and angiotensin-converting enzyme inhibitors (ACEI). Only 1.2% of cases had SCD in the 2.9 years of follow-up. The incidence of SCD was 3.6% if the patients had received the above treatments partially. The risk of SCD for the patients without revascularization was 2.1 times the risk of patients with revascularization.[53] Moreover, the time of reperfusion therapy (the time from the occurrence of the symptoms of myocardial infarction to the open of infarct-related artery) was found to be associated with induced VT and the occurrence of sudden death in future and severe ventricular arrhythmias. This study enrolled patients received primary PCI and with the LVEF ≤40%. The primary end-point was whether VT can be induced by electrophysiological examination after 3 days of myocardial infarction. The secondary end-point was the sudden death or severe ventricular arrhythmias after 2 years of follow-up (ICD treatment was needed). It was found that the shorter the time of reperfusion (it was divided into ≤3 h group, 3–5 h group, and >5 h group), the less the occurrence of primary and the secondary end-point events. Therefore, patients with STEMI should be conducted with primary PCI as early as possible, and it is very important to shorten the time of reperfusion therapy in the prevention of future SCD.

Primary percutaneous coronary intervention can reverse left ventricular remodeling

For patients with STEMI, direct PCI can reverse the structural abnormalities of the left ventricle, and improve the left ventricular function. The risk of SCD may reduce with the recovery of left ventricular function.[54] Observation of the dynamic alteration of left ventricular remodeling by consecutive echocardiography after direct PCI showed that 39% of patients achieved the criteria for the reversal of left ventricular remodeling after 6 months, which means that the reduction of the left ventricular end-systolic volume was >10% of the basic value. However, most patients cannot achieve this standard.[55] Another study compared the alteration of 5-day and 4-month left ventricular function and remodeling indexes after direct PCI. The magnetic resonance was used to measure LVEF, left ventricular end-systolic and end-diastolic volume index. It was found that for the patients with LVEF basic value <50%, if troponin I was significantly increased, LVEF and left ventricular remodeling index cannot be improved or deteriorated and left ventricular volume index was increased in 4 months after PCI.[55]

Heart failure after myocardial infarction is a high-risk factor for sudden cardiac death

The risk of SCD is significantly increased in patients with myocardial infarction combined with heart failure.[9] Primary PCI can significantly reduce the in-hospital mortality of the patients with STEMI, leading to most patients with large areas of myocardial infarction or severely diseased patients with myocardial infarction can survive to discharge from the hospital, but there is a risk of heart failure in the future for these patients. Therefore, the in-hospital mortality of patients with STEMI have been significantly reduced with the popularization and promotion of the early and optimal treatment with direct PCI as a key strategy, but the incidence of heart failure for these patients was increased.[56] A retrospective study showed that 1-year cumulative incidence of heart failure was 23.4% in over 9000 cases of STEMI patients, and the newly emerged heart failure within 1 year after discharge was 12%.[6] The study suggested that >1/5 of STEMI patients had higher risk of SCD after discharge. The CADILLAC study showed that after direct PCI, LVEF ≤40% was the most important predictive factor for 30-day and 1-year mortality.[57]

Sudden cardiac death after the direct percutaneous coronary intervention is the main manner of death

SCD is still the main reason of death for STEMI patients who discharged after direct PCI, even if standard secondary prevention of coronary heart disease is applied. A recent study analyzed the short- and long-term causes of death in over 2800 STEMI patients, with an average follow-up of 4.7 years. In all 717 cases, the causes of death, the top was cardiogenic shock (140 cases, 19.5%), which occurred at 0–3 days in the course of the acute phase; which was followed by tumor occurrence (124 cases, 17.3%) at 3.25 years (1.96–4.63 years); the third was SCD (111 cases, 15.5%) standing on 2.75 years (1.28–3.00 years); myocardial re-infarction was the fifth cause of death (45 cases, 6.3%), which occurred at 227 days in the course of disease (6–1096 days); and heart failure was the sixth one (29 cases, 4%), which occurred at 717 days in the course of disease (50–1237 days). The results of this study demonstrate that SCD is the fifth cause of death in the long-term cardiac death for the discharged patients after direct PCI, with the incidence of SCD which is markedly more than the total incidence of all other cardiac deaths, and it is 2.47 times the death of myocardial reinfarction.[58] Therefore, the prevention of SCD is based on the treatment of cardiac ischemic events, such as the prevention of myocardial reinfarction which, should be paid more attention in the long-term management of patients discharged after direct PCI.

