(Circulation. 1995;91:1749-1756.)
© 1995 American Heart Association, Inc.
Articles |
Risk Factors for Sudden Cardiac Death in Middle-Aged British Men
From the University Department of Public Health, Royal Free Hospital School of Medicine (G.W., A.G.S., M.W.), London, England, and the Department of Medical Cardiology, Royal Infirmary (P.W.M.), Glasgow, Scotland.
Correspondence to Dr Goya Wannamethee, University Dept of Public Health, Royal Free Hospital School of Medicine, Rowland Hill St, London NW3 2PF, England.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Risk factors specific to sudden cardiac death (SCD), ie, death within 1 hour after onset of symptoms, have been poorly identified, although recent findings from the present study incriminate heavy drinking and elevated heart rate. This paper examines the relations between a wide range of established and potential risk factors for ischemic heart disease (IHD) and SCD to identify independent risk factors for SCD and factors that might particularly or specifically relate to SCD.
Methods and Results We present a prospective study of a
cohort that was drawn from general practices in 24 British towns of
7735 middle-aged men who were followed up for 8 years. During 8 years
of follow-up, the men experienced 488 major IHD events (nonfatal and
fatal), of which 117 (24%) were classified as SCD. Age, preexisting
IHD, arrhythmia, systolic blood pressure, blood cholesterol, elevated
heart rate (
90 beats per minute), physical activity (all,
P<.05), and, to a lesser extent, smoking
(P=.06), HDL cholesterol (P<.07), and elevated
hematocrit (46%, P<.09) emerged as independent risk
factors for SCD after adjustment for a wide range of factors. Diabetes
was not found to be associated with SCD, and forced expiratory volume
in 1 second, body mass index, white blood cell count, and
antihypertensive drugs were not associated with risk of SCD after
adjustment. When examined in relation to non–sudden IHD deaths and
nonfatal myocardial infarction, elevated heart rate, heavy drinking,
and arrhythmia emerged as factors that appear to be specific or
particular to SCD. These three factors and age and blood cholesterol
were associated with an increased risk of SCD in men both with and
without preexisting IHD. Physical activity, systolic blood pressure,
and current smoking were associated with SCD only in men without
preexisting IHD. HDL cholesterol and hematocrit were strong predictors
of SCD only in men with preexisting IHD.
Conclusions Three risk factors appear to be specific or particular to the risk of SCD, and these and other risk factors operate differently in patients with versus those without preexisting IHD. These findings have implications for the causes and prevention of SCD.
Key Words: death, sudden • risk factors • ischemia • coronary disease
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Sudden cardiac death (SCD), ie, death within 1 hour after onset of symptoms, constitutes about a quarter of all ischemic heart disease (IHD) events and about half of all major IHD deaths. Ventricular arrhythmia is believed to be the most common direct cause, and epidemiological studies have shown that the conventional risk factors for IHD are also predictive of SCD.1 2 3 4 5 6 7 8 9 10 However, those factors that predispose specifically to SCD are poorly identified.2 5 10 11 A review12 has concluded that there is no way of identifying those at particular risk of SCD and that the only viable approach to the problem is the use of preventive measures designed to diminish the risk of coronary atherosclerosis. We recently reported that both heavy drinking (>42 UK units/wk, where 1 UK unit is equal to 8 g alcohol) and increased heart rate (
90 beats
per minute [bpm]) in a cohort of middle-aged men (The British
Regional Heart Study [BRHS]) appear to influence SCD in a manner
that
is independent of the major risk factors for
IHD.13 14 The
present article examines a wider range of established and potential
risk factors for IHD in relation to sudden and non–sudden cardiac
events (both fatal and nonfatal) to identify independent risk factors
for SCD and to determine which risk factors might specifically or
particularly determine SCD. We are also concerned with whether the
independent risk factors for SCD operate differently in men with or
without underlying IHD. |
Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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The BRHS is a prospective study of cardiovascular disease involving 7735 men, aged 40 to 59 years old at enrollment, selected from the age-gender registers of one-group general practice in each of 24 towns in England, Wales, and Scotland between January 1978 and June 1980. The criteria for selecting the town, the general practice, the subjects, and the methods of data collection have been reported.15 Research nurses administered to each man a standard questionnaire that included questions on smoking habits, alcohol intake, and medical history. Several physical measurements were made, and nonfasting blood samples were taken for measurement of biochemical and hemotologic variables. Details of the measurement of serum lipid concentrations have been reported.16 Hematocrit was estimated with a Coulter S electronic particle counter calibrated daily with Coulter $C.17 The London School of Hygiene sphygmomanometer was used to measure blood pressure twice in succession, with the subjects seated and the arm supported on a cushion. The mean of the two readings was used in the analysis, and all blood pressure readings were adjusted for observer variation within each town.18 Classification methods for smoking status, alcohol consumption, and social class have been reported.13 15 Heavy drinking was defined as regularly drinking more than six drinks daily (>42 UK units/wk). The men were asked to indicate their usual pattern of physical activity, and a score was derived for each man on the basis of frequency and type of leisure activity.19 The men were initially grouped into six broad categories based on activity level: inactive (686) and occasional (2345), light (1761), moderate (1205), moderately vigorous (1120), and vigorous (513) activity. In this paper, the inactive and occasional activity groups have been combined and the moderately vigorous and vigorous groups have been combined. Forced expiratory volume in 1 second (FEV1) was measured with a Vitalograph spirometer with the subject seated. FEV1 measurements were height-standardized to 1.73 m, the average height of the men in the present study.20 Parental history of death from heart trouble is defined as men who reported that a parent had died from heart trouble.21
Preexisting Disease
The men were asked to recall a
doctor's diagnosis of angina or
myocardial infarction, diabetes, and a number of other disorders listed
on the questionnaire. They were also asked for details concerning
administration of any regular medical treatment, including
antihypertensive drugs. The World Health Organization (WHO) (Rose)
chest-pain questionnaire was administered to all men at the initial
examination,22 and a three-lead orthogonal ECG was
recorded at rest. The men were separated into four groups, according to
the evidence of IHD present at screening: group I, men who reported
no evidence of IHD on the WHO chest pain questionnaire or ECG and had
no recall of a doctor's diagnosis of IHD (n=5792, 74.9%); group
II,
men who reported angina or possible myocardial infarction on WHO chest
pain questionnaire or recalled a doctor's diagnosis of angina but who
had no ECG evidence of myocardial ischemia or infarction
("symptomatic IHD": n=696, 9.0%); group III, men with ECG
evidence of possible or definite myocardial ischemia or possible
myocardial infarction (n=819, 10.6%); group IV, men with a previous
definite myocardial infarction on ECG or who recalled a doctor's
diagnosis of a heart attack (n=428, 5.5%). In the analyses, men in
groups II through IV had preexisting evidence of IHD.
Heart Rate
Heart rate was determined at screening from the
three-lead
orthogonal ECG. On the basis of the 8-second recording, the average RR
interval was calculated (in seconds) during that period as follows:
heart rate was equal to 60 divided by the average RR interval. Elevated
heart rate was defined as 90 bpm.14 No information is
available on measurement error for the method used or on
intraindividual variation.
Presence of Arrhythmia
A complex diagnostic tree that was
part of a larger set of
criteria used in interpreting the ECG as a whole was used in the
interpretation.23 All ECGs were reviewed by an experienced
electrocardiographer, and any errors detected in the computer-based
rhythm interpretation were corrected before results were entered into
the database. A normal rhythm was defined as sinus rhythm, coronary
sinus rhythm, or sinus arrhythmia. All other statements of rhythm were
treated as an arrhythmia, eg, sinus rhythm with ventricular
extrasystoles. As expected, 97.8% of the men in the study were in
sinus rhythm. Only 0.7% (n=54) were in atrial fibrillation, which was
a lower rate than expected in a general population of this
kind.24 At least one ventricular extrasystole was
present in the 8-second recording in 212 men (2.7%), and 113 men
(1.5%) had supraventricular-atrial extrasystoles. Other significant
abnormalities occurred with negligible frequency, eg, two men were in
complete heart block.
