Anger is a difficult emotion that involves physiological arousal and persists briefly. Siegman and colleagues (1987) proposed that the expression of anger—and not our experience of it—could result in heart disease. Examples of expressed anger include raising your voice during arguments and temper tantrums (Brannon et al., 2022).
A model based on anger inhibition, slow cardiovascular recovery, and low parasympathetic activity (vagal tone) suggests that these factors may be more consistent with the actual nature of anger in daily life and with known cardiovascular control mechanisms, potentially leading to cardiovascular disease (CVD; Brosschott & Thayer, 1998).
The relationship between anger and CVD is complex and has been recognized for a long time. Difficulties in objectively measuring emotions, including anger, pose challenges in research. However, studies have demonstrated an increase in the incidence of coronary artery disease (CAD) in patients with higher reported anger (Montenegro & Montenegro, 2018).
The multidimensional nature of anger and its assessment has been linked to the risk of both initiation and progression of CVD, with chronic feelings of anger, cynical distrust, and antagonistic behavior modestly associated with CVD risk. Anger/hostility is also connected to stress exposure and reactivity, exaggerated autonomic function, reduced heart rate variability, platelet aggregation, and inflammation (Suls, 2013).
A meta-analytic review of prospective evidence has found that anger and hostility are associated with increased CVD events in healthy populations and with poor prognosis in populations with existing CVD. The effect of anger and hostility on CVD events was found to be greater in men than in women (Chida & Steptoe, 2009).
Ironson et al. (1992) reported that anger recall reduced the ejection fraction (the ratio of blood pumped by the left ventricle during a contraction compared to its total filling volume) more significantly than exercise and other psychological stressors among patients with coronary artery disease. Dujovne and Houston (1991) linked expressed hostility with increased total cholesterol and low-density lipoprotein (LDL) in men and women. Goldman (1996) reported that individuals classified with high anger had a 2.5 times greater chance of re-clogging arteries after angioplasty. Siegman and colleagues (1992) found that training to slow speech rate and lower speech volume reduced CVR.
There is a relationship between anger and elevated nighttime blood pressure (Beatty & Matthews, 2009). Moreover, individuals who tend to ruminate on angry incidents typically have higher resting blood pressure compared to those who do not engage in rumination (Hogan & Linden, 2004).
In adolescents, anger has been linked to elevations in cardiovascular risk, with different dimensions of anger being differentially related to physical and psychological measures of cardiovascular risk (Siegel, 1984).
Provoking Anger Increases Cardiovascular Reactivity
Researchers have shown that provocation can increase cardiovascular reactivity (CVR).
CVR refers to the cardiovascular system's response to various stimuli, including stress, and can manifest as changes in blood pressure, heart rate, and vascular resistance (Page et al., 1954).
CVR is an early indicator of preclinical and clinical disease states and has the potential to inform interventions aimed at reducing the risk of CVD. Exaggerated blood pressure responses to stress, such as those measured during the cold pressor task, can predict the subsequent development of essential hypertension in initially normotensive individuals (Treiber et al., 2003).
This predictive capacity has been observed in long-term epidemiological studies spanning 20 years or more. Furthermore, CVR has been associated with other measures of subclinical disease, such as increased left ventricular mass and carotid atherosclerosis, although more research is needed to fully understand these relationships (Treiber et al., 2003).
Several factors influence the variability in CVR among individuals, including genetic predispositions, psychological stress, and physical activity levels. For instance, heightened CVR has been associated with a positive family history of essential hypertension and can be observed early in life (Rose et al., 1986).
Additionally, physical activity has been shown to benefit CVR, with aerobically trained individuals exhibiting lower sympathetic nervous system reactivity and improved cardiovascular efficiency in response to stress (Huang et al., 2013).
CVR is also emerging as a potential risk factor for hypertension and coronary heart disease, with studies suggesting that individuals with exaggerated CVR during psychologically challenging tasks. Moreover, CVR during everyday stressors, such as verbal communication, has been linked to hypertension and coronary heart disease, highlighting the relevance of CVR in behavioral health and its potential as a target for clinical interventions (Thomas et al., 1995).