The risk of sudden cardiac death after revascularization for chronic stable ischemic heart disease

CABG can decrease the risk of severe ventricular arrhythmias and SCD for patients with preserved or mid-range left ventricular function.[50] However, it could only partially prevent SCD, and the effect was largely limited for patients with significant abnormal left ventricular function. A registered Japanese study compared the impact of PCI and CABG on the prognosis of patients with three-vessel and/or left main branch lesions. After 4.7 years of follow-up, if the LVEF ≤50%, sudden death after PCI operation accounted for 32.1% of the cardiac death, while sudden death after CABG accounted for 28.3% of the cardiac death, indicating that sudden death still remains the reason for cardiac death.[59] The STICH study with 1212 cases of ischemic heart failure patients who were suitable for CABG operation and LVEF ≤35% were enrolled and the patients were randomly divided into CABG operation group and the medical therapy group. There were a total of 462 cases of death after 56 months of follow-up, with the total mortality of 38.1%. A total of 351 cases died from cardiovascular diseases, accounting for 76% of the total deaths. Sudden death was the main cause of death in cardiovascular disease-mediated deaths. Seventy-four cases in the CABG group were subjected to sudden death, accounting for 33.9% of cardiovascular deaths; 99 cases in the medical therapy group were subjected to sudden death, accounting for 40.6% of cardiovascular deaths.[10] Revascularization should be considered for patients with heart failure combined with ischemic heart disease, silent angina, or viable ischemic myocardium. However, it was of limited benefit for patients with severe heart failure (LVEF ≤35%),[60] and then CABG was recommended by the guidelines.[61] In the substudy of MADIT-II trial, the association of the course of disease with ventricular arrhythmia after revascularization was observed. In the eight-year long-term follow-up, the longer the time of revascularization, the higher the risk of severe ventricular arrhythmia (ICD treatment was needed), and the risk could increase up to 6% for each additional year.[62] Thus, in the long-term management of the patients after revascularization, the on-going prevention of SCD should be noted.


  The Prevention of Sudden Cardiac Death After Acute Myocardial Infarction Top


Thirty-day mortality had significantly reduced hospitalization of STEMI patients due to extensive development of PCI. The early-stage mortality was also significantly reduced in patients with NSTEMI who received various therapeutic strategies including revascularization in terms of risk stratification according to the guidelines. However, the long-term mortality and event rates after AMI were underestimated and the 6-month mortality rate was still as high as 12%.[63],[64] SCD was the main or the leading cause of death in all the cases of deaths, even if revascularization was completed it accounted for 24%–40% of the total deaths.[65],[66] There were a total of 720,000 cases of new or recurrent myocardial infarction in America and 200,000 cases which belonged to high-risk SCD patients who needed active prevention.[67]

