what risk factors predispose a patient to cardiac arrest

Sudden cardiac decease (SCD), ie, decease within 1 hour later on onset of symptoms, constitutes nigh a quarter of all ischemic heart illness (IHD) events and about half of all major IHD deaths. Ventricular arrhythmia is believed to be the almost mutual direct crusade, and epidemiological studies take shown that the conventional risk factors for IHD are besides predictive of SCD.^{i ii iii iv 5 six 7 8 9 x} However, those factors that predispose specifically to SCD are poorly identified.^{two v 10 11} A review¹² has concluded that at that place is no mode of identifying those at particular risk of SCD and that the but viable approach to the problem is the employ of preventive measures designed to diminish the hazard of coronary atherosclerosis. Nosotros recently reported that both heavy drinking (>42 UK units/wk, where 1 UK unit is equal to 8 m alcohol) and increased heart rate (≥xc beats per minute [bpm]) in a accomplice of heart-aged men (The British Regional Heart Study [BRHS]) appear to influence SCD in a mode that is contained of the major hazard factors for IHD.^{13 14} The present commodity examines a wider range of established and potential risk factors for IHD in relation to sudden and not–sudden cardiac events (both fatal and nonfatal) to identify contained risk factors for SCD and to determine which risk factors might specifically or specially make up one's mind SCD. We are also concerned with whether the independent risk factors for SCD operate differently in men with or without underlying IHD.

Methods

The BRHS is a prospective study of cardiovascular affliction involving 7735 men, aged 40 to 59 years old at enrollment, selected from the historic period-gender registers of ane-grouping full general practice in each of 24 towns in England, Wales, and Scotland between January 1978 and June 1980. The criteria for selecting the boondocks, the general practice, the subjects, and the methods of information 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 concrete measurements were fabricated, and nonfasting claret 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 Schoolhouse of Hygiene sphygmomanometer was used to measure blood pressure twice in succession, with the subjects seated and the arm supported on a absorber. The mean of the two readings was used in the assay, and all blood pressure readings were adapted for observer variation inside each boondocks.^xviii Classification methods for smoking condition, booze consumption, and social class have been reported.^{13 15} Heavy drinking was defined as regularly drinking more six drinks daily (>42 United kingdom units/wk). The men were asked to indicate their usual blueprint of physical activeness, 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 half-dozen broad categories based on action level: inactive (686) and occasional (2345), light (1761), moderate (1205), moderately vigorous (1120), and vigorous (513) activity. In this newspaper, the inactive and occasional activity groups have been combined and the moderately vigorous and vigorous groups take been combined. Forced expiratory volume in 1 second (FEV1) was measured with a Vitalograph spirometer with the subject seated. FEV1 measurements were top-standardized to ane.73 1000, 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 middle trouble.²¹

Preexisting Disease

The men were asked to remember a doctor'south diagnosis of angina or myocardial infarction, diabetes, and a number of other disorders listed on the questionnaire. They were besides asked for details concerning assistants of any regular medical handling, including antihypertensive drugs. The Globe Wellness 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 testify of IHD present at screening: grouping I, men who reported no prove of IHD on the WHO breast pain questionnaire or ECG and had no remember of a dr.'s diagnosis of IHD (n=5792, 74.9%); grouping II, men who reported angina or possible myocardial infarction on WHO breast pain questionnaire or recalled a dr.'s diagnosis of angina but who had no ECG evidence of myocardial ischemia or infarction ("symptomatic IHD": north=696, 9.0%); group III, men with ECG prove of possible or definite myocardial ischemia or possible myocardial infarction (north=819, 10.6%); group Iv, men with a previous definite myocardial infarction on ECG or who recalled a doctor's diagnosis of a center attack (n=428, 5.5%). In the analyses, men in groups Two through IV had preexisting evidence of IHD.

Centre Rate

Eye rate was determined at screening from the iii-atomic number 82 orthogonal ECG. On the ground of the 8-second recording, the boilerplate RR interval was calculated (in seconds) during that period as follows: heart rate was equal to 60 divided by the boilerplate RR interval. Elevated middle charge per unit was defined as ≥90 bpm.^fourteen No data is bachelor on measurement fault for the method used or on intraindividual variation.

