Guidelines and Expert Consensus Documents summarize and evaluate all currently available evidence on a particular issue with the aim to assist physicians in selecting the best management strategies for a typical patient, suffering from a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines are not substitutes for textbooks. The legal implications of medical guidelines have been discussed previously.

A great number of Guidelines and Expert Consensus Documents have been issued in recent years by the European Society of Cardiology (ESC) as well as by other societies and organizations. Because of the impact on clinical practice, quality criteria for development of guidelines have been established in order to make all decisions transparent to the user. The recommendations for formulating and issuing ESC Guidelines and Expert Consensus Documents can be found on the ESC web site (http://www.escardio.org/knowledge/guidelines/rules).

In brief, experts in the field are selected and undertake a comprehensive review of the published evidence for management and/or prevention of a given condition. A critical evaluation of diagnostic and therapeutic procedures is performed, including assessment of the risk–benefit ratio. Estimates of expected health outcomes for larger societies are included, where data exist. The level of evidence and the strength of recommendation of particular treatment options are weighed and graded according to predefined scales, as outlined in the tables below.

The experts of the writing panels have provided disclosure statements of all relationships they may have which might be perceived as real or potential sources of conflicts of interest. These disclosure forms are kept on file at the European Heart House, headquarters of the ESC. Any changes in conflict of interest that arise during the writing period must be notified to the ESC. The Task Force report was entirely …

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European guidelines on cardiovascular disease prevention in clinical practice (version 2012) : the fifth joint task force of the European society of cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of nine societies and by invited experts).

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.

Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy.

Social support has been reliably related to lower rates of morbidity and mortality. An important issue concerns the physiological mechanisms by which support influences such health endpoints. In this review, I examine evidence linking social support to changes in cardiovascular, neuroendocrine, and immune function. Consistent with epidemiological evidence, social support appears to be related to more positive “biological profiles” across these disease-relevant systems. Recent research on immune-mediated inflammatory processes is also starting to provide data on more integrative physiological mechanisms potentially linking social support to health. The implications of these links, along with future research directions are discussed.

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Social Support and Health: A Review of Physiological Processes Potentially Underlying Links to Disease Outcomes

http://hwmaint.circ.ahajournals.org/cgi/reprint/110/9/e82.pdf

ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction

CONTEXT Depression and low perceived social support (LPSS) after myocardial infarction (MI) are associated with higher morbidity and mortality, but little is known about whether this excess risk can be reduced through treatment. OBJECTIVE To determine whether mortality and recurrent infarction are reduced by treatment of depression and LPSS with cognitive behavior therapy (CBT), supplemented with a selective serotonin reuptake inhibitor (SSRI) antidepressant when indicated, in patients enrolled within 28 days after MI. DESIGN, SETTING, AND PATIENTS Randomized clinical trial conducted from October 1996 to April 2001 in 2481 MI patients (1084 women, 1397 men) enrolled from 8 clinical centers. Major or minor depression was diagnosed by modified Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria and severity by the 17-item Hamilton Rating Scale for Depression (HRSD); LPSS was determined by the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Social Support Instrument (ESSI). Random allocation was to usual medical care or CBT-based psychosocial intervention. INTERVENTION Cognitive behavior therapy was initiated at a median of 17 days after the index MI for a median of 11 individual sessions throughout 6 months, plus group therapy when feasible, with SSRIs for patients scoring higher than 24 on the HRSD or having a less than 50% reduction in Beck Depression Inventory scores after 5 weeks. MAIN OUTCOME MEASURES Composite primary end point of death or recurrent MI; secondary outcomes included change in HRSD (for depression) or ESSI scores (for LPSS) at 6 months. RESULTS Improvement in psychosocial outcomes at 6 months favored treatment: mean (SD) change in HRSD score, -10.1 (7.8) in the depression and psychosocial intervention group vs -8.4 (7.7) in the depression and usual care group (P<.001); mean (SD) change in ESSI score, 5.1 (5.9) in the LPSS and psychosocial intervention group vs 3.4 (6.0) in the LPSS and usual care group (P<.001). After an average follow-up of 29 months, there was no significant difference in event-free survival between usual care (75.9%) and psychosocial intervention (75.8%). There were also no differences in survival between the psychosocial intervention and usual care arms in any of the 3 psychosocial risk groups (depression, LPSS, and depression and LPSS patients). CONCLUSIONS The intervention did not increase event-free survival. The intervention improved depression and social isolation, although the relative improvement in the psychosocial intervention group compared with the usual care group was less than expected due to substantial improvement in usual care patients.