The high incidence of SCD in the early stage after AMI (within 30–40 days) resulted in high-risk of sudden death.[68] However, more than half of the SCDs were not caused by arrhythmias, but by reinfarction or mechanical complications that were due to left ventricular rupture and acute mitral regurgitation. In DINAMIT study, only 50% of SCDs were attributed to arrhythmia, while the rest were due to the mechanical complications of the heart.[69] In the VALIANT trial, according to the reported data of 105 cases of the autopsy, 80% of the causes of SCD were reinfarction or cardiac rupture in the 1st month after the onset of AMI, and only 20% were speculated to be caused by arrhythmia.[70] The combined data from the four ACS studies showed that approximately one-third cardiovascular deaths after NSTE ACS were caused by SCD. Accurate risk stratification can be performed by collecting the information of clinical variables of LVEF, age, diabetes, assessment of glomerular filtration rate, heart rate, myocardial infarction, peripheral vascular disease, ancestry, gender, and Killip classification.[71] Thus, there was no benefit for the early implantation (within 40 days) of ICD after AMI, in patients caused by nonarrhythmia which accounted for the most in the early stage of SCD. Although the arrhythmic death can be reduced, there was no improvement in the overall mortality.[72],[73] After AMI, with the progression of left ventricular remodeling and myocardial fibrosis, as well as the formation of cardiac scars, the alteration of electrophysiological properties of myocardial cells in the infarct area and its surrounding areas would result in the local conduction by slowing or blocking, prolonged refractory period, and the increased degree of inconsistent repolarization. Thus, the substrate generating the reentrant of ventricular arrhythmias was formed. The risk of SCD was caused by malignant ventricular arrhythmias could also be increased. ICD therapy was the most effective method to prevent the malignant ventricular arrhythmia. About 1 year after AMI, SCD caused by arrhythmia may account for half of the cases with sudden death and would reach up to 60% after 30 months.[74] Thus, in the early stages after AMI and for the prevention of SCD, it was important to concentrate on revascularization, prevention and treatment of the progress of myocardial ischemia, and refraction, as well as mechanical complications, control of heart failure, and improvement of left ventricular function. While in the long-term management of AMI patients, ICD therapy can effectively decrease the mortality of the patients whose LVEF ≤35% after AMI in 2 years,[75] which was very important for high-risk SCD patients, based on the revascularization and the secondary prevention therapy of the guidelines.

The prevention of sudden cardiac death after revascularization in the acute phase (<48 h)

The risk of SCD significantly is increased if a polymorphous VT or VF occurred after AMI and revascularization. Under these circumstances, the progression of myocardial ischemia and the possibility of reinfarction or acute stent thrombosis should be first considered. Coronary angiography should be performed immediately if this possibility cannot be excluded. Malignant ventricular arrhythmias are also common in patients combined with cardiogenic shock and severe heart failure. The following measurements to prevent the early SCD (<48 h) after revascularization were utilized [Figure 1].[13],[67],[76],[77],[78]
Figure 1: The strategies of handling severe ventricular arrhythmias after acute myocardial infarction revascularization. VT = Ventricular tachycardia, VF = Ventricular fibrillation

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  1. Routine echocardiography should be performed after revascularization to understand left cardiac function and whether it is combined with mechanical complications and then corresponding treatment should be conducted (recommendation of Class I, evidence of level C)
  2. If no contraindications, oral administration of β-blockers should be given to prevent severe ventricular arrhythmias (recommendation of Class IIa, evidence of level B)
  3. For recurrent polymorphous VT, intravenous or oral administration of β-blockers should be administered to control the seizures (recommendation of Class I, evidence of level B)
  4. Intravenous injection of amiodarone should be given to treat polymorphic VT (recommendation of Class I, evidence of level C)
  5. For recurring VT/VF, if β-blockers and amiodarone are ineffective or there is a contraindication, then lidocaine can be used (recommendation of IIb Class, evidence of level C)
  6. For sustained VT or VF, immediate electric cardioversion or defibrillation should be performed (recommendation of Class I, evidence of level C)
  7. For recurring VT/VF, if the following possibilities exist such as acute stent thrombosis, progressed myocardial ischemia, or reinfarction, then coronary angiography should be conducted immediately and the corresponding treatment based on the results of angiography should be performed (recommendation of Class I, evidence of level C)
  8. The balance of blood electrolytes should be maintained, the syndromes of hypokalemia and hypomagnesemia should be corrected (recommendation of Class I, evidence of level C)
  9. If VT/VF recur or if it is hard to control electrical storm by drugs, catheter ablation should be considered in experienced medical center based on revascularization and optimal medical therapy (recommendation of Class IIa, evidence of level C)
  10. Deep sedation should be given leading to a sleep state of the patients for the recurrence of VT/VF that is hard to be controlled by medicine or electrical storms; (recommendation of Class IIb, evidence of level C)
  11. For the recurrence of VT that is hard to be controlled by medicine and transcatheter, electrical stimulation, and speeding suppression should be conducted to control the onset of VT if catheter ablation cannot be performed (recommendation of Class IIa, evidence of level C)
  12. For the patients who have received ICD implantation previously, and if inappropriate electric shock occurs repeatedly, reprogram should be performed to avoid the electric shock (recommendation of Class I, evidence of level C)
  13. Except β-blockers, other antiarrhythmic drugs should not be used to prevent the occurrence of ventricular arrhythmias (recommendation of Class III, evidence of level B).


