Advancing from a "hemodynamic model" to a "mechanistic disease-modifying model" of cardiogenic shock.

Emerging clinical evidence has suggested that short-term mechanical augmentation of cardiac output (CO) may not consistently improve mortality in patients with cardiogenic shock (CS), despite improvements in hemodynamics. Such failures could reflect the underlying complexity of the mechanisms that contribute to malperfusion and organ dysfunction in CS. Distinct molecular and physiologic shock endophenotypes likely exist among patients with CS, with hemodynamic aberrations as the inciting insult but not necessarily the primary drivers of clinical outcomes. We propose that building a framework that moves away from the current "hemodynamic model" in preference for a "mechanistic disease-modifying model" of CS may facilitate progress toward reducing the stagnant mortality rates in this population. Such a therapeutic paradigm shift in patients with chronic systolic heart failure-the shift away from strategies that augment CO to those that modulate the systemic responses to low CO-has been one of the single most important shifts in contemporary cardiovascular medicine.