ACUTE PULMONARY EDEMA AND ELEVATED TROPONIN: WHAT IS THEIR SIGNIFICANCE? CLINICAL REVIEW

Abstract

Acute pulmonary edema (APE) is a clinical condition characterized by severe acute respiratory distress, frequently accompanied by crackling lung sounds and sudoresis. One classification system divides APE into cardiogenic or non-cardiogenic adult respiratory distress syndrome – ARDS. This study reviews cardiogenic APE, which is the most severe clinical presentation of heart failure (ADHF), and its relationship with the increase of troponin along with other factors such as abnormalities in the electrocardiogram (ECG) that may be mistaken for acute coronary syndrome (ACS). Atypical symptoms could occur in the presentation of ACS in 8,4% of cases, as has been shown in the Global Registry of Acute Coronary Events (GRACE): dyspnea (49%), sudoresis (26%), nauseas or vomiting (24%) and syncope (19%). The CK-MB enzyme was replaced by cardiac troponin (cTn) as the chosen marker of myocardial necrosis in the diagnosis of AMI in the late 90s. The cTn is a marker of cardiac damage, not just cardiac ischemia, and this may pose questions as whether there is a myocardium infarction or not. The positive results of a cTn should be interpreted considering the clinical signs of myocardial ischemia. The challenge remains and further studies are needed to aid in accurate diagnosis of both conditions (APE and ACS) as well as cases in which one results from the other because the role of coronary artery disease in acute heart failure has not been well studied in clinical trials.