bluuebunny/crossref_metadata_2025_split huggingface dataset:
Outcomes of extracorporeal membrane oxygenation with or without left ventricular unloading devices in patients with non-myocardial infarction cardiogenic shock
Authors: Kurpad K K , Sohal S S , Mehta H M , Visveswaran G V , Tayal R T , Wasty N W , Cohen M C , Waxman S W 
Published: October 2021

Abstract

Background
Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is being increasingly used to treat cardiogenic shock, however its effect on increasing left ventricular (LV) afterload may slow myocardial recovery and negatively affect survival. Percutaneous mechanical support devices have been utilized for LV unloading by reducing afterload in an attempt to improve outcomes. While the use of LV unloading devices remains debatable, its use has not been specifically studied in patients with non-acute myocardial infarction cardiogenic shock (non-AMICS).

Purpose
To study the outcomes of VA-ECMO with or without LV unloading devices in patients with non-AMICS patients.

Methods
National inpatient sample database from years 2015 to 2018 was queried to select patients admitted with non-AMICS. Patients were included in the study if they underwent VA-ECMO during admission and later categorized into 3 groups i.e. VA-ECMO, VA-ECMO plus Impella and VA-ECMO plus intra-aortic balloon pump (IABP). Baseline demographics and in-hospital outcomes were compared between the 3 pre-specified groups. Statistical significance was assigned at p&lt;0.05.

Results
178,605 patients met criteria for non-AMICS. Of these, 2190 (1.23%) patients received VA-ECMO alone, 965 (0.54%) received VA-ECMO plus IABP and 414 (0.23%) received VA-ECMO plus Impella. On univariate analysis, patients who received VA-ECMO alone had higher rates of inpatient mortality as compared to those who received VA-ECMO plus IABP or VA-ECMO plus Impella (39.04%, 33.72% and 25.81% respectively, p=0.001). On multivariate analysis, the patients who received VA-ECMO plus IABP or VA-ECMO plus Impella had lower odds of mortality when compared to VA-ECMO alone (OR: 0.61 (0.39–0.96), p=0.03), OR: 0.51 (0.23–1.08), p=0.08). The length of stay and cost were significantly higher for patients with VA-ECMO with unloading devices (IABP or Impella) compared with VA-ECMO alone (24.77±2.44 and 27.74±3.55 days vs 23.70±1.25 days respectively. p=0.001, $846,404±71169 and 860,999±121942 vs $740,274±43644 respectively, p=0.001).

Conclusions
Non AMICS patients who received VA-ECMO along with LV unloading devices (esp IABP) had lower in-hospital mortality as compared to those who received VA-ECMO alone despite having longer length of stay and higher cost. Use of LV unloading devices like IABP or Impella may improve outcomes in patients requiring VA-ECMO support for non-myocardial infarction cardiogenic shock. Further studies are needed to identify specific patient subsets that may benefit from this approach.

Funding Acknowledgement
Type of funding sources: None.
Left ventricular global longitudinal strain as an indicator of myocardial injury in non-hospitalized COVID-19 survivors
Authors: Hassan Abdelnabi M , Abdelgawad H , Saleh Y , Almaghraby A 
Published: October 2021

Abstract

Introduction
The incidence of acute cardiac injury in COVID-19 patients is frequently subclinical and can be identified by cardiac magnetic resonance imaging. Left ventricular global longitudinal strain (LV-GLS) using two-dimensional speckle-tracking echocardiography (2D-STE) provides an accurate validated method for early detection of subclinical myocardial dysfunction. So far, long-term cardiovascular complications of COVID-19 are undetermined therefore several validated methods should be used for early diagnosis and intervention in those patients.

Purpose
The aim of this work was to describe GLS as an indicator of myocardial injury in a case series of non-hospitalized COVID-19 patients complaining of persistent dyspnea after resolution of COVID-19 infection.

Methods
A total number of 18 patients who were diagnosed with COVID-19 and were not indicated for hospital admission due to mild symptoms presenting with residual persistent dyspnea following COVID-19 infection resolution. Through clinical examination and standard 2D transthoracic echocardiography with STE emphasizing on LV-GLS was performed using Philips Epic - Qlab 10 software.

