bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum phosphate level and the outcome of coronary artery disease after coronary revascularization
Authors: Tsai T.Y , Lim S.S , Yang Y.L , Chan S.C , Hsu P.F , Wu C.H , Huang S.S , Lin S.J , Pan J.P , Lu T.M , Huang P.H , Leu H.B 
Published: November 2020

Abstract

Background
Elevated serum phosphate levels have been linked with increased risk of cardiovascular disease and mortality with conflicting results. However, whether phosphate level is associated with poor outcome for CAD patients after successful percutaneous coronary intervention (PCI) remained undetermined.

Purpose
We aimed to investigate the relationship between phosphate levels and the outcome of CAD patient undergoing PCI.

Methods
We enrolled 2894 patients (2220 male 71.59±12.20 y/o) with coronary artery disease (CAD), who received successful coronary intervention, in a cohort from our hospital from 2006 to 2015. The baseline characteristics, biochemical data and procedure details were collected. Serum phosphorus levels were analyzed to correlate with long-term outcome. The primary outcome was the composite of cardiac death, nonfatal MI, nonfatal stroke (MACE). The secondary event was MACE and hospitalization for heart failure.

Results
During an average 65.06±32.1-month follow-up, there were 173 cardiovascular deaths, 211 nonfatal myocardial infarctions, 91 nonfatal strokes, 416 hospitalizations for heart failure, and 579 revascularization procedures. There was a J-curve like linear association between serum phosphorus and future adverse event. In the multivariate analysis adjusted with comorbidities including underlying renal function, subjects with increasing every 1 mg/dL in serum phosphorus level had a higher risk of MACE (HR: 1.13, 95% CI: 1.03–1.24), cardiovascular death (HR: 1.37,95% CI: 1.22–1.55), heart failure-related hospitalization (HR: 1.12, 95% CI: 1.02–1.23), and total major CV events (HR: 1.12, 95% CI: 1.05–1.21). (Figure)

Conclusion
Serum phosphate level is significantly associated with increased risk of adverse events in CAD patients after successful PCI even considering underlying renal function.
Figure 1

Funding Acknowledgement
Type of funding source: None
Coronary artery ectasia in acute myocardial infarction: to be culprit or not to be?
Authors: Maalemben Messaoud B , Maza M , Ratheau E , Debeaumarche H , Pommier T , Zeller M , Cottin Y 
Published: November 2020

Abstract

Background
Coronary artery ectasia (CAE), is only found in about 1% of acute myocardial infarction (AMI), but represents a clinical challenge in the setting of percutaneous coronary intervention (PCI), considering 1) culprit lesion or not, 2) a solely CAE or mixt 3) number, localization and size of CAE, 4) etiology and 5) therapeutic strategies. Only few studies from small cohorts have focused on infarct-related arteries. We aim to assess the impact of CAE as culprit artery on management strategy.

Methods
From 2010 to 2019, this study prospectively analyzed the characteristics, and management of 70 consecutive admitted for an AMI and with CAE at coronary angiography. Patients with ectatic infarcted-related artery (ERIA) were compared with patients without ectasia localized on infarcted-related (No ERIA).

Results
Among the 70 patients included, most had ERIA 47 (67%). ERIA patients had more frequently diabetes than patients without ERIA (32 vs 4%, p=0.01). The rate of other CV risk factors, and chronic medications, including antiplatelet agents and anticoagulants,.were similar for the 2 groups. Moreover, no difference was observed between the 2 groups for clinical parameters and biological data. Whatever the group, the ectatic artery is mainly located on the right coronary artery (RCA) (73%), of which most were ERIA (77%). ERIA group had less frequently anterior wall location STEMI (18 vs 65%, p= &lt;0.001). The rate of diffuse coronary artery disease (91 vs 92%) and maximum CAE diameter (6.36 (6.00–7.00) mm vs 6.14 (5.53–7.64) mm, p=0.571) were similar for the 2 groups. SYNTAX was lower in ERIA patients (9.5 (2.0–18.0) vs 13.5 (7.0–23.0), p=0.031). A complete reperfusion was more frequently achieved in no ERIA group (70 vs 47%, p=0.073).
PCI data and hospital mortality are shown in Table.

Conclusion
CAE management is strongly dependent on the presence of CAE on IRA. Although rare, the optimal treatment strategy of patients with AMI and CAE remains to be elucidated. The place of intravascular ultrasound imaging needs to be investigated.

