Risk Of Primary Cardiac Arrest Research Articles

Cardiac arrest: a case-based review.

Coffee is commonly consumed among young people in China. However, consumers are rarely aware of physically adverse effects as a result of excessive consumption of caffeine. A literature search using multiple databases was performed for articles published with concentration on meta-analyses, systematic reviews, and randomized controlled trials. Excess coffee consumption is also a risk of primary cardiac arrest especially in young people. Treatment modalities include activated charcoals, beta-blockers, vasopressin and hemodialysis when necessary. Coffee consumers should be advised not to routinely take more than moderate coffee.

Marathon Rat

Cardiac adaptation to intensive exercise has long intrigued cardiologists and physiologists, particularly in relation to the notion that different types of exercise drive divergent remodeling. On the basis of a meta-analysis of 59 echocardiographic studies (including 1451 male athletes 18 to 40 years of age), Pluim et al1 concluded that endurance-trained runners, who are known to develop eccentric cardiac hypertrophy, demonstrated a more pronounced left ventricular (LV) wall thickening than expected. Strength-trained sportsmen showed an unanticipated increase in LV internal diameter besides concentric cardiac hypertrophy. These adaptations accounted for a higher LV mass, whereas no differences were found between athletes and nonathletes regarding LV ejection fraction, fractional shortening, and early and late ventricular filling velocity ratio. Recently, Pelliccia and colleagues2 reported on a longitudinal assessment in young Olympic athletes engaged in rowing, canoeing, cycling, middle- and long-distance running, cross-country skiing, swimming, or participating in triathlons. The investigators concluded that extreme endurance training over long stretches of time (4 to 17 years) was not associated with significant changes in LV shape and function or the occurrence of cardiovascular symptoms and events. However, this unique study has been criticized for including only athletes who had undergone mandatory cardiovascular screening before enrollment, so those already having exercise-induced cardiac abnormalities would have been excluded.3 A second criticism was that no analysis of the right ventricle (RV) was performed, although extreme exercise can cause RV dysfunction and arrhythmias.3 Generally, the risk of primary cardiac arrest is increased among men with infrequent vigorous exercise, whereas, for those exercising habitually, the overall risk is decreased. There is a striking male predominance of sudden death among athletes. Article see p 13 What happens with the RV and the atria during long-term intensive sports training? Previous data indicated disproportional changes in the RV and LV …

The Choice of Thiazide Diuretics

Thiazide diuretics were introduced in the United States for the treatment of hypertension in 1957. The first of these, chlorothiazide, was soon accompanied by a large number of other sulfonamide derivatives, including chlorthalidone. Hydrochlorothiazide (HCTZ) rapidly became the most commonly prescribed antihypertensive drug in the United States, whereas bendroflumethiazide was most popular in the United Kingdom. The initial popularity of HCTZ in the United States was abetted by its use in the first controlled trial of the treatment of nonmalignant hypertension, the Veterans’ Affairs Cooperative Study.1 The starting dose of HCTZ was 50 mg/d, and it was used along with reserpine and hydralazine. A number of other trials published in the 1970s all used higher doses of diuretic, for example, ≥50 mg of HCTZ per day.2 For reasons unknown to me, chlorthalidone was chosen to be the diuretic in the first large controlled trial of the treatment of hypertension, the Hypertension Detection and Follow-Up Program.3 In the Hypertension Detection and Follow-Up Program, all 10 940 patients were started on chlorthalidone from 25 to 100 mg/d. Other drugs were added to achieve control of the blood pressure. In addition, half were assigned to “referred” care and the other half to more closely monitored and intensively treated “stepped” care. The stepped care–treated half achieved a 4.4% further reduction in diastolic blood pressure and a 17.0% reduction …

The interaction of vasoactive substances during exercise modulates platelet aggregation in hypertension and coronary artery disease

