I. The concept and current situation of sudden cardiac death (SCD)
Sudden cardiac death (SCD) is a natural death due to cardiac causes, in which sudden loss of consciousness occurs within one hour after the onset of acute symptoms, causing unexpected death. Patients may or may not have had cardiac manifestations during their lifetime. In the United States, 300,000 to 400,000 people die of sudden cardiac death each year, and in China, the results of the National Public Relations Project “Sudden Cardiac Death in China” show that 544,000 patients die of sudden cardiac death each year, and nearly 1,480 patients die of SCD every day, in other words, one person dies of SCD every minute. The survival rate of sudden cardiac death outside the hospital is less than 15%, and even if the patient can be admitted to the hospital in time, the survival rate at discharge is less than 20%. Sudden cardiac death of which 88% is arrhythmogenic sudden death, the most important cause of SCD is acute coronary syndrome, and about 30% is the first symptom. Wei Feng, Department of Cardiology, Bengbu First People’s Hospital
II. Risk predictors of sudden cardiac death
1. left ventricular ejection fraction (LVEF)
Most studies have confirmed that LVEF is an independent risk predictor of SCD, and the lower the LVEF, the greater the risk of sudden death, and the EF value=0.40 is usually taken as the threshold value of risk score. The incidence of sudden death in patients with LVEF <30% was more than 6 times that of patients with normal heart function. Ischemic cardiomyopathy with significant heart enlargement and reduced LVEF has a higher mortality rate.
2, cardiac insufficiency
The annual mortality rate is 6% in patients with NYHA class II and 20% in NYHA class III, 30% of which are sudden cardiac deaths. SCD is the main cause of death in patients with cardiac insufficiency. Patients with heart failure who have experienced syncope are independent risk predictors. The 1-year incidence of sudden death in heart failure patients with a history of syncope is 45%, while the 1-year incidence of sudden death in those without a history of syncope is 12%.
3, QT interval, QT dispersion (QTd)
QT interval is the process of ventricular depolarization and repolarization, normal value is 320-440ms, but it varies with heart rate, usually with corrected QT interval (QTc interval = QT/RR1/2), sudden cardiac death is associated with QT interval, >450ms in men and >470ms in women, and is an independent predictor of sudden cardiac death. prolonged QT interval is prone to ventricular tachycardia/ventricular fibrillation episodes.
QT dispersion (QTd) represents the instability and inhomogeneity of ventricular myocardial repolarization, and an increase in QTd predisposes to various ventricular arrhythmias.
QTd (ms) = longest QT interval – shortest QT interval
QTcd (ms) = longest QTc interval – shortest QTc interval
4. Impaired cardiac autonomic function
(Ventricular fibrillation threshold is significantly lower)
Heart rate variability (HRV): the change in heart rate fast or slow over time.
Time-domain indicators: SDNN: overall standard deviation of normal sinus RR intervals, SDNN <100ms, mildly impaired HRV, SDNN <50ms significantly impaired HRV.
Sinus rhythm oscillation (HRT): Abnormal parameters indicate abnormal autonomic regulation. It is the phenomenon of short-term fluctuations in sinus heart rate after the onset of ventricular prematureness. It is accelerated and then decelerated. HRT can be used as an independent predictor of SCD.
5. Positive ventricular late potentials can be used as an independent predictor of SCD.
III. Predictive value of ECG for sudden death in high-risk coronary heart disease
(i) 1. Common arrhythmias of sudden cardiac death.
a. Polymorphic ventricular tachycardia: it can cause ventricular fibrillation, syncope, sudden death, and the electrocardiogram shows continuous changes in QRS wave pattern, irregular rhythm, frequency >200 beats/min, lasting for more than 10 cardiac cycles during the attack.
b, tip-twisting ventricular tachycardia: can be caused by QT interval prolongation. QRS wave polarity, amplitude line progressive changes, twisting around the isotonic line, frequency in 200-250bpm can be terminated or progress to ventricular fibrillation.
c, bidirectional ventricular tachycardia: can metamorphose into polymorphic ventricular tachycardia or even ventricular fibrillation and sudden death.
d, ventricular fibrillation: ventricular fibrillation and ventricular tachycardia, ventricular premature homologation, can be transformed into each other.
e sympathetic electrical storm (ventricular electrical storm, electrical storm, catecholamine storm).
It is a clinical syndrome of spontaneous ventricular tachycardia/ventricular fibrillation ≥2 times within 24 hours that requires urgent treatment. The mechanism of occurrence is sympathetic hyperactivation, Na+ and Ca2+ inward flow and K+ outward flow, leading to malignant arrhythmias (VT/VF)
Clinical features: sudden onset, rapid deterioration, recurrent syncope, need for repeated electrical defibrillation, and drugs that are usually effective in treatment such as amiodarone become ineffective or have poor efficacy. It is often accompanied by elevated blood pressure and increased respiration.
