Impact of hospitalisation on behavioural and physiological stress responses associated with cardiovascular risk in visiting family members.

BACKGROUND: The hospitalisation of a patient in intensive care impacts the psychological health of family members, with a high prevalence of anxiety, depression, and post-traumatic stress symptoms reported among families of critically ill patients. Understanding of the behavioural and physiological impact is limited and presents a new area of focus. OBJECTIVES: The objective of this study was to evaluate behavioural and physiological stress responses of visiting family members following hospitalisation of their adult relative. METHODS: Prospective longitudinal evaluation included 40 family members of adult patients with admission to intensive or coronary care in a large tertiary care metropolitan hospital. Assessments were conducted at three timepoints: in-hospital within 1 week of admission and 2 weeks and 3 months post discharge. Assessments included duration and quality of sleep (self-reported and actigraphy measured), physical activity, dietary and alcohol patterns, resting heart rate and blood pressure, and morning blood cortisol and lipid levels. Assessment of a reference group of 40 non-hospital-exposed control participants was also conducted. RESULTS: At the in-hospital assessment, study participants reported lower sleep time, altered 24-h physical activity patterns, reduced dietary and alcohol intake, and higher systolic and diastolic blood pressure than a nonhospitalised reference group. Compared to in-hospital assessment, these altered behavioural and physiological responses improved over time except for systolic blood pressures which remained unchanged at 3 months post family member discharge. CONCLUSION: Hospitalisation is associated with altered behavioural and physiological responses in family members. These findings contribute to understanding of the impact of unexpected hospitalisation on family members' cardiovascular risk factors and provide insights into potential mechanisms for the proposed increased risk during this time. Elevated systolic blood pressure at 3 months post discharge suggests a prolonged cardiovascular stress response in many family members of critical care patients that requires further study, with a focus on contributing and potential modifiable factors.

Masters age football and cardiovascular risk.

BACKGROUND: Football (soccer) is popular among those of Masters age (≥35 years). Although regular exercise improves health, strenuous exercise causes a transient increase in cardiac risk. AIM: To gain insight into cardiac risk factors, symptoms, and knowledge, attitudes and beliefs about myocardial infarction (MI), and support for prevention. METHODS: A web-based survey using REDCap was completed by 153 amateur Masters footballers from A grade competition (n = 24), B or lower grade (n = 95) or social games (n = 34) in Sydney, Australia. RESULTS: Participants were aged 49.3 ± 7.5 years and primarily male (92.2%), Caucasian (88.9%) and university educated (75.2%). Risk factors included hypercholesterolaemia (37.3%), hypertension (19.6%), smoker (7.8%), overweight (40.5%) or obese (13.1%). One-fifth (21.6%) reported ≥1 potential cardiac symptom during activity in the prior year, for which one-quarter (24.2%) sought medical attention. Knowledge of typical MI symptoms was high (>80%) but lower (<40%) for less typical symptoms. Half (49.6%) were not confident to recognise MI in themselves. Half (49.0%) would remain on the field for 5-10 min with chest pain. Only 39.9% were aware that warning signs might precede MI by days. They overestimated survival from cardiac arrest (43%). Participants supported training in automatic external defibrillators (AED) and cardiopulmonary resuscitation (84%), AED at games (85%) and cardiac education (>70%). CONCLUSIONS: Cardiac risk factors are common In Masters footballers, with one in five experiencing possible cardiac symptoms in the prior year. While gaps exist in knowledge and optimal responses, strong support exists for preventive measures.

Psychological responses and coping behaviour of visiting family members during and following unplanned hospital admission.

AIMS: To describe the psychological symptoms and coping behaviours of visiting family members following the unplanned hospitalisation of their relative. BACKGROUND: Hospitalisation of a patient is recognised as a stressful time for visiting family members, who experience psychological morbidity and elevated health risk. DESIGN: This prospective longitudinal evaluation included 40 family members of patients with unplanned admission to coronary or intensive care. Assessments were conducted at 3 timepoints: in-hospital within 1 week of admission and again at 2 weeks and 3 months post-discharge. Measures included symptoms of anxiety, depression, and anger, coping strategies and social support. This paper adhered to STROBE guidelines. RESULTS: At the initial in-hospital assessment study participants reported higher anxiety, depression and anger symptoms levels compared to community matched control participants. Compared to in-hospital assessment, anxiety and depression levels were lower at 2 weeks and 3 months following hospital discharge. The use of active coping and the use of religion during early hospitalisation were associated with higher anxiety and depression symptoms at 3 months post-discharge. Conversely, use of instrumental support (getting help and advice from others), planning and venting during early hospitalisation were associated with lower depression symptoms at 3 months. Venting during the hospitalisation period was also associated with lower anxiety symptoms at 3 months. CONCLUSION: Results demonstrate the significant psychological impact of unplanned hospitalisation on visiting family members both during and following hospitalisation. The finding that prolonged psychological response is associated with individual coping strategies employed in the early hospitalised period informs potential preventative approaches for family members at risk of prolonged psychological morbidity following hospitalisation of their loved one. RELEVANCE TO CLINICAL PRACTICE: The reported psychological impact of hospitalisation on family members provides a strong imperative for nurses and health professionals to provide early individualised support to reduce the risk of long-term psychological morbidity.