BackgroundAcute vigorous exercise, associated with increased release of plasma catecholamines, transiently increases the risk of primary cardiac arrest. We tested the effect of acute submaximal exercise on vasoactive substances and their combined result on platelet function.MethodsHealthy volunteers, hypertensive patients and patients with coronary artery disease (CAD) performed a modified treadmill exercise test. We determined plasma catecholamines, thromboxane A2, prostacyclin, endothelin-1 and platelet aggregation induced by adenosine diphosphate (ADP) and collagen at rest and during exercise.ResultsOur results during exercise showed a) platelet activation (increased thromboxane B2, TXB2), b) increased prostacyclin release from endothelium and c) decreased platelet aggregation in all groups, significantly more in healthy volunteers than in patients with CAD (with hypertensives lying in between these two groups).ConclusionDespite the pronounced activation of Sympathetic Nervous System (SNS) and increased TXB2 levels during acute exercise platelet aggregation decreases, possibly to counterbalance the prothrombotic state. Since this effect seems to be mediated by the normal endothelium (through prostacyclin and nitric oxide), in conditions characterized by endothelial dysfunction (hypertension, CAD) reduced platelet aggregation is attenuated, thus posing such patients in increased risk for thrombotic complications.

Higher plasma docosahexaenoic acid is associated with reduced progression of coronary atherosclerosis in women with CAD

Fish intake, eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and in some cases alpha-linolenic acid (ALA) have been associated with reduced risk of cardiovascular events and death. The association between n-3 fatty acids in plasma lipids and the progression of coronary artery atherosclerosis was assessed among women with established coronary artery disease (CAD). A prospective cohort study involved postmenopausal women (n = 228) participating in the Estrogen Replacement and Atherosclerosis Trial. Quantitative coronary angiography was performed at baseline and after 3.2 +/- 0.6 (mean +/- SD) years. Women with plasma phospholipid (PL) DHA levels above the median, compared with below, exhibited less atherosclerosis progression, as expressed by decline in minimum coronary artery diameter (-0.04 +/- 0.02 and -0.10 +/- 0.02 mm, respectively; P = 0.007) or increase in percentage stenosis (1.34 +/- 0.76% and 3.75 +/- 0.74%, respectively; P = 0.006), and had fewer new lesions [2.0% (0.5-3.5%) of measured segments (95% confidence interval) and 4.2% (2.8-5.6%), respectively; P = 0.009] after adjustments for cardiovascular risk factors. Similar results were observed for DHA in the triglycerides (TGs). EPA and ALA in plasma lipids were not significantly associated with atherosclerosis progression. Consistent with higher reported fish intake, higher levels of plasma TG and PL DHA are associated with less progression of coronary atherosclerosis in postmenopausal women with CAD.

Exercise prescription and thrombogenesis

Lifestyle habits, such as exercise, may significantly influence risk of major vascular thrombotic events. The risk of primary cardiac arrest has been shown to transiently increase during vigorous exercise, whereas regular moderate-intensity exercise is associated with an overall reduced risk of cardiovascular diseases. What are the mechanisms underlying these paradoxical effects of vigorous exercise versus exercise training on thrombotic modification? This review analyzes research regarding effects and their underlying mechanisms of acute exercise, endurance training, and deconditioning on platelets, coagulation, and fibrinolysis. Evidence suggests that (i) light, acute exercise ( < or = 49% VO(2 max)) does not affect platelet reactivity and coagulation and increases fibrinolytic activity; (ii) moderate, acute exercise (50 to approximately 74% VO(2 max)) suppresses platelet reactivity and enhances fibrinolysis, which remains unchanged in the coagulation system; and, (iii) strenuous, acute exercise ( > or = 75% VO(2 max)) enhances both platelet reactivity and coagulation, simultaneously promoting fibrinolytic activity. Therefore, moderate exercise is likely a safe and effective exercise dosage for minimizing risk of cardiovascular diseases by inducing beneficial anti-thrombotic changes. Moreover, moderate-intensity exercise training reduces platelet reactivity and enhances fibrinolysis at rest, also attenuating enhanced platelet reactivity and augmenting hyper-fibrinolytic activity during strenuous exercise. However, these favorable effects of exercise training on thrombotic modification return to a pre-training state after a period of deconditioning. These findings can aid in determining appropriate exercise regimes to prevent early thrombotic events and further hinder the cardiovascular disease progression.

