Abstract
The pathophysiology of cardiogenic shock (CS) varies depending on its etiology, which may lead to different hemodynamic profiles (HP) and may help tailor therapy. We aimed to assess the HP of CS patients according to their etiologies of acute myocardial infarction (AMI) and acute decompensated chronic heart failure (ADCHF). We included patients admitted for CS secondary to ADCHF and AMI. HP were measured before the administration of any inotrope or vasopressor. Systemic Vascular Resistances index (SVRi), Cardiac Index (CI), and Cardiac Power Index (CPI) were measured by trans-thoracic Doppler echocardiography on admission. Among 37 CS patients, 28 had CS secondary to ADCHF or AMI and were prospectively included. The two groups were similar in terms of demographic data and shock severity criteria. AMI CS was associated with lower SVRi compared to CS related to ADCHF: 2010 (interquartile range (IQR): 1895–2277) vs. 2622 (2264–2993) dynes-s·cm−5·m−2 (p = 0.002). A trend toward a higher CI was observed: respectively 2.13 (1.88–2.18) vs. 1.78 (1.65–1.96) L·min−1·m−2 (p = 0.067) in AMICS compared to ADCHF. CS patients had different HP according to their etiologies. AMICS had lower SVR and tended to have a higher CI compared to ADHF CS. These differences should be taken into account for patient selection in future research.
Highlights
Cardiogenic shock (CS) remains a major clinical challenge with a stable incidence and a high mortality [1,2,3]
The hemodynamic profiles (HP) of CS related to acute myocardial infarction (AMI) and acute decompensated chronic heart failure (ADCHF) differed significantly
CS related to AMI was associated with significantly lower Systemic vascular resistance index (SVRi) and a trend toward a higher Cardiac Index (CI) compared to to AMI was associated with significantly lower SVRi and a trend toward a higher CI compared to those related to an ADCHF
Summary
Cardiogenic shock (CS) remains a major clinical challenge with a stable incidence and a high mortality [1,2,3]. Because of its complex pathophysiology and the limited evidence-based therapeutic interventions, the current therapeutic strategy are supported by a low level of evidences. CS involves a profound depression of myocardial contractility considered to trigger hemodynamic instability, resulting in a potentially deleterious spiral of reduced cardiac output, low blood pressure, and further coronary ischemia. Evidences suggest that there is a large variability in systemic vascular resistances (SVR) and a wide range of hemodynamic profiles in CS [6]. Acute myocardial infarction (AMI) remains a major etiology of CS, acute decompensated chronic heart failure (ADCHF) is a growing cause and may be the leading cause nowadays [2,7,8,9]
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