The effect of metoprolol and aspirin on cardiovascular risk in bereavement: A randomized controlled trial.

BACKGROUND: Bereavement is associated with an increased risk of cardiovascular disease; however, no reports exist of interventions to reduce risk. In a randomized, double-blind, placebo-controlled trial of 85 recently bereaved participants, we determined whether ß-blocker (metoprolol 25 mg) and aspirin (100 mg) reduce cardiovascular risk markers and anxiety, without adversely affecting bereavement intensity. METHODS: Participants were spouses (n = 73) or parents (n = 12) of deceased from 5 hospitals in Sydney, Australia, 55 females, 30 males, aged 66.1 ±â€¯9.4 years. After assessment within 2 weeks of bereavement, subjects were randomized to 6 weeks of daily treatment or placebo, and the effect evaluated using ANCOVA, adjusted for baseline values (primary analysis). RESULTS: Participants on metoprolol and aspirin had lower levels of home systolic pressure (P = .03), 24-hour average heart rate (P < .001) and anxiety (P = .01) platelet response to arachidonic acid (P < .001) and depression symptoms (P = .046) than placebo with no difference in standard deviation of NN intervals index (SDNNi), von Willebrand Factor antigen, platelet-granulocyte aggregates or bereavement intensity. No significant adverse safety impact was observed. CONCLUSIONS: In early bereavement, low dose metoprolol and aspirin for 6 weeks reduces physiological and psychological surrogate measures of cardiovascular risk. Although further research is needed, results suggest a potential preventive benefit of this approach during heightened cardiovascular risk associated with early bereavement.

Coping by family members of critically ill hospitalised patients: An integrative review.

OBJECTIVES: To provide a comprehensive integrative review of research literature on 1) the coping strategies that are reported by adult family members following admission of their adult loved ones to the intensive care unit (ICU), 2) identify which coping strategies are associated with psychological response during this stressful experience, and 3) the factors that are associated with coping strategies. DATA SOURCES: Electronic databases: MEDLINE, PubMed, CINAHL, PsycINFO, and EMBASE; reference lists of journal publications. REVIEW METHODS: A total of 643 citations or abstracts were initially screened for content relevance, 15 were included in the integrative review, including 7 quantitative, 3 qualitative and 5 mixed methods studies. Included studies were all conducted in the hospital intensive care unit. RESULTS: Coping approaches such as self-distraction appear to be associated with lower psychological distress, and avoidant coping and denial associated with increased psychological distress including traumatic stress symptoms. Factors including social support, gender, age, relationship with the patient, decision maker role, and prior ICU experience can influence coping by family members. Uncertainty of the patient's prognosis and recovery heightens the intensity of the emotional response experienced by family members. Such family members appear at increased risk for experiencing depressive symptoms. CONCLUSIONS: From the studies reviewed, it is unclear if coping approaches employed by family members mediate psychological responses such as anxiety and depressive symptoms, or whether coping is a response to psychological stress experienced following hospitalisation of their relative. Future research should focus on the relationship between coping and psychological, physiological and health related behaviours in family members following ICU admission that might contribute towards transient increased health risk during this time. Additionally, future research should explore potential interventions to modify coping and promote family well-being following hospitalisation.

A genome-wide association study identifies new loci for factor VII and implicates factor VII in ischemic stroke etiology.