Electrocardiographic QT Interval Prolongation and Risk of Primary Cardiac Arrest in Diabetic Patients

Sudden cardiac death, also known as primary cardiac arrest (PCA), is a major cause of mortality among diabetic patients and typically occurs in the setting of coronary heart disease. Because it can occur as the first clinical manifestation of coronary heart disease, identifying diabetic patients at risk of PCA remains challenging. Interrelated sequelae of diabetes, including QT prolongation and autonomic failure (1, 2), have been repeatedly implicated in the pathophysiology of PCA (3–6). However, it remains unknown whether the QT interval on a 12-lead electrocardiogram (ECG) has potential utility in risk stratification of diabetic patients without prior physician-diagnosed heart disease for PCA (7–12). We therefore conducted a case-control study of PCA in a large prepaid health plan, Group Health Cooperative of Puget Sound. We included patients age 18–79 years who were enrolled for ≥1 year or had four or more clinic visits in the prior year, had physician-diagnosed diabetes noted in their ambulatory care medical record or were treated with oral hypoglycemics or insulin, and had an ECG recorded before their index date (see below). We excluded enrollees with prior physician-diagnosed heart disease (Table 1). Patients were diabetic enrollees who experienced out-of-hospital PCA (a sudden, pulseless condition without a known noncardiac cause) between …

N-3 long-chain polyunsaturated fatty acids in type 2 diabetes: A review

Historically, epidemiologic studies have reported a lower prevalence of impaired glucose tolerance and type 2 diabetes in populations consuming large amounts of the n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) found mainly in fish. Controlled clinical studies have shown that consumption of n-3 LC-PUFAs has cardioprotective effects in persons with type 2 diabetes without adverse effects on glucose control and insulin activity. Benefits include lower risk of primary cardiac arrest; reduced cardiovascular mortality, particularly sudden cardiac death; reduced triglyceride levels; increased high-density lipoprotein levels; improved endothelial function; reduced platelet aggregability; and lower blood pressure. These favorable effects outweigh the modest increase in low-density lipoprotein levels that may result from increased n-3 LC-PUFA intake. Preliminary evidence suggests increased consumption of n-3 LC-PUFAs with reduced intake of saturated fat may reduce the risk of conversion from impaired glucose tolerance to type 2 diabetes in overweight persons. Reported improvements in hemostasis, slower progression of artery narrowing, albuminuria, subclinical inflammation, oxidative stress, and obesity require additional confirmation. Expected health benefits and public health implications of consuming 1 to 2 g/day n-3 LC-PUFA as part of lifestyle modification in insulin resistance and type 2 diabetes are discussed.

Strenuous, acute exercise affects reciprocal modulation of platelet and polymorphonuclear leukocyte activities under shear flow in men