Funding Acknowledgement
Type of funding source: None
The change of serum serotonin levels between acute coronary syndrome and chronic stable angina undergoing percutaneous coronary intervention
Authors: Han D , Shin D.G , Kang M.K , Choi S , Lee N , Cho J.R 
Published: November 2020

Abstract

Background
Activated platelets release serotonin (5-hydroxytryptamine, 5HT) causing vasoconstriction and aggregation of platelets in patients with acute coronary syndrome (ACS). It can lead to undergo percutaneous coronary intervention (PCI). We investigated the serial changes of serotonin level in patients with ACS and chronic stable angina (CSA) treated with PCI.

Methods
From July 2009 to April 2010, 123 consecutive patients who have undergone PCI for either ACS (n=63) or CSA (n=60) were enrolled. After the loading dose of aspirin 300mg and clopidogrel 600mg before PCI, maintenance once daily dose of 100mg and 75mg have been given from the day after PCI in all patients. Serum serotonin level (SERO) were serially measured at baseline, pre-, post-PCI, 90 min, 6 hours, 12 hours, 24 hours and 48 hours to compare between ACS and CSA groups. All demographic, biochemical variables, and clinical events were also collected for comparison in each group.

Results
SERO at post-PCI (55.2±120.0 vs 20.1±24.0, p=0.03) and peak level (94.0±170.9 vs 38.8±72.3, p=0.02) were significantly higher in ACS group. SERO after 90 min (34.4±66.1 vs 28.7±38.2, p=0.8), 6 hours (23.9±38.3 vs 10.1±10.0, p=0.34), 24 hours (55.8±108.5 vs 37.2±88.2, p=0.39) and 48 hours (43.5±122.9 vs 25.2±65.5, p=0.53) tended to be higher in ACS group than CSA group without statistical significance. SERO rebounded at 24 hours post-PCI and dropped at 48 hours.

Conclusions
SERO was more elevated in patients with ACS than those with CSA undergoing PCI, suggesting the need for more potent and sustained platelet inhibition particularly in ACS patients. SERO might be considered as a substitute marker of platelet activation. Triple antiplatelet therapy including selective serotonin receptor antagonist on top of aspirin and clopidogrel could be as an option for ACS patients undergoing PCI

Funding Acknowledgement
Type of funding source: Other. Main funding source(s): Hallym University Research Fund 2017 (HURF-2017-84)
Impact of smoking habit on platelet reactivity in a cohort of patients admitted due to an acute coronary syndrome
Authors: Gomez Polo J.C , Vivas Balcones D , Marcano Fernandez A.L , Playan Escribano J , Lugo Gavidia L.M , Bernardo E , Ortega Pozzi M.A , De La Hera Galarza J.M , Tello Montoliu A , Besteiro Vazquez A , Silva I , Marin F , Roldan Rabadan I , Gomez Hospital J.A , Ferreiro J.L 
Published: November 2020

Abstract

Background
Several pharmacodynamic studies have shown the impact of smoking habit on platelet reactivity; with a reduction on platelet aggregation. Wether this inhibition in platelet reactivity is due to tobacco effects in platelet signaling pathways or due to a pharmacodynamic interaction with antiplatelet therapies is not well stablished.

Purpose
Our aim was to study the influence of smoking habit in platelet reactivity and in the response to P2Y12 inhibitors.

Methods
Patients admitted in four tertiary care hospitals due to an acute coronary syndrome that undergone percutaneous coronary intervention (PCI) were consecutively and prospectively recruited. All the patients received dual antiplatelet therapy with aspirin and a P2Y12 inhibitor following current European Guidelines. Platelet function was assessed at day 1 and day 30 post-PCI by VerifyNow P2Y12, VASP (Vasodilator-stimulated phosphoprotein) y MEA (Multiple electrode aggregometry).

Results
A total of 1000 patients were enrolled, of whom 12 had to be excluded due to inaccurate processing of blood samples. 372 patients (37,6%) had smoking habit. Non-smoking patients showed higher prevalence of high blood pressure [423 (68.7%) vs 196 (52.7%)] and diabetes mellitus [213 (34.6%) vs 81 (21.8%)]. Smoking patients were younger [57.3 (9,6) years old vs 68.4 (11.1)], with higher incidence of acute coronary syndrome with ST segment elevation [184 patients (49,5%) vs 241 (39.1%), p&lt;0,001]. There were no differences in platelet function at day 1. When analysing platelet function 30 days post-PCI, a lower inhibition of platelet reactivity in non-smoking patients as compared with smoking patients was observed in those treated with clopidogrel, with higher prevalence of clopidogrel-resistance in non-smoking patients (VerifyNow, 51,2% prevalence of high platelet reactivity in non-smoking patients vs 34,9% 30 days after PCI, p=0,023). On the other hand, smoking patients that received ticagrelor did not show any differences. Patients with smoking habit treated with prasugrel showed a lower response of borderline statistical significance.

