bluuebunny/crossref_metadata_2025_split huggingface dataset:
Morphological characteristics of plaque erosion with noncritical coronary stenosis: an optical coherence tomography study
Authors: Fang C , Dai J , Zhang S , Wang J , Wang Y , Li L , Xing L , Hou J , Yu B 
Published: November 2020

Abstract

Background
Plaque erosion is a frequent and important mechanism of acute coronary thrombosis only secondary to plaque rupture. Recent studies suggested plaque erosion with noncritical stenosis could be treated conservatively that distinct from those with critical stenosis. However, characteristics of plaque erosions with different coronary stenosis remain unknown.

Purpose
The present study aimed to investigate morphological features of plaque erosions with different coronary stenosis using optical coherence tomography (OCT).

Methods
Consecutive ST-segment elevated myocardial infarction (STEMI) patients with OCT images of culprit lesion between August 2014 and December 2017 were enrolled and 348 cases presented with plaque erosion identified by OCT. Based on the severity of lumen area stenosis [calculated by (1-minimal lumen area/reference lumen area) * 100%], all culprit plaque erosions were divided into three groups: Group A (area stenosis&lt;50%, n=50, 14.4%); Group B (50%≤area stenosis&lt;75%, n=146, 42.0%); Group C (area stenosis≥75%, n=152, 43.7%). Clinical characteristics, lesion features detected by coronary angiography and OCT were compared among three groups.

Results
Of all 348 STEMI patients with plaque erosions, patients in Group A were youngest (p=0.008) and had the lowest frequency of hypertension (p=0.029) as compared with those in Group B and C. Angiographic analysis showed 72.0% of plaque erosions in Group A located in LAD, while 67.8% in Group B and 53.9% in Group C (p=0.039). OCT findings (Figure 1-A) showed the prevalence of fibrous plaque was significantly highest in Group A than those in Group B and C (82.0% vs. 54.8% vs. 34.9%, p&lt;0.001), whereas lipid rich plaque was most frequent in Group C (16.0% vs. 43.8% vs. 62.5%, p&lt;0.001). The prevalence of macrophage (p&lt;0.001), microvessel (p=0.009) and cholesterol crystals (p&lt;0.001) increased gradually from plaque erosion with lumen area stenosis &lt;50% to 50–75% to ≥75%. Notably, compared with Group B and C, nearby bifurcation was most common in Group A (72.0% vs. 67.1% vs. 55.3%, p=0.036). Multivariable regression analyses (Figure 1-B) showed fibrous plaque and nearby bifurcation were independently associated with plaque erosion with noncritical stenosis (area stenosis&lt;75%).

Conclusion
56.3% plaque erosion in STEMI patients presented with noncritical stenosis, having distinct morphological features from erosion with critical stenosis. Fibrous plaque and nearby bifurcation were independently associated with the presence of noncritically stenotic plaque erosion, remaining a desire to tailor treatment therapy to individual patients.
Figure 1

Funding Acknowledgement
Type of funding source: Foundation. Main funding source(s): National Key R&D Program of China
Metformin exerts cardioprotection via attenuating mitochondrial fission in cardiac ischaemia-reperfusion injury in rats
Authors: Palee S , Higgins L , Leech T , Chattipakorn S.C , Chattipakorn N 
Published: November 2020

Abstract

Background
Cardiac ischemia/reperfusion (I/R) injury following myocardial infarction reperfusion therapy is a phenomenon that results in further cardiomyocytes death and impaired cardiac contractility. Although metformin has been shown to exert cardioprotection in addition to glycemic control, its effect on cardiac I/R injury are still controversy, and the comparative doses of metformin in cardiac I/R injury have never been investigated.

Purpose
We hypothesized that metformin given acutely prior to cardiac ischaemia exerts cardioprotection in rats with cardiac I/R injury via attenuating cardiac mitochondrial dysfunction, leading to improved left ventricular (LV) function.

Methods
Forty Male Wistar rats were subjected to cardiac I/R injury. Four treatment groups were investigated. The first group received saline as a control group. The second to the fourth groups received metformin at 100, 200, and 400 mg/kg intravenously, respectively. During the I/R protocols, the LV function, arrhythmia score, and mortality rate were determined. At the end, the hearts were rapidly removed to determine infarct size, cardiac mitochondrial function, cardiac mitochondrial dynamics, and cardiac apoptosis.