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Effects of treating depression and low perceived social support on clinical events after myocardial infarction: the Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) Randomized Trial.

Background: Narrative review strategies and meta-analyses have shown that drug treatment and exercise rehabilitation regimens can reduce psychological distress and postmyocardial infarction mortality and recurrence. Objective: To question whether the addition of psychosocial interventions improves the outcome of a standard rehabilitation regimen for patients with coronary artery disease. Methods: We performed a statistical meta-analysis of 23 randomized controlled trials that evaluated the additional impact of psychosocial treatment of rehabilitation from documented coronary artery disease. Anxiety, depression, biological risk factors, mortality, and recurrence of cardiac events were the clinical end points that were studied. Mortality data were available from 12 studies, and recurrence data were available from 10 of the 23 studies. Results: The studies had evaluated 2024 patients who received psychosocial treatment vs 1156 control subjects. The psychosocially treated patients showed greater reductions in psychological distress, systolic blood pressure, heart rate, and cholesterol level (with effect size differences of 0.34, -0.24, -0.38, and -1.54, respectively). Patients who did not receive psychosocial treatment showed greater mortality and cardiac recurrence rates during the first 2 years of follow-up with log-adjusted odds ratios of 1.70 for mortality (95% confidence interval [CI], 1.09 to 2.64) and 1.84 for recurrence (CI, 1.12 to 2.99). Conclusions: The addition of psychosocial treatments to standard cardiac rehabilitation regimens reduces mortality and morbidity, psychological distress, and some biological risk factors. The benefits were clearly evident during the first 2 years and were weaker thereafter. At the clinical level, it is recommended to include routinely psychosocial treatment components in cardiac rehabilitation. The findings also suggest an urgent need to identify the specific, most effective types of psychosocial interventions via controlled research. (Arch Intern Med. 1996;156:745-752)

Psychosocial interventions for patients with coronary artery disease: a meta-analysis.

Psychosocial Interventions for Patients With Coronary Artery Disease

Alexithymia, defensiveness and cardiovascular reactivity to stress

We investigated two social determinants (i.e., availability of social support and status differentials of the provocateur) for the degree of perceived anger in two populations. Because no suitable tool was available, the conceptual and psychometric development and validation of a new vignette-based measure for anger level (STandardized Experience of Anger Measure, STEAM) is described first. Two versions of STEAM were developed: one for students and one for community-living adults. Through a series of four studies, two sets of a 12-item vignette-based questionnaire were developed and validated. The resulting test had excellent test-retest stability and high internal consistency. Using the new STEAM measure, a variety of analyses were conducted to test the hypothesized influence of social determinants of anger. In the student sample, presence of social support was associated with lessened anger, and in both samples decreasing status of the provocateur also led to lessened anger arousal. In addition, findings in both samples revealed that social support reduced anger when the provocateur was of higher status relative to situations of equal and lesser status. In the community sample, the availability of support was associated with greater intensity of the anger experience in the lesser status condition than in the equal or greater status condition. No gender main effects or interactions were noted.

Carmen Stossel

Papers

Psychosocial interventions for patients with coronary artery disease: a meta-analysis.

Psychosocial Interventions for Patients With Coronary Artery Disease

Alexithymia, defensiveness and cardiovascular reactivity to stress

Social determinants of experienced anger.