Presence of Arrhythmia

A complex diagnostic tree that was function of a larger ready of criteria used in interpreting the ECG equally a whole was used in the interpretation.²³ All ECGs were reviewed by an experienced electrocardiographer, and whatsoever 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 every bit an arrhythmia, eg, sinus rhythm with ventricular extrasystoles. As expected, 97.8% of the men in the study were in sinus rhythm. Only 0.seven% (due north=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.vii%), and 113 men (i.5%) had supraventricular-atrial extrasystoles. Other significant abnormalities occurred with negligible frequency, eg, two men were in complete center block.

Follow-upward

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-upwards was achieved in 99% of the cohort. Fatal events were defined as expiry from IHD (ICD ninth revision codes 410 to 414) as the underlying crusade. These events comprised any IHD death during the 8-year follow-up, irrespective of a previous nonfatal outcome during that menses. The certifying doctor was asked to consummate an inquiry form that asked the duration from onset of symptoms to expiry: <1 hour, 1 to 24 hours, or >24 hours. SCD was defined as an event in which death occurred within one hour after the onset of symptoms. Simply those men for whom articulate information was available regarding death within 1 hr 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 decease 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: (one) a history of astringent prolonged chest pain, (2) ECG prove of myocardial infarction, or (iii) cardiac enzyme changes associated with myocardial infarction.

Statistical Methods

The Cox proportional hazards model was used to assess the contained contributions of chance factors to the run a risk of SCDs and to obtain the relative risks adjusted for age and the other gamble 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 equally relative risks. For the quantitative (continuous) variables, such equally systolic blood pressure, the relative risks are presented to estimate the relative gamble of expiry from SCD associated with a given change in the hazard gene, which was ≈i SD (Table 4). Adjusted relative risks in the Effigy were obtained past fitting serum full cholesterol, systolic blood pressure, and HDL cholesterol (HDL-C) as four dummy variables for the 5 quintiles of each risk factor. Tests for trend were performed by plumbing fixtures the quantitative variables in their continuous grade. The distribution of white blood jail cell count was skewed, and log transformation was used. In the adjustment, age, body mass alphabetize, and biological variables, with the exception of centre rate and hematocrit, were fitted continuously. Because of the nonlinear relations between heart rate and SCD,^fourteen and between hematocrit and major IHD events,¹⁷ center rate was fitted as five categorical groups (<60, lx to 69, 70 to 79, 80 to 89, and ≥90 bpm) and hematocrit every bit a dichotomous variable (≥46% versus residue), since our earlier reports have shown a threshold effect.¹⁷ In the adjustment, physical activity was fitted as 3 dummy variables for the four groups and smoking status equally 4 dummy variables for the five levels of smoking categories (never smoked, exsmoker, 1 to 19 cigarettes per solar day, 20 cigarettes per day, ≥21 cigarettes per day). In some of the analyses, smoking is fitted as 0,i 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 co-ordinate 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, centre rate, HDL-C, hematocrit, white blood cell count, and FEV1 were entered one at a time.

Results

During the 8-year follow-upwards menstruum, 488 major IHD events occurred. These events included 217 deaths, of which 117 (53.ix%) were classified every bit 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).

Coronary Take a chance Factors

The unadjusted rates per k 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 events^{17 19 twenty 21 28 29 30 31 32 33} are presented in Tables 2 and three.

Preexisting Disease

Bear witness of a definite centre assault (group Iv), evidence of IHD on ECG (grouping III), presence of arrhythmia, and antihypertensive treatment were all strongly associated with an increased gamble of SCD, even subsequently adjustment for age. Symptomatic IHD (grouping II) and diabetes were non associated with a significant increase in risk of SCD.

Personal Characteristics

Current smoking, higher body mass index (≥28 kg/thousand²), a depression level of concrete 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 expiry from center 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 (six.1 mmol/50), all were significantly associated with chance of SCD after adjustment for age, with the exception of nonfasting claret glucose.

Multivariate Analysis

Many of the factors presented in Tables 2 and 3 are interrelated. HDL-C, heart rate, white blood prison cell count, and hematocrit are all associated to various degrees with preexisting IHD, personal characteristics, and biological factors, eg, systolic blood pressure and claret cholesterol, and they may serve as intermediate mechanisms between these variables and SCD. We take therefore examined the relation betwixt SCD and all the factors that were significantly associated with SCD, after adjusting for age, preexisting IHD, arrhythmia, antihypertensive treatment, personal characteristics, systolic claret pressure, and claret cholesterol.