The prevention of sudden cardiac death after acute myocardial infarction (>48 h)

The prognosis of the SCA or malignant arrhythmia that occurred 48 h after the onset of AMI was different from those that occurred within 48 h,[67] which was common in patients with severe heart failure and cardiogenic shock. After revascularization, underoptimal medical treatment of secondary prevention, most SCA, or sustained VTs were not related to ischemia if they occurred from 1 or several months in the course of disease after myocardial infarction. However, there was a high risk of SCD in the future. The SCD prevention was the secondary prevention for the patients. After AMI revascularization, although there was no SCA or sustained VT, the risk of SCD increased if it was combined with severe left heart dysfunction (LVEF ≤35%), unexplained syncope, frequent NSVT, or sustained VT induced by EP study. The SCD prevention was the primary prevention for the patients.

The secondary prevention

  1. After 48 h of onset of AMI, if there is no sustained VT or VF within 40 days, then it is not related to the progress of myocardial ischemia and reinfarction, and no other amendable reasons that caused VT can be found, then ICD can be implanted or wearable cardioverter defibrillator (WCD) can be used (recommendation of Class I, evidence of level B)[74],[77]
  2. 48 h after the onset of AMI and within the 40 days, polymorphic VT or VF occurs, then ICD implantation and WCD should be considered if revascularization is incomplete (revascularization cannot be performed for culprit lesion revascularization failure of significant nonculprit severe artery lesion), and the patients have left ventricular dysfunction and decreased LVEF before AMI (recommendation of Class IIb, evidence of level C)[13]
  3. 48 h after the onset of AMI, based on revascularization and the optimal drug therapy, radiofrequency catheter ablation should be considered if VT/VF or electrical storm still occurs repeatedly (recommendation of Class IIa, evidence of level C)[13]
  4. 48 h after the onset of AMI and within the 40 days, if sustained VT occurs, then catheter ablation should be considered to treat VT in experienced centers (recommendation of Class IIb, evidence of level C)[13],[74]
  5. Within 40 days after the onset of AMI, sustained VT occurs, which is not related to myocardial ischemia, then comprehensive treatments against ischemia should be performed to correct myocardial ischemia, including revascularization (revascularization should be performed for the second time if the patients have already received revascularization), and ICD should not be implanted (recommendation of Class III, evidence of level C).[74]


The primary prevention

The risk stratification of early sudden cardiac death after acute myocardial infarction

The risk stratifications are summarized below:[13],[76],[77],[79]