Extensive research has been conducted on the mechanisms underlying CVR and its role in the etiology of hypertension. It is proposed that repeated stressor episodes may lead to autoregulatory and structural changes in the resistive vessels, contributing to the development of hypertension (Cinciripini et al., 1986).
Additionally, a model of central nervous system control over peripheral response systems has been presented to explain individual differences in stress reactivity and their potential contribution to cardiovascular disease risk (Lovallo et al., 2005).
How Provoking Anger Affects Cardiovascular Health
Smith and Brown (1991) found that when provoked, women showed less CVR than men. While husbands increased their heart rate and systolic blood pressure while trying to control their wives, wives did not experience these changes when trying to control their husbands. The wives' systolic blood pressure only increased when their husbands expressed cynical hostility.
After provoking male undergraduates, Siegman, Anderson, Herbst, Boyle, and Wilkinson (1992) observed increased heart rate and blood pressure (diastolic and systolic). The participants reported experiencing considerable anger following their provocation.
Shimbo et al. (2024) found that brief experimentally-provoked anger interfered with endothelial cell relaxation, increasing peripheral resistance. Anxiety and sadness did not affect endothelial cell-mediated vasodilation.
The endothelium critically regulates vascular homeostasis. Vascular endothelial cells (ECs) maintain vascular tone and blood vessel integrity (Libby, 2018). Research indicates that endothelial dysfunction is an early pathological step in developing atherosclerosis and initiating cardiovascular disease (CVD) events (Aman & Margadant, 2023; Moreno, Sanz, & Fuster, 2009). Numerous studies have shown that mental stress tasks, like mental arithmetic or public speaking, can impair endothelium-dependent vasodilation (EDV).
Fredrickson et al. (2000) asked adult men and women to re-experience earlier anger experiences. More hostile participants produced larger, longer-duration blood pressure increases than less hostile individuals. Also, African Americans showed greater CVR than European Americans.
Bishop and Robinson (2000) studied Chinese and Indian men in Singapore who performed a difficult task with or without harassment. The harassed participants showed greater CVR than those who were not provoked.
Smith et al. (2004) reported that high-hostile husbands experienced greater cardiovascular reactivity during stressful interactions with their wives than low-hostile husbands.
Anger Expression Style Affects Physiological Responses
The influence of anger expression style on psychophysiological responses varies depending on whether individuals are exposed to an anger instigation and whether they are using their preferred mode of anger expression (Engebretson, Matthews, & Scheier, 1989). Expressed anger may contribute to heart disease by increasing cardiovascular reactivity (CVR), often revealed as increased blood pressure and heart rate in response to social stressors like a provocation. The State-Trait Anger Expression Inventory – II measures anger experience and anger expression (Spielberger, 1999).
Diamond (1982) hypothesized an anger-in dimension, which is the tendency to withhold the expression of anger, even when anger is warranted. Dembroski and colleagues (1985) reported that anger suppression could contribute to heart disease. Siegman (1994) recommended that patients develop an awareness of their anger but express it using a quiet, slow voice.
In women, the relationship between anger-in and anger-out and cardiovascular reactivity to stress has been studied, with findings indicating that moderate levels of anger-out are associated with lower blood pressure and heart rate reactions to stress (Abel, Larkin, & Edens, 1995).
Finally, suppressed anger in patients with CAD has been associated with an increased risk of adverse events, with this association being influenced by individual differences in Type D personality (Denollet et al., 2010). A Type D personality, or "distressed" personality, is characterized by high levels of negative affectivity (the tendency to experience negative emotions) and social inhibition (the tendency not to express emotions). Individuals with a Type D personality are often seen as worried, irritable, and gloomy and tend not to share these feelings because of fear of disapproval. This combination can lead to an increased risk of stress-related health problems.
The research indicates a notable association between Type D personality and cardiovascular disease Grande et al., 2011). Type D individuals tend to have worse cardiovascular outcomes, potentially due to physiological hyperreactivity to stress, unhealthy lifestyle choices, and more severe manifestations of acute coronary syndrome. However, the direct impact of Type D personality on cardiovascular function in the absence of CVD is less clear. Overall, Type D personality emerges as a risk marker for cardiovascular health, warranting attention in both clinical and general populations for its potential role in cardiovascular risk management.