Follow-up
All men were followed up for all-cause mortality
and for
cardiovascular morbidity.25 Information on death was
collected through the established "tagging" procedures provided
by the National Health Service registers. Mortality and major IHD
events (fatal IHD and nonfatal myocardial infarction) are based on 8
years of follow-up for each man; follow-up was achieved in 99% of the
cohort. Fatal events were defined as death from IHD (ICD ninth revision
codes 410 to 414) as the underlying cause. These events comprised any
IHD death during the 8-year follow-up, irrespective of a previous
nonfatal event during that period. The certifying doctor was asked to
complete an inquiry form that asked the duration from onset of symptoms
to death: <1 hour, 1 to 24 hours, or >24 hours. SCD was defined as an
event in which death occurred within 1 hour after the onset of
symptoms. Only those men for whom clear information was available
regarding death within 1 hour were included as sudden death. Men found
dead in bed were not classified as having experienced SCD. No episodes
of cardiopulmonary resuscitation that converted sudden to non–sudden
death were reported. A major nonfatal IHD event, ie, myocardial
infarction, was diagnosed according to WHO criteria,26
which included any report of myocardial infarction accompanied by at
least two of the following criteria: (1) a history of severe prolonged
chest pain, (2) ECG evidence of myocardial infarction, or (3) cardiac
enzyme changes associated with myocardial infarction.
Statistical Methods
The Cox proportional hazards model was
used to assess the
independent contributions of risk factors to the risk of SCDs and to
obtain the relative risks adjusted for age and the other risk
factors.27 For the categorical and binary (yes/no)
variables, eg, current smoking and heavy drinking, the results obtained
from the multiple-regression model are presented as relative risks.
For the quantitative (continuous) variables, such as systolic blood
pressure, the relative risks are presented to estimate the relative
risk of death from SCD associated with a given change in the risk
factor, which was 
1 SD (Table 4
). Adjusted relative
risks in the Figure were obtained by fitting serum total
cholesterol, systolic blood pressure, and HDL cholesterol (HDL-C) as
four dummy variables for the five quintiles of each risk factor. Tests
for trend were performed by fitting the quantitative variables in their
continuous form. The distribution of white blood cell count was skewed,
and log transformation was used. In the adjustment, age, body mass
index, and biological variables, with the exception of heart rate and
hematocrit, were fitted continuously. Because of the nonlinear
relations between heart rate and SCD,14 and between
hematocrit and major IHD events,17 heart rate was fitted
as five categorical groups (<60, 60 to 69, 70 to 79, 80 to 89, and
90 bpm) and hematocrit as a dichotomous variable (46% versus
rest), since our earlier reports have shown a threshold
effect.17 In the adjustment, physical activity was fitted
as three dummy variables for the four groups and smoking status as four
dummy variables for the five levels of smoking categories (never
smoked, exsmoker, 1 to 19 cigarettes per day, 20 cigarettes per day,
21 cigarettes per day). In some of the analyses, smoking is fitted as
0,1 variables; ie, current smokers versus nonsmokers. Subjects with
missing values for covariates in the various adjustments by Cox's
model were excluded from that particular analysis. Thus, the number
of men and cases available for analyses varied according to the models
used (Table 5). All the variables listed in the
adjustments in the multivariate analysis (see "Multivariate
Analysis") were included in the model and the biological factors;
eg, heart rate, HDL-C, hematocrit, white blood cell count, and FEV1
were entered one at a time.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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During the 8-year follow-up period, 488 major IHD events occurred. These events included 217 deaths, of which 117 (53.9%) were classified as SCDs, and 271 nonfatal IHD events, ie, myocardial infarctions. The incidence of IHD deaths and SCDs increased significantly with increases in age (P<.0001) (Table 1
).
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Coronary Risk Factors
The unadjusted rates per 1000 per year
and the age-adjusted
relative risk for SCD in relation to preexisting disease, personal
characteristics, and biological factors shown to be associated with
risk of major IHD
events17 19 20 21 28 29 30 31 32 33
are presented
in Tables 2 and 3.
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Preexisting Disease
Evidence of a definite heart attack
(group IV), evidence of IHD on
ECG (group III), presence of arrhythmia, and antihypertensive treatment
were all strongly associated with an increased risk of SCD, even after
adjustment for age. Symptomatic IHD (group II) and diabetes were not
associated with a significant increase in risk of SCD.
Personal Characteristics
Current smoking, higher body mass
index (28
kg/m2), a low level of physical activity, and heavy
drinking were significantly associated with an increased risk of SCD
(P<.01). Exsmokers showed slightly higher risk of SCD than
those who had never smoked. Neither parental history of death from
heart trouble or social class was significantly associated with SCD
after adjustment for age.
Biological Factors
The biological factors shown to be
independently associated with
increased risk of major IHD events in this cohort, systolic blood
pressure, blood cholesterol, HDL-C, FEV1, white blood cell count,
elevated hematocrit (46%), and elevated blood glucose (6.1 mmol/L),
all were significantly associated with risk of SCD after adjustment for
age, with the exception of nonfasting blood glucose.