Conclusion
Smoking habit was associated with a lower response to prasugrel of borderline significance, and with higher response to clopidogrel, according with previous studies suggesting a pharmacodynamics interaction between tobacco use and P2Y12 inhibitors.

Funding Acknowledgement
Type of funding source: Public grant(s) – National budget only. Main funding source(s): Fondo de Investigaciones Sanitarias (FIS)
Influence of myocardial damage on serum procalcitonin in ST-elevation myocardial infarction
Authors: Reindl M , Tiller C , Holzknecht M , Lechner I , Henninger B , Mayr A , Brenner C , Klug G , Bauer A , Metzler B , Reinstadler S.J 
Published: November 2020

Abstract

Background
Myocardial tissue injury due to acute ST-elevation myocardial infarction (STEMI) initiates an inflammatory response with a release of systemic inflammatory biomarkers including C-reactive protein (CRP) and white blood cell count (WBCc), which, however, hampers the usefulness of these routine biomarkers to identify concomitant infections. The clinical role of Procalcitonin (PCT), a promising marker of bacterial infections, to detect concomitant infections in acute STEMI is unknown, mainly because it is unclear whether myocardial injury per se induces a systemic PCT release.

Purpose
To investigate release kinetics of serum PCT in the acute setting of STEMI and possible associations with myocardial injury markers as comprehensively assessed by cardiac magnetic resonance (CMR) imaging.

Methods
In this prospective observational study, we included 141 STEMI patients treated with primary percutaneous coronary intervention (PCI). Concentrations of PCT, high-sensitivity CRP (hs-CRP), WBCc and high-sensitivity cardiac troponin T (hs-cTnT) were measured serially at day 1 and day 2 after infarction. CMR imaging to assess infarct size (IS), extent of microvascular injury (MVI) and occurrence of intramyocardial haemorrhage (IMH) was performed within the first week following STEMI.

Results
Median concentrations of PCT were 0.07μg/l at both time points. In 140 patients (99%), both PCT values were within the normal range (≤0.5μg/l). Whereas hs-CRP, WBCc, and hs-TnT were significantly correlated with CMR markers of myocardial damage, PCT did not show significant correlations (all p&gt;0.10) with IS (PCT24h: r=0.07; PCT48h: r=0.13) or MVI (PCT24h: r=−0.03; PCT48h: r=0.09). Furthermore, PCT failed to discriminate between large and small IS or MVI or between presence and absence of IMH (AUC values:0.46–0.55).

Conclusions
In the acute phase after PCI for STEMI, circulating PCT remained unaffected by the extent of myocardial and microvascular tissue damage as visualized by CMR imaging. These data highlight the clinical potential of PCT to identify concomitant infections and to guide antibiotic treatments in STEMI patients.

Funding Acknowledgement
Type of funding source: Public grant(s) – National budget only. Main funding source(s): Austrian Science Fund, Tiroler Wissenschaftsförderung
The inflammasome signaling axis in thrombi from STEMI patients is related to degree of myocardial injury
Authors: Nordeng J , Helseth R , Aakra S , Hoffman P , Schandiz H , Roald B , Bendz B , Arnesen H , Solheim S , Seljeflot I 
Published: November 2020

Abstract

Background
The NLRP3-inflammasome and the IL-6-pathways, i.e. the inflammasome signaling axis, seems to be central mechanisms in the inflammatory response related to myocardial reperfusion injury after revascularization. The beneficial results shown by treating MI-patients with canakunimab, an antibody blocking IL1-β, in the CANTOS trial*, and by treatment of NSTEMI patients with the IL6-receptor antagonist tocilizumab**, are looked upon as proof of concept for inflammasome inhibition.

Purpose
To study whether genes encoding inflammasome-related proteins are present in coronary thrombi and in circulating cells from STEMI patients, and whether these are related to the degree of myocardial injury as measured by troponin T, and time from symptoms to PCI.

Methods
Intracoronary thrombi were aspirated from 33 patients with STEMI treated with primary PCI. The thrombi were snap-frozen in RNA-later solution for gene expression analyses. Peripheral blood samples with Pax-gene tubes were drawn at end of the PCI-procedure. mRNA of NLRP3, caspase1, IL1-β, IL18, IL6, IL6-receptor (IL6-R) and gp130 were isolated from the thrombi and leukocytes in peripheral blood, and relatively quantified by RT PCR. Peak troponin was collected from clinical records.