Anger Control Predicts CVD Events
Different measures of hostility, including Anger Control, have been examined as predictors of CVD and ischemic heart disease (IHD). Low Anger Control has been shown to predict CVD events, suggesting that it may be an important factor to consider in the prevention and treatment of CVD (Haukkala et al., 2010).
Anger and hostility have been critically reviewed in the context of essential hypertension and coronary heart disease, with hostility potentially being a significant component of the Type A coronary-prone behavior pattern (Diamond, 1982).
Evidence-Based Anger Interventions
Cognitive-behavior therapy for anger has been studied for decades and found to be helpful (Beck & Fernandez, 1998). Recent reviews have found that mindfulness-based cognitive behavior therapy is especially helpful (Richard, Tazi, Frydecka, Hamid, & Moustafa, 2022).
Biofeedback, such as heart rate variability biofeedback, may also be helpful. HRV training may be useful in moderating one’s response to anger-inducing stimuli (Francis, Penglis, & McDonald, 2016) and affect physiological responses to anger provocation among patients with coronary artery disease (Lin, Lin, & Fan, 2022).
As Lehrer (2011) suggests, innovative approaches are often derived from clinical work. Dr. Inna Khazan has developed one such approach that integrates mindfulness, cognitive-behavior therapy, and biofeedback.
Dr. Inna Khazan's Perspective on Managing Anger
From Dr. Khazan's mindfulness perspective, anger is a difficult emotion. She does not describe it as a negative emotion because that would imply that we shouldn't experience it. Although we cannot control our feelings, we can choose our actions. We can identify anger triggers (e.g., sleep deprivation), disable them by changing our behavior (e.g., improving sleep hygiene), challenge our perceptions (e.g., they did not intend to hurt us), reframe (e.g., it's all small stuff), and moderate our responses to triggers using mindfulness meditation and psychophysiological self-regulation training.
Biofeedback can increase awareness of early anger warning signs (e.g., cold hands and muscle tension). Heart rate variability biofeedback can increase prefrontal cortex regions' (ventromedial prefrontal cortex and the orbitofrontal cortex) control of structures that generate anger (amygdala and anterior cingulate cortex) and reduce cardiovascular reactivity. We can develop rescue skills like pausing or leaving the situation when we are angry and have already taken unhelpful actions. Dr. Khazan's (2021) FLARE technique can help us choose a more helpful response to anger. Feel: Recognize early anger signs (e.g., a trigger, cognitions, emotions, and physiological changes). Label: Distance yourself by labeling your experience as anger or frustration. Allow: Permit yourself to feel angry. Respond: Select the most beneficial response. Expand Awareness: Zoom out from your negative experience, placing it within the perspective of all the positive and negative events in your internal and external environments.
Conclusion
The relationship between anger and cardiovascular disease (CVD) is multifaceted and significant, as various studies have indicated. Anger not only provokes physiological arousal but also contributes to cardiovascular reactivity (CVR), which has been linked to the progression and initiation of CVD. The expression of anger, highlighted by Siegman et al. (1987) and others, can manifest through behaviors like raised voices or temper tantrums, potentially increasing the risk of heart disease. Additionally, inhibition of anger expression, coupled with slow cardiovascular recovery and low vagal tone, may further predispose individuals to CVD, as suggested by Brosschott & Thayer (1998). Moreover, chronic anger and hostility correlate with increased stress reactivity, autonomic dysfunction, and inflammatory responses, all of which are risk factors for CVD. Research such as that by Goldman (1996) directly links high anger levels to increased occurrences of re-clogged arteries post-angioplasty, underscoring the clinical implications of effectively managing anger to mitigate CVD risks.
In light of these findings, Dr. Inna Khazan offers a mindfulness-based approach to managing anger, emphasizing that while anger is a difficult emotion, it is not inherently negative. According to Dr. Khazan, by identifying triggers and utilizing techniques like mindfulness meditation and heart rate variability biofeedback, individuals can enhance their control over anger responses. This approach not only helps in recognizing early warning signs of anger but also in choosing healthier responses, thereby potentially reducing cardiovascular reactivity and improving overall cardiovascular health. Dr. Khazan's methods, including the FLARE technique, represent a proactive strategy for mitigating the impact of anger on cardiovascular disease, aligning well with the broader body of research advocating for integrated emotional and physiological health interventions.
