(1)
Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, NC, USA
Synopsis
Sudden cardiac death (SCD), also labeled as primary cardiac arrest (PCA) is generally defined as sudden death occurring within 1 h after the onset of symptoms when no other cause of death is evident. SCD is often the first manifestation of coronary heart disease (CHD). From various arrhythmias ventricular tachycardia and ventricular fibrillation play an important role as mechanisms of SCD. QT prolongation is thought to be a marker of increased risk of SCD.
In a case-control study among patients who experienced SCD (including about 45 % women) treated for hypertension but free from recognized heart disease, the risk for SCD was increased after adjustment for other risk factors for three continuous variables: and index for QT prolongation (QTI), an index for cardiac injury containing a variety of ventricular excitation and repolarization variables and an ECG index for left ventricular hypertrophy containing the Cornell voltage and body weight. These variables were stronger predictors when used as continuous variables as the same variables used as dichotomized variables.
In another case-control study (32 % women) among diabetic patients excluding prior physician-diagnosed heart disease the risk for PCA was increased 3.5-fold in the fourth versus first QTI quartile, corresponding rate-adjusted QT prolongation 7 % above the QTI in reference normal men and women.
In the large Rotterdam Heart Study in 4,878 women and 3,105 men 55 years old and older, the multivariable-adjusted for risk for SCD was increased 2.5-fold. Stratified by sex and adjusted for age, the SCD risk was increased 2.5-fold in women and 2.6-fold in men.
In the Atherosclerosis Research in Communities (ARIC) Study in 7,684 middle-aged women and 5,937 men free from CVD at baseline, the strongest predictor of SCD in women and men was Ѳ(Tp|Tref) with 2.59-fold increased risk of SCD in women and 2.22-fold increased risk in men. Ѳ(Tp|Tref) is a measure of deviant spatial direction of the regional repolarization sequence in the lateral wall of the left ventricle. TaVR amplitude was a significant predictor of SCD in women (2.59-fold increased risk) and in men (2.2-fold increased risk). The rate-adjusted QTe was a significant predictor in men only (1.94-fold increased risk). Overall, increased TaVR amplitude was the most uniform predictor of CHD death and SCD in men and in women. The presence of a positive, flat or less negative than −100 μV (−1 mm) TaVR amplitude in men and women with CVD calls for additional diagnostic evaluation and possibly stronger therapeutic measures for prevention of CHD death and SCD.
Abbreviations and Acronyms
ARIC
Arteriosclerosis research in communities
CHD
Coronary heart disease
DBP
Diastolic blood pressure
HR
Hazard ratio
PAR
Population attributable risk
PCA
Primary cardiac arrest
QTcBz
QTe adjusted by Bazett’s formula
QTe
QTend interval
QTea
Rate-adjusted QTe
QTI
QT prolongation index
QTp
QTpeak interval
QTpa
Rate-adjusted QTp
SBP
Systolic blood pressure
SCD
Sudden cardiac death
VF
Ventricular fibrillation
VT
Ventricular tachycardia
WHI
Women’s health initiative
Ѳ(Tinit|Tterm)
Spatial angle between the initial and terminal T vectors
Ѳ(Tp|Tref)
Spatial angle between Tp vector and the mean Tp vector in normal reference group (Tref)
6.1 Introduction
SCD is generally defined as sudden death occurring within 1 h after the onset of symptoms when no other cause of death is evident. From various arrhythmias ventricular tachycardia and ventricular fibrillation (VF) play an important role as mechanisms of sudden cardiac death (SCD). Ventricular ectopic (VE) activity is generally prognostically less important than other ventricular arrhythmias although frequent VEs have in some reports been found to predict adverse events such as incident stroke [1]. Ventricular arrhythmias include frequent VEs ventricular tachycardias (VT, runs of three or more VEs) and ventricular fibrillation (VF). Only VT and VF will be considered here in the context of sudden cardiac death (SCD). Epidemiological aspects of VE were covered in reference [2].
6.2 Sudden Cardiac Death: Prevalence and Risk Factors
A variety of factors have been related to the risk of SCD, including even less obvious factors such as diet. For the latter factor the association with SCD was evaluated in a prospective study in 93,122 postmenopausal women from the Women’s Health Initiative (WHI) study [3]. The average follow-up was 10.5 years. A score was assigned according to how closely the reported diet resembled the Mediterranean diet. A higher Mediterranean diet score was associated with lower risk of SCD (HR: 0.64; 95 % CI: 0.43–0.94) after adjustment for age, total energy, race, income, smoking, and physical activity.
