bluuebunny/crossref_metadata_2025_split huggingface dataset:
P2Y12 inhibitors in patients with non-ST-segment elevation acute coronary syndrome: systematic review and network meta-analysis of randomized trials
Authors: Fujisaki T , Kuno T , Briasoulis A , Misumida N , Takagi H , Latib A 
Published: October 2021

Abstract

Background
Based on a recent randomized control trial (RCT), prasugrel is recommended in preference to ticagrelor for patients with non-ST-segment elevation ACS (NSTE-ACS), however, limited data exists.

Objectives
We aimed to investigate the effect of P2Y12 inhibitors on ischemic and bleeding events in NSTE-ACS patients.

Methods
Clinical trials enrolling NSTE-ACS patients were identified and relevant data was extracted. We performed a network meta-analysis on efficacy and safety outcomes.

Results
Our study including a total of 37, 268 patients with NSTE-ACS from 11 RCTs. Prasugrel decreased major adverse cardiovascular events (MACE) when compared to clopidogrel (Hazard ratio (HR): 0.84; 95% confidence interval (CI) [0.71–0.99]). For MACE, prasugrel showed the highest likelihood of event reduction (P-score=0.97) in comparison to ticagrelor (P-score=0.29) and clopidogrel (P-score=0.24). Prasugrel decreased myocardial infarction (HR: 0.82; 95% CI [0.68–0.99]) but increased major bleeding without statistical significance (HR: 1.30; 95% CI [0.97–1.74]) when compared to clopidogrel. Ticagrelor reduced cardiovascular death (HR: 0.79; 95% CI [0.66–0.94]) but increased major bleeding (HR: 1.33; 95% CI [1.00–1.77], p=0.049) in comparison to clopidogrel. There was no significant difference between prasugrel and ticagrelor for each endpoint, but prasugrel had higher likelihood of event reduction than ticagrelor for all endpoints except cardiovascular death.

Conclusions
Prasugrel and ticagrelor had comparable risk for each endpoint, but prasugrel had the highest probability being the best treatment in reducing the primary endpoint. This study highlights the need for further large-scale RCTs to investigate the optimal P2Y12 inhibitor selection in NSTE-ACS patients.

Funding Acknowledgement
Type of funding sources: None.
Association of beta-blockers or inhibitors of renin-angiotensin system with clinical outcomes in patients with mid-range left ventricular ejection fraction after acute myocardial infarction
Authors: Joo S , Lee J , Kim S , Beom J , Boo K , Choi J , Jeong M ,   KAMIR-NIH registry investigators
Published: October 2021

Abstract

Background
In the era of the initial optimal interventional and medical therapy for acute myocardial infarction (AMI), a number of patients with mid-range left ventricular ejection fraction (EF) (&gt;40%, &lt;50%) becomes increasing.

Purpose
This observational study aimed to investigate the association between oral beta-blockers or inhibitors of renin-angiotensin system (RAS) and 2-year clinical outcomes in patients with mid-range EF after AMI.

Methods
Among 13,624 patients enrolled in the Korea Acute Myocardial Infarction Registry-National Institute of Health (KAMIR-NIH), propensity-score matched patients who survived the initial attack and had mid-range EF were selected according to beta-blocker or RAS inhibitor therapy at discharge.

Results
Beta-blocker therapy at discharge was associated with lower 2-year major adverse cardiac events (MACE) of cardiac death, MI, revascularization or re-hospitalization due to heart failure (8.7 vs. 12.8/100 person-year; hazard ratio [HR] 0.68; 95% confidence interval [CI] 0.50–0.93; P=0.015), and no significant interaction between EF ≤45% and &gt;45% was observed (P for interaction=0.354). This association was mainly driven by lower MI in patients with beta-blockers (1.6 vs. 3.1/100 person-year; HR 0.50; 95% CI 0.26–0.95; P=0.035). Inhibitors of RAS at discharge were not associated with lower 2-year MACE, but with lower re-hospitalization due to heart failure (1.8 vs. 3.5/100 person-year; HR 0.53; 95% CI 0.33–0.86; P=0.010) without significant interaction between EF ≤45% and &gt;45% (P for interaction=0.333).