Results
The mean age of the included patients was 37.44±6.33 years, the mean time from COVID-19 diagnosis was 48.1±15.45 days, all patients (100%) had persistent dyspnea grade II. The mean left ventricular ejection fraction (LVEF) was 62.9±3.46% while the mean LV-GLS was −15.55±2.16%. Clinical and echocardiographic data is presented in Table 1.

Conclusion
In a case series of non-hospitalized COVID-19 survivors who complained of persistent dyspnea, GLS was low in comparison to the normally reported values of LV-GLS although they had normal LVEF indicating the persistence of myocardial injury even in mild cases of COVID-19 long after infection resolution. Further close follow-up of even mild and moderate COVID-19 survivors is certainly required to detect long-term cardiovascular sequelae. 2D STE with LV-GLS can be used as a readily available validated technique to detect early or persistent myocardial dysfunction succeeding COVID-19 infection.

Funding Acknowledgement
Type of funding sources: None.
Is GLP-1 insufficiency a coronary risk factor? A multicenter observational study, BOREAS-CAD2
Authors: Nagase C , Tanno M , Kouzu H , Miki T , Nishida J , Murakami N , Kokubu N , Nagano N , Nishikawa R , Yoshioka N , Tsuchida A , Kita H , Ohnishi H , Miura T 
Published: October 2021

Abstract

Background and aim
Glucagon-like peptide-1 (GLP-1) regulates insulin secretion and also affords pleiotropic effects including protective effects on blood vessels. Multiple factors regulate GLP-1 secretion after meals, but a group of apparently healthy subjects showed blunted responses of GLP-1 secretion in our previous study. In this study, we examined the possibility that the reduced capacity of GLP-1 secretion is associated with increased extent of coronary artery stenosis in non-diabetic patients.

Methods and results
Non-diabetic patients who were admitted for coronary angiography without a history of coronary interventions were enrolled. Coronary artery stenosis was quantified by Gensini score (GS), and GS ≥10 was used as an outcome variable based on results of earlier studies indicating its predictive value for cardiovascular events. The patients (mean age, 66.5±8.8 years; 71% males, n=173) underwent oral 75 g-glucose tolerant tests for determination of glucose, insulin and active GLP-1 levels. The area under the curve of plasma active GLP-1 (AUC-GLP-1) was determined as an index of GLP-1 secretion capacity. AUC-GLP-1 was not correlated with fasting glucose, AUC-glucose, serum lipids, indices of insulin sensitivity or estimated glomerular filtration rate. In multivariate logistic regression analysis for GS ≥10, AUC-GLP-1 &lt; median, age and hypertension were selected as explanatory variables, though fasting GLP-1 level was not selected.

Conclusion
The findings indicate significant association of reduced GLP-1 secretion capacity with increased extent of coronary artery stenosis in non-diabetic patients. A causal relationship between change in GLP-1 secretion capacity and coronary stenosis remains to be examined by a longitudinal study

Funding Acknowledgement
Type of funding sources: Private company. Main funding source(s): This study was supported in part by a research grant from Investigator-Initiated Studies Program of Merck Sharp & Dohme Corp./MSD K.K.
Mechanisms of cardiac protection by pirfenidone in the post-myocardial infarction setting
Authors: Aimo A , Iborra Egea O , Bayes-Genis A , Galvez-Monton C , Burchielli S , Passino C , Emdin M 
Published: October 2021

Abstract

Background
A high proportion of patients with ST-segment elevation myocardial infarction (STEMI) experience adverse left ventricular (LV) remodelling despite guideline-recommended therapy. An excessive and dysregulated fibrotic response is involved in LV remodelling, and could be targeted by anti-fibrotic drugs such as pirfenidone, which is an approved treatment for idiopathic pulmonary fibrosis.

Methods
We evaluated the mechanisms of action of pirfenidone in the post-MI setting through sampling method-based mathematical models, enriched with transcriptomic data of swine experimental models of MI translated to the human proteome.

