Dipyridamole versus verapamil for treatment of no‐reflow during primary angioplasty

Tanzilli, Gaetano; Greco, Cesare; Pasceri, Vincenzo; Pelliccia, Francesco; Arrivi, Alessio; Placanica, Attilio; Madon, E

doi:10.1002/ccd.22724

Cited by 14 publications

(6 citation statements)

References 30 publications

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“…No-reflow is an important complication of primary percutaneous coronary intervention (PPCI) with poor clinical outcomes, occurring more frequently in the setting of acute ST-elevation myocardial infarction (STEMI) [4]. The angiographic no-reflow phenomenon is defined as severely impaired forward coronary flow (Thrombolysis in Myocardial Infarction (TIMI) < 3) in the absence of residual stenosis, dissection or thrombosis [5–9]. Although the underlying mechanisms of no-reflow remain obscure, microvascular plugging, thrombotic debris, cellular edema, reperfusion injury, endothelial dysfunction, coronary vasospasm and microvascular spasm are likely to be closely related [4, 6, 7, 10].…”

Section: Introductionmentioning

confidence: 99%

The role of insulin-like growth factor-1 in development of coronary no-reflow and severity of coronary artery disease in patients with acute myocardial infarction

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et al. 2014

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IntroductionInsulin-like growth factor-1 (IGF-1) has atheroprotective effects via reduction in oxidative stress, cellular apoptosis, pro-inflammatory signaling, and endothelial dysfunction.AimWe hypothesized that low levels of IGF-1 may be associated with the severity and extent of coronary artery disease and development of the coronary no-reflow phenomenon in patients with acute ST-elevation myocardial infarction (STEMI) and investigated the role of the IGF-1 molecule in the coronary no-reflow phenomenon and severity of coronary artery disease (CAD) in patients with acute STEMI in a tertiary hospital.Material and methodsThe study was conducted among 113 patients undergoing primary percutaneous coronary intervention (PPCI) for STEMI, of whom 49 patients developed the no-reflow phenomenon. Coronary no-reflow was defined as Thrombolysis In Myocardial Infarction (TIMI) flow grade 2 or less after intervention. Insulin-like growth factor-1 levels were measured in both groups. The severity and extent of CAD were evaluated according to the Gensini and Syntax scores.ResultsAlthough IGF-1 levels were lower in the no-reflow group, there was not a statistically significant difference between the no-reflow group and the control group (116.65 ±51.72 vs. 130.82 ±48.76, p = 0.130). Gensini and Syntax scores were higher in the no-reflow group. There was no association between Gensini and Syntax scores and IGF-1 levels (r = –0.071, r = 0.479, r = –0.158, p = 0.113).ConclusionsIn this study, IGF-1 levels were not statistically different between patients developing the no-reflow phenomenon and controls. There was no association between development of the no-reflow phenomenon and severity of CAD or IGF-1 levels. Nevertheless, large scale studies are needed to verify these results.

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Section: Introductionmentioning

confidence: 99%

The role of insulin-like growth factor-1 in development of coronary no-reflow and severity of coronary artery disease in patients with acute myocardial infarction

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“…126 The use of vasodilators (calcium-channel antagonist, dypiridamole) or metabolic drugs (ranolazine) at discharge needs future research having as endpoint reversion of CMVO, improved remodelling, and clinical outcome. 127,128 Finally, endothelin-1 may be another promising therapeutic target of. 129,130 Inadequate therapies Intra-aortic balloon pumping (IABP) is able to reduce myocardial oxygen demand due to systolic left ventricular unloading and increases myocardial perfusion.…”

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confidence: 99%

Coronary Microvascular Obstruction in Acute Myocardial Infarction

2018

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The success of a primary percutaneous intervention (PCI) in the setting of ST elevation myocardial infarction depends on the functional and structural integrity of coronary microcirculation. Coronary microvascular dysfunction and obstruction (CMVO) occurs in up to half of patients submitted to apparently successful primary PCI and is associated to a much worse outcome. The current review summarizes the complex mechanisms responsible for CMVO, including pre-existing coronary microvascular dysfunction, and highlights the current limitations in the assessment of microvascular function. More importantly, at the light of the substantial failure of trials hitherto published on the treatment of CMVO, this review proposes a novel integrated therapeutic approach, which should overcome the limitations of previous studies.

