The Impact of Mental Stress on Cardiovascular Health—Part II

Abstract

Endothelial dysfunction is one of the earliest manifestations of atherosclerosis, contributing to its development and progression. Mental stress induces endothelial dysfunction through increased activity of the sympathetic nervous system, release of corticotropin-releasing hormone from the hypothalamus, inhibition of nitric oxide (NO) synthesis by cortisol, and increased levels of pro-inflammatory cytokines. Mental-stress-induced increased output of the sympathetic nervous system and concomitant withdrawal of the parasympathetic inflammatory reflex results in systemic inflammation and activation of a neural–hematopoietic–arterial axis. This includes the brainstem and subcortical regions network, bone marrow activation, release of leukocytes into the circulation and their migration to the arterial wall and atherosclerotic plaques. Low-grade, sterile inflammation is involved in all steps of atherogenesis, from coronary plaque formation to destabilisation and rupture. Increased sympathetic tone may cause arterial smooth-muscle-cell proliferation, resulting in vascular hypertrophy, thus contributing to the development of hypertension. Emotional events also cause instability of cardiac repolarisation due to brain lateralised imbalance of cardiac autonomic nervous stimulation, which may lead to asymmetric repolarisation and arrhythmia. Acute emotional stress can also provoke severe catecholamine release, leading to direct myocyte injury due to calcium overload, known as myocytolysis, coronary microvascular vasoconstriction, and an increase in left ventricular afterload. These changes can trigger a heart failure syndrome mimicking acute myocardial infarction, characterised by transient left ventricular dysfunction and apical ballooning, known as stress (Takotsubo) cardiomyopathy. Women are more prone than men to develop mental-stress-induced myocardial ischemia (MSIMI), probably reflecting gender differences in brain activation patterns during mental stress. Although guidelines on CV prevention recognise psychosocial factors as risk modifiers to improve risk prediction and decision making, the evidence that their assessment and treatment will prevent CAD needs further evaluation.

Temporal characteristics and associated factors of discontinuation and outcomes after percutaneous coronary intervention

“…However, the existing literature also shows that other outcomes and psychological symptoms after PCI have a similar temporal characteristic ( Gu et al, 2016 ; Williams et al, 2021 ; Murad et al, 2022 ; Vulcanescu et al, 2023 ). Therefore, in addition to the effect of medication adherence on outcomes, this temporal characteristic may also reflect the physical and psychological stress effect of ischemic heart disease or PCI ( Vilchinsky et al, 2017 ; Birk et al, 2019 ; Kronish et al, 2020 ; Henein et al, 2022 ; Princip et al, 2023 ). The stress effect diminishes over time, resulting in a trend toward a decrease in associated medication nonadherence, psychological symptoms, and clinical outcomes.…”

“…Thus, medication nonadherence after PCI may also be a consequence of patient maladaptation to the stress of the disease and/or PCI ( Vilchinsky et al, 2017 ; Kronish et al, 2020 ; Narisawa et al, 2021 ; Princip et al, 2023 ). Clinical outcomes, on the other hand, may be influenced by both medication nonadherence and the stress of disease and/or PCI ( Vilchinsky et al, 2017 ; Henein et al, 2022 ; Princip et al, 2023 ). Future work is needed to test these possibilities and to explore the possibility of developing medication adherence interventions from a stress perspective for patients undergoing PCI ( Birk et al, 2019 ; von Känel et al, 2022 ).…”

Heartbeats and high scores: esports triggers cardiovascular and autonomic stress response

“…Considering these responses is crucial when addressing the health risks associated with esports, as gamers may be at risk of experiencing chronic stress outcomes. While short episodes of stress may not pose a significant health risk, repeated and prolonged cardiovascular activation can lead to vascular hypertrophy, progressively increasing peripheral resistance and contributing to the development of established hypertension ( 57 , 58 ).…”

Clinical and psychological associations and coping strategies for personality type D and depression in patients with coronary artery disease

“…Коморбидность проявлений психологического дистресса и сердечно-сосудистых заболеваний носит комплексный характер. С одной стороны, психосоциальные факторы предрасполагают к развитию и прогрессированию патологии кардиоваскулярной патологии [1]. С другой стороны, развитие серьезного заболевания (например, инфаркта миокарда) может способствовать возникновению психологических проблем, вплоть до развития психозов и депрессии [2].…”