Nicardipine Augments Local Myocardial Perfusion after Coronary Artery Reperfusion in Dogs

Jang, Young Ho; Kim, Jin Mo

doi:10.3346/jkms.2003.18.1.23

Cited by 4 publications

(1 citation statement)

References 17 publications

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“…In an animal model, intracoronary nicardipine infusion augmented the local myocardial perfusion as demonstrated by a thermal diffusion microprobe following the release of coronary occlusion. 11 Also, in patients with minimally diseased coronary artery disease, intracoronary nicardipine offered more potent and prolonged vasodilation with fewer systemic side effects compared to other calcium channel blockers (CCB) including diltiazem and verapamil. 12 We hypothesized that intracoronary nicardipine would decrease the incidence and severity of myonecrosis associated with PCI resulting in reduction in cardiac enzyme leakage.…”

Section: Introductionmentioning

confidence: 99%

Effect of Intracoronary Nicardipine on Cardiac Enzymes After Elective Percutaneous Coronary Intervention

Arora

Alfayoumi

Khawaja

et al. 2009

Clinical Cardiology

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Background: Elevation in cardiac enzymes after percutaneous coronary intervention (PCI) is common and is associated with adverse clinical outcomes. Hypothesis: Administration of intracoronary nicardipine-a calcium channel blocker will reduce cardiac enzyme levels in patients undergoing elective PCI. Methods: In a single center, prospective, double-blind placebo-controlled trial, 193 patients undergoing elective PCI (with or without stenting) for chronic stable angina and/or an abnormal stress test were randomized to receive 200 mcg of intracoronary nicardipine (n = 93) or saline solution (n = 100) prior to intervention. Cardiac enzyme levels were measured immediately and at 8 and 16 hours after the procedure. Major adverse clinical events (MACE) were assessed at 30 days and at 6 months. Results: Incidence of periprocedural myonecrosis defined as elevation of troponin I levels >1× the upper limit of normal was similar in both groups (placebo 15.4% vs drug 10.6%; P = 0.47). There was no significant difference in peak troponin I levels after PCI between the 2 groups (placebo 0.58 ng/mL ± 1.08 ng/mL vs drug 0.97 ng/mL ± 3.6 ng/mL; P = 0.35). Major adverse clinical events at 6 months were infrequent and not statistically different in the 2 groups (placebo 3.4% vs drug 1.2%; P = 0.52). Multivariate analysis revealed that pretreatment with nicardipine was not associated with reduction in the incidence of troponin I elevation (odds ratio [OR]: 0.54; 95% confidence interval [CI]: 0.18-1.6; P = 0.28). Conclusions: In low-risk patients undergoing elective PCI, intracoronary nicardipine administration did not produce a significant cardioprotective effect in reducing postprocedural cardiac enzymes leakage.

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Section: Introductionmentioning

confidence: 99%

Effect of Intracoronary Nicardipine on Cardiac Enzymes After Elective Percutaneous Coronary Intervention

Arora

Alfayoumi

Khawaja

et al. 2009

Clinical Cardiology

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Role of apoptosis in reperfusion injury

Eefting¹,

Rensing²,

Wigman³

et al. 2004

Cardiovascular Research

370

263

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Many changes occur during reperfusion of the myocardium after ischemic damage. Necrosis and apoptosis appear to be ongoing during ischemia, while apoptosis is boosted by the reperfusion event. In the past 10 years, distinct intracellular pathways important for hypertrophy, apoptosis, cardiac failure, ischemic preconditioning and reperfusion damage have been recognized. The eventual response of the cardiomyocyte will depend on energy and time available as well as changes in pH and ion handling and the delicate balance of activation of signaling molecules and transcription factors. There is agreement on the central role of mitochondria and nitric oxide (NO) in programmed cell death. However, although many groups analyzed the contribution of NO to cell death, still the circumstances and levels required for cardioprotection or death are unclear. Growth factors, cytokines, and downstream signaling molecules have been shown to influence programmed cell death through mechanisms reminiscent of preconditioning. Here, the role of apoptosis in ischemia reperfusion-related cell death is reviewed. Important data have been obtained in isolated cells, intact hearts and intact animals. Both pharmacological as well as genetic interventions are discussed. Proof for apoptosis in man post-myocardial infarction (MI) treated through primary Percutaneous Trans-luminal Coronary Angioplasty or other reperfusion therapy is reviewed. Finally, the currently available quantification methods for apoptosis post-MI are mentioned.

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The Systemic Hemodynamic and Renal Effects of Nicardipine Administration Followed by Supraceliac Aortic Cross Clamping and Unclamping in Experimental Dogs

Hong

Choe

Bae

et al. 2004

Korean J Anesthesiol

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Background:The incidence of renal insufficiency is reported about 18-27% during the thoracoabdominal aneurysm surgery. The possible mechanisms are reduction and maldistribution of renal blood flow, activation of renin angiotensin system, release of various mediators. In this study, we observed the effect of nicardipine, one of the calcium channel blockers that commonly used, on the systemic hemodynamics and the renal fuctions.Methods: A total of 13 mongrel dogs were divided into two groups: control group (C, n = 7), nicardipine administration group (N, n = 6). After brachial arterial and Swan-Ganz catheterization, midline abdominal incision was made. For the aortic cross clamping the supraceilac aorta was exposed and the doppler flowmeter probe was placed on the left renal artery. The thermal diffusion microprobe was inserted in the renal parenchyme to measure local renal perfusion. At sixty minutes after aortic cross clamping, systemic hemodynamic data, renal blood flow and local renal perfusion were measured and at 1, 2, 3, 4, 5 and 6 hours after unclamping the same parameters were measured.Results: There were no differences on renal blood flow, renal perfusion and oxygen extraction ratio between two groups. The renal blood flow and renal perfusion did not recover to the baseline level after unclamping in both groups. The plasma renin activity, serum creatinine concentration and cystatin-c did not show any difference between groups respectively.Conclusions: We concluded that the administration of nicardipine after supraceliac aortic unclamping to improve the renal function was not effective in experimental dogs. (Korean J Anesthesiol 2004; 46: 467∼474) ꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏꠏ

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Nicardipine Augments Local Myocardial Perfusion after Coronary Artery Reperfusion in Dogs

Cited by 4 publications

References 17 publications

Effect of Intracoronary Nicardipine on Cardiac Enzymes After Elective Percutaneous Coronary Intervention

Effect of Intracoronary Nicardipine on Cardiac Enzymes After Elective Percutaneous Coronary Intervention

Role of apoptosis in reperfusion injury

The Systemic Hemodynamic and Renal Effects of Nicardipine Administration Followed by Supraceliac Aortic Cross Clamping and Unclamping in Experimental Dogs

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