ECG features: sympathetic electrical storm often preceded by sinus tachycardia, ventricular premature is the aura, clustered ventricular tachycardia/ventricular fibrillation follows, ventricular premature can be monomorphic, polymorphic, multi-source, the association interval is mostly short, VT is mostly polymorphic, torsional, ventricular rate is usually in the range of 250-350 bpm, very easy to deteriorate into ventricular fibrillation.
f, slow arrhythmia: Ⅲ degree AV block especially when the junctional escape frequency is very slow, or ventricular escape rhythm, may cause SCD, simple Ⅰ degree, Ⅱ degree AV block usually does not cause SCD. but if Ⅱ degree AV block occurs on the basis of very slow sinus rhythm, SCD may occur.
(ii) ECG prediction of sudden death in patients with acute coronary syndrome
1. ECG manifestations of left main stem lesions.
① ECG of acute left main stem occlusion
◆ Extensive anterior wall lead ST-segment elevation combined with positive posterior wall myocardial infarction: Ⅰ, aVL, ST-segment elevation in leads V1-V6; ST-segment elevation in leads V7-V9; ST-segment elevation in lead aVR>0.05mV; STⅡ↑>STⅢ↑ when combined with ST-segment elevation in inferior wall leads
Extensive ST-segment elevation in anterior wall leads combined with atrial infarction: PTa-segment elevation
Extensive ST-segment downshift in the anterior wall leads
②Electrocardiogram of myocardial ischemia caused by severe left main stem lesions
◆ Ⅰ, aVL lead ST segment downshift, V4 ~ V6 lead ST segment downshift (≥ 2mm), Ⅱ, Ⅲ, aVF lead ST segment downshift (Ⅱ lead downshift is the most obvious), aVR lead ST segment elevation > V1 lead ST elevation, i.e., manifestation of 8+2 phenomenon
2, giant R waveform ST-segment elevation
QRS wave and ST-T fusion together, ST segment is spike-like or downward sloping elevation, J point disappears, R wave descending branch and ST-T fusion into a diagonal line down, resulting in QRS wave, ST segment and T wave form a single triangle, a peak-tip side straight bottom wide wave, it is difficult to identify the junction of the wave segments, similar to The “giant R waveform”.
The giant R waveform is often found in the leads with the most significant ST-segment elevation.
When regular giant R waveforms with ST-segment elevation appear consecutively, especially when the heart rate is fast, the P wave is not easily identified by fusion in the preceding T wave, and is easily misdiagnosed as ventricular tachycardia or supraventricular tachycardia with differential transmission or bundle branch block, and needs to be differentiated.
3.Tombstone-shaped ST-segment elevation
The raised ST segment has a peak higher than the R wave, the R wave is short, and the time limit is usually less than 0.04s. The raised ST segment is fused with the ascending T wave after it, and it is difficult to identify the separate T wave, and the T wave is often not inverted. Tombstone-shaped ST-segment elevation is a manifestation of severe myocardial injury in the early or hyperacute phase of acute infarction. Clinical observation shows that tombstone-shaped ST-segment elevation in acute infarction is associated with transmural infarction, pump failure, severe arrhythmia, complete atrioventricular block/bundle branch block, and infarct extension within 1 week of admission, and significantly increased mortality.
Coronary angiography revealed complete occlusion of the anterior descending branch of acute myocardial infarction with tombstone-shaped ST-segment elevation and no collateral circulation, and a high incidence of three-branch coronary occlusion.
4. Ischemic J wave
J wave is a small semicircular wave immediately following the QRS wave group, which was described in more detail by Osborn in 1953 in experiments on dogs, also known as Osborn wave. When a severe acute myocardial ischemic event occurs due to an obstructive lesion or functional spasm in the coronary artery, the ECG may show a new J wave or a pre-existing J wave with increased amplitude or prolonged duration, called an ischemic J wave. Ischemic J wave is an electrocardiographic change in the hyperacute phase of severe myocardial ischemia. Ischemic J waves are a hallmark manifestation of electrode instability, with greater myocardial repolarization dispersion, and are prone to malignant arrhythmias. Ischemic J waves are an early warning indicator of high risk of sudden death. Ischemic J wave with ST-segment elevation is an early warning indicator of higher risk of sudden death.
5.T wave alternans (TWA)
T-wave alternans (TWA) refers to the wave-by-wave alternation of T-wave amplitude and morphology on the ECG during regular heart rhythm. TWA indicates severe repolarization instability and inconsistency in the myocardium. Recent studies have confirmed that TWA is a highly sensitive predictor of sudden cardiac death and critical arrhythmias. The coexistence of ischemic J-wave, ST-segment elevation and T-wave alternans is the strongest warning indicator of ventricular fibrillation and sudden death.