scholarly journals Apolipoprotein C3 and Necrotic Core Volume Are Correlated but Also Associated With Future Cardiovascular Events

Author(s):  
Takayuki Ohwada ◽  
Takayuki Sakamoto ◽  
Satoshi Suzuki ◽  
Yukiko Sugawara ◽  
Kazuhiko Nakazato ◽  
...  

Abstract We aimed to clarify the relationship between apolipoprotein C3 (apo-C3) and vascular composition of lesion plaque in stable coronary disease (SCD) before percutaneous coronary intervention (PCI) and to investigate major adverse cardiovascular events (MACEs) within 4 years. Data of 98 consecutive patients with SCD who underwent PCI between November 1, 2012, and March 10, 2015, were analyzed. Laboratory evaluation and virtual histology-intravascular ultrasound (VH-IVUS) examination of culprit lesions were conducted before PCI. Patients were divided according to the median apo-C3 value into low apo-C3 (≤8.5 mg/dL) and high apo-C3 (>8.5 mg/dL) groups. VH-IVUS data indicated that the percentage of necrotic core volume (%NC) was significantly higher in the high apo-C3 group than in the low apo-C3 group. Moreover, the %NC significantly correlated with the apo-C3 level (R=0.2109, P=0.037). Kaplan–Meier curve analysis revealed that freedom from MACEs decreased more in the high apo-C3 group than in the low apo-C3 group and in the high %NC group than in the low %NC group. Multivariate Cox hazards analysis showed that the %NC and high apo-C3 were independent predictors of 4-year MACEs. Apo-C3 may be a useful marker for future MACEs in patients with SCD after PCI and contribute to %NC growth.

Author(s):  
Hendra Wana Nur’amin ◽  
Iwan Dwiprahasto ◽  
Erna Kristin

Objective: Antiplatelet therapy is recommended in patients with coronary heart disease (CHD) who had the percutaneous coronary intervention (PCI) procedure to reduce major adverse cardiovascular events (MACE). There has been a lack of population-based studies that showed the superior effectiveness of ticagrelor over clopidogrel and similar studies have not been conducted in Indonesia yet. The aim of the study was to investigate the effectiveness of ticagrelor compared to clopidogrel in reducing the risk of MACE in patients with CHD after PCI.Methods: A retrospective cohort study with 1-year follow-up was conducted. 361 patients consisted of 111 patients with ticagrelor exposure and 250 patients with clopidogrel exposure. The primary outcome was MACE, defined as a composite of repeat revascularization, myocardial infarction, or all-cause death. The association between antiplatelet exposure and the MACE was analyzed with Cox proportional hazard regression, adjusted for sex, age, comorbid, PCI procedures and concomitant therapy.Results: MACE occurred in 22.7% of the subjects. Clopidogrel had a significantly higher risk of MACE compared with ticagrelor (28.8%, vs 9.0%, hazard ratio (HR): 1.96 (95% CI 1.01 to 3.81, p=0.047). There were no significant differences in risk of repeat revascularization (20.40% vs 5.40%, HR: 2.32, 95% CI 0.99 to 5.42, p = 0.05), myocardial infarction (11.60% vs 3.60%, HR: 2.08, 95% CI, 0.73 to 5.93, p = 0.17), and death (1.60% vs 1.80%, HR: 0.77, 95% CI, 0.14 to 4.25, p = 0.77).Conclusion: Clopidogrel had a higher risk of MACE compared to clopidogrel in patients with CHD after PCI, but there were no significant differences in the risk of repeat revascularization, myocardial infarction, and all-cause death. 