Vigorous exercise transiently increases the risk of primary cardiac arrest. The reciprocal modulation of platelet and polymorphonuclear leukocyte (PMN) activities is important in the pathogenesis of thrombosis. This study investigates how strenuous, acute exercise affects platelet-PMN reciprocal modulation by closely examining 18 sedentary men who exercised strenuously on a bicycle ergometer. Shear-induced platelet activation, PMN interaction with surface-adherent platelets under shear flow, and PMN-dependent inhibition of platelet activation were measured both before and immediately after exercise. Analytical results can be summarized as follows: (i) shear-induced platelet adhesion on fibronectin-coated surface as well as ADP-induced release of platelet soluble P-selectin release and elevation of [Ca2+]i significantly increases after strenuous exercise; (ii) strenuous exercise is associated with higher velocity and percentage of rolling PMNs and lower numbers of PMNs remaining bound to surface-adherent platelets under shear flow than at rest; (iii) PMN-dependent inhibition of platelet [Ca2+]i elevation and soluble P-selectin release after strenuous exercise is much greater than that at rest; and (iv) strenuous exercise increases PMN-derived nitric oxide metabolite level and reduces oxidized low-density lipoprotein-promoted interaction between platelets and PMNs. Therefore, we conclude that platelet activity may be sensitized by strenuous exercise. However, strenuous exercise can also simultaneously enhance the antiplatelet effect of PMNs. The finding provides a new insight into the negative feedback of PMNs against exercise-evoked platelet-related thrombotic risk.

Digoxin therapy and the risk of primary cardiac arrest in patients with congestive heart failure: Effect of mild–moderate renal impairment

Background and Objective: The cardiac safety of digoxin therapy for congestive heart failure (CHF) is a source of concern, especially among those with renal impairment. Methods: Using a case–control design, we examined the risk of primary cardiac arrest (PCA) associated with digoxin therapy within three levels of renal function. Results: After adjustment for other clinical characteristics, digoxin therapy for CHF was not associated with an increased risk of PCA [odds ratio (OR) = 0.97, 95% confidence interval (CI) 0.59–1.62] among patients with normal renal function (serum creatinine ⩽1.1 mg/dL). In contrast, digoxin therapy was associated with a modest increase in risk (OR = 1.58, CI 0.89–2.80) among patients with mild renal impairment (serum creatinine = 1.2–1.4 mg/dL); and a twofold increase in risk (OR = 2.39, CI 1.37–4.18) among patients with moderate renal impairment (serum creatinine = 1.5–3.5 mg/dL). Conclusions: These findings suggest that the risks of digoxin may offset the benefits among patients with moderately impaired renal function, but not among patients with normal renal function.

Exposure to ambient fine particulate matter and primary cardiac arrest among persons with and without clinically recognized heart disease.

The authors studied the association between incidence of primary cardiac arrest and daily measures of fine particulate matter (</=2.5 micro m) using a case-crossover study of 1,206 Washington State out-of-hospital cardiac arrests (1985-1994) among persons with (n = 774) and without (n = 432) clinically recognized heart disease. The authors compared particulate matter levels on the day of the cardiac event and the 2 days preceding the event with levels from matched reference days. The estimated relative risk for a 13.8- micro g/m(3) increase in fine particulate matter (nephelometry: 0.54 x 10(-1) km(-1 )bsp) on the day prior to cardiac arrest was 0.94 (95% confidence interval: 0.88, 1.02). Pollutant levels measured on the same day as the event and on the 2 days preceding the event demonstrated similar results. No increased risk was found among all cases with preexisting cardiac disease (odds ratio = 0.97, 95% confidence interval: 0.89, 1.07); however, an unexpected association appeared between current smokers with preexisting heart disease and increased particulate matter levels 2 days prior to the event (odds ratio = 1.29, 95% confidence interval: 1.06, 1.55). This association was not present in the 0- or 1-day lag analyses or in persons with other diseases. There was no consistent association between increased levels of fine particulate matter and risk of primary cardiac arrest.