Conclusions
Beta-blockers or RAS inhibitors at discharge were associated with better 2-year clinical outcomes without significant interaction between ≤45% and &gt;45% in patients with mid-range EF after AMI.&lt;/ef&lt;50%)&gt;

Funding Acknowledgement
Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Korea Centers for Disease Control and Prevention. 2-year clinical outcomes
Associations between metabolic syndrome at index PCI and 1-year outcomes
Authors: Chandrasekhar J , Chowdhury E , Eccleston D , Delacroix S , Worthley S 
Published: October 2021

Abstract

Background
The prevalence of obesity, diabetes and metabolic syndrome is rising, with negative health consequences for the community.

Purpose
We sought to examine the prevalence and impact of metabolic syndrome (MetS) on 1-year outcomes from an Australian cohort of all-comer PCI patients.

Methods
We retrospectively analysed the GenesisCare Outcomes multicentre Registry of prospectively collected data in patients undergoing PCI from 2008–2020. Metabolic syndrome was defined as presence of any 3 features including hypertension, diabetes, obesity with body mass index ≥30 kg/m2 and dyslipidaemia. We examined 1-year outcomes for death and MACE (death, MI or TLR), and the adjusted risk after accounting for each of the defining variables.

Results
During the study period from 2005–2018, 14,405 were included, of which 5480 (38%) had metabolic syndrome. MetS patients were somewhat younger without sex differences (∼76% men). They had greater prevalence of defining characteristics, and smoking and lower prevalence of myocardial infarction presentation compared to non-MetS patients. MetS patients had higher prevalence of B2/C type lesions, restenosis, chronic total occlusions and multivessel disease. At 30-days MetS patients had lower risk of re-infarction (0.1% vs. 0.3%, p=0.011) but from 30-days to 1-year they had greater risk of MI (1.1% vs. 0.5%, p&lt;0.01), TLR (1.5% vs. 1.1%, p=0.03), readmissions (21.8% vs. 19.8%, p=0.008) and MACE (3.6% vs. 2.7%, p=0.03) without differences in mortality (1.3% in both, p=0.88). Unadjusted models showed trend for greater risk of 1-year MACE with MetS, HR 1.15 (95% CI 1.00–1.33), p=0.054. In multivariable models, this risk was lost after adjusting individually for hypertension, dyslipidaemia and insulin-treated diabetes, but not after adjustment for obesity and non-insulin diabetes (See Figure).

Conclusions
Metabolic syndrome was noted in over one-third of all-comer PCI patients, and was associated with greater risk of 1-year MACE. This risk appeared to be related to hypertension, dyslipidaemia and insulin-treated diabetes but not obesity.

Funding Acknowledgement
Type of funding sources: None.
TMAO (trimethylamine n-oxide) as a potential biomarker of individual severe stress perception in posttraumatic stress disorder (PTSD)-vulnerable patients after acute myocardial infarction
Authors: Von Lewinski D , Enko D , Rotenhaeusler H P , Amouzadeh-Ghadikolai O , Harpf H , Harpf L , Traninger H , Obermayer-Pietsch B , Von Lewinski F , Schweinzer M , Braun C , Meinitzer A , Baranyi A 
Published: October 2021

Abstract

Background
Acute myocardial infarction is not only a somatic disease but potentially triggers psychological effects, too. Post-traumatic stress disorder (PTSD) is a common stress-related disorder. It is characterized by numerous symptoms, such as flashbacks, intrusions, nightmares and severe anxiety, as well as uncontrollable, intense and disturbing thoughts and feelings related to the traumatic experience. However, with regard to the development of PTSD, individual stress perception might be crucial since not every serious traumatic experience leads to PTSD. To date, almost no biological correlates of an individual's perception of stress have been identified as being associated with the long-term development of PTSD.