Results
Metformin 200 mg/kg exerted the highest level of cardioprotection through the attenuated incidence of arrhythmia, decreased infarct size (Fig. 1), improved cardiac mitochondrial function, and decreased mitochondrial fission (Fig. 1) and cardiac apoptotic markers, leading to improved cardiac function during I/R injury. Although Metformin at all doses effectively decreased infarct size, improved cardiac mitochondrial function and LV function, Metformin at 200 mg/kg exerted the best efficacy (Fig. 1).

Conclusions
Metformin exerts cardioprotection by attenuating mitochondrial dysfunction and decreased mitochondrial fission, leading to decreased infarct size and ultimately improved LV function after acute cardiac I/R injury in rats. These findings also indicate the potential biphasic effects of metformin on infarct size which are dose-dependent.
Figure 1

Funding Acknowledgement
Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Science and Technology Development Agency Thailand (NC), and Thailand Research Fund (SCC)
Characterization of thromboembolic and bleeding risks in cancer patients with acute myocardial infarction under the use of guideline-recommended dual-antiplatelet therapy
Authors: Hayashi H , Kataoka Y , Hosoda H , Nakashima T , Honda S , Fujino M , Nakao K , Yoneda S , Otsuka F , Asaumi Y , Noguchi T , Izumiya Y , Yoshiyama M , Yasuda S 
Published: November 2020

Abstract

Background
Atherosclerotic cardiovascular disease including acute myocardial infarction (AMI) has become one of major co-existing diseases in cancer patients due to their improved survival rate. Current guideline recommends dual-antiplatelet therapy (DAPT) in patients with AMI. Given that the presence of cancer elevates not only coagulability but bleeding risks, these substrate may further worsen cardiovascular outcomes and bleeding risks in cancer subjects with AMI receiving DAPT.

Methods
We retrospectively analyzed 712 AMI patients treated by primary PCI with drug-eluting stent and DAPT between 2007 and 2017. The diagnosis of cancer was determined through medical record review. Clinical characteristics, thromboembolic (=all-cause death+non-fatal MI+stroke) and bleeding events were compared in AMI subjects with vs. without cancer.

Results
Cancer was identified in 11.1% (=79/712) of study subjects. Of these, around 40% of them had gastrointestinal cancer (=35/79), followed by lung cancer (=5/79) and breast cancer (=8/79). Cancer patients were more likely to be older (77±7 v. 69±13 years, p&lt;0.001) with a history of Af (25 v. 10%, p&lt;0.001), CKD (eGFR&lt;60: 60 v. 42%, p=0.002), anemia (hemoglobin: 12.8±1.8 v. 13.9±1.8 g/dl, p&lt;0.001). Under anti-thrombotic (DAPT=86%, triple-antiplatelet therapy=14%) and optimal medical therapies (ACE-I=90%, beta-blocker=76%, statin=96%), more frequent occurrence of thromboembolic events was observed in patients with cancer (34.2 v. 12.6%, p=0.004, Picture). Furthermore, the presence of cancer was associated with more than four times greater risk of bleeding events compared to non-cancer subjects (18.9 v. 4.3%, p&lt;0.001, Picture). In particular, the frequency of both major (10.1 vs. 3.3%, p=0.003) and minor (8.9 vs. 0.9%, p&lt;0.001) bleeding events was significantly higher in patients with cancer. In multivariate analysis, cancer independently predicted bleeding events (Table).

Conclusions
Under the use of guideline recommended DAPT, the concomitance of cancer in AMI subjects was a predictor for thromboembolic as well as bleeding events. In particular, the relationship between cancer and bleeding was significant. These observations underscore the appropriate selection and duration of anti-thrombotic agents in AMI subjects with cancer.
Cardiac/Bleeding Events in AMI Subjects

Funding Acknowledgement
Type of funding source: None
Ischemic and bleeding risk stratification in diabetic patients after acute coronary syndrome based on insulin requirement
Authors: Cavallari I , Sagazio E , Antonucci E , Calabro' P , Gragnano F , Cirillo P , Gresele P , Palareti G , Pengo V , Pignatelli P , Marcucci R , Patti G 
Published: November 2020

Abstract

Background
Diabetes is a known risk factor for a first or recurrent cardiovascular event, however, its association with an increased risk of bleeding is controversial. To date, no study has explored the prognostic weight of insulin therapy in the setting of ACS.

