Background: Post-traumatic stress disorder (PTSD) may develop in the aftermath of an acute myocardial infarction (MI). Whether PTSD is a risk factor for cardiovascular disease (CVD) is elusive. The biological mechanisms linking PTSD with atherosclerosis are unclear.
Design: A critical review of 31 studies in the English language pursuing three aims: (i) to estimate the prevalence of PTSD in post-MI patients; (ii) to investigate the association of PTSD with cardiovascular endpoints; and (iii) to search for low-grade systemic inflammatory changes in PTSD pertinent to atherosclerosis.
Methods: We located studies by PubMed electronic library search and through checking the bibliographies of these sources.
Results: The weighted prevalence of PTSD after MI was 14.7% (range 0-25%; a total of 13 studies and 827 post-MI patients). Two studies reported a prospective association between PTSD and an increased risk of cardiovascular readmission in post-MI patients and of cardiovascular mortality in combat veterans, respectively. In a total of 11 studies, patients with PTSD had increased rates of physician-rated and self-reported cardiovascular diseases. Various cytokines and C-reactive protein were investigated in a total of seven studies suggesting that PTSD confers a pro-inflammatory state.
Conclusions: Increasing evidence suggests that PTSD specifically related to MI develops considerably frequently in post-MI patients. More research is needed in larger cohorts applying a population design to substantiate findings suggesting PTSD is an atherogenic risk factor and to understand better the suspected behavioural and biological mechanisms involved.
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http://dx.doi.org/10.1097/01.hjr.0000214606.60995.46 | DOI Listing |
Kardiol Pol
January 2025
Department of Electrocardiology and Heart Failure, Medical University of Silesia in Katowice, Katowice, Poland.
Background: Sleep-disordered breathing (SDB) impairs exercise capacity after myocardial infarction (MI).
Aims: This study aimed to evaluate the impact of SDB on the efficacy of post-MI cardiac rehabilitation (CR).
Methods: The study evaluated consecutive patients up to 28 days after MI who participated in outpatient CR as part of the Polish Managed Care after Acute Myocardial Infarction program.
Eur J Cardiovasc Nurs
January 2025
Department of Clinical Sciences Malmö, Lund University, Box 117, 221 00 Lund, Malmö, Sweden.
Aims: Improved dietary habits are important for successful secondary prevention after myocardial infarction (MI), with counselling and support on healthy dietary habits constituting a cornerstone of cardiac rehabilitation (CR). However, there is limited knowledge on how to optimize CR organization to motivate patients to adopt healthy dietary habits. We aimed to explore associations between CR programme structure, processes, and self-reported dietary habits 1 year post-MI.
View Article and Find Full Text PDFMetabolites
December 2024
Department of Cardiology, Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland.
Vitamin D deficiency is one of the most common metabolic disorders in the European population. A low level of 25-OH vitamin D3 is related to an elevated risk of myocardial infarction (MI). The aim of our study was to examine the relationship between calcidiol and calcitriol serum concentration and left ventricular ejection fraction early after interventional treatment for acute coronary syndrome.
View Article and Find Full Text PDFJ Cardiovasc Nurs
December 2024
Background: Research has shown that younger patients who have had a myocardial infarction (MI) experience more emotional distress than their older counterparts.
Objective: In this study, we aimed to compare emotional distress 2 months post-MI (follow-up 1) between younger (<55) vs older (≥55) patients in Sweden, and investigate its impact on working status and 4 secondary preventive goals 1 year after MI (follow-up 2).
Methods: Data (N = 50 213) from the SWEDEHEART National Quality Registers for Cardiac Care, which covers approximately 90% of all MIs in Sweden, were used.
J Physiol
December 2024
Daniel Baugh Institute for Functional Genomics and Computational Biology, Department of Pathology and Genomic Medicine, Thomas Jefferson University, Philadelphia, PA, USA.
Loss of cardiac physiological function following myocardial infarction (MI) is accompanied by neural adaptations in the baroreflex that are compensatory in the short term, but then become associated with long-term disease progression. One marker of these adaptations is decreased baroreflex sensitivity, a strong predictor of post-MI mortality. The relative contributions of cardiac remodelling and neural adaptation in the sensory, central brainstem and peripheral ganglionic loci to baroreflex sensitivity changes remain underexplored.
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