scholarly journals Prognostic Impacts of Comorbid Significant Coronary Stenosis and Coronary Artery Spasm in Patients With Stable Coronary Artery Disease

2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Kiyotaka Hao ◽  
Jun Takahashi ◽  
Yoku Kikuchi ◽  
Akira Suda ◽  
Koichi Sato ◽  
...  

BACKGROUND Stable coronary artery disease is caused by a variable combination of organic coronary stenosis and functional coronary abnormalities, such as coronary artery spasm. Thus, we examined the clinical importance of comorbid significant coronary stenosis and coronary spasm. METHODS AND RESULTS We enrolled 236 consecutive patients with suspected angina who underwent acetylcholine provocation testing for coronary spasm and fractional flow reserve (FFR) measurement. Among them, 175 patients were diagnosed as having vasospastic angina (VSA), whereas the remaining 61 had no VSA (non‐VSA group). The patients with VSA were further divided into the following 3 groups based on angiography and FFR: no organic stenosis (≤50% luminal stenosis; VSA‐alone group, n=110), insignificant stenosis of FFR>0.80 (high‐FFR group, n=36), and significant stenosis of FFR≤0.80 (low‐FFR group, n=29). The incidence of major adverse cardiovascular events, including cardiovascular death, nonfatal myocardial infarction, urgent percutaneous coronary intervention, and hospitalization attributed to unstable angina was evaluated. All patients with VSA received calcium channel blockers, and 28 patients (95%) in the low‐FFR group underwent a planned percutaneous coronary intervention. During a median follow‐up period of 656 days, although the incidence of major adverse cardiovascular events was low and comparable among non‐VSA, VSA‐alone, and high‐FFR groups, the low‐FFR group had an extremely poor prognosis (non‐VSA group, 1.6%; VSA‐alone group, 3.6%; high‐FFR group, 5.6%; low‐FFR group, 27.6%) ( P <0.001). Importantly, all 8 patients with major adverse cardiovascular events in the low‐FFR group were appropriately treated with percutaneous coronary intervention and calcium channel blockers. CONCLUSIONS These results indicate that patients with VSA with significant coronary stenosis represent a high‐risk population despite current guideline‐recommended therapies, suggesting the importance of routine coronary functional testing in this population.

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. 


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.


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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