Objective
The aim of the study was to determine whether blood levels of TMAO vary immediately after AMI (1) in patients with or without depression, and (2) in patients with AMI induced PTSD symptomatology (subsyndromal PTSD and full PTSD). Furthermore, we investigated whether TMAO is a potential biomarker that might be useful in the prediction of PTSD symptomatology in the long term.

Method
A total of 114 AMI patients were assessed with standardized clinical psychiatric interviews based on the Hamilton Depression Scale (HAMD-17) after admission to the hospital and 6 months later. In addition, the CAPS-5 was used to explore PTSD symptoms (subsyndromal PTSD and full PTSD) 6 months after AMI. To assess patients' TMAO status, serum samples were collected at hospitalization and 6 months after AMI.

Results
Study participants with post-myocardial infarction PTSD symptomatology (subsyndromal PTSD and full PTSD) had significantly higher TMAO levels immediately after AMI than patients without PTSD symptoms (ANCOVA: TMAO (PTSD x time), F = 4.544, df = 1, p=0.035). In contrast, depressive symptomatology 6 months after AMI had no influence on TMAO levels (TMAO (depression x time), F = 0.083, df = 1, p=0.774). With the inclusion of additional clinical predictors in a hierarchical logistic regression model, TMAO becomes a significant predictor of PTSD symptomatology.

Conclusions
An elevated TMAO level immediately after AMI might reflect severe stress in PTSD-vulnerable patients, which might also lead to a short-term increased gut permeability to trimethylamine (TMA), the precursor of TMAO. Thus, elevated TMAO might be a biological correlate for stress that is associated with vulnerability to PTSD and might help to identify patients at increased risk.

Funding Acknowledgement
Type of funding sources: None.
The prevalence and characteristics of patients with ST-elevation myocardial infarction during the first two months of the COVID-19 pandemics
Authors: Steinmetz Y , Wolff R , Farkash R , Dadon Z , Levi N , Anguizola F , Taha L , Shaheen F , Glikson M , Asher E ,   For the Jerusalem Platelets Thrombosis and Intervention in cardiology (JUPITER-7) study group
Published: October 2021

Abstract

Background
ST-Segment elevation MI (STEMI) is one of the leading cause of mortality in the western world. The coronavirus disease-2019 (COVID-19) pandemic might have implications of the treatment of STEMI patients. Our aim was to evaluate the treatment of STEMI patients during 2 months of the COVID-19 pandemic as compared with the year before.

Methods
Data of 90 STEMI patients treated at the Shaare Zedek Medical Center intensive coronary care unit (ICCU) Between March-April 2019 and March-April 2020 were collected. Patients were divided into 2 groups: The pre COVID-19 group and the COVID-19 era group. Data regarding complications upon arrival and during hospitalization, door to balloon time and echocardiographic exams.

Results
Fifty one (56%) patients were admitted with STEMI in the pre COVID-19 group and only 39 (44%) in the COVID-19 era group. Of them 13.7% vs. 20.5% were female, p=0.392 with a mean age of 62.1 (±13.5) vs. 63.4 (±11) years old, p=0.635 in the pre vs. post COVID-19 era group, respectively. Interestingly, more Jewish vs. non-Jewish were admitted with STEMI in the COVID-19 era group. There were no differences regarding baseline characteristics, catheterization access, culprit vessel and percutaneous coronary intervention rate. Door to balloon time was also similar in both pre and post COVID-19 era groups 35.4 (±32) vs. 30.5 (±29.1) minutes (p=0.896). Moreover, there was no difference regarding infarct size. Complications including acute renal failure, cardiogenic shock, and the use of intra-aortic balloon pump were similar in both groups. 30-day mortality rate was low and similar in both pre and post COVID-19 era groups (5.9% vs. 2.6%, respectively, p=0.426).

