Sudden cardiac arrest (SCA) remains one of the most devastating and unpredictable medical emergencies, with survival rates that vary widely depending on rapid intervention. Out-of-Hospital Cardiac Arrest (OHCA), a specific subset of SCA, is a leading global cause of mortality, with survival hinging on immediate access to resuscitation and emergency medical services (EMS). While traditional risk factors such as cardiovascular disease are well-documented, recent research highlights the impact of psychological stress and major life events as potential triggers for SCA.

This article synthesizes key findings from multiple studies to provide a comprehensive view of OHCA incidence, survival trends, and the emerging connection between stress and fatal cardiac events.

While we traditionally associate SCA aetiology with structural heart disease or coronary artery blockages, an increasing body of evidence suggests a more elusive culprit: stress.

Could life’s emotional upheavals—bereavement, financial hardship, or even natural disasters—play a role in triggering fatal arrhythmias?

Recent studies provide compelling evidence that stress and anxiety may significantly influence cardiac electrical stability, potentially leading to SCA.

The enigma of Unexplained Sudden Cardiac Arrest (USCA)

A considerable proportion of SCA cases, particularly in younger individuals without known cardiovascular disease, remain unexplained. In these cases, traditional risk factors fail to provide answers. This has led researchers to explore psychosocial contributors, including stressful life events (SLEs), anxiety, and mental stress. The autonomic nervous system (ANS), which governs the balance between sympathetic and parasympathetic activity, emerges as a key player in this interaction. Current research suggests that acute stress can heighten sympathetic activation, increasing calcium influx into cardiac cells and potentially triggering fatal arrhythmias. 

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Stressful life events and SCA risk

A study conducted by Dalhousie/Western University compared SCA survivors with age- and sex-matched controls. Strikingly, individuals with unexplained SCA (USCA) had significantly higher Life Change Unit (LCU) scores, a measure of stress exposure, than those with explained SCA (ESCA) (308 ± 237 LCU vs. 163 ± 183 LCU; P = .030). However, when comparing the entire SCA cohort to controls, no significant difference was observed, highlighting the complexity of this relationship.

Similarly, Jeong et al. (2018) found that major life events occurring within six months before SCA were associated with a 2.26-fold increased risk of cardiac arrest. However, contrasting findings from Liu et al. (2020) indicated no significant difference in stress-generating potential between SCA survivors and controls. These discrepancies suggest that individual susceptibility and the timing of stress exposure may be crucial in determining cardiac risk.

Interestingly, research also suggests that chronic stress, rather than a single acute stressful event, may be a key risk factor. Long-term exposure to stress hormones such as cortisol can have deleterious effects on cardiovascular function, including increased blood pressure, inflammation, and endothelial dysfunction—all of which can contribute to arrhythmogenesis. Moreover, studies have shown that individuals with high levels of work-related stress or caregiving responsibilities have a greater risk of cardiovascular mortality.

Anxiety and mental stress

Batelaan et al. (2022) provided further interesting insights into this phenomenon. Their meta-analysis found that individuals with high baseline anxiety had a 2.44-fold increased risk of sudden cardiac death (SCD). Interestingly, natural disasters such as earthquakes have been consistently linked to increased SCA incidence, reinforcing the role of acute psychological stress in triggering fatal arrhythmias.

Specific case studies further emphasize the importance of stress as a trigger. For instance, studies following major sporting events, particularly high-stakes football matches, have documented a significant increase in cardiac events among spectators. This phenomenon, sometimes termed “sports-related sudden cardiac arrest,” underscores the role of acute emotional stress in destabilizing cardiac electrophysiology. The exact mechanisms remain under investigation, but increased sympathetic outflow and heightened platelet aggregation are likely contributors.

Biological mechanisms: From brain to heart

The interplay between stress and SCA is mediated through a complex neurocardiac pathway. The amygdala, a critical brain region for processing emotions, has been implicated in cardiovascular events. Stress-induced activation of the amygdala can influence cardiac ion channels through autonomic pathways, predisposing individuals to arrhythmias. Batelaan et al. (2022) emphasize the need for further research into neurotransmitter regulation—specifically the roles of GABA and glutamate—in altering cardiac electrophysiology.

Furthermore, the impact of inflammation and oxidative stress in stress-related cardiovascular risk is an emerging area of interest. Chronic stress is known to contribute to systemic inflammation, which in turn can promote atherosclerotic plaque instability and arrhythmogenesis. Elevated levels of inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) have been associated with an increased risk of SCA, highlighting potential pathways for targeted intervention.

Clinical and public health implications

Clinicians must consider stress and mental health as potential contributors to SCA, particularly in patients without conventional risk factors. Routine assessments of psychosocial stressors should become an integral part of cardiovascular evaluations.

Targeted interventions for at-risk individuals

Identifying individuals with chronic anxiety, recent major life events, or high-stress occupations may enable targeted interventions. Stress management programs, cognitive behavioral therapy (CBT), and mindfulness-based interventions could play a pivotal role in mitigating risk. Moreover, wearable technology capable of monitoring heart rate variability (HRV) and other autonomic markers could provide real-time insights into stress-induced physiological changes.

Future research priorities

Despite the growing body of evidence, significant knowledge gaps remain. Further research is needed to:

• Define optimal timeframes for assessing stress-induced cardiac risk.
• Investigate the efficacy of behavioral and pharmacological interventions in preventing stress-induced arrhythmias.
• Explore the role of brain function and neurotransmitters in modulating cardiac vulnerability.
• Examine the intersection between genetics, stress susceptibility, and cardiovascular outcomes. 

The emerging link between stress, anxiety, and SCA underscores the need to broaden our understanding of cardiovascular risk. While traditional factors remain crucial, psychosocial contributors must not be overlooked. Integrating mental health assessment into routine cardiac care may provide new avenues for prevention and ultimately save lives. As research continues to unravel this intricate connection, one thing is clear: our hearts are not immune to the weight of our emotions. By recognizing and addressing the profound impact of stress on cardiac health, we may move closer to a future where fewer lives are lost to sudden cardiac arrest.