Psychophysiology and the development of Cardiovascular Disease Flashcards
What is cardiovascular disease (CVD)?
It is a class of diseases that involve the heart and/or blood vessels
It has symptoms such as angina, MI, stroke
CVD is the single biggest killer in the UK
Describe Coronary Heart Disease (CHD).
- Can be ischaemic (heart is damaged due to oxygen deprivation, caused by restricted blood flow) or nonischaemic (cardiomyopathy)
- Underlying condition is usually coronary atheroschlerosis, a process of arterial wall thickening due to lipid deposition, inflammation and smooth muscle infiltration (Hansson 2005)
- Acute coronary syndromes (ACS). These include myocardial infarction (MI), unstable angina, and sudden cardiac death (SCD).
Describe the onset of acute coronary syndrome (ACS)
Chronic risk factors, atherosclerosis –> vulnerable arterial plaque –> plaque disruption, rupture/erosion (also impacted by acute factors - cardiovascular activation, coronary vasoconstriction and prothrombotic blood) –> Myocardial infarction, unstable angina, ventricular tachycardia/arrhythmia
What are the chronic, acute and episodic risk factors of CVD?
Chronic: e.g., elevated low-density lipoprotein (LDL) cholesterol, smoking, hypertension
Acute: transient pathophysiologic change (immediate change) resulting from exposure to external physical or psychological factors that can trigger events such as ischaemia, infarction or sudden death.
Episodic: behavioural characteristics that are neither acute nor chronic (e.g., depression)
Expand on cardiac arrhythmias.
Approximately 85-90% of sudden cardiac death (SCD) is due to the first arrhythmic event
80% of SCD events are caused by ventricular arrhythmias:
VT: ventricular tachycardia
VF: ventricular fibrillation
What does QT interval represent and how does it predict arrhythmic events and SCD?
- Echocardiographic representation of ventricular repolarization time
- Increased variability is a significant predictor of arrhythmic events and SCD
- Difference greatest at 6am
What are the triggers of arrhythmic events?
- PHYSICAL - exertion, activity
- time of day/year (peak @ 6am)
- PSYCHOLOGICAL: anger, mental stress, anxiety, mood disturbance, behavioural
Describe substrate-trigger interactions.
Increased intensity of stessors (trigger), as well as an increase in severity of personal vulnerability factors, leads to cardiac event
What are some behavioural triggers of CVD?
- Poor sleep associated prospectively with risk of CHD mortality (Mallon et al. 2002)
- Smoking increases risk of CHD (increases CA & cortisol levels, heart rate and blood pressure); but little evidence of triggering of ACS
- Alcohol: J-shaped relationship between consumption and mortality; evidence for heavy drinking as trigger lacking
- Vigorous physical activity has been found to trigger MI and SCD. Relative risk estimates of 2.1-5.9 (Mittleman et al 1993; Willich et al 1993)
Describe anger as a trigger of CVD?
- Mittleman et al 1995: Elevated reports of anger episodes within 2 hours prior to MI (2.4%)
- SHEEP study (1999) absolute incidence of intense anger in hour before onset was 1.2%
OR of acute MI in 2 hours after anger episode relative to no anger was 4.0 (1.9-9.4) - Risk of anger triggering inversely related to SES
Describe emotional triggers of CVD.
- Emotional factors can act as triggers of acute cardiac events in susceptible people (see Exercise 1 today and TED talk in Canvas)
- Susceptible because tendency of a heightened psychophysiological response profile
- Death of a partner associated with a range of major CV events in the immediate weeks and months after bereavement (Carey et al., 2014)
- In the month following 9-11, arrhythmic events more likely in ICD population.
- Triggering more common in people of lower SES and undergoing work stress
Describe psychobiological processes underlying acute triggering.
- Haemodynamic response: increased BP, HR and cardiac output, regional changes in blood flow
- Autonomic dysfunction: PNS withdrawal (decreased HR variability) /SNS activation
- Neuroendocrine activation: increases in HPA activity and in catecholamine levels (esp noradrenaline)
- Inflammatory processes activated
- Platelet activation can stimulate plaque disruption, promote thrombus formation & induce electrical instability
Describe the neurobiological processes underlying acute triggering.
- natural disasters are good to look at acute cardiac events
- Earthquake studies have shown (see Dar et al 2020):
- increased risk for acute cadriovascular complications such as MI, left ventricular dysfunction, and arrhythmias
- relative increase in SNS activity; increases in heart rate, low-frequency/high-frequency heart rate variability ratio, and risk of thromboembolism
- Coronary microvascular constriction during acute mental stress is hypothesized to be important mechanism behind stress-induced MI
- CAD patients with high peripheral vasoconstriction show increased stress activation (vs.low vasoconstrictors) in insula/parietal cortices and decreased activation in prefrontal cortex (Shah et al 2019).