Conclusions
During the beginning of COVID-19 era there was a reduction in STEMI admission rate, while no significant difference was found regarding baseline characteristics, door to balloon time, infarct size and mortality rate

Funding Acknowledgement
Type of funding sources: None.
Prediction of endogenous thrombolytic activity in patients with coronary artery disease
Authors: Suh J W , Kang H , Kim J , Cho H W , Lee W , Yoon C H , Youn T J , Chae I H 
Published: October 2021

Abstract

Background
Endogenous thrombolytic activity (ETA) has been suggested as an essential factor related to the acute coronary syndrome. However, there have been little data regarding clinical characteristics of ETA in East Asians.

Method
As an interim study of the entire cohort (n=2,000), we analyzed a total of 278 patients who underwent percutaneous coronary intervention (PCI) due to coronary artery disease (CAD). Informed consent was obtained from all research subjects. Blood samples of patients were brought before the procedure. The Global Thrombosis Test (GTT, Thromboquest, UK), a novel test for examining ETA, was used. Lysis time (LT), which means the time interval between blood flow occlusion and restart, was used as an indicator for ETA. Clinical, laboratory and angiographic characteristics were obtained. LT=3000 seconds was used as a cut-off value to divide patients into two groups. P value&lt;0.05 was regarded as significant.

Results
LT of Korean CAD patients showed bimodal distribution. Median value was 1695 [IQR: 1099, 5932] and it was higher than previous data from Europeans (Figure 1). Patients with impaired ETA (LT&gt;3000) were older and more diabetic. They showed higher creatinine, aPTT, fibrinogen, D-dimer, c-reactive protein, and proBNP values. Moreover, they had lower hemoglobin and platelet levels. Intracoronary thrombus was more frequently observed in LT&gt;3000 group. In the multivariable regression analysis, hemoglobin (per g/dL, odds ratio 0.766, 95% confidence interval (CI) 0.632–0.928) and fibrinogen level(per 10mg/L, odds ratio 1.054, 95% CI 1.015–1.095) could significantly predict impaired ETA.

Conclusion
East Asian patients showed a right-shifted distribution of ETA compared to that of Europeans. Patients with impaired ETA had different clinical, laboratory and angiographic characteristics from those with intact ETA. Hemoglobin and fibrinogen level were significantly associated with impaired ETA. Further studies are warranted to confirm causal relationship among these factors.

Funding Acknowledgement
Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Research Foundation, Republic of Korea
Impact of smoking habit on baseline and on-treatment platelet reactivity in STEMI patients treated with 3rd generation P2Y12
Authors: Canonico M E , Scudiero F , Sanna G D , Siciliano R , Guarino S , Saba P S , Esposito G , Parodi G 
Published: October 2021

Abstract

Background
Smoking habit is a well known risk factor for cardiovascular disease. High on-treatment platelet reactivity has been associated with high risk of ischemic events in STEMI patients. The relationship between platelet reactivity and smoking habit was investigated only in few studies, and the impact of smoke on platelet reactivity in STEMI patients treated with 3rd generation P2Y12 inhibitor is still lacking.

Purpose
This study aim to assess the impact of smoking habits on baseline and on-treatment platelet reactivity in STEMI patients treated with 3rd generation P2Y12 inhibitor.

Methods
Overall, 429 STEMI patients were enrolled in this study. Patients were divided into two groups according to smoking habit. Platelet reactivity was assessed by VerifyNow at baseline and after 3rd generation P2Y12 inhibitor (ticagrelor or prasugrel) loading dose (LD). Blood samples were obtained at baseline (T0), and after 1 hour (T1), 2 hours (T2), 4–6 hours (T3) and 8–12 hours (T4) after LD.