Presence of IHD (group Three and 4), arrhythmia, current smoking, concrete activity, claret cholesterol, systolic blood force per unit area, middle rate, hematocrit, and white claret cell count remained significantly associated with the take a chance of SCD, even later adjustments were made (all P<.05). Even so, the increased risk seen with heavy drinking was reduced and was of marginal significance (relative risk [RR]=1.61; P=.06) later on adjustments were made. The risk associated with antihypertensive treatment was substantially reduced and was no longer pregnant (RR=1.27; 95% CI, 0.77 to 2.xi) after these adjustments. No significant clan was seen with body mass index and FEV1 after adjustment.

Additional Aligning for HDL-C, Heart Rate, and Hematocrit

Hematocrit and white blood prison cell count are strongly correlated (r=.26), and since the association between white blood prison cell count and SCD diminished after adjusting farther for middle charge per unit and HDL-C, white blood cell count was omitted from the aligning. We have therefore adapted HDL-C, center rate, and hematocrit to appraise the independence of and to decide 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 meaning or marginally significant are presented. To illustrate the clan of the quantitative take chances factors with SCD, we accept likewise presented the adjusted relative risks by levels of each factor (Effigy).

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 increment in adventure, and this clan increased to greater than fivefold in those with definite myocardial infarction (group 4). In that location was a progressive decline in take a chance of SCD as the level of physical activity increased (RR=1.00, 0.86, 0.67, and 0.54 for the iv groups of men classified co-ordinate to level of physical activity, respectively) (meet "Methods"; exam for trend, P<.05). The take a chance 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 i.46, and the increased risk was now of marginal significance (P=.06), indicating that function 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 ane.48 to 1.forty, and was of marginal significance (P=.09). Elevated centre 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 take a chance (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 everyman quintile compared with the second quintile. Men in the peak quintile of HDL-C showed a 40% reduction in gamble.

Specificity of Risk

The factors shown to be independently predictive of SCD (Table iv) were as well examined in relation to nonfatal myocardial infarction and not–sudden IHD decease, after adjusting for each of the other variables to appraise whether any factors were specifically or particularly associated with SCD (Tabular array 4). Arrhythmia was not shown to be associated with nonfatal events and was only weakly and nonsignificantly associated with non–sudden IHD death simply was strongly associated with SCD. Elevated center charge per unit was non shown to be associated with nonfatal myocardial infarction. An elevated middle rate was associated with a marginally significant increase in risk of not–sudden IHD death (P=.08) and a strongly significant increase in adventure of SCD. Heavy drinking posed a lower risk of nonfatal myocardial infarction (RR=0.77) and of not–sudden IHD deaths (RR=0.4) simply was associated with a significantly increased gamble 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 decease or nonfatal IHD events.

Effect of Preexisting IHD

The contained chance factors for SCD were examined separately in men with IHD (groups II through IV combined) and without IHD (group I) adapted 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 betwixt the 2 groups rather than with evaluation of the statistical significance of the relations, although these are presented (Table 5).

Historic period, arrhythmia, increased middle charge per unit, heavy drinking, and hypercholesterolemia were positively associated with an increased run a risk of SCD in both groups, although the magnitude of the relative risk for arrhythmia, heavy drinking, and especially center rate was greater in those without preexisting IHD. However, the absolute take chances of SCD is much higher in men with preexisting IHD overall (1.0 in 1000 versus 4.viii in yard per twelvemonth); thus, the lower estimated relative risks may however stand for substantial excess risk. Physical inactivity and current smoking were independently associated with an increased hazard of SCD simply in men without preexisting IHD. Systolic blood pressure showed a pregnant positive clan with take chances of SCD in men without preexisting IHD. In men with preexisting IHD, a J-shaped relation was seen betwixt systolic blood pressure and run a risk of SCD, with the highest chance seen in those in the lowest quintile and the lowest risk in those in the second quintile, with hazard increasing thereafter so that a test for overall linear trend was nonsignificant. This phenomenon will be presented and discussed in a dissever publication. Elevated hematocrit and low HDL-C were associated with an increased adventure of SCD only in men with preexisting IHD. Farther adjustment for the grades of preexisting eye disease (groups 2 through IV) made little difference in the associations seen in men with IHD.

Discussion

In the present report, every bit in near 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.^{one two 3 iv 5 6 vii eight ix x} In add-on, physical activity (inversely), heart charge per unit, arrhythmia, heavy drinking, and, to a lesser extent, hematocrit and HDL-C (inversely), take been shown to be independently associated with the risk of SCD. Diabetes, FEV1, and white blood cell count did not sally equally 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 non differ from the risk factors in those who succumbed more slowly to IHD,^{one two 3 4 v 6 seven 8 ix 10} but most of these studies examined only conventional run a risk factors. Early on reports from the The 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 nowadays study, we have identified three factors that appear to exist critical to SCD, ie, elevated heart charge per unit, arrhythmia on ECG, and heavy drinking, and the latter two factors appear to be specific to SCD.

