Revascularization in cardiogenic shock
- PDF / 519,078 Bytes
- 5 Pages / 595 x 792 pts Page_size
- 86 Downloads / 183 Views
Anne Freund1,2 · Steffen Desch1,2 · Holger Thiele1 1
Department of Internal Medicine/Cardiology, Heart Center Leipzig at University of Leipzig, Leipzig, Germany 2 German Center for Cardiovascular Research (DZHK), Berlin, Deutschland
Revascularization in cardiogenic shock Between 5 and 13% of patients with acute myocardial infarction (AMI) develop cardiogenic shock (CS; [1–4]). As a result, 60,000–70,000 patients are affected by CS complicating AMI each year in Europe [5]. Despite major advances in interventional and intensive care treatment, the mortality rate of infarct-related CS remains high, reaching 50% at 30 days after hospital admission [6, 7]. Coronary revascularization represents a cornerstone in the treatment of infarct-related CS. This review therefore aims to provide an overview of the pathophysiology of CS, the advantage of early revascularization, revascularization strategies, as well as the role of mechanical support and adjunctive anticoagulant and antithrombotic therapy.
Pathophysiology and clinical presentation of cardiogenic shock In CS subsequent to AMI, reduction of cardiac output is evoked by systolic and diastolic dysfunction of the myocardium. The most frequent causes of infarct-related CS are (in descending order): left heart failure, ischemic mitral valve insufficiency, infarct-related ventricular septal defects, right heart failure, and pericardial tamponade (. Fig. 1; [8]). A reduction in cardiac output promotes peripheral vasoconstriction leading to an increase in systemic vascular resistance and thus afterload. As a consequence, cardiac output is further reduced. This vicious circle is further intensified by a systemic inflammatory response syndrome leading to a release of nitric oxide with subsequent reduction
of systemic vascular resistance and catecholamine sensitivity. An increased risk of bleeding due to invasive procedures, antithrombotic therapy, and inflammation additionally enhances this “shock spiral” through loss of volume and oxygen carriers as well as aggravated systemic inflammation [9, 10]. The clinical presentation of CS varies considerably. Often, persistent hypotension is paramount. However, it must be emphasized that especially at early stages of CS, arterial blood pressure can be normal or elevated due to vasoconstriction. Other symptoms include pulmonary congestion, oliguria, cold and clammy skin, and mental impairment. Arterial lactate serves as a very sensitive but not specific laboratory marker, which is often increased early in the development of shock. An early diagnosis of CS is of immense importance in order to influence the prognosis by initiating specific therapies in time.
Early revascularization in infarct-related cardiogenic shock Two decades ago, the randomized SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) trial demonstrated a significant benefit of early revascularization in patients with ST-elevation myocardial infarction (STEMI), new left bundle brunch block, or posterior infarction (with ST-depression in anterior lead
Data Loading...
