scholarly journals New Interventional Therapies beyond Stenting to Treat ST-Segment Elevation Acute Myocardial Infarction

2021 ◽  
Vol 8 (9) ◽  
pp. 100
Author(s):  
Pablo Vidal-Calés ◽  
Pedro L. Cepas-Guillén ◽  
Salvatore Brugaletta ◽  
Manel Sabaté
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
St Segment Elevation ◽  
St Segment

Myocardial infarction remains the principal cause of death in Europe. In patients with ST-segment-elevation myocardial infarction (STEMI), a promptly revascularization with primary percutaneous intervention (PCI) has transformed prognosis in the last decades. However, despite increasing successful PCI procedures, mortality has remained unchanged in recent years. Also, due to an unsatisfactory reperfusion, some patients have significant myocardial damage and suffer left ventricular adverse remodeling with reduced function—all that resulting in the onset of heart failure with all its inherent clinical and socioeconomic burden. As a consequence of longer ischemic times, distal thrombotic embolization, ischemia-reperfusion injury and microvascular dysfunction, the resultant myocardial infarct size is the major prognostic determinant in STEMI patients. The improved understanding of all the pathophysiology underlying these events has derived to the development of several novel therapies aiming to reduce infarct size and to improve clinical outcomes in these patients. In this article, based on the mechanisms involved in myocardial infarction prognosis, we review the new interventional strategies beyond stenting that may solve the suboptimal results that STEMI patients still experience.

Abstract 17348: Necrostatin 7 Limits Myocardial Infarct Size and Reduces Cardiac Remodeling After Permanent Coronary Occlusion in Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yuri Dmitriev ◽  
Sarkis Minasian ◽  
Anna Dracheva ◽  
Andrey Karpov ◽  
Svetlana Chefu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Rat Model ◽  
Coronary Occlusion ◽  
Ventricular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Morphological Characteristics ◽  
Left Ventricular ◽  
Myocardial Infarct Size

Background: Reduction of irreversible myocardial ischemia-reperfusion injury (IRI) remains important. One of the promising strategies aimed at myocardial IRI alleviation is modulation of programmed cell death (PCD) pathways. PCD mode displaying morphological characteristics of necrosis, and amenable to pharmacological manipulation is referred to as necroptosis. Necroptosis inhibitor necrostatin-1 has been shown to exert cardio- and neuroprotective effects. In the present work, the effect of necrostatin-7 (Nec-7) on myocardial injury in the rat model of permanent coronary occlusion was studied. Methods: Male Wistar rats (n = 19) were anesthetized with pentobarbital. The animals were subjected to permanent coronary occlusion (PCO) and intraperitoneal (i.p.) Nec-7 administration 1 h prior to PCO at a dose of 14.5 mg/kg in dimethyl sulfoxide (DMSO) or DMSO alone at a dose of 3.1 g/kg. Control rats were treated with saline. Three weeks after PCO, serum levels of NT-proBNP were measured, and histological outcomes were assessed. The infarct size (IS, %) and infarct length (IL, mm) were analyzed morphometrically. Results: DMSO caused significant reduction in serum NT-proBNP level vs. Control (0.3 ± 0.19 vs. 0.5 ± 0.22 ng/ml, p = 0.001), while Nec-7 further decreased NT-proBNP level in comparison with DMSO (0.2 ± 0.14 ng/ml, p = 0.008 vs. DMSO). Compared with Control, DMSO reduced adverse left ventricular remodeling, as evidenced by reduction in IS (16.0 ± 2.92 and 12.9 ± 1.72%, p = 0.015) and IL (6.2 ± 0.89 and 3.8 ± 0.35 mm, p = 0.008). Nec-7 treatment resulted in additional reduction of both IS and IL vs. DMSO group (9.0 ± 4.91 % and 2.9 ± 1.62 mm, respectively; p = 0.013 and p = 0.011 vs. DMSO, respectively). Conclusion: Nec-7 has cardioprotective properties, reducing myocardial wall stress and myocardial remodeling in the rat model of myocardial infarction.

