The effect of verapamil on the restoration of myocardial perfusion and functional recovery in patients with angiographic no-reflow after primary percutaneous coronary intervention

Umemura, Satoshi; Nakamura, Shinya; Sugiura, Tetsuro; Tsuka, Yoshiaki; Fujitaka, Keisuke; Yoshida, Susumu; Baden, Masato; Iwasaka, Toshiji

doi:10.1097/00006231-200603000-00007

Cited by 14 publications

(9 citation statements)

References 27 publications

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“…The P‐glycoprotein multidrug resistance 1 (MDR1) transports PS to the outer leaflet of the plasma membrane bilayer [25], and P‐glycoprotein‐deficient mice are protected against post‐IRI in the kidney [26]. The reported efficacy of verapamil in attenuating the no‐reflow phenomenon following coronary thrombosis in humans [8,10] is also consistent with the role of PS externalization in reperfusion injury. Increased intracellular calcium levels promote PS externalization [11], and verapamil is a calcium entry blocker.…”

Section: Discussionmentioning

confidence: 89%

“…Various pharmaceutical treatments, including adenosine, nicorandil, nitroprusside, verapamil, clopidogrel, and IIb/IIIa in-hibitors, have been administered at the time of PCI in an attempt to decrease the extent of the microvascular perfusion defect [2][3][4][5][6][7][8][9][10]. However, apart from the use of clopidogrel and IIb/IIIa inhibitors, these agents are not routinely used in clinical practice to reduce no-reflow.…”

Section: Introductionmentioning

confidence: 99%

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Diannexin Reduces No-Reflow after Reperfusion in Rabbits with Large Ischemic Myocardial Risk Zones

Hale¹,

Allison²,

Kloner³

2010

Cardiovascular Therapeutics

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SUMMARY Introduction and Aims:In patients with ST-segment elevation myocardial infarction who receive percutaneous coronary intervention and stenting, a large zone with no-reflow is associated with adverse outcomes. During myocardial ischemia/reperfusion, phosphatidylserine (PS) translocates to the surface of endothelial cells triggering attachment of platelets and leukocytes, thus impairing microvascular blood flow. Diannexin, a recombinant dimer of the endogenous human annexin V protein, binds PS and thus inhibits the adverse effects of PS. It has been shown to attenuate postischemic reperfusion injury in several experimental models. We speculated that Diannexin would reduce no-reflow in the heart after coronary artery occlusion (CAO) and reperfusion. Rabbits received: (1) Diannexin 5 min pre-CAO (diannexin pre ischemia [DPI], 400 μg/kg, n = 17), or (2) Diannexin 5 min pre-coronary reperfusion (diannexin pre reperfusion [DPR], 400 μg/kg, n = 20), or (3) saline (Cont, n = 18), with 30 min CAO and 3 h reperfusion. In a secondary analysis, rabbits were divided into two groups based on the overall average risk zone size of 29% of the left ventricle (LV): small (<29% of LV) and large (>29% of LV). Results: Overall, risk zones and infarct size, and the no-reflow zone were similar in all groups. In hearts with large risk zones the noreflow area was significantly smaller in both drug-treated groups (DPI, 22 ± 5% and DPR, 22 ± 3% vs. control 40 ± 3%, P < 0.006), the hemorrhagic areas were significantly smaller, and infarct size was reduced at the P < 0.06 level compared with control. In animals with small risk zones there were no significant differences. Diannexin treatment did not affect hemodynamics or LV function. Conclusion: Diannexin was cardioprotective in rabbits with a severe ischemic insult. This is important, because large infarcts accompanied by no-reflow in humans are associated with increased complications. In animals with small risk zones, no significant drug effect was observed.

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Diannexin Reduces No-Reflow after Reperfusion in Rabbits with Large Ischemic Myocardial Risk Zones

Hale¹,

Allison²,

Kloner³

2010

Cardiovascular Therapeutics

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“…Various mechanisms have been implicated in liver ischemia-reperfusion injury, including reactive oxygen species generation, lipid peroxidation, alterations in calcium homeostasis, mitochondrial dysfunction, activation of Kupffer cells, and cytokine production [15][16][17]. However, mechanisms that coordinate and integrate this pathologic response are still unclear.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of Verapamil on hepatic ischemia–reperfusion injury during hepatectomy in the cirrhotic patients with hepatocellular carcinoma

Xia

Wang

Chen

et al. 2009

Langenbecks Arch Surg

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“…Intracoronary nicardipine is given at a median dose of 400 μg. 23 To date, multiple small studies have demonstrated the benefit of verapamil and diltiazem in treating no-reflow [24][25][26][27] . Further, a meta-analysis showed improved outcomes in individuals who received intracoronary verapamil or diltiazem.…”

Section: Calcium Channel Blockersmentioning

confidence: 99%

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

et al. 2021

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Coronary 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.

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The effect of verapamil on the restoration of myocardial perfusion and functional recovery in patients with angiographic no-reflow after primary percutaneous coronary intervention

Abstract: Intracoronary verapamil restored myocardial perfusion in patients with angiographic no-reflow after PCI and lead to better functional recovery after acute myocardial infarction.

Cited by 14 publications

References 27 publications

Diannexin Reduces No-Reflow after Reperfusion in Rabbits with Large Ischemic Myocardial Risk Zones

Diannexin Reduces No-Reflow after Reperfusion in Rabbits with Large Ischemic Myocardial Risk Zones

Protective effect of Verapamil on hepatic ischemia–reperfusion injury during hepatectomy in the cirrhotic patients with hepatocellular carcinoma

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

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