The relationship between non-alcoholic fatty liver disease and acute coronary syndrome severity: is non-alcoholic fatty liver disease a risk marker of coronary atherosclerotic disease?

Abstract

Background/Introduction Non-alcoholic fatty liver disease (NAFLD) has been significantly associated with atherosclerotic disease independent of classical risk factors. However, the role of NAFLD in this context remains unclear. The systemic inflammation described in NAFLD related to liver disease progression may be one factor that can influence the progression and instability of atherosclerotic disease and, consequently, in the clinical characteristics of acute coronary syndrome (ACS). Purpose To assess the potential relationship between NAFLD and ACS severity. Methods We performed a retrospective study in adult patients with ACS who presented to the emergency room of a quaternary care medical centre between March 2015 and March 2016 and selected 99 patients without previously known coronary artery disease or liver disease, without a history of significant alcohol consumption, terminal disease, other acute illness, use of statins, amiodarone, or other steatogenic drugs. The diagnostic criteria for acute myocardial infarction (AMI) with ST-segment elevation (STEMI) were ST elevation ≥1mm in ≥2 contiguous leads (2mm for leads V1 to V3). The acute myocardial infarction without ST-segment elevation (NSTEMI) diagnostic was established in patients who did not meet the criteria for STEMI and who had elevated necrosis markers (creatine kinase-MB isoform and troponin I). Unstable angina (UA) diagnostic was established in patients who did not meet the criteria for STEMI and NSTEMI but had more than three cardiovascular risk factors and typical thoracic pain. The presence of steatosis and its degrees was assessed using ultrasound, and the diagnosis of NAFLD was based on the presence of steatosis and clinical history. Results The diagnosis of UA, NSTEMI and STEMI was established in 40, 33 and 26 patients, respectively, and NAFLD was observed in 30%, 66.6% and 76.9% of these patients. NAFLD patients were 5.8 times more likely to have a diagnosis of AMI than UA (p<0.001), were 7.88 times more likely to have a diagnosis of STEMI than UA (p<0.001) and were 4.7 times more likely to have a diagnosis of NSTEMI than UA (p<0.01). Patients with grades 2 and 3 liver steatosis were 4.2 times more likely to have a diagnosis of AMI than UA (p<0.01) and were 8.2 times more likely to have a diagnosis of STEMI than UA (p<0.01). There was no significant relationship between other variables evaluated and the clinical presentation of ACS. Conclusion(s) In this study, the frequency of AMI presentation in NAFLD patients with ACS was significantly higher than the frequency of UA, suggesting a significant relationship between NAFLD and the severity of ACS, independent of the classic risk factors assessed. The results also suggest that the steatosis degree can proportionally influence this context. Therefore, NAFLD could be considered a potential risk marker for coronary atherosclerotic disease progression and instability. FUNDunding Acknowledgement Type of funding sources: None.

"Atherosclerotic Coronary Artery Disease and Nonalcoholic Fatty Liver Disease: Exploring the Possible Correlation"

“…The frequent, significant, and sometimes independent association between NAFLD and CVD, especially atherosclerotic disease, has been demonstrated in different ways and has reinforced the hypothesis that this liver disease is at least one risk marker for CVD [25]. Among the possible links between CVD and NAFLD is the systemic inflammatory response related mainly to NASH [6].…”

“…Regarding the correlation between the severity of NAFLD and the severity of CAD, in a cross-sectional study, severe NAFLD was related to the presence of coronary plaques, especially those at high risk, regardless of traditional risk factors [24]. Furthermore, a retrospective study showed a significant relationship between NAFLD and the severity of acute coronary syndrome (ACS), with the results also suggesting a correlation between the severity of both [25]. In a prospective cohort study, NAFLD was related to an increased risk of developing obstructive atherosclerotic lesions >50% and of percutaneous coronary interventions [26].…”

Features of myocardial infarction with ST segment elevation in patients with non-alcoholic liver steatosis and steatohepatitis

“…Метаболически-ассоциированная жировая болезнь печени (МАЖБП, старое название -неалкогольная жировая болезнь печени), развивающаяся в рамках метаболической дисфункции организма, рассматривается как фактор риска острого коронарного синдрома (ОКС) и может оказывать влияние на течение инфаркта миокарда (ИМ) [1]. В ряде исследований доказано, что у пациентов с МАЖБП наблюдается более тяжелое поражение коронарных артерий [2][3][4]. Тем не менее, связь между стеатозом печени и стеатогепатитом, т.е.…”

“…В связи с выполнением чрескожных вмешательств несколькими операторами рассчитывали значения κ Коэна для всех ангиографических показателей. Для оценки влияния набора факторов на вероятность наступления неблагоприятных событий в течение 18 5 (11,4) 3 (6,8) 6 (13,6) 15,5 (10;18,5) 0,453 0,568 0,816 0,950 0,847 0,128 0,048 <0,001 0,117 0,178 0,897 0,003 0,008 0,061 <0,001 <0,001 <0,001 <0,001 0,260 0,835 0,345 0,815 0,879 0,875 0,879 0,547 0,317 0,956 0,822 0,880 0,270 0,356 0,547 0,712 0,402 0,402 0,014 0,115 0,066 0,327 0,003 0,011 0,712 0,221 0,722 0,933 0,944 0,890 0,150 Примечание: ФВ ЛЖ -фракция выброса левого желудочка, ФПфибрилляция предсердий, ИМТ -индекс массы тела, ЧКВчрескожное вмешательство на коронарных артериях сосудов (извитость, кальциноз, признаки коллатерального кровотока) существенные различия между двумя группа не выявили. Итоговые значения шкалы SYN-TAX также не достоверно не отличались.…”

“…КЛИНИЧЕСКАЯ ФАРМАКОЛОГИЯ И ТЕРАПИЯ, 2023, 32 (4) Количество похожих исследований, в которых изучалось значение стеатогепатита в развитии ОКС, меньше, однако они свидетельствуют о самостоятельной патогенетической роли МАЖБП. При неалкогольном стеатогепатите наблюдается увеличение количества факторов риска атеросклероза и ИМ [44], а дестабилизация атеросклеротической бляшки может быть следствием высокой концентрации медиаторов воспаления и повышенной активности эффекторных клеток врожденного иммунитета.…”