Key result
PCPS stabilizes refractory cardiogenic shock caused by no-reflow during primary PCI.
Why the study?
Does percutaneous cardiopulmonary support (PCPS) improve hemodynamics and survival in patients with refractory no-reflow and cardiogenic shock during primary PCI?
Case Report (n=1)
Does percutaneous cardiopulmonary support (PCPS) improve hemodynamics and survival in patients with refractory no-reflow and cardiogenic shock during primary PCI?
Percutaneous cardiopulmonary support (PCPS) can serve as an effective rescue therapy for hemodynamic stabilization in patients with refractory no-reflow and cardiogenic shock during primary PCI who do not respond to maximal pharmacotherapy and IABP.
Answers are grounded in this paper and cite their sources.
May stabilize refractory no-reflow shock after IABP failure; leaves open survival benefit in prospective studies.
Coronary no-reflow is defined as inadequate myocardial perfusion of a given coronary segment without angiographic evidence of mechanical vessel obstruction. No-reflow is visualized angiographically as a reduction in thrombolysis in myocardial infarction (TIMI) flow grade and is typically accompanied by chest pain, electrocardiographic changes with ST-segment shift and possible hemodynamic compromise. No-reflow during primary percutaneous coronary intervention (PCI) results in increasing mortality and morbidity. Therefore, treatment of noreflow is associated with improved clinical outcomes. Generally, the treatment of no-reflow is based on pharmacotherapy. In this case, despite maximal pharmacotherapy and intraaortic balloon pump (IABP), refractory no-reflow accompanied with cardiogenic shock was successfully treated with percutaneous cardiopulmonary support (PCPS).
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Son et al. (2010) conducted a case report in Refractory no-reflow with cardiogenic shock after acute myocardial infarction (n=1). Percutaneous cardiopulmonary support (PCPS) was evaluated on Hemodynamic stabilization. Percutaneous cardiopulmonary support successfully stabilized hemodynamics in a patient with refractory no-reflow and cardiogenic shock during primary PCI, despite maximal pharmacotherapy and IABP.
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