Endothelial dysfunction in patients with myocardial ischemia or infarction and nonobstructive coronary arteries

Şimşek, Ersin Çağrı; Sarı, Cenk; Kucukokur, Murat; Ekmekçi, Cenk; Çolak, Ayfer; Özdoğan, Öner

doi:10.1002/jcu.22902

Cited by 8 publications

(8 citation statements)

References 41 publications

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“…Endothelial dysfunction as measured by flow-mediated dilation (FMD) or acetylcholine-dependent plethysmography in peripheral arteries represents an early correlate of atherosclerosis and has predictive value for future cardiovascular events and accordingly has broad diagnostic implications [11]. Patients with IHD (comprising coronary artery disease and acute coronary syndrome) [12][13][14][15][16][17], heart failure [18,19] and myocardial infarction [20,21] display impaired endothelial function. Of note, endothelial dysfunction is directly correlated with oxidative stress and vascular inflammation [14,22], representing a strong diagnostic tool to investigate cardiovascular pathophysiology, morbidity and mortality [23,24].…”

Section: Reactive Oxygen and Nitrogen Species Related Pathomechanism Of Endothelial Dysfunction And Cardiovascular Damagementioning

confidence: 99%

Discovery of new therapeutic redox targets for cardioprotection against ischemia/reperfusion injury and heart failure

Daiber¹,

Andreadou

Oelze³

et al. 2021

Free Radical Biology and Medicine

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Section: Reactive Oxygen and Nitrogen Species Related Pathomechanism Of Endothelial Dysfunction And Cardiovascular Damagementioning

confidence: 99%

Discovery of new therapeutic redox targets for cardioprotection against ischemia/reperfusion injury and heart failure

Daiber¹,

Andreadou

Oelze³

et al. 2021

Free Radical Biology and Medicine

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“…Many vasodilators have different dilation effects on large and small vessels, which can affect some specific diseases. For example, the dilation of large vessels, such as the coronary artery, can alleviate myocardial ischemia ( Simsek et al, 2021 ), while the dilation of small vessels increases peripheral resistance ( Jensen et al, 2019 ). At present, our research is carried out on only the rabbit thoracic aorta, which is a large vessel.…”

Section: Discussionmentioning

confidence: 99%

Vasodilatory Effect of Guanxinning Tablet on Rabbit Thoracic Aorta is Modulated by Both Endothelium-Dependent and -Independent Mechanism

Ling

Shi²,

et al. 2021

Front. Pharmacol.

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Vasodilatory therapy plays an important role in the treatment of cardiovascular diseases, especially hypertension and coronary heart disease. Previous research found that Guanxinning tablet (GXNT), a traditional Chinese compound preparation composed of Salvia miltiorrhiza (Danshen) and Ligusticum chuanxiong (Chuanxiong), increase blood flow in the arteries, but whether vasodilation plays a role in this effect remains unclear. Here, we found that GXNT significantly alleviated the vasoconstriction of isolated rabbit thoracic aorta induced by phenylephrine (PE), norepinephrine (NE), and KCl in a dose-dependent manner with or without endothelial cells (ECs). Changes in calcium ion levels in vascular smooth muscle cells (VSMCs) showed that both intracellular calcium release and extracellular calcium influx through receptor-dependent calcium channel (ROC) declined with GXNT treatment. Experiments to examine potassium channels suggested that endothelium-denuded vessels were also regulated by calcium-activated potassium channels (Kca) and ATP-related potassium channels (KATP) but not voltage-gated potassium channels (kv) and inward rectifying potassium channels (KIR). For endothelium-intact vessels, the nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) contents in vascular tissue obviously increased after GXNT treatment, and pretreatment with the NO synthase inhibitor Nw-nitro-L-arginine methyl ester (L-NAME) or guanylyl cyclase inhibitor methylthionine chloride (MB) significantly inhibited vasodilation. An assessment of NO-related pathway protein expression revealed that GXNT enhanced the expression of phosphorylated endothelial NO synthase (eNOS) in a dose-dependent manner but had no effect on total eNOS, p-Akt, Akt, or PI3K levels in human umbilical vein ECs (HUVECs). In addition to PI3K/AKT signaling, Ca2+/calmodulin (CaM)-Ca2+/CaM-dependent protein kinase II (CaMKII) signaling is a major signal transduction pathway involved in eNOS activation in ECs. Further results showed that free calcium ion levels were decreased in HUVECs with GXNT treatment, accompanied by an increase in p-CaMKII expression, implying an increase in the Ca2+/CaM-Ca2+/CaMKII cascade. Taken together, these findings suggest that the GXNT may have exerted their vasodilative effect by activating the endothelial CaMKII/eNOS signaling pathway in endothelium-intact rings and calcium-related ion channels in endothelium-denuded vessels.