Arrhythmia

Ventricular fibrillation is the well-nigh common crusade of SCD,³⁶ and although SCD may appear to be unexpected in a detail 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 rest had high-form atherosclerotic stenosis merely no recent vascular alter. 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 (northward=xi) or supraventricular (n=four) extrasystoles. One of 6 men with atrial fibrillation also had prove of ventricular extrasystoles. In males <65 years of age, information technology is accepted that up to 10 supraventricular or 10 ventricular extrasystoles per hour would exist constitute in normal individuals on a 24-60 minutes ECG recording. It could be argued that the presence of an extrasystole in an 8-2d 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%). Ii hundred twelve individuals had at least one ventricular extrasystole, and of these, 12 experienced SCD (5.vii%). One hundred 13 men had at least i 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 pb to both underreporting and overreporting of preexisting IHD, the prevalence found is similar to that observed in other epidemiological studies of middle-aged men. About studies notice that near half the patients who experienced SCD have preexisting IHD (variously defined),^{6 7 38} and in this study, sixty% of men who experienced SCD had evidence of IHD at screening (see Table two). 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 only without definite myocardial infarction, in keeping with other studies.^{10 39} Those with "symptomatic IHD" (chest hurting without ECG changes) were not unduly decumbent to SCD. These findings are similar to those in a Finnish study,^vii 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" (grouping 2) showed an increased risk of non–sudden death and nonfatal myocardial infarction like 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.^{six 38} In the present report, nigh of the chance 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 chance factors separately in subjects with versus those without preexisting IHD, few of the conventional adventure factors have been predictive of SCD in those with IHD.^{half-dozen 7 38} In particular, no association has been found between systolic blood force per unit area and hazard of SCD. In near of these studies, a linear relation with systolic blood pressure has been assumed and no positive association has emerged. In the present written report, we observed a J-shaped relation between systolic claret pressure and SCD in men with preexisting IHD, then that the overall trend, every bit in other studies, was nonsignificant. As in many other studies, cigarette smoking was non predictive of SCD in those with preexisting IHD. The finding that blood cholesterol is predictive of SCD in these men is like to the findings of the Finnish study.^vii Even so, no such association was observed in the Framingham Study.⁶ Nosotros observed pregnant associations betwixt both hematocrit and HDL-C with SCD only in men with preexisting IHD. Hematocrit is strongly influenced past presence of IHD,⁴⁰ but the positive association remained after adjusting for grades of preexisting IHD, suggesting that the findings were independent of caste of severity of IHD in this grouping. Few studies accept examined HDL-C and hematocrit in relation to SCD separately in men with versus those without preexisting IHD. The Framingham report did not find hematocrit to be predictive of SCD in men with IHD, simply hematocrit was an contained predictor in women.⁶ The emergence of hematocrit and HDL-C as predictive factors simply in men with preexisting IHD requires confirmation from other studies.

Implications for Prevention

A review of SCD concluded that there is no mode of identifying those at particular risk and that the merely 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 item in other studies appear to exist specifically or particularly related to SCD rather than to only the overall run a risk of IHD, ie, heavy drinking, increased heart rate, and cardiac arrhythmia.

Heavy drinking (>42 Great britain units/wk) is clearly a modifiable factor, and SCD should be added to the list of problems associated with heavy drinking. Middle charge per unit is conditioned to a considerable degree by the design of habitual physical activity and by the caste of concrete fitness attained. Both physical action and heart rate appear to have contained relations to the gamble of IHD in this study, but information technology 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 β-Blockade is a standard therapeutic process in hypertension and angina and in subjects who have survived a myocardial infarction, and its benefits may exist related to its effect on eye charge per unit every bit much as to its antiarrhythmic and claret pressure–lowering effects.⁴² β-Blockers are also widely used in subjects with ectopic beats and supraventricular tachycardias. A contempo review of the efficacy of β-adrenoreceptor–blocking drugs in preventing SCD suggests that they are the most constructive of all therapeutic measures currently available.⁴³

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Figure ane. Graphs showing relative hazard of sudden cardiac death in relation to blood cholesterol (top), systolic blood pressure (middle), and HDL cholesterol (lesser). Adjusted (×) for historic period, preexisting ischemic heart disease, arrhythmia, antihypertensive treatment, physical activity, trunk mass alphabetize, smoking, heavy drinking, hematocrit, center rate, and, where appropriate, for systolic blood pressure, blood cholesterol, and HDL cholesterol.

