Multivessel disease in patients with acute myocardial infarction and high-risk unstable angina: culprit versus non-culprit intervention
Francesco Saia, David Antoniucci
Abstract
Francesco Saia, David Antoniucci
Abstract
Multivessel disease in patients with acute coronary syndromes • The ‘vulnerable’ patient • Multivessel percutaneous coronary intervention in patients with ST elevation myocardial infarction • Multivessel percutaneous coronary intervention in patients with left ventricular dysfunction or cardiogenic shock • Multivessel percutaneous coronary intervention in patients with unstable angina non-ST elevation myocardial infarction • Conclusions The definition ‘acute coronary syndromes’ (ACS) includes three different clinical entities, i.e. ST elevation acute myocardial infarction (STEMI), unstable angina (UA), and non-ST elevation myocardial infarction (NSTEMI), which share a common underlying pathophysiological mechanism, i.e. atherosclerotic plaque rupture or erosion, with differing degrees of superimposed thrombosis and distal embolization, and enhanced vasoreactivity. Hence, ACS are most of the time triggered by a single ‘culprit’ lesion, although sometimes there are multiple lesions which could be equally responsible for the clinical event.
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Multivessel disease in patients with acute coronary syndromes • The ‘vulnerable’ patient • Multivessel percutaneous coronary intervention in patients with ST elevation myocardial infarction • Multivessel percutaneous coronary intervention in patients with left ventricular dysfunction or cardiogenic shock • Multivessel percutaneous coronary intervention in patients with unstable angina non-ST elevation myocardial infarction • Conclusions The definition ‘acute coronary syndromes’ (ACS) includes three different clinical entities, i.e. ST elevation acute myocardial infarction (STEMI), unstable angina (UA), and non-ST elevation myocardial infarction (NSTEMI), which share a common underlying pathophysiological mechanism, i.e. atherosclerotic plaque rupture or erosion, with differing degrees of superimposed thrombosis and distal embolization, and enhanced vasoreactivity. Hence, ACS are most of the time triggered by a single ‘culprit’ lesion, although sometimes there are multiple lesions which could be equally responsible for the clinical event.
Key concepts: Culprit, Medicine, Unstable angina, Myocardial infarction, Internal medicine, Cardiology, Disease, Intervention (counseling)