2018 ◽  
Vol 27 (5) ◽  
pp. 459-465 ◽  
Author(s):  
Erdal Aktürk ◽  
Lütfü Aşkın ◽  
Hakan Taşolar ◽  
Serdar Türkmen ◽  
Hakan Kaya

Objective: We evaluated the relationship between various risk scores (SYNTAX score [SS], SYNTAX score-II [SS-II], thrombolysis in myocardial infarction [TIMI] risk scores, and Global Registry of Acute Coronary Events [GRACE] risk scores) and major adverse cardiovascular events (MACE) in non-ST elevation myocardial infarction (NSTEMI) patients undergoing percutaneous coronary intervention (PCI). Subjects and Methods: The study population were selected from among 589 patients who underwent coronary angiography with a diagnosis of NSTEMI. TIMI and GRACE risk scores were calculated. SS and SS-II were calculated in all patients, and points were added according to the predefined algorithm, taking into account the other 6 clinical variables being monitored (age, sex, left ventricular ejection fraction, creatinine clearance, chronic obstructive pulmonary disease, and peripheral artery disease). Patients were classified into tertile 1 (SS < 22), tertile 2 (SS 23–32), and tertile 3 (SS > 32). Results: The group with high SS-II for PCI values in the risk scores were observed from tertile 1 to tertile 3 (from 25.0 ± 7.7 to 31.6 ± 9.4, p < 0.001, respectively). The SS-II score in patients with PCI was an independent predictor of MACE, in-hospital mortality, nonfatal myocardial infarction, and stent thrombosis (OR 1.082, 95% CI 1.036–1.131, p < 0.001). The overall MACE, in-hospital mortality, and nonfatal myocardial infarction rates were significantly higher in the high SS-II for PCI group (p < 0.001). Conclusion: TIMI and GRACE risk scores were able to predict MACE. In addition to these, SS-II was also able to predict in-hospital mortality, nonfatal myocardial infarction, and stent thrombosis.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Kazuhiro Fujiyoshi ◽  
Yoshiyasu Minami ◽  
Kohki Ishida ◽  
Miwa Ishida ◽  
Ken-ichiro Wakabayashi ◽  
...  

Introduction: Sleep apnea syndrome (SAS) is a risk factor of cardiovascular disease. However, the impact of SAS on the clinical course after percutaneous coronary intervention (PCI) remains to be elucidated. Methods: A total of 206 consecutive patients who underwent PCI were included. The incidence of major adverse cardiovascular events (MACE) at 3-year was compared among patients with untreated SAS (untreated SAS group; n=60), those with SAS treated by continuous positive alveolar pressure (CPAP group; n=20) and those without SAS (non-SAS group; n=96). MACE included cardiac death, non-fatal myocardial infarction, target vessel revascularization (TVR), and non-TVR (NTVR). Results: There was no significant difference in baseline clinical characteristics among the untreated SAS group, the CPAP group and the non-SAS groups, other than in age (74.1 ± 9.6 vs. 71.2 ± 0.33 vs. 68.2 ± 10.7, p = 0.002) and hemoglobin A1c levels (6.54 ± 0.87 vs. 6.61 ± 0.58 vs. 6.09 ± 0.70 %, p < 0.001). The incidence of MACE, TLR and TVR was significantly higher in the untreated SAS group than in the CPAP group and the Non-SAS group although there was no significant difference in the incidence of NTVR among the three groups (Figure). The untreated SAS was independently associated with the incidence of 3-year MACE (odds ratio 3.24, 95% confidence interval 1.36-8.20, p = 0.008). Conclusions: The incidence of MACE was significantly higher in patients with untreated SAS than in those treated with CPAP and those without SAS after PCI. The present findings may highlight the importance of SAS management in patients requiring PCI.


2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Lidija Savic ◽  
Igor Mrdovic ◽  
Milika Asanin ◽  
Sanja Stankovic ◽  
Gordana Krljanac ◽  
...  