  1. All the patients should receive the measurement of LVEF before discharging from the hospital (recommendation of Class I, evidence of level C)
  2. LVEF should be retested after 40-day postmyocardial infarction for patients who have not received revascularization, and LVEF should be retested after 90 days for the patients who have completed revascularization (PCI or CABG), leading to uncover the patients with severe left ventricular dysfunction (LVEF ≤35%), thereby the ICD can be an indication of primary prevention for SCD (recommendation of Class I, evidence of level B)
  3. 24-h dynamic ECG should be performed before discharging from the hospital to measure ventricular arrhythmias (NSVT and frequent premature ventricular contractions) and evaluate the ventricular arrhythmias (monomorphic or polymorphic VT, ventricular rate at VT, duration, and number of clusters of PVCs) (recommendation of Class IIa, evidence of level C)
  4. Electrophysiological examination should be performed for the patients with LVEF ≤40% and evaluate the risk of SCD according to the induction of sustained VT (recommendation of Class IIb, evidence of level B)
  5. It is not recommended to use noninvasive (such as microvolt T-wave alternans, autonomic function test, or signal-averaged ECG) for risk stratification at the early-stage post-AMI; (recommendation of Class III, evidence of level B).


The primary prevention of sudden cardiac death after myocardial infarction

According to the guidelines and principles of secondary prevention of coronary artery disease, long-term medical treatment after myocardial infarction is very important in the reduction of the overall mortality rate and SCD, including lifestyle intervention and control of risk factors, antiplatelet agents, lipid-lowering drugs, β-blockers, ACEI or angiotensin receptor blockers, and aldosterone antagonists.[80],[81] However, it was not sufficient to depend on revascularization and the optimal treatment of the secondary prevention of coronary heart disease for the patients with a high-risk of SCD, whereas the implantation of ICD can effectively reduce SCD.[38],[39],[43],[44],[51],[52],[53] At present, all the guidelines involving coronary heart disease, heart failure, ventricular arrhythmias and sudden death, and implantable device therapy emphasized that ICD should be used for the primary prevention of SCD, which were based on sufficient evidence provided by a number of clinical trials.[8],[11],[13],[61],[74],[76],[79],[82]

The Primary Prevention of Sudden Cardiac Death After 40-Day Postmyocardial Infarction or After 90-Day Postrevascularization

  1. ICD should be implanted at least 40 days after myocardial infarction, or at least 90 days after revascularization, with LVEF ≤35%, and NYHA of Class II or Class III (recommendation of Class I, evidence of level A)[11],[77],[82]
  2. ICD should be implanted at least 40 days after myocardial infarction or at least 90 days after revascularization, with LVEF ≤30% and NYHA of Class I. (Recommendation of Class I, evidence of level A).[11],[82]


The Primary Prevention of Sudden Cardiac Death Within 40 days After Myocardial Infarction or Within 90 days After Revascularization

In general, LVEF should be measured within 40 days after myocardial infarction or 90 days after revascularization, cardiac function, and clinical status should be evaluated before deciding whether it was suitable to implant ICD for primary prevention of SCD. The recommendation from the guidelines was based on the negative results of DINAMIT and RIS.[72],[73] But in clinical trials, the evidence generated by the research results and the recommendations of the guidelines did not cover the real and special clinical situations due to the limitations of inclusion and exclusion conditions of selected patients. To address this practical clinical problem, a consensus was published by experts of the three Institutes of America's HRS/ACC/AHA in 2014 which elaborated on how to use ICD to prevent SCD when clinical trials cannot be used or reflected the special circumstances.[74] Due to the lack of clinical evidence, the statements of “is recommended,” “is not recommended,” “can be useful,” and “may be useful” were used in the consensus to express the standpoints of using ICD under different conditions. However, it did not use the common expressions of Class I, Class II, and Class III recommended by the guideline.