Results
The mean age of the enrolled population was 62±12 and male rate was 75%. Patients with smoking habit were younger (75.8% vs 38.9%, p&lt;0.001 for age &lt;65 years), with higher prevalence of family history of CAD, while with a lower rate hypertension (43.4% vs 65.9%, p&lt;0.001) and previous myocardial infarction (5.3% vs 11.4%, p=0.022) (Table). Smoker patients had lower platelet reactivity either at baseline [T0: 249 (205–285) vs 284 (230–324), p&lt;0.001] or at 2 hours after the LD [T2: 107 (18–279) vs 136 (51–260), p=0.003] (Table). Similarly, Smoker patients experienced a lower rate of in-hospital composite adverse event of death, reinfarction, stroke or acute kidney injury (1.6% vs 12.4%; p≤0.001) (Table). Multivariate analysis demonstrated that left ventricular ejection fraction at admission (OR= 0.916, 95% CI 0.865–0.969; p=0.002), and platelet reactivity at baseline (OR= 1.013, 95% CI 1.002–1.024; p=0.024) were independent predictors of in-hospital composite adverse event.

Conclusions
Smoker status is associated with lower platelet reactivity either at baseline or after LD and with a better short-term prognosis in STEMI patients treated by dual antiplatelet therapy with ticagrelor or prasugrel.

Funding Acknowledgement
Type of funding sources: None.
Frequency and predictors of thin-cap fibroatheroma progression: a comprehensive and dynamic in-vivo OCT study
Authors: He L , Xu Y , Hu S , Qin Y , Weng Z , Feng X , Zhao C , Zeng M , Chen X , Yi B , Xie C , Zhang D , Hou J , Jia H , Yu B 
Published: October 2021

Abstract

Purpose
To assess the evolution of thin-cap fibroatheroma (TCFA) and to explore predictors for its progression by using optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS).

Methods
We enrolled ACS patients with non-culprit TCFA at baseline and corresponding OCT images at follow-up of 9 to 15 months. Clinical, angiographic and OCT data were collected and analyzed according to established methods. TCFA was defined as a lipid plaque with maximum lipid arc &gt;90° and fibrous cap thickness &lt;65μm. Considering the resolution of OCT, the regression of TCFA was defined as an increase of fibrous cap thickness &gt;10μm. Inversely, TCFA progression was defined as a decrease, constant or ≤10μm increase of fibrous cap thickness.

Results
41 patients with 55 non-culprit TCFAs were taken into final analysis. 17 patients (41.5%) had patient-level progression and 22 TCFAs (40.0%) progressed at plaque-level with a median follow-up duration of 371 days. 11 (20.0%) of the 55 TCFAs happened subclinical rupture at follow-up, including 10 with the formation a new layer and 1 without the detection of the new layer. Besides, another patient suffered re-myocardial infarction because of the rupture of TCFA induced acute thrombosis and lumen occlusion during follow-up. The baseline clinical and angiographic characteristics were similar between the two cohorts. The progression group had a significantly higher prevalence of macrophage infiltration and vasa vasorum at baseline than the non-progression group (Figure 1). Multivariate analysis identified macrophage infiltration (odds ratio [OR]: 5.30; 95% confidence interval [CI]: 1.01 to 27.91; p=0.049]) as the independent predictor of TCFA progression. When it came to the evolution of lesion morphology and lipid components, the progression cohort had a higher percent change of lumen stenosis and lipid length (Figure 2).

Conclusions
About 40% of non-culprit TCFAs in ACS patients progressed in fibrous cap thickness at a median interval of 1 year. Macrophage infiltration was the independent predictor of non-culprit TCFA progression. The progression of fibrous cap thickness was usually accompanied with an aggressive evolution of other lesion characteristics.

Funding Acknowledgement
Type of funding sources: Foundation. Main funding source(s): the National Key R&D Program of China Baseline OCT characteristicsPercent change of lesion morphology
A contemporary presentation of the incidence and management of spontaneous coronary artery dissection (SCAD) in New Zealand: an ANZACS-QI study
Authors: Mbizvo R M , Alfadhel M , Williams M J A , Coffey S , Kerr A , Webster M , Lee M 
Published: October 2021

Abstract

Background/Purpose
Spontaneous coronary artery dissection (SCAD) is an underdiagnosed and poorly understood condition that frequently affects younger women without cardiovascular risk factors. In this project we aimed to describe the present landscape of SCAD in New Zealand (NZ).