Table iv. Adjusted Relative Risk for Nonfatal Myocardial Infarction, Non–Sudden Ischemic Eye Affliction Expiry, and Sudden Cardiac Death in 6826 Men With Information on Covariates

	Sudden Cardiac Death (n=106)	Nonfatal MI (n=231)	Non–Sudden IHD Death (northward=87)
Age, increase in 5 y	1.561	ane.133	one.64two
IHD (vs none)
Grouping II	1.28	1.842	1.48
Group 3	2.661	one.50iii	1.40
Group IV	5.151	two.22one	iv.611
Smoking, yeah/no	1.464	one.373	1.79ii
Physical activity, moderately vigorous–vigorous vs never-occasionally	0.543	0.97	0.63three
Cholesterol, increment in one mmol/L	1.481	1.371	i.xiii
SBP, increase in 20 mm Hg	i.223	one.322	ane.20iv
HDL, increase in 0.3 mmol/L	0.804	0.843	0.87
Hematocrit ≥46% vs rest	1.40v	1.xxx4	0.92
Arrhythmia, yes/no	2.511	0.84	1.27
Heart charge per unit, ≥90 vs <60 beats/min	three.35two	0.69	one.915
Heavy drinking, aye/no	ane.793	0.77	0.404

Table v. Relative Risk of Sudden Cardiac Death Associated With Risk Factors in Men With vs Men Without Preexisting Ischemic Heart Illness

Gamble Factors	No Preexisting IHD (n=5181 men, twoscore cases)	Whatsoever Preexisting IHD (n=1731 men, 66 cases)
Age, 55-59 vs <50	1.eightone	three.seven1
Arrhythmia, yes/no	three.v1	2.22
Heavy drinking, aye/no	two.03	1.half-dozen
Eye rate, ≥90 vs <60	7.51	ii.1
Cholesterol, quintile 5 vs i	three.5one	2.91
Smoking, yes/no	two.twotwo	1.2
Physical activeness, moderately vigorous–vigorous vs never-occasionally	0.three2	0.viii
SBP, quintile 5 vs ane	3.ix1	1.0
Hematocrit, ≥46 vs residue	0.ix	i.nine2
HDL-C, quintile 5 vs 1	i.1	0.three1

Tabular array 1. Rate per 1000 per Twelvemonth (No. of Events) for All Ischemic Heart Disease Events and Deaths and Sudden Cardiac Deaths by Age

Age	No. of Men	IHD		Sudden Cardiac Deaths
		Major Events	Deaths
40-44	1838	2.8 (40)	0.6 (9)	0.iv (6)
45-49	1898	6.nine (104)	2.4 (36)	i.iii (nineteen)
50-54	1974	9.0 (142)	3.vi (58)	2.1 (33)
55-59	2025	12.5 (202)	7.0 (114)	3.half dozen (59)
All	7735	7.nine (488)	iii.5 (217)	one.9 (117)
Test for trend		P<.0001	P<.0001	P<.0001

Table 2. Unadjusted Rates per m per Year and Age-Adapted Relative Risks for Sudden Cardiac Expiry in Relation to Various Risk Factors