Multivariate Analysis
Many of the factors presented in Tables
2
and 3 are
interrelated. HDL-C, heart rate, white blood cell count, and hematocrit
are all associated to various degrees with preexisting IHD, personal
characteristics, and biological factors, eg, systolic blood pressure
and blood cholesterol, and they may serve as intermediate mechanisms
between these variables and SCD. We have therefore examined the
relation between SCD and all the factors that were significantly
associated with SCD, after adjusting for age, preexisting IHD,
arrhythmia, antihypertensive treatment, personal characteristics,
systolic blood pressure, and blood cholesterol.
Presence of IHD (group III and IV), arrhythmia, current smoking, physical activity, blood cholesterol, systolic blood pressure, heart rate, hematocrit, and white blood cell count remained significantly associated with the risk of SCD, even after adjustments were made (all P<.05). However, the increased risk seen with heavy drinking was reduced and was of marginal significance (relative risk [RR]=1.61; P=.06) after adjustments were made. The risk associated with antihypertensive treatment was substantially reduced and was no longer significant (RR=1.27; 95% CI, 0.77 to 2.11) after these adjustments. No significant association was seen with body mass index and FEV1 after adjustment.
Additional Adjustment for HDL-C,
Heart Rate, and
Hematocrit
Hematocrit and white blood cell count are strongly
correlated
(r=.26), and since the association between white blood cell
count and SCD diminished after adjusting further for heart rate and
HDL-C, white blood cell count was omitted from the adjustment. We have
therefore adjusted HDL-C, heart rate, and hematocrit to assess the
independence of and to determine the role of these factors as possible
intermediate mechanisms. Data were available on all covariates for 6914
men (106 SCDs). The adjusted relative risks for preexisting disease and
personal characteristics and for a given change in the biological
factors are presented in Table 4. Only factors that were
significant or marginally significant are presented. To illustrate
the association of the quantitative risk factors with SCD, we have also
presented the adjusted relative risks by levels of each factor
(Figure).
The additional adjustments made no major
differences to the
associations with age, arrhythmia, preexisting IHD, and physical
activity with SCD. Presence of IHD without myocardial infarction (group
III) and arrhythmia were associated with a greater than twofold
increase in risk, and this association increased to greater than
fivefold in those with definite myocardial infarction (group IV). There
was a progressive decline in risk of SCD as the level of physical
activity increased (RR=1.00, 0.86, 0.67, and 0.54 for the four groups
of men classified according to level of physical activity,
respectively) (see "Methods"; test for trend, P<.05).
The risk in heavy drinkers was increased because of the strong
association between heavy drinking and HDL-C. Because HDL-C, heart
rate, and hematocrit are all strongly associated with smoking,
adjustment for these factors reduced the increased risk seen in current
smokers from 1.70 to 1.46, and the increased risk was now of marginal
significance (P=.06), indicating that part of the increased
risk of SCD attributable to smoking is mediated by these factors. The
increased risk observed with elevated hematocrit was slightly reduced,
from 1.48 to 1.40, and was of marginal significance (P=.09).
Elevated heart rate was associated with a greater than threefold
increase in risk of SCD. Men in the top quintile of the cholesterol
distribution compared with the lowest quintile showed a 2.5-fold
increase in risk (Figure). Men in the top quintile of systolic
blood
pressure showed the highest risk; risk was slightly but not
significantly raised in those in the lowest quintile compared with the
second quintile. Men in the top quintile of HDL-C showed a 40%
reduction in risk.
Specificity of Risk
The factors
shown to be independently predictive of SCD (Table 4)
were also examined in relation to nonfatal myocardial infarction and
non–sudden IHD death, after adjusting for each of the other variables
to assess whether any factors were specifically or particularly
associated with SCD (Table 4). Arrhythmia was not shown to be
associated with nonfatal events and was only weakly and
nonsignificantly associated with non–sudden IHD death but was strongly
associated with SCD. Elevated heart rate was not shown to be associated
with nonfatal myocardial infarction. An elevated heart rate was
associated with a marginally significant increase in risk of
non–sudden IHD death (P=.08) and a strongly significant
increase in risk of SCD. Heavy drinking posed a lower risk of nonfatal
myocardial infarction (RR=0.77) and of non–sudden IHD deaths
(RR=0.4)
but was associated with a significantly increased risk of SCD. These
findings suggest that heavy drinking and arrhythmia are risk factors
specific to SCD and that an elevated heart rate is more particularly
associated with SCD than with non–sudden death or nonfatal IHD
events.
