Combination of Xuesaitong and Aspirin Based on the Antiplatelet Effect and Gastrointestinal Injury: Study Protocol

Bao-Chen Zhu1, Chun-Miao Xue1, Rui Lang2

  • 1Department of Pharmacy, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China.

Insights

This clinical trial investigates the combined effects of aspirin and Xuesaitong (Panax notoginseng saponins) for coronary heart disease. The study aims to evaluate their synergistic antiplatelet and gastrointestinal protective benefits.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Gastroenterology

Background:

  • Aspirin is a primary treatment for coronary heart disease (CHD) but can cause gastrointestinal issues.
  • Xuesaitong, containing Panax notoginseng saponins (PNS), inhibits platelet aggregation and may reduce aspirin-induced gastrointestinal injury.
  • Clinical evidence is needed to confirm the synergistic effects of combining Xuesaitong and aspirin.

Purpose of the Study:

  • To evaluate the synergistic antiplatelet and gastrointestinal protective effects of combining Xuesaitong with aspirin in CHD patients.
  • To provide evidence for rational drug combination therapy in CHD management.

Main Methods:

  • A prospectively planned, open-labeled, parallel-grouped, single-centered clinical trial.
  • 480 participants will be randomized into three groups: aspirin alone, Xuesaitong alone, and the combination.
  • Primary outcomes include changes in platelet aggregation rate and calprotectin activity; secondary outcomes include PAC-1, P-selectin, P2Y12, I-FABP activity, and fecal occult blood.

Main Results:

  • This section is to be filled upon study completion.

Conclusions:

  • This study is expected to provide high-quality evidence on the combined efficacy of Xuesaitong and aspirin.
  • Results will support the clinical application of this drug combination for CHD treatment and prevention.
Abstract

Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
774
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
845
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
184
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
722
Coronary Artery Disease V: Interprofessional Care01:27

Coronary Artery Disease V: Interprofessional Care

Interprofessional care for coronary artery disease includes pharmacological therapy and revascularization procedures.Pharmacological therapy for Coronary Artery Disease (CAD) aims to manage symptoms, prevent complications, and improve patient outcomes through various classes of medications:Antiplatelet Agents:Aspirin and Clopidogrel: These medications inhibit platelet aggregation, preventing blood clots, which is crucial for avoiding heart attacks and strokes. Doctors often prescribe these...
74
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
631