Results
Genes coding for the 7 different markers were present in 76–100% of the thrombi. The expression of NLRP3 in thrombi significantly correlated to peak troponin T (r=0.468, p=0.024). Dividing peak troponin T values into quartiles, the median value of NLRP3 mRNA in Q4 was 2.0-fold higher compared to Q1–3 (p=0.012). Peak troponin T also correlated with the expression in circulating leukocytes of NLRP3 (r=0.420, p=0.0149) and IL1-β (r=0.394, p=0.023), and borderline to caspase1 (r=0.321, p=0.069) and IL18 (r=0.310, p=0.079).
IL6-R expression in thrombi correlated significantly to peak troponin T (r=0.434, p=0.019), with a 2.5-fold higher median level in Q4 vs Q1–3 of troponin T (p=0.017). gp130 expression in thrombi correlated inversely with peak troponin T (r=−0.398, p=0.050), as did IL6-R expression in circulating leukocytes (r=−0.421, p=0.015). There were no significant correlations between genes expressed in the thrombi and time from symptom to PCI (median 152 minutes), whereas genes for IL6 in circulating leukocytes correlated inversely (r=−0.385, p=0.027).

Conclusion
The inflammasome signaling pathway was actively regulated in coronary thrombi and in circulating leukocytes from patients with STEMI. Genes encoding NLRP3 and IL6-R were increasingly expressed in thrombi from patients with increased myocardial damage, measured by troponin T, supporting the beneficial effects of medically targeting this pathway.

Funding Acknowledgement
Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): Stein Erik Hagens Foundation for Clinical Heart Research
Meta-inflammation in monocytes of patients with Acute Coronary Syndrome
Authors: Canonico F , Vinci R , Pedicino D , Pisano E , Ciampi P , Bonanni A , Ponzo M , D'Aiello A , Di Sario M , Severino A , D'Amario D , Niccoli G , Biasucci L.M , Crea F , Liuzzo G 
Published: November 2020

Abstract

Background
Several studies suggest that an alteration of monocyte metabolism might be implicated in inflammatory diseases. Enhanced glycolysis might be a hallmark of pro-inflammatory monocyte subsets. Improved glycolysis enables the immune cells to generate sufficient ATP and biosynthetic intermediates to carry out its particular effector functions. For macrophages this includes phagocytosis and inflammatory cytokine production. Pyruvate Kinase isozyme M2 (PKM-2) catalyzes the final step of glycolysis producing pyruvate and ATP. Latest studies have shown that a member of Jumonji family (JMJD8) acts as a positive regulator in TNF-induced NF-kB signaling leading to pro-inflammatory pathways in macrophages and is involved in angiogenesis and cellular metabolism through interacting with PKM-2 in endothelial cells.

Purpose
The aims of the study are to assess the expression of the glycolytic key enzyme PKM-2 in CD14+ monocytes obtained from patients with non-ST-elevation myocardial infarction (NSTEMI) or with stable angina (SA). Furthermore, the expression of JMJD8 was evaluated.

Methods
30 patients with NSTEMI and 30 patients with SA were enrolled. Peripheral blood mononuclear cells were obtained from whole blood samples. For cytoplasmatic protein identification, cells were fixed and permeabilized and then incubated with fluorochrome-conjugated mAbs anti-CD14, anti-PKM-2 and anti-JMJD8. For analysis we used Two-tailed Mann-Whitney non parametric Comparison test.

Results
CD14+ monocytes from NSTEMI patients showed reduced expression of the key glycolytic enzyme PKM-2 as compared to CD14+ monocytes from SA patients (p=0.02) (Figure 1). JMJD8 expression in NSTEMI patients is increased compared with SA patients (p=0.02) (Figure 2).

Conclusion
This study introduces a role for immune-metabolism in the immunity dysregulation described in ACS patients and provides novel insights into the mechanisms responsible for coronary instability. Taking their potential interaction into account, our data suggest that in acute setting glycolysis key enzyme PKM2 expression is downregulated. Besides, JMJD8 protein levels increase in NSTEMI patients acting as potential limiting factor of PKM2 function. Moreover, our data propose the potential roles of immune-metabolism to detect novel therapeutic targets, associated with an accurate patient stratification based on immune-metabolic profiles, for prevention and treatment of atherosclerosis, in the perspective of a personalized medicine approach.