Another prospective study in 161,808 women from the WHI clinical trials and observational studies estimated the annual incidence rate of SCD and identified risk factors for SCD [4]. The participants were enrolled between 1993 and 1998, and followed until August 2009. Incident SCD was defined as death occurring within 1 h of symptom onset or within 1 h after the participant was last seen without symptoms and death that occurred in the absence of a potentially lethal non-coronary disease process. Adjudicated SCD occurred in 418 women. Of interest was the fact that nearly one-half of women who experienced sudden cardiac death had no previous diagnosis of coronary heart disease. The incidence rate of SCD was 2.4/10,000 women/year (95 % confidence interval: 2.2–2.7). The study identified 11 independent risk factors for SCD including 6 traditional risk factors for CHD (older age, tobacco use, diabetes, history of myocardial infarction, previous CHD, and hypertension). Besides these risk factors for CHD, the additional risk factors for sudden cardiac death in postmenopausal women included African-American race, higher pulse, higher waist-to-hip ratio, elevated white blood cell count, and heart failure. Overall, population-attributable fractions were greatest for hypertension, waist-to-hip ratio, and myocardial infarction. Population attributable risk (PAR) was defined as:
![$$ \mathrm{P}\mathrm{A}\mathrm{R}=\left[\mathrm{Prev}\times \left(\mathrm{R}\mathrm{R}-1\right)/\mathrm{Prev}\times \left(\mathrm{R}\mathrm{R}-1\right)+1\right], $$](/wp-content/uploads/2016/10/A333161_1_En_6_Chapter_Equa.gif)
where Prev is the prevalence of the exposure, and relative risk RR is the relative risk taken as the hazard [5].
Ventricular fibrillation (VF) is considered as the main mechanism of sudden cardiac arrhythmic death, and QT prolongation is thought to be a marker of increased risk for this fatal outcome. The mechanism of primary cardiac arrest is generally VF which in a strict sense is not a cardiac arrest. However, a person even immediately after the onset of ventricular fibrillation is found pulseless because in VF the left ventricular filling time is so short that no pulse is felt. This is why the condition is called cardiac arrest.
6.3 ECG Predictors of Sudden Cardiac Death
Some studies have focused specifically on ECG predictors of arrhythmic SCD often labeled as primary cardiac arrest (PCA). Table 6.1 is a summary table of selected studies on ECG predictors of arrhythmic SCD. The source data for the first two of the studies in the table come from a large prepaid health plan, Group Health Cooperative of Puget Sound in Seattle and surrounding King County, Washington.
Table 6.1
A summary table for selected reports on ECG predictors of SCD
Study | Predictor variables/test group criteria | Hazard ratio (95 % CI) | Adjustment |
|---|---|---|---|
Siscovick et al. [6] | aQTI | 1.8 (1.3–2.7) | dClinical factors |
Group Health Cooperative of Puget Sound, WA | bCIIS | 1.7 (1.2–2.5) | |
Treated hypertensive patients, free from recognized heart disease | cLVMI | 1.4 (1.0–2.0) | |
Case-control study; cases (n = 131), controls (n = 562) | (Quintile 5 vs. quintile 1 for each criterion) | ||
Women 46 % of controls, 44 % of cases | |||
Whitsel et al. [11] | cQTI | Primary cardiac arrest risk increased 3.5-fold | eSampling design, age, and race |
Group Health Cooperative of Puget Sound, WA | |||
Enrollees with physician-diagnosed diabetes or treated with oral hypoglycemics or insulin. Enrollees with prior physician-diagnosed heart disease were excluded. Cases (n = 79), controls (n = 214). Women 32 % of cases and controls | Definite QT prolongation (QTI >107 %) vs. mean normal QTI (100 %) | ||
Rotterdam Heart Study. Straus et al. [12]. Women (n = 4,878) and men (n = 3,105), 55 years old and older; 125 SCD events during an average follow-up 6.7 years | QTcBz women and men | 2.5 (1.3–4.7) | Demographic/clinical factors |
QTcBz women | 2.5 (1.0–7.1) | Age | |
QTcBz men | 2.6 (1.1–5.8) | Age | |
Baseline prevalence: hypertension 33.6 %, diabetes 10.5 %, ECG-MI 6.3 %, HF3.2 %, | Women QTcBz >470 ms vs. < 450 ms | ||
Definite prolonged QTcBz: 8.5 % | Men QTcBz >450 ms vs. <430 ms | ||
ARIC Study, Rautaharju et al. [13] | fѲ(Tp|Tref) women | 2.59 (1.39–4.82) | Single ECG variable risk models multivariable-adjusted for demographic/clinical factors; |
CVD-free subgroup of 5,937 men and 7,684 women, 45–65 years old, predominantly white (70 %), approximately 30 % hypertensives, 10 % diabetics. Average follow-up 14 years | fѲ(Tp|Tref) men | 2.22 (1.43–3.43) | HR evaluated for quintile 5 for each predictor variable as the test group, with quintiles 1–4 as the reference groupi |
gѲ(Tinit|Tterm) women | 1.47 (0.79–2.72) | ||
gѲ(Tinit|Tterm) men | 1.68 (1.07–2.62) | ||
TaVR women | 1.79 (0.97–3.29) | ||
TaVR men | 1.64 (1.04–2.58)
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