Effect of Preexisting IHD
The independent
risk factors for SCD were examined separately in
men with IHD (groups II through IV combined) and without IHD (group I)
adjusted for each of the other factors (Table 5). Because of
the
relatively small number of SCD cases when those with and without IHD
are analyzed separately, we are primarily concerned with whether the
associations differ between the two groups rather than with evaluation
of the statistical significance of the relations, although these are
presented (Table 5).
Age, arrhythmia, increased heart rate, heavy drinking, and hypercholesterolemia were positively associated with an increased risk of SCD in both groups, although the magnitude of the relative risk for arrhythmia, heavy drinking, and especially heart rate was greater in those without preexisting IHD. However, the absolute risk of SCD is much higher in men with preexisting IHD overall (1.0 in 1000 versus 4.8 in 1000 per year); thus, the lower estimated relative risks may still represent substantial excess risk. Physical inactivity and current smoking were independently associated with an increased risk of SCD only in men without preexisting IHD. Systolic blood pressure showed a significant positive association with risk of SCD in men without preexisting IHD. In men with preexisting IHD, a J-shaped relation was seen between systolic blood pressure and risk of SCD, with the highest risk seen in those in the lowest quintile and the lowest risk in those in the second quintile, with risk increasing thereafter so that a test for overall linear trend was nonsignificant. This phenomenon will be presented and discussed in a separate publication. Elevated hematocrit and low HDL-C were associated with an increased risk of SCD only in men with preexisting IHD. Further adjustment for the grades of preexisting heart disease (groups II through IV) made little difference in the associations seen in men with IHD.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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In the present study, as in most other studies, the conventional risk factors for IHD, such as smoking, hypertension, raised blood cholesterol, and preexisting IHD, have been shown to be strongly predictive of SCD.1 2 3 4 5 6 7 8 9 10 In addition, physical activity (inversely), heart rate, arrhythmia, heavy drinking, and, to a lesser extent, hematocrit and HDL-C (inversely), have been shown to be independently associated with the risk of SCD. Diabetes, FEV1, and white blood cell count did not emerge as independent predictors of SCD, supporting observations made in other studies.2 3 6 7 8 9
In most studies, the risk factors in men who experienced SCD did not differ from the risk factors in those who succumbed more slowly to IHD,1 2 3 4 5 6 7 8 9 10 but most of these studies examined only conventional risk factors. Early reports from the United States suggested that heavy drinking34 and increased heart rate35 might be specific to SCD, and recent reports from the BRHS have focused attention on these risk factors.13 14 In the present study, we have identified three factors that appear to be critical to SCD, ie, elevated heart rate, arrhythmia on ECG, and heavy drinking, and the latter two factors appear to be specific to SCD.
Arrhythmia
Ventricular fibrillation is the most common cause
of
SCD,36 and although SCD may appear to be unexpected in a
particular individual, it rarely comes "out of the blue." In an
anatomical study of sudden coronary deaths in London, almost three
quarters of the persons studied had a recent coronary thrombotic lesion
with underlying atherosclerosis. The remainder had high-grade
atherosclerotic stenosis but no recent vascular change. In this group,
the myocardium showed scarring from previously healed infarction; such
scarring acted as a substrate for reentrant ventricular
arrhythmia.37 Sympathetic hyperactivity in the presence of
an ischemic myocardium is clearly a setting for potential disaster. In
the present study, those subjects with arrhythmia who sustained SCD
(n=21) either had atrial fibrillation (n=6) or ventricular
(n=11) or
supraventricular (n=4) extrasystoles. One of 6 men with atrial
fibrillation also had evidence of ventricular extrasystoles. In males
<65 years of age, it is accepted that up to 10 supraventricular or 10
ventricular extrasystoles per hour would be found in normal individuals
on a 24-hour ECG recording. It could be argued that the presence of an
extrasystole in an 8-second recording implies a frequency that is
considerably in excess of the normal incidence. Of the 54 men with
atrial fibrillation, 6 experienced SCD (11.1%). Two hundred twelve
individuals had at least one ventricular extrasystole, and of these, 12
experienced SCD (5.7%). One hundred thirteen men had at least one
supraventricular extrasystole, and of these, 4 sustained SCD
(3.5%).