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“…In contrast, the clinical treatment of the no-reflow phenomenon in patients undergoing a percutaneous coronary intervention (PCI) for the treatment of acute myocardial infarction are consistent with our experimental findings in murine models of ischemic AKI. Indeed, it has become routine practice to treat the no-reflow phenomenon in patients undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction by direct injection of adenosine or dipyridamole into the coronary circulation (66,67). Due to the fact that ischemic AKI is in most cases treated medically without vascular intervention, direct injection of adenosine or dipyridamole into the renal artery following ischemic AKI is usually not a treatment option.…”

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confidence: 99%

Equilibrative nucleoside transporter 1 (ENT1) regulates postischemic blood flow during acute kidney injury in mice

Grenz¹,

Bauerle²,

Dalton³

et al. 2017

Journal of Clinical Investigation

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A complex biologic network regulates kidney perfusion under physiologic conditions. This system is profoundly perturbed following renal ischemia, a leading cause of acute kidney injury (AKI) -a life-threatening condition that frequently complicates the care of hospitalized patients. Therapeutic approaches to prevent and treat AKI are extremely limited. Better understanding of the molecular pathways promoting postischemic reflow could provide new candidate targets for AKI therapeutics. Due to its role in adapting tissues to hypoxia, we hypothesized that extracellular adenosine has a regulatory function in the postischemic control of renal perfusion. Consistent with the notion that equilibrative nucleoside transporters (ENTs) terminate adenosine signaling, we observed that pharmacologic ENT inhibition in mice elevated renal adenosine levels and dampened AKI. Deletion of the ENTs resulted in selective protection in Ent1 -/-mice. Comprehensive examination of adenosine receptor-knockout mice exposed to AKI demonstrated that renal protection by ENT inhibitors involves the A2B adenosine receptor. Indeed, crosstalk between renal Ent1 and Adora2b expressed on vascular endothelia effectively prevented a postischemic no-reflow phenomenon. These studies identify ENT1 and adenosine receptors as key to the process of reestablishing renal perfusion following ischemic AKI. If translatable from mice to humans, these data have important therapeutic implications. IntroductionAcute kidney injury (AKI) is clinically defined by an abrupt reduction in kidney function (e.g., a decrease in glomerular filtration rate [GFR]), occurring over a period of minutes to days. AKI is frequently caused by an obstruction of renal blood flow (renal ischemia) and represents an important cause of morbidity and mortality of patients (1-3). Indeed, a recent study revealed that only a mild increase (0.3 mg/dl) in the serum creatinine level is associated with a 70% greater risk of death than in patients without this increase (2, 3). Particularly for surgical patients, AKI represents a significant threat. For example, surgical procedures requiring cross-clamping of the aorta and renal vessels are associated with a rate of AKI of up to 30% (4). Similarly, AKI after cardiac surgery occurs in up to 10% of patients under normal circumstances and is associated with dramatic increases in mortality (5). In addition, patients with sepsis frequently go on to develop AKI, and the combination of moder-

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Dipyridamole versus verapamil for treatment of no‐reflow during primary angioplasty

Abstract: Dipyridamole is a safe and effective first-line drug for treatment of no-reflow. Dipyridamole can also be successfully used in patients with incomplete response to verapamil.

Cited by 14 publications

References 30 publications

The role of insulin-like growth factor-1 in development of coronary no-reflow and severity of coronary artery disease in patients with acute myocardial infarction

The role of insulin-like growth factor-1 in development of coronary no-reflow and severity of coronary artery disease in patients with acute myocardial infarction

Coronary Microvascular Obstruction in Acute Myocardial Infarction

Equilibrative nucleoside transporter 1 (ENT1) regulates postischemic blood flow during acute kidney injury in mice

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