  1. Within the 40-day postmyocardial infarction, LVEF was ≤35%, permanent pacemaker should be implanted due to bradycardia. It is recommended to implant ICD if predicted that LVEF is difficult to recover to a value of >35% or cannot be determined after 40 days. If pacemaker is implanted within 40-day postmyocardial infarction, it should be replaced by ICD if LVEF was still ≤35% (this is with high possibility) because it is suitable to the indications of Class I of ICD
  2. If syncope occurs in 40-day postmyocardial infarction, it is presumably associated with severe ventricular arrhythmias (for instance, NSVT is recorded by ECG, electrophysiological examination can induce sustained VT or VF), then the implantation of ICD may be useful
  3. ICD has been implanted before myocardial infarction and ICD battery is depleted within 40 days after myocardial infarction, it is recommended to replace ICD if the clinical status of the patient is permitted
  4. If the condition of the primary prevention of SCD for implanting ICD is met before myocardial infarction, then the implantation of ICD may be useful when it is predicted that LVEF is likely to recover to a value >35% in 40-day postmyocardial infarction and within the 90-day postrevascularization
  5. Within the 90-day postrevascularization after myocardial infarction and LVEF is ≤35%, it is recommended to implant ICD because permanent pacemaker should be implanted due to bradycardia and because it is unlikely or cannot be determined for the LVEF recovering to a value >35%
  6. If syncope occurs within 90-day postrevascularization after myocardial infarction, it is presumably caused by server ventricular arrhythmias (according to the history of disease, NSVT recorded by ECG, or sustained VT induced by electrophysiological examination), then the implantation of ICD may be useful
  7. For the patients who have ICD implantation previously and battery depletion within the 90-day postrevascularization, it is recommended to replace ICD if the clinical condition is permitted
  8. After 40 days of myocardial infarction and within the 90-day postrevascularization, the implantation of ICD may be useful during the period when the patients are waiting for heart transplantation or waiting for the implantation of artificial heart assist device.


The prevention of sudden cardiac death after revascularization for stable coronary heart disease

Revascularization can reduce ventricular arrhythmias and the risk of SCD for stable coronary disease patients with preserved cardiac function or with mild heart failure.[50] However, for the patients combined with severe left ventricular dysfunction (LVEF ≤35%), SCD still remains the cause of death even if CABG was used to carry out complete revascularization, which accounted for one-third of the overall cardiovascular death, dramatically more than the overall mortality caused by pump failure, myocardial infarction, and cerebrovascular disease.[10] Recently, long-term follow-up studies showed that SCD was the main cause of death for discharged STEMI patients after direct PCI. Therefore, the implantation of ICD should be considered for the patient with high risk of SCD, based on the secondary prevention of the treatment of coronary heart disease after revascularization. Monitoring and prevention of high-risk SCD patients postrevascularization are shown in [Figure 2], [Figure 3], [Figure 4].
Figure 2: Monitoring of the patients with high risk of sudden cardiac death after revascularization of coronary heart disease. LVEF = Left ventricular ejection fraction, PVC = Frequent premature ventricular contractions (>10 times/h), VT = Sustained ventricular tachycardia, NSVT = Nonsustained ventricular tachycardia, ICD = Implantable cardioverter defibrillator, CRT-D = Cardiac resynchronization therapy defibrillator, PCI = Percutaneous coronary intervention

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Figure 3: Prevention of cardiac sudden death after revascularization of coronary heart disease. PCI = Percutaneous coronary intervention, CABG = Surgical coronary artery bypass surgery, LVEF = Left ventricular ejection fraction, SCA = Sudden cardiac arrest, SVT = Sustained ventricular tachycardia, NSVT = Nonsustained ventricular tachycardia, VF = Ventricular fibrillation, ICD = Implantable cardioverter defibrillator, WCD = Wearable cardioverter defibrillator, OMI = Old myocardial infarction, NYHA = New York Heart Association, CRT-D = Cardiac resynchronization therapy defibrillator

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Figure 4: Streamlining processes of sudden cardiac death prevention after revascularization of coronary heart disease. PCI = Percutaneous coronary intervention, CABG = Surgical coronary artery bypass surgery, LVEF = Left ventricular ejection fraction, SCD = Sudden coronary death

