Pathophysiology of Acute Coronary Syndromes—Diagnostic and Treatment Considerations

Theofilis, Panagiotis; Oikonomou, Evangelos; Chasikidis, Christos; Tsioufis, Κonstantinos; Tousoulis, Dimitris

doi:10.3390/life13071543

Cited by 8 publications

(6 citation statements)

References 64 publications

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“…The gradual increase in coronary artery plaques leads to a narrowing of the arterial lumen, resulting in reduced blood flow to the heart and the occurrence of myocardial ischemia. The further progression of coronary artery plaques can lead to sudden rupture, forming a thrombus that obstructs the artery, causing a sudden reduction in blood flow and thus triggering UA [46].…”

Section: Discussionmentioning

confidence: 99%

Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization

Xu,

Dirsch,

Dahmen

2024

JCM

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Background: Patients with angina are often suffering from comorbidities such as varying degrees of hepatic dysfunction. However, the impact of angina on the incidence of hepatic failure (HF) remains unclear. Methods: The genetic data were retrieved from genome-wide association studies. Five Mendelian randomization methods were used to investigate the causal relationship between unstable angina (UA), stable angina (SA), and HF. The result of the Inverse variance weighted (IVW) method was deemed the principal result. In addition, we performed a comprehensive sensitivity analysis to verify the robustness of the results. Results: The IVW results showed that UA (Odds ratio (OR): 2.055, 95% confidence interval (CI): 1.171–3.606, p = 0.012) was causally associated with the incidence of HF. SA (OR: 1.122, 95% CI: 0.738–1.706, p = 0.591) was not causally associated with the incidence of HF. Sensitivity analysis did not identify any bias in the results. Conclusions: UA turned out to be a risk factor for HF. SA does not have a significant causal effect on HF. Therefore, it is highly recommended that patients with chronic liver disease seek prompt medical attention and undergo regular monitoring of liver function when experiencing UA. This may help them to reduce the risk of HF.

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Section: Discussionmentioning

confidence: 99%

Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization

Xu,

Dirsch,

Dahmen

2024

JCM

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“…When plaque rupture occurs, the thrombogenic lipid-rich core is exposed to circulation, leading to platelet activation and aggregation. This results in the development of an occlusive thrombus causing myocardial ischemia and potentially myocardial infarction [9].…”

Section: Plaque Rupturementioning

confidence: 99%

“…Coronary artery disease (CAD) and acute coronary syndromes (ACS) represent a significant global public health burden, contributing significantly to morbidity and mortality in the population [1] . Cardiovascular disease (CVD) is the most common cause of mortality and morbidity worldwide, primarily affecting low-and middle-income countries.…”

Section: Introductionmentioning

confidence: 99%

Acute coronary syndrome: Definition, pathophysiology, diagnosis, and management

Erick Alexander Cabrera Estrada,

Epitafio Rafael Mestre Sequeda,

Jairo Enrique Barcinilla Barros

et al. 2024

World J. Adv. Res. Rev.

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Acute coronary syndrome (ACS) represents the most severe form of presentation of ischemic heart disease and imposes a significant burden on morbidity and mortality worldwide, particularly in low- and middle-income countries. Within the clinical spectrum of coronary syndrome are ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. Although primarily caused by atherosclerotic plaque thrombosis or non-atherosclerotic causes, its pathophysiological mechanisms are not fully understood. Currently, the main mechanisms include plaque rupture, plaque erosion, calcified nodules, and non-atherosclerotic causes such as coronary vasospasm. For ACS diagnosis, the electrocardiogram (ECG) is recommended primarily, along with high-sensitivity cardiac troponins (hs-cTn), following recommended algorithms to determine the testing interval. Non-invasive diagnostic tools such as echocardiography, computed tomography (CT), and cardiac magnetic resonance (CMR) are also available. These are mainly indicated in patients with inconclusive ECG and hs-cTn results and for establishing differential diagnoses. The management of ACS should be multidisciplinary, encompassing pharmacological, invasive techniques, and non-pharmacological approaches. It should be individualized considering each patient's characteristics.

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“…Calcified nodules refer to discrete calcified structures within the coronary arteries that can contribute to luminal narrowing and subsequent ischemic events. The formation of calcified nodules in coronary arteries involves a complex interplay of biological processes, including inflammation, osteogenic transformation, and matrix remodeling [ 5 ]. Chronic inflammation within atherosclerotic plaques triggers the release of pro-inflammatory cytokines and growth factors, stimulating the migration and differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells.…”

Section: Plaque Phenotypesmentioning

confidence: 99%

Coronary Plaque Erosion: Epidemiology, Diagnosis, and Treatment

Theofilis,

Vlachakis,

Papanikolaou

et al. 2024

IJMS

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Plaque erosion (PE), a distinct etiology of acute coronary syndromes (ACSs), is often overshadowed by plaque ruptures (PRs). Concerning its epidemiology, PE has garnered increasing recognition, with recent studies revealing its prevalence to be approximately 40% among ACS patients, challenging earlier assumptions based on autopsy data. Notably, PE exhibits distinct epidemiological features, preferentially affecting younger demographics, particularly women, and often manifesting as a non-ST-segment elevation myocardial infarction. There are seasonal variations, with PE events being less common in winter, potentially linked to physiological changes and cholesterol solidification, while peaking in summer, warranting further investigation. Moving to molecular mechanisms, PE presents a unique profile characterized by a lesser degree of inflammation compared to PR, with endothelial shear stress emerging as a plausible molecular mechanism. Neutrophil activation, toll-like receptor-2 pathways, and hyaluronidase 2 expression are among the factors implicated in PE pathophysiology, underscoring its multifactorial nature. Advancements in intravascular imaging diagnostics, particularly optical coherence tomography and near-infrared spectroscopy coupled with intravascular ultrasound, offer unprecedented insights into plaque composition and morphology. Artificial intelligence algorithms show promise in enhancing diagnostic accuracy and streamlining image interpretation, augmenting clinician decision-making. Therapeutically, the management of PE evolves, with studies exploring less invasive approaches such as antithrombotic therapy without stenting, particularly in cases identified early through intravascular imaging. Additionally, the potential role of drug-coated balloons in reducing thrombus burden and minimizing future major adverse cardiovascular events warrants further investigation. Looking ahead, the integration of advanced imaging modalities, biomarkers, and artificial intelligence promises to revolutionize the diagnosis and treatment of coronary PE, ushering in a new era of personalized and precise cardiovascular care.

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Pathophysiology of Acute Coronary Syndromes—Diagnostic and Treatment Considerations

Cited by 8 publications

References 64 publications

Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization

Causal Relationship between Angina and Hepatic Failure as Revealed by Mendelian Randomization

Acute coronary syndrome: Definition, pathophysiology, diagnosis, and management

Coronary Plaque Erosion: Epidemiology, Diagnosis, and Treatment

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