Purpose
To investigate the differential role of insulin versus no insulin therapy on ischemic and bleeding risks in patients with diabetes and ACS.

Methods
START-ANTIPLATELET is a prospective, real-world multicenter registry including consecutive patients admitted for ACS. For the purpose of this analysis, patients were stratified according to diabetes status and insulin therapy. We compared 1-year rates of major adverse cardiovascular events, a composite of cardiovascular death, myocardial infarction and stroke, and of any bleeding, according to diabetes status (no diabetes, diabetes not on insulin therapy, diabetes on insulin therapy). In addition, we evaluated the net clinical benefit of dual antiplatelet therapy with the newer P2Y12 inhibitors (ticagrelor or prasugrel) vs dual antiplatelet therapy with clopidogrel according to diabetes status.

Results
In an overall population of 907 patients, 198 had diabetes, 10.6% of whom were on insulin. From non-diabetic patients to diabetic patients not on insulin and diabetic patients on insulin there was a stepwise decrease of MACE-free survival (log-rank p 0.039) with incidence of events at 1 year being 3.8%, 6.8% (adjusted p vs no diabetes 0.49) and 12.5% (adjusted p vs no diabetes 0.047), respectively (Figure, panel A). The rates of any bleeding were higher in patients on insulin (20.8% vs 8.8% in those without diabetes and 5.8% in diabetic patients not receiving insulin; log-rank p 0.028; Figure, panel B). Multivariable analysis demonstrated an almost 5-fold increase of any bleeding in diabetic patients with vs without insulin (OR 4.98, 95% CI 1.46–16.92; p=0.010). In the overall population, the incidence of the net composite endpoint including MACE or major bleeding with the use of ticagrelor/prasugrel on top of aspirin was significantly lower compared to use of clopidogrel (4.7% vs 8.4%; OR 0.54, 95% CI 0.30–0.94, p=0.031). This net clinical benefit in patients receiving a newer P2Y12 inhibitor was regardless of the diabetes status (p for interaction 0.48).

Conclusions
In this cohort of ACS patients, the presence of diabetes stratified by insulin therapy was associated with a graded increase in the 1-year rates of MACE. Conversely, insulin therapy significantly contributed to the overall increase of bleeding risk in diabetes.

Funding Acknowledgement
Type of funding source: None
Short and medium chain acylcarnitines as markers of outcome in diabetic and non-diabetic subjects with acute coronary syndromes
Authors: Davies A , Li X , Obeid S , Roffi M , Klingenberg R , Mach F , Raber L , Windecker S , Templin C , Muller O , Nanchen D , Matter C , Wang Z , Hazen S , Luescher T 
Published: November 2020

Abstract

Background
Dietary carnitine that is not absorbed can serve as a precursor for gut microbiota-dependent generation of trimethylamine N-oxide (TMAO), a pro-atherogenic and pro-thrombosis promoting metabolite. Gut microbiome-derived metabolites of dietary carnitine, including TMAO and g-butyrobetaine, may accelerate atherosclerosis, increase platelet reactivity and in vivo thrombosis. Carnitine metabolism also produces numerous molecular species of short, medium and long chain acylcarnitines, which play important roles in energy metabolism and intracellular fatty acid transport.

Purpose
We sought to evaluate the differences between diabetics and non-diabetics presenting with ACS with respect to acylcarnitines, and to explore their relationship with incident cardiovascular outcomes.

Methods
Using a large, prospectively recruited cohort of patients presenting to the cardiac cath lab with suspected acute coronary syndromes, we measured levels of plasma acylcarnitines, carnitine and its gut microbial-derived metabolites to assess their relationship with independently adjudicated major adverse cardiac events (MACE = myocardial infarction, stroke or TIA, need for revascularization or all-cause mortality) amongst diabetics and non-diabetics.

Results
We analysed 1683 patients who presented with ACS, were treated according to current guidelines and had undergone acylcarnitine analysis. There were 294 diabetics and 1389 non-diabetics. Diabetics had significantly higher plasma levels of all acyl carnitine metabolites than non-diabetics (P&lt;0.001), but not of carnitine itself. Baseline plasma levels of all gut microbiome derived carnitine metabolites (TMAO, g-butyrobetaine and crotonobetaine) were also significantly higher in those who subsequently experienced a MACE. All carnitine metabolites, apart from octenoylcarnitine, were significantly associated with MACE on univariate analysis, while acetylcarnitine and crotonobetaine were independently associated with MACE after multivariate adjustment.