Funding Acknowledgement
Type of funding source: Private hospital(s). Main funding source(s): Fondazione Policlinico A. Gemelli
Effect of postprandial hyperglycaemia on culprit plaque rupture in diabetic patients with non-ST segment elevation acute coronary syndrome
Authors: Su G , Zhuang S.W , Zhang T , Yang H.X , Dai W.L , Mi S.H 
Published: November 2020

Abstract

Background
Postprandial hyperglycemia was reported to play a key role in established risk factors of coronary artery diseases (CAD) and cardiovascular events. Serum 1,5-anhydroglucitol (1,5-AG) levels are known to be a clinical marker of postprandial hyperglycemia and short-term glycemic excursions. Low serum 1,5-AG levels have been associated with occurrence of CAD; however, the relationship between 1,5-AG levels and coronary plaque rupture has not been fully elucidated. The aim of this study was to evaluate 1,5-AG as a predictor of coronary plaque rupture in diabetic patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS).

Methods
A total of 132 diabetic patients with NSTE-ACS were included in this study. All patients underwent intravascular ultrasound examination, which revealed 38 patients with plaque rupture and 94 patients without plaque rupture in the culprit lesion. Fasting blood glucose (FBS), hemoglobin A1c (HbA1c) and 1,5-AG levels were measured before coronary angiography. Fasting urinary 8-iso-prostaglandin F2α (8-iso-PGF2α) level was measured and corrected by creatinine clearance.

Results
Patients with ruptured plaque had significantly lower serum 1,5-AG levels and a tendency of higher hemoglobin A1c levels than patients without ruptured plaque in our study population. In multivariate analysis, low 1,5-AG levels were an independent predictor of plaque rupture (odds ratio 3.3; p=0.006) in diabetic patients with NSTE-ACS, but HbA1c was not. The area under the receiver-operating characteristic curve for 1,5-AG (0.678, p=0.001) to predict plaque rupture was superior to that for HbA1c (0.618, p=0.034). Levels of 1,5-AG were significantly correlated with urinary 8-iso-PGF2α (r=−0.224, p=0.010).

Conclusions
Postprandial hyperglycaemia appeared to be superior to long-term average blood glucose levels in predicting plaque rupture in culprit lesions, which may be useful to assess the cardiovascular outcomes in diabetic patients.

Funding Acknowledgement
Type of funding source: Public Institution(s). Main funding source(s): Outstanding Clinical Discipline Project of Shanghai Pudong, Beijing Health Special Foundation
Efficacy of early intravenous landiolol, an ultrashort-acting beta-blocker on infarct size and its safety in patients with myocardial infarction undergoing primary PCI: a randomized, controlled study
Authors: Miyamoto M , Miyoshi T , Osawa K , Mori A , Oka T , Ito H 
Published: November 2020

Abstract

Background
Previous clinical studies showed that early intravenous metoprolol before reperfusion in patients with ST-elevation myocardial infarction (STEMI) undergoing primary PCI reduced infarct size. However, intravenous beta-blockers in acute phase of STEMI can be associated with adverse effects such as cardiogenic shock and atrioventricular block. Landiolol is an ultrashort-acting beta-blocker with a half-life of 3 min that is eight times more cardioselective than esmolol.

Purpose
We evaluate the efficacy of intravenous infusion of landiolol on infarct size and its safety in STEMI patients undergoing primary PCI.

Methods
This study is a multicenter randomized control trial. A total of 47 patients with Killip class II or less STEMI undergoing PCI within 12 hours of symptoms onset were randomized to receive intravenous landiolol (n=23) or not (control, n=24). Patients allocated to landiolol group delivered an intravenous continuous dose of 3μg/min/kg before reperfusion and then continued until a total dose of 50mg. All patients started oral metoprolol or carvedilol within 12 hours. The primary end point was myocardial salvage index (MSI) on magnetic resonance imaging performed 5 to 7 days after PCI. MSI was defined as the difference between the area at risk and the area of necrosis analyzed using a commercial software.

Results
Magnetic resonance imaging was performed in 35 patients (17 patients in landiolol group and 18 patients in the control group), and ischemia duration time was 229 minutes in the landiolol group and the 242 minutes in control. In adjusting for confounding variables, the areas of myocardium at risk were not difference in both groups (54.4g in the landiolol group, and 46.8g in the control group; p=0.31). However, MSI in the landiolol group was significantly reduced than that in the control group (36.8% and 57.0%; p&lt;0.001).
In both group blood pressure was not difference in recruitment (142mmHg in landiolol group, and 144 in control) and starting PCI (163mmHg in landiolol group, and 165 in control). Regarding safety, the composite of death, malignant ventricular arrhythmia, cardiogenic shock, and atrioventricular block at 24 hours did not differ between the landiolol and the control groups (8.7% and 8.3%, respectively, p=0.93).

Conclusion
Early intravenous landiolol before starting primary PCI reduced infarct size in STEMI patients without significant hemodynamic adverse effects.

Funding Acknowledgement
Type of funding source: None