Results
The analysis of proteins modulated by pirfenidone shows that pirfenidone has a strong impact on several pathways involved in post-MI remodeling (Figure). The inhibition of p38γ-MAPK12 and furin displays the most prominent role on post-MI remodeling when compared to the other pirfenidone targets (PAI-1 and GLI2). p38γ-MAPK12 blockade inhibits cardiomyocyte apoptosis mediated by BCL2 and BAX. Myocardial hypertrophy and inflammation might be modulated by pirfenidone through the regulation of proteins downstream to p38γ-MAPK12, such as the NFATC1/NFATC2/NFATC3 pathway, and the transcription factors FOXO1, FOXO3 and NFκB, which are involved in TNFα regulation. The transcription factor AP-1 (homo-heterodimers of c-JUN/c-FOS), also downstream to p38γ-MAPK12, regulate the expression of genes involved in hypertrophy, fibrosis and inflammation (for example, IFNγ) By blocking both p38γ-MAPK12 and furin, pirfenidone can modulate extracellular matrix remodelling and cardiac fibrosis by targeting the TGFβ1-SMAD2/3 pathway, known to be highly involved in the progression of myocardial fibrosis, and other effector proteins such as MMP2 and MMP14 metalloproteases, PDGFA/B, and IGF1, many found to be involved also in myocardial fibrosis, impaired myocyte contractility and cell hypertrophic response.

Conclusions
We have identified several possible mechanisms of action of pirfenidone with beneficial effects in the post-MI LV remodelling. These findings support future research regarding pirfenidone's clinical benefit in post-MI patients.

Funding Acknowledgement
Type of funding sources: None.
Clinical characteristics and prognosis in patients with multi-vessel coronary spasm – comparison with those in patients with single-vessel coronary spasm
Authors: Teragawa H , Oshita C , Akazawa R , Uchimura Y , Orita Y 
Published: October 2021

Abstract

Background
We have sometimes experienced patients with vasospastic angina (VSA), who showed multi-vessel spasm (MVS) on coronary angiography (CAG) and spasm provocation test (SPT). However, it has not been clarified what clinical characteristics VSA patients with MVS have or whether such patients have poor prognosis. Therefore, we compared the clinical characteristics and prognosis in VSA patients with MVS with those in VSA patients with single-vessel spasm (SVS).

Methods
One hundred and fifty-two patients (mean age: 67 yrs, 74 men and 78 women) with VSA, in which presence of coronary spasm was assessed in both left coronary artery (LCA) and right coronary artery (RCA) on SPT, were subjected. We defined VSA as the presence of more than 90% narrowing of the epicardial coronary artery on angiograms, accompanied by the usual chest symptoms and/or ischemic ST-T changes on electrocardiogram. On SPT, MVS was defined as the presence of spasm on ≥ two major coronary arteries. Base on the presence of MVS, patients were divided into the following 2 groups: MVS group and SVS group. The frequencies of conventional coronary risk factors, the average times of anginal attack (per month), the findings of SPT such as spasm provocation induced by low dose of acetylcholine (LDA) and total occlusion due to coronary spasm (TOC), the number of coronary vasodilators at discharge, and the major cardiovascular events (MACE) including death of any cause and readmission due to heart failure, acute coronary syndrome and unstable angina, were compared in the two groups.

Results
There were 98 patients (64%) in the MVS group and 54 patients (36%) in the SVS groups. The frequencies of conventional coronary risk factors and the average times of anginal attacks (4/month in both groups) were not different in the two groups. The frequencies of LDA (33% in MVS and 17% in SVS, p&lt;0.05) and TOC (12% in MVS, 0% in SVS, p&lt;0.01) were higher in the MVS group than in the SVS group. The average numbers of coronary vasodilators was higher in the MVS group (1.1±0.4) than in the SVS group (0.9±0.4, p&lt;0.01). The frequency of MACE did not differ in the two groups as follows (figure).

Conclusions
These findings suggest that there was no clinical characteristic, suggesting the presence of MVS in VSA patients. Such patients may have higher VSA activity on SPT and have more aggressive medications, leading to the similar prognosis in VSA patient with SVS.

Funding Acknowledgement
Type of funding sources: None.
Impact of wall shear stress affected by anatomical difference between acute and chronic coronary syndrome in patients with LAD proximal disease
Authors: Naniwa S , Yamada S , Awano K , Yoshida A , Takami K , Tagashira T , Tsuda S , Terashita D , Takada H , Akita T , Takata K , Kunigita T , Nishijo K 
Published: October 2021