scholarly journals Plasma apelin level in acute myocardial infarction and its relation with prognosis: A prospective study

2021 ◽  
Vol 10 ◽  
pp. 204800402096397
Author(s):  
Ozge Guzelburc ◽  
Refik Demirtunc ◽  
Servet Altay ◽  
Tugba Kemaloglu Oz ◽  
Gulsah Tayyareci
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Control Group ◽  
Prognostic Parameters ◽  
St Segment Elevation ◽  
St Segment ◽  
Plasma Apelin

Objective Apelin is a novel adipocytokine with a significant role in ischemia/reperfusion injury that is synthesized and secreted in myocardial cells and coronary endothelium. There is debate on its value for the diagnosis and prognosis of myocardial infarction. We aimed to investigate plasma apelin level in patients with acute ST segment elevation (STEMI) and non-ST segment elevation (NSTEMI) myocardial infarction and its relationship with left ventricular function and prognostic parameters. Methods Forty-one patients with STEMI, 21 patients with NSTEMI and 10 patients as control group with normal coronary angiograms were included. Plasma apelin level at presentation was investigated regarding its relationship with other diagnostic and prognostic parameters. Results Apelin level was significantly higher in acute myocardial infarction (0.31 ± 0.56 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Likewise, it was found to be significantly higher in STEMI group (0.45 ± 0.73 ng/mL) compared to control group (0.08 ± 0.05 ng/mL) (p < 0.01). Although apelin was higher in NSTEMI group (0.13 ± 0.10 ng/mL) compared to control group (0.08 ± 0.05 ng/mL), this difference was not statistically significant (p > 0.05). No correlation was found between apelin and NT-proBNP, hsCRP, troponin, ejection fraction (EF) and Killip score (p > 0.05). A positive correlation was found between apelin and TIMI, GRACE and Gensini scores (p < 0.05). Only GRACE score was found to be correlated with apelin in MI groups. Conclusion Apelin level was found to be high in acute myocardial infarction. With its inotropic and vasodilator effects, apelin was thought to have a protective role against severe ischemia.

scholarly journals Phosphatidylserine Supplementation as a Novel Strategy for Reducing Myocardial Infarct Size and Preventing Adverse Left Ventricular Remodeling

2021 ◽  
Vol 22 (9) ◽  
pp. 4401
Author(s):  
David Schumacher ◽  
Adelina Curaj ◽  
Mareike Staudt ◽  
Franziska Cordes ◽  
Andreea R. Dumitraşcu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Ventricular Remodeling ◽  
Heart Function ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Novel Strategy

Phosphatidylserines are known to sustain skeletal muscle activity during intense activity or hypoxic conditions, as well as preserve neurocognitive function in older patients. Our previous studies pointed out a potential cardioprotective role of phosphatidylserine in heart ischemia. Therefore, we investigated the effects of phosphatidylserine oral supplementation in a mouse model of acute myocardial infarction (AMI). We found out that phosphatidylserine increases, significantly, the cardiomyocyte survival by 50% in an acute model of myocardial ischemia-reperfusion. Similar, phosphatidylserine reduced significantly the infarcted size by 30% and improved heart function by 25% in a chronic model of AMI. The main responsible mechanism seems to be up-regulation of protein kinase C epsilon (PKC-ε), the main player of cardio-protection during pre-conditioning. Interestingly, if the phosphatidylserine supplementation is started before induction of AMI, but not after, it selectively inhibits neutrophil’s activation, such as Interleukin 1 beta (IL-1β) expression, without affecting the healing and fibrosis. Thus, phosphatidylserine supplementation may represent a simple way to activate a pre-conditioning mechanism and may be a promising novel strategy to reduce infarct size following AMI and to prevent myocardial injury during myocardial infarction or cardiac surgery. Due to the minimal adverse effects, further investigation in large animals or in human are soon possible to establish the exact role of phosphatidylserine in cardiac diseases.

Sign in / Sign up

Export Citation Format

Share Document