Preexisting IHD
We consider the methods used to determine the
prevalence of IHD
appropriate for an epidemiological study in which more precise
measurements cannot be used. Although these methods could lead to both
underreporting and overreporting of preexisting IHD, the prevalence
found is similar to that observed in other epidemiological studies of
middle-aged men. Most studies find that about half the patients who
experienced SCD have preexisting IHD (variously
defined),6 7 38 and in this study, 60% of
men who
experienced SCD had evidence of IHD at screening (see Table 2).
Risk of
SCD was particularly marked in those with history of definite
myocardial infarction. Increased risk was also seen in men with
evidence of ischemia on ECG but without definite myocardial infarction,
in keeping with other studies.10 39 Those with
"symptomatic IHD" (chest pain without ECG changes) were not
unduly prone to SCD. These findings are similar to those in a Finnish
study,7 in which it was suggested that those with ECG
changes represent men with more advanced IHD. However, in the
present study, those with "symptomatic IHD" (group II) showed
an increased risk of non–sudden death and nonfatal myocardial
infarction similar to those with ECG changes.
Risk Factors and Preexisting IHD
Results from the Framingham
Study indicate that the predictors of
SCD differ in those with versus those without
IHD.6 38 In
the present study, most of the risk factors for SCD were operative
in both groups, although the relative risks (eg, heart rate and
arrhythmia) were somewhat stronger in those without IHD. In studies
that have examined the risk factors separately in subjects with versus
those without preexisting IHD, few of the conventional risk factors
have been predictive of SCD in those with
IHD.6 7 38 In
particular, no association has been found between systolic blood
pressure and risk of SCD. In most of these studies, a linear relation
with systolic blood pressure has been assumed and no positive
association has emerged. In the present study, we observed a
J-shaped relation between systolic blood pressure and SCD
in men with preexisting IHD, so that the overall trend, as in other
studies, was nonsignificant. As in many other studies, cigarette
smoking was not predictive of SCD in those with preexisting IHD. The
finding that blood cholesterol is predictive of SCD in these men is
similar to the findings of the Finnish study.7 However, no
such association was observed in the Framingham Study.6 We
observed significant associations between both hematocrit and HDL-C
with SCD only in men with preexisting IHD. Hematocrit is strongly
influenced by presence of IHD,40 but the positive
association remained after adjusting for grades of preexisting IHD,
suggesting that the findings were independent of degree of severity of
IHD in this group. Few studies have examined HDL-C and hematocrit in
relation to SCD separately in men with versus those without preexisting
IHD. The Framingham study did not find hematocrit to be predictive of
SCD in men with IHD, but hematocrit was an independent predictor in
women.6 The emergence of hematocrit and HDL-C as
predictive factors only in men with preexisting IHD requires
confirmation from other studies.
Implications for Prevention
A review of SCD concluded that
there is no way of identifying
those at particular risk and that the only viable approach to the
problem is the use of preventive measures designed to diminish the risk
of coronary atherosclerosis.12 In the present study,
some factors not previously explored in detail in other studies appear
to be specifically or particularly related to SCD rather than to only
the overall risk of IHD, ie, heavy drinking, increased heart rate, and
cardiac arrhythmia.
Heavy drinking (>42 UK units/wk) is clearly a modifiable factor, and SCD should be added to the list of problems associated with heavy drinking. Heart rate is conditioned to a considerable degree by the pattern of habitual physical activity and by the degree of physical fitness attained. Both physical activity and heart rate appear to have independent relations to the risk of IHD in this study, but it would seem that maintaining moderately vigorous or vigorous levels of physical activity is likely to diminish the risk of SCD and reduce the overall risk of heart attack.41 ß-Blockade is a standard therapeutic procedure in hypertension and angina and in subjects who have survived a myocardial infarction, and its benefits may be related to its effect on heart rate as much as to its antiarrhythmic and blood pressure–lowering effects.42 ß-Blockers are also widely used in subjects with ectopic beats and supraventricular tachycardias. A recent review of the efficacy of ß-adrenoreceptor–blocking drugs in preventing SCD suggests that they are the most effective of all therapeutic measures currently available.43
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Acknowledgments |
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The BRHS is a British Heart Foundation Research Group that is also supported by the UK Department of Health and the Stroke Association.
Received August 1, 1994; revision received October 20, 1994; accepted October 31, 1994.
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