Conclusion
Serum short- and medium- chain acylcarnitine levels are significantly higher in diabetic patients presenting with ACS and predict MACE. After multivariate adjustment, acetylcarnitine and crotonobetaine remained an independent predictor of MACE.

Funding Acknowledgement
Type of funding source: Foundation. Main funding source(s): Zurich Heart House - Foundation for Cardiovascular Research
C-reactive protein increases myocardial damage after STEMI
Authors: Garlichs C.D , Ries W , Torzewski J , Pfluecke C , Heigl F , Darius H , Ince H , Mitzner S , Nordbeck P , Butter C , Sheriff A 
Published: November 2020

Abstract

Background
The CAMI-1 study dealt with the depletion of CRP by apheresis in patients with acute myocardial infarction (AMI). CRP, the prototype human acute phase protein, has been known as a marker of poor prognosis in AMI and independently predicts 30-day mortality.

Methods
66 STEMI patients were enrolled in the study following complete coronary revascularization (2–12 h after the onset of symptoms). 32 patients received CRP apheresis, whereas 34 patients treated by standard protocols served as controls. CRP apheresis started 24±12 h and 48±12 h after onset of symptoms. In case of a rapid increase in CRP plasma levels following the 2nd session, a 3rd session was carried out another 24 h later. A specific CRP adsorber removed up to 79% of the original CRP. In each apheresis session, 6000 ml of plasma was treated via peripheral venous access. Primary study endpoint was myocardial infarction size as determined by Cardiac Magnetic Resonance Imaging (CMR) 2–9 days after STEMI.

Results
Aphereses sessions were well tolerated with no relevant side effects. Peak CRP plasma levels after STEMI ranged from 9 to 279 mg/l. The expected peak CRP level after AMI can be calculated precisely with 2–3 CRP quantifications during the first 24 h after the onset of symptoms. The regression coefficient for this analysis is 0.91. This mathematical step allows for the comparison of the CRP-apheresis group and the controls on the basis of their individual CRP peak levels. The statistical evaluation shows that the CRP concentration is significantly associated with the damage (infarct size, LVEF, circumferential strain) in the controls. This association was lost in the aphereses patients: they performed significantly better at all endpoints (infarct size, LVEF, circumferential strain) than the controls. The CRP apheresis significantly reduced myocardial damage. To our surprise, two apheresis patients had an infarct size of 0%.

Conclusions
For the first time we find an unequivocal association between myocardial infarct size and the CRP concentration. This is in some respects a surprise, since the basic assumption in AMI is that the vascular occlusion leads to primary damage and the reperfusion to secondary damage, which would not have led one to expect such a clear dose-response relationship as that observed here. In addition, our results show a significant beneficial effect of CRP apheresis on myocardial infarction size and wall motion. Selective CRP apheresis is now being further evaluated as a therapeutic approach in the treatment of acute myocardial infarction in a registry (CAMI registry).

Funding Acknowledgement
Type of funding source: Private company. Main funding source(s): Pentracor GmbH
Extend of coronary lesion, in-hospital complications in patients with STEMI, treated with PCI and high levels of CD14++CD16+ monocytes subpopulation
Authors: Dovhan O.V , Parkhomenko A.N , Talayeva T.V , Tretyak I.V , Shumakov O , Gurjeva O.S 
Published: November 2020

Abstract

Aims
Acute myocardial infarction with the ST elevation (STEMI) is accompanied by the development of an inflammatory reaction, in particular, activation of monocytes. To date, the relationship between the levels and dynamics of monocyte populations in patients with STEMI and the prevalence of coronary atherosclerosis on the one hand (and with the clinical course of the disease, on the other hand) is not well understood.

