Kop & Gottdiener (2014). The interaction between psychologic distress and biobehavioral processes in cardiovascular disease – Article summary

Myocardial infarction and sudden cardiac death can be triggered by emotional distress. The vulnerability for these diseases is determined by the presence of coronary artery disease or structural myocardial damage. The gradual progress of cardiovascular disease can be influenced by psychiatric, psychological and social conditions.

There are three phases of progression of cardiovascular disease:

1. Gradual subclinical disease progression
2. Vulnerable disease stage
3. Presentation of acute coronary syndromes

There are three groups of psychological risk factors:

1. Acute psychological risk factors (e.g. outbursts of anger)
   This refers to risk factors that act as triggers of cardiac events within one hour.
2. Episodic psychological risk factors (e.g. depression)
   This refers to risk factors that last from several weeks to two years.
3. Chronic psychological risk factors (e.g. personality traits)
   This refers to near-permanent risk factors that promote the gradual progression of coronary artery disease.

Chronic risk factors are associated with increased reactivity to acute stressors and promote the risk of development of episodic risk factors. Episodic risk factors are associated with an increased emotional and biological response to acute stressors.

Psychological distress refers to a negative internal state of the individual that is dependent on interpretation or appraisal of threat, harm or demand. Distress refers to the psychological reaction to environmental challenges (i.e. stressors). It is important to evaluate psychological distress in terms of its environmental precipitants (i.e. life events) and factors that may increase vulnerability to these events as well as psychological and social factors that can act as buffers.

Psychological distress and related psychologic factors (e.g. anxiety, hostility) contribute to cardiovascular disease progression. Prolonged and repeated exposure to short-term stressors and resulting acute distress responses may result in cumulative effects relevant to gradual cardiac and vascular disease progression.

Substantial increases in central and autonomic nervous system activity are a common phenomenon that link acute psychologic, psychiatric and neurologic events to major cardiac pathologies. Myocardial infarctions that are triggered by acute physical or emotional stressors are not necessarily associated with more severe underlying coronary disease and not associated with a worse prognosis. Acute coronary symptoms can result from psychological distress (e.g. stress regarding earthquake).

Myocardial ischemia develops when cardiac demand exceeds coronary blood supply to the heart muscle. Severe and sustained myocardial ischemia causes infarctions. Acute challenges (e.g. exercise, psychological distress) can induce transient myocardial ischemia by increasing cardiac workload. Acute psychological distress may cause decreased coronary supply as a result of coronary constriction. This is related to the magnitude of stress-induced blood pressure reactivity.

Acute psychological distress can act as a trigger for life threatening arrhythmias and sudden cardiac death. Acute stress leads to arrhythmias vulnerability. Acute distress-related cardiac electrical instability may play a role.

The takotsubo syndrome (i.e. stress cardiomyopathy) consists of substantial left ventricular dysfunction, apical ballooning, minimal underlying coronary artery disease and no or limited evidence of cardiac damage. It typically develops in post-menopausal women. Extensive sympathetic stimulation is a critical component. It can occur after acute emotional distress. However, there is a fast and uncomplicated recovery.

Myocardial infarction is associated with a higher prevalence of work, home and financial stress (1), major life events (2), lower locus of control (3) and more depression (4). There is predictive value of distress for adverse cardiovascular outcomes. The onset of depressive episodes in cardiac patients can be precipitated by environmental challenges associated with distress that are unrelated to cardiac disease.

Dysfunctional cognitions and maladaptive response to loss (e.g. health; important person) are antecedents of depression. The functional severity of cardiac disease is related to depressive symptoms. Social factors may also promote the onset of depression. Depression is predictive of first and recurrent myocardial infarction and sudden cardiac death. It is also predictive of heart failure rehospitalization and mortality. Depression is often undiagnosed and untreated which makes it a major risk factor for cardiac disease.

Fatigue, lack of energy and irritability are observed more frequently in cardiac patients with depression than in other patients. Prior diagnoses of mental disorders are a stronger predictor than diagnoses during admission for cardiac problems for post-MI mortality.

Vital exhaustion refers to a lack of energy (1), increased irritability (2) and feelings of demoralization (3). It is not sure whether vital exhaustion reflects the same thing as depression. Somatic depressive symptoms are associated with better predictive value of post-MI mortality and hospitalization than cognitive-affective depressive symptoms. Exhaustion may reflect the end-stage of prolonged uncontrollable psychological distress.

Depression and exhaustion in cardiac patients is not an artefact of underlying disease. Episodic risk factors may not be long enough to initiate and sustain an atherosclerotic process. Plaque activation, rather than gradual disease progression, may be primarily involved in the adverse risk associated with episodic psychological risk factors.

Chronic psychologic risk factors may promote the onset of initial stages of atherosclerosis by various biobehavioural pathways starting in young adulthood. This includes sympathetic nervous system-mediated processes (1) and adverse health behaviours (2) and their associations with known CAD risk factors. At advanced disease stages, chronic psychological factors may increase the effects of acute psychological risk factors.

There is an association between hostility and the severity of underlying coronary disease and an association with incident myocardial infarction. The association between hostility and myocardial infarction is stronger in younger men. The type D (i.e. distressed) personality refers to a chronic form of distress characterized by an individual’s inclination to experience negative emotions combined with social inhibition. It reflects a general propensity to psychological distress that adversely affects cardiovascular outcomes.

Post-traumatic stress disorder is a chronic risk factor and is predictive of increased healthcare use (1), adverse cardiovascular risk factors (2) and increased cardiovascular morbidity and mortality (3). Part of the association between PTSD and adverse cardiac outcomes is related to underlying psychological vulnerability factors. It is also possible that it is related to rumination about the adverse event.

Biologic responses to acute exogeneous stressors are adaptive. Prolonged exposure to stressors may lead to an imbalance of normal homeostatic functions. The allostatic load may be of relevance to the relationship between episodic and chronic distress as related to cardiovascular disease.

Psychologic distress is associated with sympathetic adrenomedullary (SAM) activation.         This includes circulating catecholamine levels and hypothalamic-pituitary-adrenal hormones. It is also associated with a shift toward increased sympathetic nervous system activity and decreased parasympathetic activity. Exhaustion and atypical forms of depression are characterized by inactivation of the CRH system, reduced norepinephrine levels and dampened hemodynamic reactivity to challenge tasks. Neurohormonal and autonomic nervous system dysregulation contribute to a disruption of homeostasis and contribute to cardiovascular disease progression.

The effects of prolonged psychological distress on the immune system is associated with elevated risk for acute coronary syndromes. Low-grade inflammation may alter the stability of atherosclerotic plaques and increase the risk of plaque rupture leading to acute coronary syndromes. Part of the association between depression and cardiovascular diseases can be explained by inflammation-related processes.