Factor VII (FVII) is an important component of the coagulation cascade. Few genetic loci regulating FVII activity and/or levels have been discovered to date. We conducted a meta-analysis of 9 genome-wide association studies of plasma FVII levels (7 FVII activity and 2 FVII antigen) among 27 495 participants of European and African ancestry. Each study performed ancestry-specific association analyses. Inverse variance weighted meta-analysis was performed within each ancestry group and then combined for a trans-ancestry meta-analysis. Our primary analysis included the 7 studies that measured FVII activity, and a secondary analysis included all 9 studies. We provided functional genomic validation for newly identified significant loci by silencing candidate genes in a human liver cell line (HuH7) using small-interfering RNA and then measuring F7 messenger RNA and FVII protein expression. Lastly, we used meta-analysis results to perform Mendelian randomization analysis to estimate the causal effect of FVII activity on coronary artery disease, ischemic stroke (IS), and venous thromboembolism. We identified 2 novel (REEP3 and JAZF1-AS1) and 6 known loci associated with FVII activity, explaining 19.0% of the phenotypic variance. Adding FVII antigen data to the meta-analysis did not result in the discovery of further loci. Silencing REEP3 in HuH7 cells upregulated FVII, whereas silencing JAZF1 downregulated FVII. Mendelian randomization analyses suggest that FVII activity has a positive causal effect on the risk of IS. Variants at REEP3 and JAZF1 contribute to FVII activity by regulating F7 expression levels. FVII activity appears to contribute to the etiology of IS in the general population.

Triggering of Acute Coronary Occlusion by Episodes of Vigorous Physical Exertion.

BACKGROUND: There is increasing recognition that heavy exertion can occasionally trigger an acute myocardial infarction (MI), although some uncertainties exist regarding the link. The primary aim of this study was to compare the relative risk (RR) of MI following vigorous exertion between those with confirmed coronary occlusion and those with a non-occluded culprit artery on acute angiography. Secondary aims were to determine if the risk of coronary occlusion is modified by the type of exercise (dynamic or isometric resistance), the frequency of regular exertion or whether the exertion was emotionally charged. METHODS: Seven hundred sixty-two (762) participants with MI (410 with coronary occlusion TIMI 0,1), and 352 (46%) with a non-occluded culprit artery (TIMI 2,3) completed a questionnaire within 4days of admission, detailing episodes of physical exertion in the 28hours prior to symptom onset and the usual frequency of such exertion. Exertion exposures within 1hour prior to symptom onset were compared to subjects' usual yearly exposure, with case-crossover methodology. RESULTS: The RR of symptom onset following heavy physical exertion level ≥6 (exertion scale 1-8), was higher in those with TIMI 0,1 compared to those with TIMI 2,3 flow (RR 6.30, 95% CI 4.70-8.50 vs 3.93, 2.89-5.30). The increased risk of coronary occlusion following vigorous exertion was observed following both dynamic exertion and isometric resistance, and did not differ between exertion types. The highest risk of coronary occlusion following exertion was observed in those who were sedentary (regular vigorous exertion <1day weekly) (RR=77, 95% CI 46-132), whereas in those who frequently perform regular vigorous physical exertion (>4days weekly), the RR of symptom onset during exertion was significantly lower, RR 2.3 (95% CI 1.5-3.6). There was no significant difference in relative risk based on whether the exertion was reported as emotionally charged. CONCLUSIONS: The relative risk that heavy exertion will trigger a non-fatal MI with an occluded artery is greater than for a non-occluded culprit artery. Both dynamic and isometric exertion increase the relative risk of event, while exposure to regular vigorous exertion reduces the relative risk.

Genome-Wide Association Transethnic Meta-Analyses Identifies Novel Associations Regulating Coagulation Factor VIII and von Willebrand Factor Plasma Levels.