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Section: Discussionunclassified

“…Кроме того, для пациентов с ИМБОКА наличие хронического воспаления было показано ранее [4,6]. При этом очагами воспаления у пациентов с ИМБОКА могут являться как нестенозирующие атеросклеротические бляшки, так и дисфункциональное микрососудистое русло [4][5][6]. Так, было выявлено повышение концентрации СРБ, снижение резерва коронарного кровотока и взаимосвязь с хроническим воспалением у пациентов со стабильной стенокардией без стенозирующего атеросклероза [29].…”

Section: Discussionunclassified

“…обнаружили выраженную эндотелиальную дисфункцию у пациентов ИМБОКА в сравнении со стабильными пациентами при необструктивном поражении коронарных артерий, что также свидетельствует в пользу наличия хронического воспаления в стенке коронарных сосудов [6].…”

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Serum cytokines levels in patients with myocardial infarction with non-obstructive and obstructive coronary arteries

et al. 2021

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Aim. To compare the concentrations of proinflammatory and anti-inflammatory cytokines in patients with myocardial infarction with non-obstructive (MINOCA) and obstructive coronary arteries (MIOCA) in the early postinfarction period and after 1-year follow-up.Material and methods. The study included 40 patients with myocardial infarction (experimental group, 19 patients; control group, 21 patients). Three (15,7%) patients with diagnosed acute myocarditis were excluded from the final analysis. Blood samples were taken upon admission, on the 2nd, 4th and 7th days from hospitalization, and also after 1-year follow-up. Twenty-three parameters were analyzed using multiplex analysis and the Multiplex Instrument FLEXMAP 3D system (Luminex Corporation), as well as the MILLIPLEX map Human Cytokine/ Chemokine Panel II.Results. According to multiplex analysis of blood serum of the studied groups, a comparable increase in proinflammatory cytokines CCL-15, CCL-26, CCL-27 in the early postinfarction period and after 1-year follow-up, as well as antiinflammatory and regenerative cytokines CXCL-12, TPO in the early postinfarction period and after 1-year follow-up. In patients with MINOCA, higher concentrations of the following proinflammatory cytokines were determined: IL-16 upon admission (p=0,03), IL-20 on days 2 and 4 of the early postinfarction period (p=0,005 and p = 0.03), as well as CCL-15 on days 4 and 7 (p=0,05 and p=0,02). After 1-year follow-up, among the proinflammatory cytokines, a greater increase in CCL-21 (p=0,02) was noted in the patients of experimental group. Also, in patients with MINOCA, a greater increase in TPO was determined upon admission and on the 2nd day (p=0,02 and p=0,02), SCF — on the 7th day and after 1-year follow-up (p=0,04 and p=0,04), and LIF on the 4th day of early postinfarction period (p=0,007). In contrast, MIOCA patients showed a greater increase in CXCL-12 levels upon admission (p=0,04). At the same time, patients with MINOCA showed a higher level of C-reactive protein on the 1st day, as well as a higher relative monocyte count after 1-year follow-up.Conclusion. Despite a comparable increase in the cytokines CCL-8, CCL-13, CCL26, CCL-27 in patients of both groups, in patients with MINOCA there was a greater increase in proinflammatory cytokines IL-16, IL-20, CCL-15, CCL-21, and also CXCL-12, LIF, TPO, SCF, which have anti-inflammatory and regenerative activity. After 1 year follow-up, MINOCA patients showed a significant increase in CCL-21 and SCF, with a comparable increase in other proinflammatory cytokines in patients of both groups. A greater increase in proinflammatory cytokines in patients with MINOCA may indicate a more aggressive atherosclerosis course and lead to plaque destabilization followed by ischemic event.

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Endothelial dysfunction in patients with myocardial ischemia or infarction and nonobstructive coronary arteries

Cited by 8 publications

References 41 publications

Discovery of new therapeutic redox targets for cardioprotection against ischemia/reperfusion injury and heart failure

Discovery of new therapeutic redox targets for cardioprotection against ischemia/reperfusion injury and heart failure

Vasodilatory Effect of Guanxinning Tablet on Rabbit Thoracic Aorta is Modulated by Both Endothelium-Dependent and -Independent Mechanism

Serum cytokines levels in patients with myocardial infarction with non-obstructive and obstructive coronary arteries

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