Abstract

Recent hemodynamic studies have demonstrated that progression of coronary atherosclerosis occurs at low wall share-stress site, whereas plaque rupture frequently occurs at high share stress site. It is well recognized that wall shear stress is relatively low along the outer walls of the bifurcation.
We investigated consecutive 140 patients (77 with acute coronary syndrome (ACS) and 63 with chronic coronary syndrome (CCS) performed PCI for LAD proximal lesions (AHA seg.6) from January 2016 to December 2019. In CCS group, entry criteria included stenosis of at least 90% in the LAD proximal lesion or at least 70% in the LAD proximal lesion and objective evidence of myocardial ischemia (inducible ischemia with either exercise or pharmacologic vasodilator stress or with pressure wire). Exclusion criteria were patients with maintenance dialysis, chronic total occlusion lesions, in-stent restenosis, and clinically diagnosed unstable angina without troponin I elevation. We measured the distance from LMT distal carina to the culprit site (Distance) and plaque location (Location) with intravascular ultrasound and angle between LMT and LAD with cardiovascular angiography analysis system (CAAS) (Angle).
The two groups were generally well balanced with regard to baseline clinical characteristics. The mean (±SD) age of the patients was 69.0±11.8 years, and 75% were men. Medication at baseline was also similar between two groups except higher prevalence of statin prescription in CCS group. The Distance was shorter and Angle was steeper in CCS group than in ACS group. The number of patients with Angle less than 150 degrees and with Location in the lateral wall side was much more in CCS group.
In this study, plaques in CCS were frequently observed at low shear stress site, whereas those in ACS at high shear stress site. Plaque progression in CCS may be associated with low wall shear stress, and high shear stress may play key role in plaque rupture in ACS. This anatomical difference can partly explain the different mechanisms of onset between of ACS and CCS.

Funding Acknowledgement
Type of funding sources: None. Anatomical differenceCharacteristics and results
Angiography vs physiology-based deferral of revascularization in patients with reduced left ventricular ejection fraction: a 10-year clinical follow-up
Authors: Gallinoro E , Paolisso P , Bermpeis K , Peregrina E F , Candreva A , Esposito G , Fabbricatore D , Sonck J , Di Gioia G , Vanderheyden M , Bartunek J , Collet C , De Bruyne B , Barbato E 
Published: October 2021

Abstract

Background
Deferring percutaneous coronary intervention (PCI) in patients with non-ischemic coronary stenoses based on fractional flow reserve (FFR) and preserved left ventricular ejection fraction (LVEF) is associated with favorable long-term clinical outcomes. In patients with reduced LVEF, the role of reversible/residual ischemia in deferring revascularization is still debated.

Purpose
To investigate whether FFR provides additive clinical benefit compared to coronary angiography in deferring revascularization in patients with intermediate coronary stenoses and reduced LVEF.

Methods
Among 4577 coronary angiographies performed between 2002 and 2010, consecutive patients with reduced LVEF (≤50%) and at least one intermediate coronary stenosis [diameter stenosis (DS)% 40–70%] in whom revascularization was deferred based either on FFR (FFR-guided) or angiography (Angiography-guided) were screened. The primary endpoint of the study was cumulative incidence of death at 10 years.

Results
A total of 843 patients were included (209 in the FFR-guided and 634 in the Angio-guided group). Median clinical follow-up was 7.1 years (IQR 3.2–11.2 years). After 1:1 propensity score matching, baseline characteristics between the two groups were similar. All-cause death at 10 years was significantly lower in the FFR-guided compared with the Angiography-guided group (94 [45%] vs 115 [55%], HR 0.72 [95% CI 0.55–0.95], p&lt;0.05). Similarly, the incidence of major adverse cardiovascular and cerebrovascular events (MACCE, composite of all-cause death, myocardial infarction, any revascularization and stroke) was lower in the FFR guided group (125 [60%] vs 140 [67%], HR 0.77 [95% CI 0.61–0.98], p&lt;0.05).

Conclusions
In patients with reduced LVEF and associated coronary artery disease, deferring revascularization of intermediate stenoses based on FFR is associated with lower incidence of death and MACCE at 10 years.

Funding Acknowledgement
Type of funding sources: None.
Effect of PM2.5 on circulating inflammatory cells and microRNA expression in acute coronary syndrome
Authors: Cecconi A , De La Fuente H , Blanco Dominguez R , Navarrete G , Garcia-Guimaraes M , Vera A , Lopez Melgar B , Rivero F , Sanz Garcia A , Lozano Prieto M , Martin P , Sanchez-Madrid F , Alfonso F , Jimenez-Borreguero L J 
Published: October 2021

Abstract

Background
Air pollutants increase the risk of myocardial infarction. Air pollution-induced atherosclerotic plaque destabilization may be related to inflammation, but the specific inflammatory alterations remain unclear.

