Pathophysiology, Diagnosis, and Management of Coronary No-Reflow Phenomenon

2022 ◽  
Author(s):  
Gagan Kaur ◽  
Patrick Baghdasaryan ◽  
Balaji Natarajan ◽  
Prabhdeep Sethi ◽  
Ashis Mukherjee ◽  
...  
Keyword(s):  
Ventricular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Left Ventricular Remodeling ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Clinical Predictors ◽  
Catheterization Laboratory ◽  
Cardiac Catheterization Laboratory ◽  
No Reflow ◽  
No Reflow Phenomenon

AbstractCoronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but they have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.

scholarly journals Pathophysiology, Diagnosis, and Management of Coronary No-Reflow Phenomenon

2021 ◽  
Author(s):  
Gagan Kaur ◽  
Patrick Baghdasaryan ◽  
Balaji Natarajan ◽  
Prabhdeep Sethi ◽  
Ashis Mukherjee ◽  
...  
Keyword(s):  
Ventricular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Left Ventricular Remodeling ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Clinical Predictors ◽  
Catheterization Laboratory ◽  
Cardiac Catheterization Laboratory ◽  
No Reflow ◽  
No Reflow Phenomenon

AbstractCoronary no-reflow phenomenon is a lethal mechanism of ongoing myocardial injury, following successful revascularization of an infarct-related coronary artery. Incidence of this phenomenon is high following percutaneous intervention, and is associated with adverse in-hospital and long-term outcomes. Several mechanisms such as ischemia-reperfusion injury and distal microthromboembolism in genetically susceptible patients and those with preexisting endothelial dysfunction have been implicated. However, the exact mechanism in humans is still poorly understood. Several investigative and treatment strategies within and outside the cardiac catheterization laboratory have been proposed, but have not uniformly shown success in reducing mortality or in preventing adverse left ventricular remodeling resulting from this condition. The aim of this article is to provide a brief and concise review of the current understanding of the pathophysiology, clinical predictors, and investigations and management of coronary no-reflow phenomenon.

scholarly journals Cardiac mTOR protects the heart against ischemia-reperfusion injury

2012 ◽  
Vol 303 (1) ◽  
pp. H75-H85 ◽  
Author(s):  
Toshinori Aoyagi ◽  
Yoichiro Kusakari ◽  
Chun-Yang Xiao ◽  
Brendan T. Inouye ◽  
Masaya Takahashi ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Ventricular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Interstitial Fibrosis ◽  
Ex Vivo ◽  
Left Ventricular Remodeling ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation

Cardiac mammalian target of rapamycin (mTOR) is necessary and sufficient to prevent cardiac dysfunction in pathological hypertrophy. However, the role of cardiac mTOR in heart failure after ischemic injury remains undefined. To address this question, we used transgenic (Tg) mice with cardiac-specific overexpression of mTOR (mTOR-Tg mice) to study ischemia-reperfusion (I/R) injury in two animal models: 1) in vivo I/R injury with transient coronary artery ligation and 2) ex vivo I/R injury in Langendorff-perfused hearts with transient global ischemia. At 28 days after I/R, mortality was lower in mTOR-Tg mice than littermate control mice [wild-type (WT) mice]. Echocardiography and MRI demonstrated that global cardiac function in mTOR-Tg mice was preserved, whereas WT mice exhibited significant cardiac dysfunction. Masson's trichrome staining showed that 28 days after I/R, the area of interstitial fibrosis was smaller in mTOR-Tg mice compared with WT mice, suggesting that adverse left ventricular remodeling is inhibited in mTOR-Tg mice. In the ex vivo I/R model, mTOR-Tg hearts demonstrated improved functional recovery compared with WT hearts. Perfusion with Evans blue after ex vivo I/R yielded less staining in mTOR-Tg hearts than WT hearts, indicating that mTOR overexpression inhibited necrosis during I/R injury. Expression of proinflammatory cytokines, including IL-6 and TNF-α, in mTOR-Tg hearts was lower than in WT hearts. Consistent with this, IL-6 in the effluent post-I/R injury was lower in mTOR-Tg hearts than in WT hearts. These findings suggest that cardiac mTOR overexpression in the heart is sufficient to provide substantial cardioprotection against I/R injury and suppress the inflammatory response.

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