Antiplatelet Therapy Changes for Patients With Myocardial Infarction With Recurrent Ischemic Events: Insights Into Contemporary Practice From the TRANSLATE‐ACS (Treatment With ADP Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events After Acute Coronary Syndrome) Study

Kaltenbach, Lisa A.; Peterson, Eric D.; Akhter, Mohammed W.; Effron, Mark B.; Henry, Timothy D.; Wang, Tracy Y.

doi:10.1161/jaha.117.007982

Cited by 3 publications

(1 citation statement)

References 45 publications

(89 reference statements)

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“…Since reperfusion is still the main treatment method to rescue infraction for myocardial ischemic infarction patients, the ischemic/reperfusion (I/R) injury is still clinical challenge (1)(2)(3). Many molecular mechanisms and signaling pathways are involved during the I/R process, including activation of cell apoptosis pathways (4), induction of mitochondrial damage (5) and ATP dysfunction (6) and also the increase of oxidative stress (7).…”

Section: Introductionmentioning

confidence: 99%

CFTR improves myocardial ischemic/reperfusion injury through activating FUNDC1-mediated mitophagy and regulating ATP and mitochondrial functions

Zhang¹,

Ding²,

Yi³

et al. 2020

Preprint

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Background To investigate the potential role of CFTR in myocardial ischemic/reperfusion (I/R) injury and its relationship with mitophagy. Methods Wild type (WT) and age matched CFTR−/− male mice were used to establish the myocardial I/R model. CFTR activator forskolin (FSK) was used to activate CFTR in mice. Hypoxia/reoxygenation (H/R) treatment was used for in vitro model in WT or CFTR−/− cardiomyocytes. The autophagy inhibitor 3-MA and activator rapamycin was used for inhibition or activation of autophagy, respectively. The mitochondrial membrane potential (MMP) and ATP concentration were detected. Immunofluorescence was performed for measurement of mitochondria. Oxidative factors reactive oxygen species (ROS), superoxide dismutase (SOD), malondiadehycle (MDA) and glutathione peroxidase (GSH-PX) were detected. The expression of CFTR, MMP-9, TNF-α, IL-8, LC3 II/I, beclin1, caspase-3, caspase-8, caspase-9, bax, bcl-2, p-62 and FUNDC1 was determined using western blotting or PCR. Results Knockdown of CFTR significantly increased the infraction volume and decreased the expression of autophagy related proteins beclin1 and LC3II/I in mice. In H/R cardiomyocytes, deficiency of CFTR by induced dysfunction of mitochondrial, decrease of ATP concentration and enhanced oxidative stress, as well as inhibited mitophagy and increased cell apoptosis related protein levels. When treated with 3-MA, the effects of overexpression of CFTR was remarkably reversed, while treatment of rapamycin significantly reversed the effects of inhibiting CFTR on both mitophagy, oxidative stress and cell apoptosis related proteins. The inhibition of FUNDC1 also reversed the above effects of overexpressing CFTR. Conclusion Inhibition of CFTR could promote myocardial I/R injury by suppressing FUNDC1-mediated mitophagy and activating of oxidative stress.

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Section: Introductionmentioning

confidence: 99%

CFTR improves myocardial ischemic/reperfusion injury through activating FUNDC1-mediated mitophagy and regulating ATP and mitochondrial functions

Zhang¹,

Ding²,

Yi³

et al. 2020

Preprint

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Drug-eluting stent thrombosis: current and future perspectives

Kuramitsu

Sonoda

Ando

et al. 2021

Cardiovasc Interv and Ther

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Risk Factors and Outcomes of Recurrent Drug‐Eluting Stent Thrombosis: Insights From the REAL‐ST Registry

Enomoto

Kuramitsu

Shinozaki

et al. 2021

JAHA

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Background Stent thrombosis (ST) after drug‐eluting stent (DES) implantation remains a life‐threatening complication. Recurrent ST (RST) is not a rare phenomenon, potentially contributing to high mortality after the index ST events. However, little evidence is available about the incidence, risk factors, and clinical outcomes of definite RST after DES thrombosis. Methods and Results From REAL‐ST (Retrospective Multicenter Registry of ST After First‐ and Second‐ Generation DES Implantation), this study evaluated 595 patients with definite ST (first‐generation DES thrombosis, n=314; second‐generation DES thrombosis, n=281). During a median follow‐up of 31 months, we identified 32 patients with definite RST after first‐generation DES thrombosis (n=18) and second‐generation DES thrombosis (n=15). Cumulative incidence of RST was 4.5% and 6.0% at 1 and 5 years, respectively, which did not significantly differ between first‐generation DES thrombosis and second‐generation DES thrombosis. Independent predictors of definite RST were early ST (hazard ratio [HR], 2.38; 95% CI, 1.06–5.35 [ P =0.035]) and multivessel ST (HR, 3.47; 95% CI, 1.03–11.7 [ P =0.044]). Definite RST was associated with a 2.8‐fold increased risk of mortality (adjusted HR, 2.78; 95% CI, 1.35–5.73 [ P =0.006]). Conclusions Cumulative incidence of definite RST did not significantly differ between first‐generation DES thrombosis and second‐generation DES thrombosis. Early ST and multivessel ST were risk factors of definite RST. Definite RST significantly increased mortality after DES thrombosis, highlighting the clinical importance of preventing RST to improve outcomes of patients with ST. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: UMIN000025181.

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Antiplatelet Therapy Changes for Patients With Myocardial Infarction With Recurrent Ischemic Events: Insights Into Contemporary Practice From the TRANSLATE‐ACS (Treatment With ADP Receptor Inhibitors: Longitudinal Assessment of Treatment Patterns and Events After Acute Coronary Syndrome) Study

Cited by 3 publications

References 45 publications

CFTR improves myocardial ischemic/reperfusion injury through activating FUNDC1-mediated mitophagy and regulating ATP and mitochondrial functions

CFTR improves myocardial ischemic/reperfusion injury through activating FUNDC1-mediated mitophagy and regulating ATP and mitochondrial functions

Drug-eluting stent thrombosis: current and future perspectives

Risk Factors and Outcomes of Recurrent Drug‐Eluting Stent Thrombosis: Insights From the REAL‐ST Registry

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