Risk Factors for Upper Gastrointestinal Bleeding in Patients Undergoing Percutaneous Coronary Intervention on Dual

Chun-Ting Shih1, Ting-Hsin Huang1, Chih-Ming Liang2

  • 1Division of Cardiology.

PubMed

Insights

Prophylactic anti-ulcer medications like PPIs or H2RAs did not significantly reduce upper gastrointestinal bleeding (UGIB) in coronary care unit patients after percutaneous coronary intervention (PCI) with dual antiplatelet treatment (DAPT). High-risk patients still require vigilant monitoring.

Area of Science:

  • Cardiology
  • Gastroenterology
  • Clinical Pharmacology

Background:

  • Patients in coronary care units (CCU) undergoing percutaneous coronary intervention (PCI) with dual antiplatelet treatment (DAPT) face a heightened risk of upper gastrointestinal bleeding (UGIB).
  • The efficacy of histamine-2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs) in preventing UGIB in this high-risk population remains unclear.

Purpose of the Study:

  • To evaluate the effectiveness of prophylactic anti-ulcer medications (H2RAs and PPIs) in preventing UGIB among CCU patients treated with DAPT post-PCI.
  • To identify risk factors associated with UGIB within 72 hours and beyond 72 hours after PCI in this patient cohort.

Main Methods:

  • A retrospective study involving 288 CCU patients who underwent PCI and received DAPT.
  • Assessed UGIB incidence at two time points: within 72 hours and after 72 hours post-catheterization.
  • Analyzed patient history, medication regimens (including PPIs, H2RAs, and absence of prophylaxis), and clinical factors.

Main Results:

  • Acute UGIB (within 72 hours) occurred in 8.3% of patients; cerebrovascular accident history and higher Killip grade were identified as risk factors.
  • Delayed UGIB (beyond 72 hours) occurred in 4.9% of patients; chronic kidney disease and higher Killip grade were significant risk factors.
  • No significant difference in UGIB rates was observed between groups receiving PPIs, H2RAs, or no prophylactic medication (p = 0.264). TriMatch analysis confirmed similar rates (7.5%, 7.5%, 5.0%; p = 0.875).

Conclusions:

  • Prophylactic anti-ulcer medications did not significantly reduce UGIB incidence in CCU patients post-PCI with DAPT.
  • Vigilant monitoring and consideration of prophylactic medication are recommended for high-risk UGIB patients in the CCU setting.
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...
436
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...
55
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
111
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
327
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...
323
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
72