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      Behavior in a stressful situation, personality factors, and disease severity in patients with acute myocardial infarction: baseline findings from the prospective cohort study SECAMI (The Secondary Prevention and Compliance following Acute Myocardial Infarction-study)

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          Abstract

          Background

          Psychosocial stress has been identified as a risk factor in association with cardiovascular disease but less attention has been paid to heterogeneity in vulnerability to stress. The serial Color Word Test (CWT) measures adaptation to a stressful situation and it can be used to identify individuals that are vulnerable to stress. Prospective studies have shown that individuals with a maladaptive behavior in this test are exposed to an increased risk of future cardiovascular events. The aim of the present study was to investigate whether maladaptive behavior in the serial CWT alone or in combination with any specific personality dimension was associated with severity of myocardial infarction (MI).

          Methods

          MI-patients (n = 147) completed the test and filled in a personality questionnaire in close proximity to the acute event. The results were analyzed in association with four indicators of severity: maximum levels above median of the cardiac biomarkers troponin I and creatine kinase-MB (CKMB), Q-wave infarctions, and a left ventricular ejection fraction (LVEF) ≤ 50%.

          Results

          Maladaptive behavior in the serial CWT together with low scores on extraversion were associated with maximum levels above median of cardiac troponin I (OR 2.97, CI 1.08-8.20, p = 0.04) and CKMB (OR 3.33, CI 1.12-9.93, p = 0.03). No associations were found between the combination maladaptive behavior and low scores on extraversion and Q-wave infarctions or a decreased LVEF.

          Conclusions

          Maladaptive behavior in combination with low scores on extraversion is associated with higher cardiac biomarker levels following an MI. The serial CWT and personality questionnaires could be used to identify individuals vulnerable to the hazardous effects of stress and thereby are exposed to an increased risk of a more severe infarction.

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          Most cited references29

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          Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

          Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.
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            DS14: standard assessment of negative affectivity, social inhibition, and Type D personality.

            Type D personality-a joint tendency toward negative affectivity (NA) and social inhibition (SI)-is related to poor cardiac prognosis, but there is no standard for assessing Type D. This study reports on the Type D Scale-14 (DS14) as a standard measure of NA, SI, and Type D. The study included 3813 participants (2508 from the general population, 573 cardiac patients, 732 hypertension patients). They all filled out the DS14, containing 7-item NA and SI subscales; 275 subjects also completed the NEO-FFI, and 121 patients filled out the DS14 twice. Factor analysis of the DS14 yielded 2 dominant traits; all of the NA and SI items loaded between 0.62 to 0.82 on their corresponding factor (N = 3678). The NA scale covered dysphoria, worry, and irritability; the SI scale covered discomfort in social interactions, reticence, and lack of social poise. The NA and SI scales were internally consistent (alpha = 0.88/0.86; N = 3678), stable over a 3-month period (test-retest r = 0.72/0.82) and not dependent on mood and health status (N = 121). NA correlated positively with neuroticism (r = 0.68); SI correlated negatively with extraversion (r = -0.59/-0.65). Scale-level factor analysis confirmed the construct validity of the DS14 against the NEO-FFI. Using a cutoff of 10 (NA > or =10 and SI > or =10), 1027 subjects (28%) were classified as Type D, 21% in the general population versus 28% in coronary heart disease and 53% in hypertension (p < or = .001). Age, sex, and Type D (odds ratio, 3.98; 95% confidence interval, 3.2-4.6; p <.0001) were independently associated with cardiovascular morbidity. The DS14 is a brief, psychometrically sound measure of negative affectivity and social inhibition that could readily be incorporated in epidemiologic and clinical research.
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              Psychological stress and cardiovascular disease.

              There is an enormous amount of literature on psychological stress and cardiovascular disease. This report reviews conceptual issues in defining stress and then explores the ramifications of stress in terms of the effects of acute versus long-term stressors on cardiac functioning. Examples of acute stressor studies are discussed in terms of disasters (earthquakes) and in the context of experimental stress physiology studies, which offer a more detailed perspective on underlying physiology. Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors' contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress "causes" the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients' suffering and enhance their quality of life.
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                Author and article information

                Journal
                BMC Cardiovasc Disord
                BMC Cardiovascular Disorders
                BioMed Central
                1471-2261
                2011
                21 July 2011
                : 11
                : 45
                Affiliations
                [1 ]Department of Clinical Sciences, Lund University, Skåne University Hospital, Malmö, Sweden
                [2 ]Department of Neurology, Skåne University Hospital, Malmö, Sweden
                [3 ]Department of Cardiology, Lund University, Skåne University Hospital, Malmö, Sweden
                Article
                1471-2261-11-45
                10.1186/1471-2261-11-45
                3160986
                21777467
                aca10d38-d23c-409d-82c9-f281caf01644
                Copyright ©2011 André-Petersson et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 December 2010
                : 21 July 2011
                Categories
                Research Article

                Cardiovascular Medicine
                Cardiovascular Medicine

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