BACKGROUND: Factor VIII (FVIII) and its carrier protein von Willebrand factor (VWF) are associated with risk of arterial and venous thrombosis and with hemorrhagic disorders. We aimed to identify and functionally test novel genetic associations regulating plasma FVIII and VWF. METHODS: We meta-analyzed genome-wide association results from 46 354 individuals of European, African, East Asian, and Hispanic ancestry. All studies performed linear regression analysis using an additive genetic model and associated ≈35 million imputed variants with natural log-transformed phenotype levels. In vitro gene silencing in cultured endothelial cells was performed for candidate genes to provide additional evidence on association and function. Two-sample Mendelian randomization analyses were applied to test the causal role of FVIII and VWF plasma levels on the risk of arterial and venous thrombotic events. RESULTS: We identified 13 novel genome-wide significant ( P≤2.5×10-8) associations, 7 with FVIII levels ( FCHO2/TMEM171/TNPO1, HLA, SOX17/RP1, LINC00583/NFIB, RAB5C-KAT2A, RPL3/TAB1/SYNGR1, and ARSA) and 11 with VWF levels ( PDHB/PXK/KCTD6, SLC39A8, FCHO2/TMEM171/TNPO1, HLA, GIMAP7/GIMAP4, OR13C5/NIPSNAP, DAB2IP, C2CD4B, RAB5C-KAT2A, TAB1/SYNGR1, and ARSA), beyond 10 previously reported associations with these phenotypes. Functional validation provided further evidence of association for all loci on VWF except ARSA and DAB2IP. Mendelian randomization suggested causal effects of plasma FVIII activity levels on venous thrombosis and coronary artery disease risk and plasma VWF levels on ischemic stroke risk. CONCLUSIONS: The meta-analysis identified 13 novel genetic loci regulating FVIII and VWF plasma levels, 10 of which we validated functionally. We provide some evidence for a causal role of these proteins in thrombotic events.

Triggers and Timing of Acute Coronary Syndromes.

Previous studies have shown that an acute coronary syndrome (ACS) may be triggered by external activities; however, their frequency, predictors, and significance are uncertain. We evaluated data from the National Israel Survey of Acute Coronary Syndromes, which was conducted in 2004 (February to March) in all 25 coronary care units and cardiac wards in Israel. Demographic and clinical data were recorded for consecutive participants, including potential triggers and time of symptom onset of ACS. Among the 1,849 patients who completed the trigger question, 1/4 (25.9%) reported a possible trigger, comprising heavy physical exertion (15.2%), emotional stress (8.3%), anger (1.1%), heavy meal (1.3%), and sexual activity (0.5%). Predictors of a triggered ACS were age <65 years, previous angina, no previous angiotensin-converting enzyme inhibitors/angiotensin 2 receptor blockers, impaired functional class, not having typical chest pain on admission, and a final diagnosis of unstable angina. The highest proportion of triggered ACS was between noon and 6 p.m. Physical exertion as a trigger was associated with reduced in-hospital mortality (0.4% vs 2.8%, p <0.05) and 1-year mortality. Emotional stress as a trigger did not influence in-hospital or 1-year mortality; however among those discharged from hospital, it was associated with increased 30-day rehospitalization (27.6% vs 19.3%, p <0.05) and a trend toward increased mortality (4.1% vs 2.0%, p = 0.10).

Triggering of acute myocardial infarction by respiratory infection.

BACKGROUND: Respiratory infection has been associated with an increased short-term risk of myocardial infarction (MI). However, previous studies have predominantly been conducted without angiographic confirmation of MI. The possibility can therefore not be excluded that raised troponin levels or electrocardiogram abnormalities that may be seen with respiratory infections are due to non-ischaemic causes. AIMS: To investigate the association between respiratory infection and angiographically confirmed MI. METHODS: Interviews were conducted within 4 days of hospitalisation in 578 patients with angiographically confirmed MI, to assess for recent exposure to respiratory infection symptoms and the usual annual frequency of these symptoms. Using case-crossover methodology, exposure to respiratory infection prior to the onset of MI was compared against the usual frequency of exposure in the past year. RESULTS: Symptoms of respiratory infection were reported by 100 (17%) and 123 (21%) within 7 and 35 days, respectively, prior to MI. The relative risk (RR) for MI occurring within 1-7 days after respiratory infection symptoms was 17.0 (95% confidence interval (CI) 13.2-21.8), and declined with subsequent time periods. In a subgroup analysis, the RR tended to be lower in groups taking regular cardiac medications. For those who reported milder, upper respiratory tract infection symptoms, the RR for the 1-7-day time period was 13.5 (95% CI 10.2-17.7). CONCLUSION: These findings confirm that respiratory infection can trigger MI. Further study is indicated to identify treatment strategies to decrease this risk, particularly in individuals who may have increased susceptibility.

Anxiety and anger immediately prior to myocardial infarction and long-term mortality: Characteristics of high-risk patients.