Glossary
amygdala: a small, almond-shaped structure in the temporal lobe, the amygdala is critical for emotional processing and is particularly known for its role in the perception of threats and the generation of fear and anger responses. It triggers immediate emotional reactions, including aggression.
anterior cingulate cortex (ACC): positioned in the front part of the cingulate cortex, the ACC is involved in a wide range of functions, including error detection, attention, motivation, and emotional regulation. It plays a role in controlling emotional responses and behavioral adaptation, helping to moderate responses to perceived threats or conflict, such as anger.
anger-in: a pattern where individuals hold in or suppress their feelings of anger rather than express them outwardly. This can be a risk factor for adverse health outcomes, particularly in patients with coronary artery disease (CAD), as it may be associated with increased stress and cardiovascular reactivity.
anger-out: the tendency to express anger outwardly, in an aggressive or confrontational manner. It contrasts with anger-in and is characterized by externalizing feelings of anger through verbal or physical actions.
cardiovascular reactivity (CVR): the cardiovascular system's response to stress, including changes in heart rate, blood pressure, and vascular resistance. High cardiovascular reactivity can be a risk factor for developing cardiovascular diseases
coronary artery disease (CAD): a condition characterized by the narrowing or blockage of the coronary arteries, usually due to atherosclerosis. This can lead to reduced blood flow to the heart muscle, causing chest pain (angina), shortness of breath, or other symptoms, and can result in a heart attack if a coronary artery becomes completely blocked.
endothelium: a thin layer of simple squamous epithelial cells that lines the interior surface of blood vessels. This layer forms an interface between circulating blood in the lumen and the rest of the vessel wall, playing critical roles in vascular function, including regulating blood flow, vascular tone, and blood coagulation.
endothelium-dependent vasodilation (EDV): the widening of blood vessels that results from the relaxation of the blood vessel walls. This process is mediated by the endothelium and is crucial for maintaining proper blood flow and blood pressure. EDV is typically triggered by substances released by endothelial cells in response to various stimuli, including physical activity or chemical signals.
ejection fraction: a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction. A normal ejection fraction is typically between 55% and 70%. It is a key indicator of heart function and is often used to diagnose and track heart failure.
ischemic heart disease (IHD): also known as coronary artery disease (CAD), IHD occurs when the blood supply to the heart muscle is restricted, typically due to blockage in one or more coronary arteries. This leads to insufficient oxygen supply to the heart tissue, which can cause chest pain (angina), heart attacks, and other cardiovascular complications.
low-density lipoprotein (LDL): LDL, often called "bad" cholesterol, carries cholesterol particles throughout your body. LDL cholesterol builds up in the walls of your arteries, making them hard and narrow, which increases the risk of cardiovascular disease.
orbitofrontal cortex (OFC): situated above the eye sockets, the OFC is integral to impulse control and the modulation of emotions based on the expected rewards or punishments of an action. It helps regulate anger and aggression through its role in understanding social cues and consequences.
total cholesterol: the sum of all cholesterol types in the blood, including low-density lipoprotein (LDL), high-density lipoprotein (HDL), and very low-density lipoprotein (VLDL) cholesterol. It is a broad measure of an individual's cholesterol levels, crucial for assessing cardiovascular health.
Type D Personality: a personality characterized by high levels of negative affectivity (NA) and social inhibition (SI). Individuals with a Type D personality tend to experience negative emotions across time and situations. They are hesitant to share these emotions in social interactions because they fear rejection or disapproval. This personality type has been associated with worse cardiovascular outcome
vascular endothelial cells (ECs): cells that line the interior surface of blood vessels. They form a barrier between the vessel wall and the blood, and play a crucial role in regulating blood flow, vascular tone, and blood vessel integrity.
ventromedial prefrontal cortex (vmPFC): located in the lower frontal lobes, the vmPFC is involved in emotional regulation, decision-making, and risk assessment. It plays a crucial role in controlling aggressive and angry responses by evaluating social and emotional information.
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