Background/Aim. The RISK-PCI is a simple score for the prediction of 30-day major adverse cardiovascular events (MACE) and mortality in patients treated with primary PCI (pPCI). The aim of the present study is to evaluate the prognostic performance of the RISK-PCI score in predicting MACE and mortality in the long-term follow-up of STEMI patients treated with pPCI. Method. The present study enrolled 2,096 STEMI patients treated with pPCI included in the RISK-PCI trial. Patients presenting with cardiogenic shock were excluded. The composite end-point MACE comprising cardiovascular mortality, nonfatal reinfarction and stroke. Patients were followed up at 6 years after enrollment. Results. One-year and 6-year MACE occurred in 229 (10.9%) and 285 (13.6%) patients, respectively; and 1-year and 6-year mortality occurred in 128 (6.2%) and 151 (7.2%) patients, respectively. The RISK-PCI score was an independent predictor for 1-year MACE (HR 1.24, 95% CI 1, 18–1.31, p<0.001), 6-year MACE (HR 1.22, 95% CI 1.16–1.28, p<0.001), 1-year mortality (HR 1.21, 95% CI 1.13–1.29, p<0.001), and 6-year mortality (HR 1.23, 95% CI 1.15–1.31, p<0.001). The discrimination of the RISK-PCI score to predict 1-year and 6-year MACE and mortality was good: for 1-year MACE c-statistic 0.78, for 6-year MACE c-statistic 0.75, for 1-year mortality c-statistic 0.87, and for 6-year mortality c-statistic 0.83. The nonsignificant Hosmer–Lemeshow goodness-of-fit estimates for 1-year MACE (p=0.619), 6-year MACE (p=0.319), 1-year mortality (p=0.258), and 6-year mortality (p=0.540) indicated a good calibration of the model. Conclusion. The RISK-PCI score demonstrates good characteristics in the assessment of the risk for the occurrence of MACE and mortality during long-term follow-up after pPCI.


Circulation ◽  
2019 ◽  
Vol 140 (9) ◽  
pp. 751-764 ◽  
Author(s):  
Yulin Li ◽  
Boya Chen ◽  
Xinying Yang ◽  
Congcong Zhang ◽  
Yao Jiao ◽  
...  

Background: Myocardial ischemia-reperfusion (MI/R) injury is a significant clinical problem without effective therapy. Unbiased omics approaches may reveal key MI/R mediators to initiate MI/R injury. Methods: We used a dynamic transcriptome analysis of mouse heart exposed to various MI/R periods to identify S100a8/a9 as an early mediator. Using loss/gain-of-function approaches to understand the role of S100a8/a9 in MI/R injury, we explored the mechanisms through transcriptome and functional experiment. Dynamic serum S100a8/a9 levels were measured in patients with acute myocardial infarction before and after percutaneous coronary intervention. Patients were prospectively followed for the occurrence of major adverse cardiovascular events. Results: S100a8/a9 was identified as the most significantly upregulated gene during the early reperfusion stage. Knockout of S100a9 markedly decreased cardiomyocyte death and improved heart function, whereas hematopoietic overexpression of S100a9 exacerbated MI/R injury. Transcriptome/functional studies revealed that S100a8/a9 caused mitochondrial respiratory dysfunction in cardiomyocytes. Mechanistically, S100a8/a9 downregulated NDUF gene expression with subsequent mitochondrial complex I inhibition via Toll-like receptor 4/Erk–mediated Pparg coactivator 1 alpha/nuclear respiratory factor 1 signaling suppression. Administration of S100a9 neutralizing antibody significantly reduced MI/R injury and improved cardiac function. Finally, we demonstrated that serum S100a8/a9 levels were significantly increased 1 day after percutaneous coronary intervention in patients with acute myocardial infarction, and elevated S100a8/a9 levels were associated with the incidence of major adverse cardiovascular events. Conclusions: Our study identified S100a8/a9 as a master regulator causing cardiomyocyte death in the early stage of MI/R injury via the suppression of mitochondrial function. Targeting S100a8/a9-intiated signaling may represent a novel therapeutic intervention against MI/R injury. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03752515


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