Inhaled beta-2 adrenergic receptor agonists and primary cardiac arrest

Purpose We sought to investigate if short-acting, inhaled β 2-adrenergic receptor agonists were associated with higher risk of primary cardiac arrest in patients with asthma or chronic obstructive pulmonary disease (COPD). Subjects and methods We conducted a population-based study involving 454 patients enrolled in a health maintenance organization, aged 40 to 79 years, who had asthma or COPD and who experienced primary cardiac arrest during 1980 to 1994. We randomly selected 586 controls from strata of enrollees, defined by age, sex, calendar year, and prior heart disease. Medication use was assessed from computerized pharmacy data, and risk factors from medical record review. Results Use of inhaled β-agonists was associated with a twofold increased risk of primary cardiac arrest (odds ratio [OR] = 1.9; 95% confidence interval [CI]: 1.1 to 3.3) among patients with asthma, but not among those with COPD (OR = 1.3; 95% CI: 0.6 to 2.7), after adjustment for risk factors. This association was observed only with use of two or more canisters of metered-dose, inhaled β-agonists for 3 months, and when inhaled steroids were not used. Conclusion These results support current guidelines recommending inhaled steroids as first-line asthma therapy.

Sudden death and myocardial infarction in first degree relatives as predictors of primary cardiac arrest

The hypothesis that family history (FH) of myocardial infarction (MI) and FH of sudden death (SD) are both independent risk factors for primary cardiac arrest (PCA) was examined in a case–control study. PCA cases were attended by paramedics (1988–1994) and community-based age and sex matched controls were identified. Subjects (25–74 years) were free of prior clinically-recognized heart disease and major co-morbidity. Interviewers obtained a detailed history of MI and SD in first-degree relatives from spouses of 235 cases and 374 control subjects. A parental history of early-onset SD (age <65) was associated with an increased risk of PCA (odds ratio (OR)=2.69, 95% CI=1.35–5.36), after adjustment for parental history of MI and other risk factors. A parental history of late-onset SD was not associated with PCA risk (OR=0.94, 95% CI=0.55–1.62). Additionally, parental history of SD was related to early-onset PCA (OR=1.89, 95% CI=1.08–3.30) but not to late-onset PCA (OR=0.89, 95% CI=0.49–1.61). In contrast, parental MI (early/late) was related to PCA (early/late), after adjustment for other risk factors and parental history of SD. Similar results were observed in first-degree relatives. Findings suggest a potential role of familial factors related to both MI and SD in PCA. Stronger findings for a familial patterning of PCA were noted for early onset disease in cases and their relatives.

Omega-3 fatty acids and cardiovascular disease: The epidemiological evidence.

Epidemiological studies in the last 40 years suggest that omega-3 fatty acids derived from fish and fish oil decrease the risk of coronary heart disease, hypertension and stroke, and their complications. The beneficial effects of omega-3 fatty acids include effects on lipids, blood pressure, cardiac and vascular function, eicosanoids, coagulation, and immunological responses. However, not all population studies have shown that omega-3 fatty acids are associated with reduced rates of coronary mortality. Such studies suffer either from small numbers of subjects or the population already had a high intake of fish. When comparing the highest intake of fish to that of the lowest fish intake, the beneficial effects of omega-3 fatty acids have been shown. In population-based case-control studies, the patients consuming modest amounts of fish, the equivalent of one fatty fish meal per week, had a significant lower risk of primary cardiac arrest compared with those who did not eat fish at all. In case-control studies, the intake of eicosapentaenoic acid and docosahexaenoic acid as reflected in adipose tissue content is inversely associated with risk of myocardial infarction.

Cell Membrane Trans -Fatty Acids and the Risk of Primary Cardiac Arrest

The relation of trans-fatty acid intake to life-threatening arrhythmias and primary cardiac arrest is unknown. We investigated the association of trans-fatty acid intake, assessed through a biomarker, with the risk of primary cardiac arrest in a population-based case-control study. Cases, aged 25 to 74 years, were out-of-hospital cardiac arrest patients attended by paramedics in Seattle, Washington from 1988 to 1999 (n=179). Controls, matched to cases by age and sex, were randomly identified from the community (n=285). Participants were free of previous clinically diagnosed heart disease. Blood was obtained at the time of cardiac arrest (cases) or at the time of an interview (controls) to assess trans-fatty acid intake. Higher total trans-fatty acids in red blood cell membranes was associated with a modest increase in the risk of primary cardiac arrest after adjustment for medical and lifestyle risk factors (odds ratio for interquintile range, 1.5; 95% CI, 1.0 to 2.1). However, trans isomers of oleic acid were not associated with risk (odds ratio for interquintile range, 0.8; 95% CI, 0.5 to 1.2), whereas higher levels of trans isomers of linoleic acid were associated with 3-fold increase in risk (odds ratio for interquintile range, 3.1; 95% CI, 1.7 to 5.4). These findings suggest that dietary intake of total trans-fatty acids is associated with modest increase and trans isomers of linoleic acid with a larger increase in the risk of primary cardiac arrest. These associations need to be confirmed in future studies that distinguish between trans isomers of linoleic acid and trans isomers of oleic acid.