Gamble Factors	Sudden Cardiac Death
	Rate (northward) per 1000 per Year	Age-Adjusted Relative Hazard (95% CI)
Preexisting IHD
None (n=5792)	i.0 (46)	ane.0
II (northward=696)	1.four (8)	one.3 (0.6,two.8)
III (due north=819)	three.vii (24)	three.two (2.0,5.three)
Four (n=428)	11.four (39)	eight.3 (5.iv,12.9)
Arrhythmia
No (northward=7320)	1.half dozen (96)	1.0
Yep (n=407)	6.4 (21)	3.ii (ii.0,five.3)
Antihypertensive handling
No (northward=7360)	one.half dozen (95)	one.0
Yes (n=375)	7.3 (22)	3.2 (2.0,v.two)
Diabetes
No (n=7617)	one.9 (115)	1.0
Yes (northward=118)	two.1 (2)	i.0 (0.2,four.0)
Smoking
Never smoked (n=1819)	1.0 (xiv)	1.0
Exsmoker (n=2715)	1.seven (38)	one.4 (0.eight,ii.9)
Current smoker (north=3185)	ii.6 (65)	2.iii (1.2,4.0)
BMI
<22 (n=971)	ane.5 (12)	ane.0
22- (n=1549)	ane.2 (15)	0.8 (0.4,1.viii)
24- (n=2080)	1.9 (32)	one.3 (0.6,2.six)
26- (due north=1638)	2.one (27)	one.iii (0.6,2.6)
28- (north=1494)	2.6 (31)	1.half dozen (0.ix,3.2)
Test for tendency		P<.01
Concrete activity
None-occasional (north=3131)	2.6 (65)	ane.0
Lite (n=1761)	ane.9 (27)	0.7 (0.5,i.1)
Moderate (north=1205)	one.vi (15)	0.half dozen (0.4,1.1)
Moderately vigorous–vigorous (n=1633)	0.8 (10)	0.iv (0.ii,0.7)
Test for trend		P<.0001
Heavy drinking
No (n=6903)	1.eight (98)	ane.0
Yes (north=832)	ii.9 (19)	1.8 (i.1,three.0)
Parental history
No (north=5604)	i.vii (74)	1.0
Aye (north=2077)	two.5 (42)	1.4 (0.nine,2.0)
Social grade
Nonmanual labor (n=3061)	1.5 (37)	0.8 (0.five,1.2)
Transmission labor (n=4428)	2.ane (73)	1.0
Armed forces (due north=231)	3.2 (6)	ane.7 (0.7,four.0)

Table iii. Unadjusted Rates per g per Year and Age-Adapted Relative Risks for Sudden Cardiac Death in Relation to Biological Factors

Run a risk Factors	Sudden Cardiac Death
	Rate (n)	Relative Take a chance (Top Fifth vs Bottom 5th)
SBP, mm Hg (northward)
<128 (1611)	i.two (sixteen)
128- (1462)	0.seven (8)
138- (1493)	1.3 (16)	2.2 (1.two,iii.9)1
148- (1703)	2.0 (27)
161- (1497)	4.0 (48)
Cholesterol, mmol/L (north)
<5.v (1613)	1.two (15)
five.5- (1384)	1.three (14)
6.0- (1493)	i.iii (15)	3.3 (1.8,6.0)1
6.five- (1703)	2.0 (27)
7.ii- (1497)	3.8 (46)
HDL cholesterol, mmol/Fifty (due north)
<0.93 (1520)	3.0 (36)
0.93- (1580)	2.1 (27)
1.06- (1332)	2.0 (21)	0.iv (0.2,0.8)1
1.18- (1484)	1.3 (xvi)
1.33- (1504)	1.2 (14)
FEV1, L (n)
<2.75 (1532)	3.8 (47)
2.75- (1509)	ii.2 (27)
3.nineteen- (1528)	one.9 (23)	0.3 (0.1,0.7)ane
iii.55- (1550)	0.9 (eleven)
three.94- (1532)	0.half dozen (vii)
White claret cell count, ×109/Fifty (n)
<five.eight (1505)	0.9 (11)
five.viii- (1397)	1.0 (11)
6.six- (1573)	2.1 (27)	3.0 (1.half-dozen,vi.two)one
7.5- (1423)	2.v (28)
eight.six- (1449)	2.9 (34)
Heart charge per unit, beats/min (northward)
<60 (1429)	0.9 (10)
lx- (2475)	ane.6 (32)
lxx- (2101)	two.0 (33)	4.8 (ii.2,10.0)1
80- (1031)	ii.1 (17)
ninety- (644)	iv.v (23)
Hematocrit ≥46% (n)
No (4884)	1.four (54)	≥46% vs balance
Aye (2462)	2.9 (57)	2.1 (1.4,three.ane)
Glucose ≥6.1 mmol/L (n)
No (6256)	i.8 (88)	≥half dozen.1 vs rest
Yes (1429)	2.5 (29)	1.3 (0.9,2.0)

The BRHS is a British Heart Foundation Research Group that is also supported by the UK Department of Health and the Stroke Association.

Footnotes

Correspondence to Dr Goya Wannamethee, University Dept of Public Wellness, Royal Complimentary Hospital Schoolhouse of Medicine, Rowland Hill St, London NW3 2PF, England.

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Source: https://www.ahajournals.org/doi/10.1161/01.CIR.91.6.1749

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