OBJECTIVE: Acute high levels of anger and anxiety are associated with an elevated risk of myocardial infarction (MI) in the following two hours. MIs preceded by these acute negative emotions may also have a poor long-term prognosis, but information about high-risk patients is lacking. We examined whether young age and female sex are associated with MIs that are preceded by negative emotions and whether age and sex moderate the subsequent increased mortality risk following MI preceded by negative emotions. METHODS: We conducted a secondary analysis of the Determinants of Myocardial Infarction Onset Study (N=2176, mean age=60.1±12.3years, 29.2% women). Anxiety and anger immediately prior to (0-2h) MI and the day before (24-26h) MI were assessed using a structured interview. Subsequent 10-year all-cause mortality was determined using the US National Death Index. RESULTS: Anxiety during the 0-2h pre-MI period was associated with younger age (OR=0.98,95% CI=0.96-0.99 per year) and female sex (OR=1.50,95% CI=1.11-2.02). Anger in the 0-2h pre-MI period was also associated with younger age (OR=0.95,95% CI=0.94-0.96) but not with sex (OR=0.93,95% CI=0.67-1.28). During follow-up, 580 (26.7%) patients died. Mortality rate was higher if MI occurred immediately after high anxiety, particularly in patients ≥65years (HR=1.80,95% CI=1.28-2.54) vs. younger patients (HR=0.87,95% CI=0.55-1.40; p-interaction=0.015). Other interactions with sex or anger were not significant. CONCLUSIONS: Patients with high anxiety or anger levels in the critical 2-hour period prior to MI are younger than those without such emotional precipitants. In addition, pre-MI anxiety is associated with an elevated 10-year mortality risk in patients aged ≥65years.

The impact of hospitalisation on a visiting family member: A case study and discussion.

Evidence suggests that when an immediate family member of a spouse is hospitalised, the partner's risk of death significantly increases. Hospitalisation can represent a time of great vulnerability and imposed stress for both the patient and their family members. Family members have been reported to give priority to the welfare of their ill relative and in their heightened emotional state, often adversely put their own health at risk. The paper presents a case study highlighting how an intensive care hospitalisation and discharge to rehabilitation experience for a patient's mother triggered an episode of myocardial infarction for her adult son. Discussion focuses on the caregiving burden and potential mechanisms for how hospitalisation may contribute to the health risk of immediate family members of hospitalised patients. Discussion also highlights the importance of family members receiving clear, continuous and consistent information from a limited number of clinicians to help reduce the stress associated with caregiving during acute hospitalisation.

Increased heart rate is associated with a prothrombotic state: The Framingham Heart Study.

Background Although a higher heart rate is associated with an increased risk of cardiovascular disease, the mechanism is not well understood. As thrombosis has an important role in plaque development and acute coronary syndromes, the increase related to heart rate may result from a prothrombotic imbalance. Methods We investigated the relation between heart rate and thrombotic potential in 3451 participants from the Offspring Cohort of the Framingham Heart Study (mean age 54 years, 55% women). Participants were divided into quintiles based on heart rate derived from a resting electrocardiogram. Results Higher heart rates were associated with significant age-adjusted increases in fibrinogen, viscosity, factor VII antigen, and impaired fibrinolytic potential (plasminogen activator inhibitor and tissue plasminogen activator antigen) among men and women, and von Willebrand factor antigen among men. Fibrinogen levels were 9% higher among men with a heart rate of 80.9 ± 8.1 beats/min (quintile 5) vs. 50.0 ± 3.9 beats/min (quintile 1) (314 vs. 287 mg/dl, p < 0.001 for linear trend) and 13% higher among women (83.5 ± 7.7 beats/min vs. 53.7 ± 3.5 beats/min (330 vs. 291 mg/dl, p < 0.001). The significant relations persisted after multivariate adjustment, other than among men, in whom factor VII was not significant and fibrinogen was borderline significant ( p = 0.065). Conclusions Higher heart rates are associated with a prothrombotic state. Because these factors are also associated with endothelial dysfunction and inflammation, these findings are consistent with an injurious effect of higher heart rates on the endothelium. Measures to reduce thrombotic potential may be of particular value in people with higher heart rates.

Biomarkers for the prediction of venous thromboembolism in the community.

BACKGROUND &OBJECTIVES: Venous and arterial thrombosis share common pathophysiology. Multiple biomarkers reflecting various biological pathways can predict arterial thrombosis. We studied whether this approach could identify persons at risk of first venous thromboembolism (VTE).

Gene-centric approach identifies new and known loci for FVIII activity and VWF antigen levels in European Americans and African Americans.