Long-chain n-3 polyunsaturated fatty acids and out-of-hospital primary cardiac arrest: clinical and public health implications of observational studies and clinical trials*1

GISSI-Prevenzione findings provide additional support for the association of dietary intake of long-chain n-3 polyunsaturated fatty acids (PUFAs) from seafood [eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3) with the risk of coronary heart disease (CHD) mortality and sudden cardiac death. The findings also complement evidence from animal-experimental studies, cell biology and dietary intervention trials that suggest that long-chain n-3 PUFAs may protect against the life-threatening ventricular arrhythmias that result in sudden cardiac death. In this report, we review (1) several issues initially raised in the interpretation of clinical epidemiological studies of the association of long-chain n-3 PUFAs and the risk of CHD and (2) findings from a population-based case-control study of dietary intake and cell-membrane levels of long-chain n-3 PUFAs from seafood and the risk of primary cardiac arrest, that complements the findings from the GISSI-Prevenzione trial. Taken together, the available data supports both the role of low-dose, long-chain n-3 PUFAs in the prevention of sudden cardiac death and further targeted clinical research to examine more fully the effects of lowdose, long-chain n-3 PUFAs on the occurrence of life-threatening ventricular arrhythmias in other clinically defined, high-risk populations.

A Case-Crossover Analysis of Particulate Matter Air Pollution and Out-of-Hospital Primary Cardiac Arrest

Numerous epidemiologic studies have reported increases in the daily incidence of cardiovascular mortality and morbidity associated with increases in daily levels of particulate matter air pollution. We studied the association between the incidence of primary cardiac arrest and two daily measures of particulate matter using a case-crossover study of 362 cases of out-of-hospital cardiac arrest. All cases were attended by paramedics and had no history of clinically recognized heart disease or life-threatening comorbidities. We compared particulate matter levels at index times with particulate matter levels from referent days matched on day of week within strata defined by month and year. The estimated relative risk at a lag of 1 day for an interquartile range (IQR) change in nephelometry (0.51 x 10(-1) km(-1)) was 0.893 (95% CI = 0.779-1.024). The estimated relative risk at a lag of 1 day for an IQR change in PM10 (19.3 microg m(-3)) was 0.868 (95% CI = 0.744-1.012). Other lag periods gave similar results. We did not find evidence of confounding by carbon monoxide or sulfur dioxide. Analysis of effect modification by individual-level variables did not reveal any susceptible subgroups. These findings do no support an association between particulate matter and increased risk of primary cardiac arrest among persons without clinically recognized heart disease. The null results of this study may result from several factors, including the highly selected nature of this case series and the relatively low particulate matter levels in the Seattle metropolitan area.

RR interval variation, the QT interval index and risk of primary cardiac arrest among patients without clinically recognized heart disease.