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The secondary prevention

  1. ICD should be implanted if SCA is caused by VF or VT and is not associated with myocardial ischemia, and no other correctable or reversible reasons can be found (recommendation of Class I, evidence of level A)[11],[13],[82]
  2. ICD should be implanted if sustained VT occurred and no reversible reasons that caused VT can be found (recommendation of Class I, evidence of level B)[11],[13],[82]
  3. Catheter ablation should be used to treat the endless attacking on VT or electrical storm that is not associated with myocardial scars (recommendation of Class I, evidence of level B)[13]
  4. For the patients who had implanted ICD, catheter ablation can be used to treat the repeated electric shocks that are caused by sustained VT (recommendation of Class I, evidence of level B)[13]
  5. For the patients who had ICD implanted, catheter ablation should be used after the first sustained VT (recommendation of Class IIa, evidence of level B).[13]


The primary prevention

  1. Left ventricular systolic function (LVEF) is measured by conventional echocardiography for all the patients with stable coronary heart disease to screen patients who have high-risk of SCD (recommendation of Class I, evidence of level C)[83]
  2. ICD should be implanted after at least 90-day postrevascularization if NYHA is Class II or III and LVEF is ≤35% (recommendation of Class I, evidence of level A)[11],[13],[61],[82]
  3. Combined with syncope, ICD should be implanted if it is clinically presumable that syncope is associated with electrophysiological examination that can induce sustained VT and VF and also obviously affect the hemodynamics (recommendation of Class I, evidence of level B)[11],[13],[82]
  4. ICD should be implanted for chronic myocardial infarction at least 90-day postrevascularization, NYHA is Class I and LVEF is ≤30% (recommendation of Class I, evidence of level A)[11],[82]
  5. ICD should be implanted for chronic myocardial infarction at least 90-day postrevascularization, LVEF is ≤40% and combined with NSVT, in addition to the electrophysiological examination that can induce sustained VT and VF (recommendation of Class I, evidence of level B)[11]
  6. For chronic myocardial infarction, if unexplained syncope occurs after revascularization and LVEF retains, electrophysiological examination can be performed to stimulate VF, and based on the results of stimulation one can determine whether ICD should be implanted or not (recommendation of Class IIa, evidence of level C)[13]
  7. It is recommended to implant ICD within 90-day postrevascularization if there are indications of implanting permanent pacemaker due to severe bradycardia and LVEF is ≤35%, in addition to it is predicted that it is hard to recover to a value >35% in the future (recommendation of Class IIa, evidence of level C)[74]
  8. For the patients who had implanted ICD, and within 90-day postrevascularization, ICD battery is required to be replaced due to depletion, it is recommended to replace ICD if clinical status is permitted after evaluating the patients and the risk and complications of replacing ICD (recommendation of Class IIa, evidence of level C)[74]
  9. The implantation of ICD should be considered during the period of waiting for a heart transplantation or a left ventricular assist device after revascularization (recommendation of Class IIa, evidence of level C)[13],[74]
  10. The implantation of ICD should be considered if syncope occurs after 90 days of revascularization, which is presumably related to severe ventricular arrhythmias (NSVT can be recorded based on the history of disease, clinical performance, and ECG, or electrophysiological examination can induce sustained VT) (recommendation of Class IIb, evidence of level C)[74]
  11. The implantation of ICD can be considered if unexplained syncope occurs after revascularization and the reason of syncope cannot be found by electrophysiological examination or noninvasive examination, but its association with severe arrhythmias cannot be excluded (recommendation of Class IIb, evidence of level C)[11]


Situations unsuitable for the implantation of implantable cardioverter defibrillator

The details are given as follows:[11]

  1. The expected survival time is <1 year (evidence of level C)
  2. Endless VT or VF (evidence of level C)
  3. Combined with severe mental illness, it obviously affects the surgical procedure of ICD implantation and the follow-up of ICD (evidence of level C)
  4. Late stage of severe heart failure (NYHA IV Class) when drug therapy is not effective, at the same time, heart transplantation or CRT-D implantation is not suitable (evidence of level C).