Summarise acute triggering
- Converging evidence for supporting role of acute mental stress and heightened (negative) emotional processing in the acute triggering of cardiac events, may be moderated by SES
- Include processes that may promote plaque rupture, vascular environment encouraging thrombus formation, and neuroendocrine /autonomic processes that stimulate rhythmic disturbances
- Brain areas involved in fear inhibition and visuospatial processing of threat likely to be involved in stress-related vascular function, particularly coronary microvascular constriction
- Suggests the critical role of management techniques intended to reduce exposure to triggers and precautions in high-risk situations (e.g., natural disasters) in reducing the risk of acute cardiac events
What are risk factors?
- Risk factor in epidemiological terms is a variable associated with an increased risk of disease; disease often results from multiple risk factors (act as confounders; need to control for)
- Confer an independent risk on prognosis
- Have a direct dose-dependent relationship; increase in risk factor associated with concomitant increase in mortality (gradation effect)
- Established operational pathway (plausibility)
- Reduction in the risk factor leads to a concomitant improvement in survival
What are risk markers?
A variable that is quantitatively associated with a disease (or outcome) however direct manipulation of the marker does not necessarily alter the risk of the outcome
Lie somewhere on the causal pathway between a third pathway and cardiac prognosis
Give examples of psychological factors as potential risk factors for CVD.
Depression Anxiety Acute and chronic stress Anger & hostility Personality Psychosocial variables: Social support Socioeconomic status
Describe depression.
- Depression characterised by melancholic mood and symptoms such as changes in appetite, sleep patterns, diminished interest/pleasure in usual activities
- Distinguish between Adjustment Disorder (resolves quickly with appropriate support) with Depressed Mood and Major Depressive Disorder:
- – Between 30% and 50% of cardiac patients may have depressive symptoms (compared to 13% in population) – can resolve with psychoeducation, social support etc.
- – Major depressive disorder rates are higher in cardiac patients esp post MI (16-23%); maladaptive response, needs targetted intervention
What is the role of depression with CVD?
- Affects morbidity and mortality in CVD patients
- Independently associated with a more than threefold increased risk of sudden cardiac death in coronary artery disease (CAD; Lahtinen et al 2018)
- Depression diagnosis following CAD diagnosis associated with 2-fold higher risk of death (May et al 2017).
- More severe symptoms of depression predict shocks for VF/VT in ICD patients (TOVA cohort)
- Frequency of laughter independently associated with CVD incidence (HR=1.62 for low frequency laughers) after adjusting for multiple risk factors (Sakurada et al 2019)
look at ppt for table linking depression and CVD
Describe anxiety and CVD.
- Anxiety is common in cardiac patients, associated with poor health status and QoL
- Evidence that anxiety is independently associated with increased mortality in CVD
- Anxiety and depression tend to co-occur in post-MI patients
- Many studies have found a relationship between anxiety and adverse clinical events
Describe studies linking anxiety and CVD
Shen et al (2008) in a study of 735 older men (60+) without a history of CHD found that anxiety characteristics independently and prospectively predicted MI incidence after controlling for confounders (e.g., age, education, marital status, fasting glucose, BMI, systolic BP)
- These relationships remained significant after controlling for health behaviours, as well as depression, anger and hostility
- 2016 meta-analysis of 37 studies (n=1565699); Anxiety was associated with a 52% increased incidence of CVD (HR = 1.52; Batelaan et al)
look at ppt for table on depression & anxiety
Describe stress and its link with CVD.
- Conceptual issues in defining stress
- Can trigger events but less clear that it ‘causes’ events (at least for low-level stressors)
- Can be acute or chronic
- Excessive ‘stress reactivity’ may be a risk factor for CAD
- Permanent ‘stress’ (high levels of chronic stress) at work or home was associated with >2.1 times the risk of MI (Interheart study 2004)
- Whitehall II study (1998) found a 2.15 x increased risk for new CHD in men who experienced a mismatch between effort and reward at work
- Swedish cohort followed for 5 yrs (Orth-Gomer et al 2000) studied impact of work & marital stress on subsequent incidence of CV events in Stockholm women. Marital stress was associated with a 2.9 x increased risk of coronary events but work stress did not predict subsequent coronary events
Describe Chida & Steptoe’s study linking anger & hostility with CVD.
Chida & Steptoe meta-analysis(2009):
- reported a 20% increased risk of both incident CHD in initially healthy people and poor prognosis in CHD patients
- harmful effects of (trait) anger & hostility in healthy pops was greater in men
- when behavioural covariates (smoking, physical activity, BMI, SES) are controlled for effects no longer significant
What are the challenges with anger & hostility?
Not all anger the same: Anger-Out tendencies to express aggression outwardly; Anger-In tendencies to suppress or withhold anger
Correlations among anger measures tend to be low-to-moderate, which partly reflects multi-dimensional nature of anger
Self-reported ‘cynical hostility’ and intensity/frequency of anger more frequently show effects (Suls, 2013)