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Acute coronary syndrome
Influence of ranitidine on gastrointestinal haemorrhage and thrombosis induced by dual antiplatelet therapy after percutaneous coronary intervention
  1. Zhangqiang Chen,
  2. Lang Hong,
  3. Hong Wang,
  4. Qiulin Yao,
  5. Heng Li Lai,
  6. Linxiang Lu
  1. Jiangxi Provincial People's Hospital, Jiangxi, China

Abstract

Background Percutaneous coronary intervention (PCI) is an effective treatment. method of coronary heart disease, particularly acute coronary syndrome. A large number of evidence-based medicine has shown that patients with coronary heart disease after PCI obtain clinical significant benefit in conjunction with clopidogrel and aspirin therapy, while the most common side effects of antiplatelet drugs is of gastric injury, that can lead to gastric bleeding, Thus, the American Heart Association/American Gastroenterological Association/American Heart Association guidelines proposed the patients for the acceptance of dual antiplatelet therapy were treated with proton pump inhibitor (PPI) to reduce gastrointestinal complications such as ulcers and bleeding risk in 2008. But recently, the observation of basic and clinical research suggests that proton pump inhibitor (PPI) can reduce clopidogrel inhibitory effect on platelet aggregation, increasing major adverse cardiac events (MACE). H2 receptor antagonist ranitidine do not pass cytochrome P450 metabolism, would such gastric mucosa protective agents affect the clopidogrel and aspirin antiplatelet effect and increase the occurrence of cardiovascular events in patients with coronary heart disease after PCI? None reported in the literature, this study was to explore the efficacy and security of ranitidine in the prevention of upper gastrointestinal haemorrhage from dual antiplatelet drugs after PCI, and provide the basis for clinical treatment after PCI.

Methods One hundred and twenty patients with CHD were divided into ranitidine group (60 patients) and control group (60 patients). We examined the blood express levels of CD62p, GPαb/βa and FIB-C from before treatment, then the patients in ranitidine group received ranitidine capsule treatment for 12 weeks (two capsule twice daily), and compared the results with control group.

Results In patients with coronary heart disease, The levels of CD62p, GPαb/βa and plasma FIB-C and platelet aggregation rate were significantly higher than that of healthy controls (all p<0.01), after PCI, the levels of CD62p, GPαb/βa, FiB-C and platelet aggregation rate were significantly higher than that before the operation (respectively, p<0.01, p<0.05, p<0.01, p<0.05). The levels of CD62p, GPαb/βa, FiB-C and platelet aggregation rate were no statistical difference between the ranitidine group and conventional group after 12-week treatment (all p>0.05). Followed up for 6 months, two cases of thrombosis events occurred in both ranitidine group and control group, no gastrointestinal bleeding occurred in the ranitidine group, while six cases of gastrointestinal bleeding occurred in control group.

Conclusion Ranitidine can prevent dual antiplatelet drug-induced gastrointestinal bleeding complications in patients with CHD after PCI, no interference with antiplatelet activity of clopidogrel and the incidence of thrombosis no increasing.

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