The application of cardiac resynchronization therapy in the prevention of sudden cardiac death

After revascularization, for the patients combined with heart failure, reduced LVEF, and wide QRS, CRT-D can be considered if the criteria for ICD implantation are also met. Cardiac resynchronization therapy can reverse left ventricular remodeling, improve left ventricular function, increase LVEF, and decrease the overall mortality.[84],[85] In the primary prevention of SCD, the risk of SCD could be decreased and the occurrence of severe arrhythmias that requires ICD treatment could be significantly reduced with the improvement of cardiac functions and the increase of LVEF.[86] The incidence of severe arrhythmias that required ICD treatment could be reduced to a minimum value when LVEF is recovered to ≥45%.[87] The long-term follow-up results of 7 years' of MADIT-CRT research confirmed that, compared with ICD, CRT-D can reduce the risk of all-cause death by 41% for the heart failure patients with widened QRS accompanying complete left bundle branch block.[88] Although cardiac resynchronization therapy pacing (CRT-P) can reduce the risk of SCD,[86],[87],[89] it was still possible for the occurrence of SCD and its risk did not reduce to zero even for the patients who were superresponders to cardiac resynchronization therapy (heart function improves significantly, LVEF recovered to >55%).[86] Therefore, from the point of view of SCD prevention, the patients were not suitable to replace CRT-D with CRT-P.[54],[90] As the primary prevention of SCD, the indications of the application of CRT-D were as follows:[13]

  1. Patients are included in NYHA III Class or ambulatory NYHA IV Class. After the optimal drug therapy for at least 3 months, LVEF is ≤35% and it is expected to survive with a certain quality of life for >1 year:


    1. Sinus rhythm, complete left bundle branch block (LBBB): width of QRS >150 ms (recommendation of Class I, evidence of level A) and width of QRS between 120 ms and 150 ms (recommendation of Class I, evidence of level B)
    2. Sinus rhythm, non-LBBB: the width of QRS >150 ms (recommendation of Class IIa, evidence of level B) and the width of QRS between 120 ms and 150 ms (recommendation of Class IIb, evidence of level B)


  2. Patients are with NYHA Class III or ambulatory NYHA Class IV. After the optimal drug therapy for at least 3 months, LVEF is ≤35%, permanent atrial fibrillation, width of QRS ≥120 ms, and it is expected to survive with a certain quality of life for >1 year. Hence, CRT therapy should be considered (recommendation of Class IIa, evidence of level B). To ensure that the proportion of biventricular pacing reaches 100% as much as possible, catheter ablation of atrioventricular node can be considered to improve the proportion of biventricular pacing (recommendation of Class IIa, evidence of level B)
  3. Patients are with NYHA Class II, as well as with sinus rhythm and LBBB, the width of QRS is ≥120 ms, after the optimal drug therapy for at least 3 months, LVEF is ≤30%. Then, it is expected to survive with a certain quality of life for >1 year (recommendation of Class I, evidence of level A)
  4. Patients with NYHA Class II as well as with sinus rhythm and non-LBBB, the width of QRS is ≥150 ms, after the optimal drug therapy for at least 3 months, LVEF is ≤35%. Then, it is expected to survive with a certain quality of life for >1 year (recommendation of Class IIb, evidence of level A)


Taskforce members (arranged in alphabetical order by authors' last name):

Jiyan Chen, Keping Chen, Lin Chen, Yundai Chen, Yansheng Ding, Wei Gao, JunBo Ge, Tao Guo, Yaling Han, Wei Hua, Congxin Huang, Dejia Huang, Lan Huang, Yong Huo, Jie Jiang, Guangping Li, Shumin Li, Bing Liu, Weiliang Liu, Jinghua Liu, Shubin Qiao, Chunguang Qiu, Farong Shen, Xi Su, Baopeng Tang, Yida Tang, Lin Tao, Jian'an Wang, Jingfeng Wang, Shulin Wu, Xiaolin Xue, Lixia Yang, Xinchun Yang, Bo Yu, Zuyi Yuan, Shu Zhang, Yinxin Zhao, Jing Zhou, Shenghua Zhou, Yujie Zhou, Jiangang Zou.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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