Purpose
The aim of this prospective study was to assess the inflammatory changes in circulating immune cells and microRNAs in patients with acute coronary syndrome related to short-term exposure to PM2.5.

Methods
We prospectively included all consecutive patients admitted between March 2017 and July 2018 with the diagnosis of acute coronary syndrome (STEMI, NSTEMI, unstable angina) and coronary angiography in the acute phase of the disease. We also included a control group of patients with stable angina. For each patient we collected air concentrations of PM2.5 from the closest meteorological station to the patient residence obtaining the previous 24-hour average before hospital admission. All patients underwent systematic circulating inflammatory cell analysis. A selection of patients underwent miRNAs analysis.

Results
A total of 261 patients were included. According to PM2.5 exposure, 31 patients were selected for miRNA analyses. STEMI patients exposed to PM2.5 showed a reduction of CD4+ regulatory T (Treg) cells (Figure 1A). In the microRNA assessment, PM2.5 exposure was associated with higher circulating levels of let-7f-5p, miR-223-3p, miR-423-3p, miR-197-3p, miR-335–5, miR-376c-3p and miR-501-3p. Regarding clinical presentation, PM2.5 exposure in STEMI and NSTEMI patients was associated with an increase of miR-let-7f-5p, whereas miR-423-3p and miR-146a-5p were increased only in STEMI patients (Figure 1B).

Conclusions
STEMI related to PM2.5 short-term exposure is associated to specific changes involving CD4+CD25+Foxp3+ Treg cells and miR-146a-5p.

Funding Acknowledgement
Type of funding sources: Other. Main funding source(s): Ministerio de Ciencia e Innovaciόn; Fundaciόn BBVA Equipos de Investigaciόn Científica 2018 and from Caixa Banking Foundation; Sociedad Espanola de Cardiologia; Ministerio de Ciencia, Innovaciόn y Universidades, Carlos III Institute of Health-Fondo de Investigaciόn Sanitaria; Comunidad de Madrid; Fondo Europeo de Desarrollo Regional
Differential prognostic value of resistin for cardiovascular death in patients with stable coronary artery disease according to the presence of metabolic syndrome
Authors: Kosmas N , Katsimardos A , Kountouri A , Zolindaki M , Rallidis L 
Published: October 2021

Abstract

Background
Resistin is associated with atherosclerosis progression by affecting inflammation and insulin resistance. There are controversial data regarding the prognostic value of resistin in patients with coronary artery disease (CAD).

Purpose
We prospectively investigated the long-term prognostic value of resistin in patients with stable CAD.

Methods
A total 741 consecutive patients with stable CAD were followed for a median of 5.5 years. Serum resistin, lipids, high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6) levels were measured at baseline. Primary endpoints were cardiac death (CD) and secondary hospitalizations for acute coronary syndrome, arrhythmic event or stroke.

Results
Follow-up data were obtained from 703 patients of whom 79 had a CD (11.2%) and 205 (29.2%) met the secondary endpoints. Resistin was positively correlated with hsCRP (r=0.159, p&lt;0.001) and IL-6 (r=0.165, p=0.002), and negatively with HDL-cholesterol (r=−0.176, p&lt;0.001). Resistin levels could not predict CD [HR: 1.044; 95% CI: 0.994 to 1.096; p=0.087] neither secondary endpoints [HR: 1.025; 95% CI: 0.983 to 1.068; p=0.250). Among 298 patients (42.4%) with metabolic syndrome (MS) resistin levels were independent predictors of CD after adjustment for conventional risk factors and left ventricular ejection fraction (LVEF) [HR: 1.145; 95% CI: 1.057 to 1.240; p=0.001]. Patients with resistin values ≥7.6 ng/mL (median level) had 2.8 times higher risk of CD compared to those with resistin levels &lt;7.6 ng/mL after adjustment for traditional risk factors and LVEF (HR: 2.882; 95% CI: 1.311 to 6.336; p=0.008).

Conclusions
Resistin is an independent long-term predictor of CD in patients with stable CAD and MS.

Funding Acknowledgement
Type of funding sources: None. Figure 1