Methods and results
The 50 STEMI patients (pts) were studied prospectively. All the pts underwent the PCI (alone, or followed by angioplasty/stenting) and have the monocytes (Mc) population analysis data obtained at 1st and 7th–10th days. According to the angiography data, pts were divided into three groups: “single-vessel lesion” (group 1, n=13), “two-vessel lesion” (group 2, n=14) and “three-vessel lesion” (group 3, n=23). There was an in-hospital increase in CD14++CD16-, CD14++CD16+ and CD14+CD16++ populations of Mc in 3rd group (+5%, +43% and +44%, respectively, p&lt;0.05 for all), whereas in subgroups 1 and 2 there was an increase in CD14+CD16++ population (+70% in group 1, p&lt;0.05 and +90% in group 2, p&lt;0.001), without significant dynamics of CD14++CD16− and CD14++CD16+ populations. In addition, there was an increase in the CD14+CD16++ population only in pts with 1–3 coronary lesions (+72%, p&lt;0.001 versus −12% of decrease in pts with more than 3 lesions, p&gt;0.1). The number of CD14++CD16+ Mc on day 1 of STEMI correlated positively with levels of C-reactive protein (C-RP, r=0.34, p&lt;0.05), erythrocyte sedimentation rate (ESR, r=0.39, p&lt;0.01), and with left ventricle (LV) end-systolic volume (r=0.33, p&lt;0.05) and negatively – with LV ejection fraction (r=−0.22, p&lt;0.1), while there were only slight correlations of CD14++CD16- Mc levels with left ventricle (LV) end-systolic volume (r=0.28, p&lt;0.05) and with LV ejection fraction (r=−0.23, p&lt;0.1). According to the hospital follow-up, the 1st day count of CD14++CD16+ Mc was higher in patients with in-hospital complications (mean 42.9±6.9x106/L vs 26.6±5.3x106/L in uncomplicated cases, p&lt;0.05), and was correlated with number of in-hospital complications per patient (r=0.25, p=0.05).

Conclusion
Higher baseline number of CD14++CD16+ Mc correlates with other “pro-inflammatory” indices (C-RP, ESR) and indicates the worse baseline cardio-hemodynamic and unfavorable course of in-hospital period in pts with STEMI, treated with PCI. Incremental in-hospital dynamic of all Mc populations was observed in multi-vessel lesion cases.

Funding Acknowledgement
Type of funding source: None
Coronary plaque natural history displays significant longitudinal heterogeneity along the length of individual coronary plaques
Authors: Wentzel J.J , Papafaklis M , Antoniadis A , Takahashi S , Cefalo N.V , Cormier M , Saito S , Coskun A , Stone P.H 
Published: November 2020

Abstract

Background
The natural history of plaque growth is, among other systemic risk factors, related to the blood flow induced local shear stress. Especially at regions of low shear stress plaques are initiated. Upon plaque encroachment into the lumen, plaques will be exposed to high shear stress. Interestingly, it has been observed that individual plaques are very heterogeneous regarding the local shear stress exposure and remodeling patterns along the plaque length. However no information is available on the spatial heterogeneity of temporal changes in plaques burden. We studied the longitudinal spatial heterogeneity of plaque burden progression, regression, quiescence in human coronary plaques.

Methods
591 coronary arteries from 302 patients with coronary artery disease who presented with an acute coronary syndrome from the PREDICTION study were investigated for local plaque progression, regression, quiescence patterns after 6–10 months follow up. Arterial geometry was derived from angiography/IVUS-based vascular profiling and reported in 3 mm segments. Plaques were defined as &gt;3 consecutive segments with maximal wall thickness&gt;0.5 mm. Plaque progression was defined as &gt;5% increase, regression as &lt;−5% decrease, and quiescence as no change in plaque burden (plaque area/ total vessel area * 100%). Logistic mixed model regression analysis was performed with plaque progression features as outcome and plaque length as independent variable with vessel as random factor to account for clustering of the data.

Results
5658 3mm-segments of 661 plaques were analyzed. Plaque burden changes over time ranged from −22% to +20%, with an average of −0.4%±4% which was not significant different from 0. Among all plaques, 56% showed segments with plaque progression of more than 5%, 60% with plaque regression (&lt;−5%) and 96% of the plaques had segments that did not change over time (quiescence). On average, 17% of the plaque length displayed plaque progression, 20% regression and 63% was quiescent. The presence and number of features (progression, regression, quiescence) within the plaque were significantly related to the plaque length (figure).

Conclusion
Plaques are very heterogeneous in plaque progression patterns. Most of the plaques show within the plaque length simultaneously more than one plaque progression feature (segments that do not change in plaque burden, segments that regress or progress). The number of observed plaque progression features was related to the plaque length.

Funding Acknowledgement
Type of funding source: None