Acute gastrointestinal bleeding can produce hypovolemia, hypotension, and diminished oxygen-carrying capacity, causing myocardial ischemia and necrosis. Activation of the sympathetic nervous system can further increase myocardial oxygen demand and worsen ischemia. These processes would be expected to be most important in patients with obstructive coronary artery disease, a group that is also at risk for gastrointestinal bleeding.1,2 Studies examining the relationship between gastrointestinal bleeding and myocardial ischemia suggest that the prevalence of acute myocardial infarction in patients with gastrointestinal hemorrhage ranges from 1 to 14%.1-3 Cardiac troponins are highly specific and sensitive markers of myocardial injury.6-8 However, there has been no systematic study using troponin to define myocardial injury in patients with acute gastrointestinal bleeding and anemia. Prior studies that included patients with acute anemia and myocardial injury, defined by troponin elevation, were designed to evaluate patients hospitalized with any critical illness.9,10 Furthermore, there is no general agreement about risk stratification of myocardial injury in patients with acute upper gastrointestinal bleeding. There is some suggestion that those with a greater number of coronary risk factors, a history of coronary artery disease, a lower blood pressure on admission, older age, severe illnesses, and/or lower hemoglobin are at greater risk of myocardial infarction.1-5 The aim of the present study is to examine the relationship between hemoglobin and the risk of myocardial injury, defined as an elevation of troponin I, in patients with anemia secondary to upper gastrointestinal bleeding and no other clinical signs or symptoms of coronary insufficiency on enrollment. These findings and other possible predictors of myocardial injury were examined during the hospitalization.

Anemia and ischemia: Myocardial injury in patients with gastrointestinal bleeding

BELLOTTO, FABIO;PLEBANI, MARIO;ILICETO, SABINO
2005

Abstract

Acute gastrointestinal bleeding can produce hypovolemia, hypotension, and diminished oxygen-carrying capacity, causing myocardial ischemia and necrosis. Activation of the sympathetic nervous system can further increase myocardial oxygen demand and worsen ischemia. These processes would be expected to be most important in patients with obstructive coronary artery disease, a group that is also at risk for gastrointestinal bleeding.1,2 Studies examining the relationship between gastrointestinal bleeding and myocardial ischemia suggest that the prevalence of acute myocardial infarction in patients with gastrointestinal hemorrhage ranges from 1 to 14%.1-3 Cardiac troponins are highly specific and sensitive markers of myocardial injury.6-8 However, there has been no systematic study using troponin to define myocardial injury in patients with acute gastrointestinal bleeding and anemia. Prior studies that included patients with acute anemia and myocardial injury, defined by troponin elevation, were designed to evaluate patients hospitalized with any critical illness.9,10 Furthermore, there is no general agreement about risk stratification of myocardial injury in patients with acute upper gastrointestinal bleeding. There is some suggestion that those with a greater number of coronary risk factors, a history of coronary artery disease, a lower blood pressure on admission, older age, severe illnesses, and/or lower hemoglobin are at greater risk of myocardial infarction.1-5 The aim of the present study is to examine the relationship between hemoglobin and the risk of myocardial injury, defined as an elevation of troponin I, in patients with anemia secondary to upper gastrointestinal bleeding and no other clinical signs or symptoms of coronary insufficiency on enrollment. These findings and other possible predictors of myocardial injury were examined during the hospitalization.
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2441802
Citazioni
  • ???jsp.display-item.citation.pmc??? 9
  • Scopus 39
  • ???jsp.display-item.citation.isi??? 31
  • OpenAlex ND
social impact