Autonomic tone influences RR interval variation (RRV) and the heart rate-corrected QT interval index (QTI). Together, QTI and RRV may improve characterization of sympathovagal control and estimation of risk of primary cardiac arrest. We therefore examined effects of QTI and short-term RRV from standard, 12-lead electrocardiograms on risk of primary cardiac arrest among persons without clinically recognized heart disease. We analysed data from a case-control study of risk factors for primary cardiac arrest among enrollees in a large health plan. Cases (n=505) were enrollees aged 18 to 79 years without history of heart disease who had primary cardiac arrest between 1980 and 1994. Controls (n=529) were a demographically similar, stratified random sample of enrollees. We determined enrollee characteristics from ambulatory medical records, QTI and RRV from standard, 12-lead electrocardiograms, and medication use from automated pharmacy files. Low and high values of QTI and RRV were designated as the first and fifth quintiles of QTI (96% and 107%) and RRV (35 ms and 120 ms) among controls. In a model adjusting for clinical predictors of primary cardiac arrest, RRV modified the association between QTI and risk of primary cardiac arrest (P=0.05). Compared to high RRV and low QTI, the risk of primary cardiac arrest (odds ratio [95% CI]) was 0.95 [0.73-1.23] at low RRV and QTI, 1.23 [0.97-1.57] at high RRV and QTI, and 1.55 [1.16-2.06] at low RRV and high QTI. Risk remained elevated after adjustment for other electrocardiographic predictors and medication use. Autonomic dysfunction, characterized by high QTI and low RRV on the standard, 12-lead electrocardiogram, is associated with an increased risk of primary cardiac arrest among persons without clinically recognized heart disease.

Influenza vaccination and the risk of primary cardiac arrest.

Influenza epidemics are associated with an excess of mortality not only from respiratory diseases but also from other causes, and cardiovascular mortality increases abruptly during influenza epidemics, with little evidence of a lag period. In a population-based case-control study, the authors examined whether influenza vaccination was associated with a reduced risk of out-of-hospital primary cardiac arrest (PCA), a major contributor to cardiovascular mortality in the community. Cases of PCA (n = 342) without prior heart disease or life-threatening comorbidity that occurred in King County, Washington, were identified from paramedic incident reports from October 1988 to July 1994. Demographically similar controls (n = 549) were identified from the community by using random digit dialing. Spouses of subjects were interviewed to assess treatment with influenza vaccine during the previous year and other risk factors. After adjustment for demographic, clinical, and behavioral risk factors, influenza vaccination was associated with a reduced risk of PCA (odds ratio = 0.51, 95 percent confidence interval: 0.33, 0.79). The authors suggest that while the association of influenza vaccination with a reduced risk of PCA is consistent with cohort studies of influenza vaccination and total mortality, further studies are needed to determine whether the observed association reflects protection or selection.

Dietary intake of long-chain n−3 polyunsaturated fatty acids and the risk of primary cardiac arrest

Whether the dietary intake of long-chain n-3 polyunsaturated fatty acids (PUFAs) from seafood reduces the risk of ischemic heart disease remains a source of controversy, in part because studies have yielded inconsistent findings. Results from experimental studies in animals suggest that recent dietary intake of long-chain n-3 PUFAs, compared with saturated and monounsaturated fats, reduces vulnerability to ventricular fibrillation, a life-threatening cardiac arrhythmia that is a major cause of ischemic heart disease mortality. Until recently, whether a similar effect of long-chain n-3 PUFAs from seafood occurred in humans was unknown. We summarize the findings from a population-based case-control study that showed that the dietary intake of long-chain n-3 PUFAs from seafood, measured both directly with a questionnaire and indirectly with a biomarker, is associated with a reduced risk of primary cardiac arrest in humans. The findings also suggest that 1) compared with no seafood intake, modest dietary intake of long-chain n-3 PUFAs from seafood (equivalent to 1 fatty fish meal/wk) is associated with a reduction in the risk of primary cardiac arrest; 2) compared with modest intake, higher intakes of these fatty acids are not associated with a further reduction in such risk; and 3) the reduced risk of primary cardiac arrest may be mediated, at least in part, by the effect of dietary n-3 PUFA intake on cell membrane fatty acid composition. These findings also may help to explain the apparent inconsistencies in earlier studies of long-chain n-3 PUFA intake and ischemic heart disease.