Methods
All patients in NZ who were admitted to hospital with a diagnosis of Acute Coronary Syndrome (ACS) from July 2019 to December 2020 and underwent coronary angiography were identified from the All NZ Coronary Syndrome Quality Imporvment (ANZACS-QI) registry.

Results
Of 12,053 patients admitted to hospital with an ACS, 122 had SCAD (1.0%). 80% of those with SCAD were female, with mean age of 57 years, and fewer traditional cardiovascular risk factors. Non-ST elevation myocardial infarction was the most common presentation (82.0%), while 16.4% presented with ST elevation myocardial infarction. The majority of patients were managed conservatively (91.8%) while 8.2% underwent PCI. 56.6% of SCAD patients had normal LV function. Nearly 80% of patients were discharged on Acetylsalicylic acid (ASA) therapy, while 60.7% had a P2Y12 inhibitor. Beta blockers, Statins and ACEI/ARB were part of the management strategy in 62.5%, 59.8% and 42.6% of patients respectively while 47.5% had a combination of all 3. Amongst 122 patients, only 1 in-hospital death and 1 inpatient recurrent MI occurred, with 3 patients having bleeding of any kind.

Conclusion
In NZ, incidence of SCAD is approximately 1%. Most patients affected in NZ are female with fewer traditional cardiovascular risk factors. Management is predominantly conservative, and there is a low rate of early adverse outcomes.

Funding Acknowledgement
Type of funding sources: None.
Rationale for CDR132L, an antisense inhibitor of miR-132, for a novel therapy for ventricular remodelling after myocardial infarction
Authors: Aimo A , Iborra Egea O , Bayes-Genis A , Passino C , Emdin M 
Published: October 2021

Abstract

Background
Heart failure (HF) development is a common complication of myocardial infarction (MI), which warrants a search for novel therapies able to prevent left ventricular remodelling after an MI. CDR132L is a synthetic antisense inhibitor of miR-132. In a pig model of reperfused MI, monthly intravenous administration of CDR132L proved safe and effective in preventing HF development. They expect CDR132L to have an additive, and possibly synergistic, effect to standard-of-care therapies (beta-blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers [ACEi/ARB], and mineralocorticoid receptor antagonists [MRA]) because of their distinct first targets. Nonetheless, a degree of overlap in the final effects of CDR132L and current therapies might exist, given that ACEi/ARB and MRA ultimately modulate myocardial inflammation and fibrosis, as CDR132L do. We assessed this point by searching for similar changes in protein expression between MI therapies and CDR132L.

Methods
We retrieved the 14 mRNAs significantly altered in the myocardium of pigs receiving CDR132L compared with control pigs: BMPR2, ADRA1D, GCLC, CD44, PRDX1, ECM1, LEP, GATA3, GPX1, EIF4G1, ACE2, HMOX1, RTN4 and LIFR. Except for RTN4, all these mRNAs were downregulated by CDR132L. We assumed a close correlation between changes in mRNA levels and the expression of the corresponding proteins. By using massive public databases, such as Drugbank, the Open Targets Platform and the Human Protein Atlas, we identified all approved, investigational and experimental drugs reported to modulate the expression of at least one of these 14 proteins in any setting.

Results
We did not find any drug modulating more than one of the 14 proteins. Therefore, no drug, including ACEi/ARB or MRA, proved able to mimic the effects of CDR132L on protein expression.

Conclusions
CDR132L might have an additive or synergistic action to standard drugs, given the different effects on protein expression profiles. CDR132L might then help prevent post-MI remodelling even on top of optimal medical therapy. This point should be verified in dedicated studies.

Funding Acknowledgement
Type of funding sources: None.