Coagulation factor VIII and von Willebrand factor (VWF) are key proteins in procoagulant activation. Higher FVIII coagulant activity (FVIII :C) and VWF antigen (VWF :Ag) are risk factors for cardiovascular disease and venous thromboembolism. Beyond associations with ABO blood group, genetic determinants of FVIII and VWF are not well understood, especially in non European-American populations. We performed a genetic association study of FVIII :C and VWF:Ag that assessed 50,000 gene-centric single nucleotide polymorphisms (SNPs) in 18,556 European Americans (EAs) and 5,047 African Americans (AAs) from five population-based cohorts. Previously unreported associations for FVIII :C were identified in both AAs and EAs with KNG1 (most significantly associated SNP rs710446, Ile581Thr, Ile581Thr, P = 5.10 × 10(-7) in EAs and P = 3.88 × 10(-3) in AAs) and VWF rs7962217 (Gly2705Arg,P = 6.30 × 10(-9) in EAs and P = 2.98 × 10(-2) in AAs. Significant associations for FVIII :C were also observed with F8/TMLHE region SNP rs12557310 in EAs (P = 8.02 × 10(-10) ), with VWF rs1800380 in AAs (P = 5.62 × 10(-11) ), and with MAT1A rs2236568 in AAs (P51.69 × 10(-6) ). We replicated previously reported associations of FVIII :C and VWF :Ag with the ABO blood group, VWF rs1063856(Thr789Ala), rs216321 (Ala852Gln), and VWF rs2229446 (Arg2185Gln). Findings from this study expand our understanding of genetic influences for FVIII :C and VWF :Ag in both EAs and AAs.

The effect of omega-3 polyunsaturated fatty acids on fibrin and thrombin generation in healthy subjects and subjects with cardiovascular disease.

Hypercoagulability plays a key role in the progression of cardiovascular disease (CVD). Although omega-3 polyunsaturated fatty acid (PUFA) intake has been inversely related to the risk of cardiovascular events, the mechanisms are not fully understood. The aim of this study was to investigate the effects of omega-3 on novel markers of global coagulation. The generation of fibrin and thrombin, measured via overall hemostasis potential (OHP) assay and calibrated automated thrombography, respectively, was determined in 40 healthy subjects and 16 patients with CVD at baseline and after 4 weeks of 640 mg/day omega-3 PUFA. In healthy subjects, fibrin generation was significantly reduced, as measured by overall coagulation potential (p = 0.013), OHP (p < 0.001), velocity of fibrin polymerization (p = 0.002), and significant increase in delay to fibrin generation (p = 0.002). The peak of generated thrombin was significantly reduced (p = 0.043). In subjects with CVD, omega-3 PUFA significantly reduced OHP and significantly increased the lag time to thrombin generation (both p < 0.001). Treatment with omega-3 PUFA had no effect on other fibrin and thrombin generation parameters in CVD patients. Four-week omega-3 PUFA supplementation reduced thrombotic potential in healthy subjects, as shown by reduced fibrin generation and peak thrombin. There was a greater effect on fibrin generation in healthy subjects compared with those with CVD.

Triggering of acute coronary occlusion by episodes of anger.

AIMS: The aim of this study was to report the association between episodes of anger and acute myocardial infarction (MI) in patients with angiographically confirmed coronary occlusion. METHODS AND RESULTS: 313 participants with acute coronary occlusion (Thrombolysis In Myocardial Infarction 0 or 1 at emergency angiography) reported frequency of anger episodes in the 48 h prior to MI. In primary analysis, anger exposures within 2 h and 2-4 h prior to symptom onset were compared with subjects' own usual yearly exposure to anger using case-crossover methodology. Anger level ≥5 (on an anger scale of 1-7) was reported by seven (2.2%) participants within 2 h of MI. Compared with usual frequency, the relative risk of onset of MI symptoms occurring within 2 h of anger level ≥5 (defined as very angry) was 8.5 (95% confidence interval 4.1-17.6). Anger level <5 was not associated with onset of MI symptoms. Compared with 24-26 h pre MI, anxiety scores >75th percentile on State-Trait Personality Inventory were associated with a relative risk of 2.0 (95% confidence interval 1.1-3.8) and in those above the 90th percentile, the relative risk of MI symptom onset was 9.5 (95% confidence interval 2.2-40.8). CONCLUSION: Findings confirm that episodes of intense anger, defined as being 'very angry, body tense, clenching fists or teeth' (within 2 h) are associated with increased relative risk for acute coronary occlusion. Additionally, increased anxiety was associated with coronary occlusion. Further study, including the role of potential modifiers, may provide insight into prevention of MI during acute emotional episodes.