Reducing Infarct Size and improving Cardiac Function after Acute Myocardial Infarction (AMI)
PiCSOAMI Therapy aims to improve myocardial perfusion and cardiac function in patients with myocardial infarction by redistributing blood flow into the damaged area during PCI.
Pre-clinical and clinical studies demonstrated that PiCSO, in addition to standard PCI, may significantly reduce the infarct size after acute myocardial infarction. Infarct size has shown to be strongly predictive of subsequent all-cause mortality and rehospitalization for heart failure after primary PCI.
Most recent data, presented at TCT 2016 in Washington, DC, confirm the positive effects of PiCSO during PCI in STEMI patients.
Figure 1: Microvascular Obstruction and Infarct Size in STEMI patients treated with PiCSO during PCI1
Figure 1 shows that significantly less STEMI patients treated with PiCSO during PCI experience Microvascular Obstruction (MVO) compared to patients treated with standard PCI only. These patients show a significantly smaller infarct size 5 days after the intervention, confirmed by cardiac magnetic resonance imaging (cMRI).1
Figure 2: Improved Cardiac Function in STEMI patients treated with PiCSO during PCI1
Figure 2 shows that STEMI patients treated with PiCSO during PCI show significantly improved cardiac function indices as compared to patients treated by PCI only. This is demonstrated by an improved Left Ventricular Ejection Fraction (LVEF), a smaller Left Ventricular End-Diastolic Volume (LVEDV) and a smaller Left Ventricular End-Systolic Volume (LVESV).1
PiCSO during Percutaneous Coronary Intervention (PCI)
PiCSOAMI Therapy is applied immediately following flow restoration and during coronary artery stenting in patients presenting with acute myocardial infarction. The therapy is automatically adapted to the patient’s individual anatomy and hemodynamics and extends average cath lab time by only 20-30 minutes.
The PiCSOAMI Impulse System consists of a balloon tipped catheter and a driving console. The PiCSOAMI Impulse Catheter is inserted in a standard manner via the femoral vein and placed in the coronary sinus using a steerable guide sheath (Figure 2). Intermittent coronary sinus occlusion is controlled by the PiCSOAMI Impulse Console using the unique, proprietary ‘Wien Algorithm’ which continuously monitors coronary sinus pressure dynamics and automatically sets the time of occlusion and release phases based on venous pressure.
Figure 3: PiCSOAMI Impulse Catheter Placement in the Coronary Sinus
Unique Modes of Action
The PiCSOAMI principle is based on the fact that coronary sinus pressure will increase when the vessel is occluded and drainage of venous blood into the right atrium is inhibited. During occlusion, pressure will rise from normal right atrial pressure to a pressure plateau, without effecting arterial systemic pressure (Figure 3). This pressure build-up translates into an increase in (arterial) wedge pressure over the ischemic area.
Figure 4: Coronary Sinus Pressure Increase during PiCSO
Clinical and pre-clinical studies have shown that the effectiveness of PiCSOAMI Therapy is based on three main modes of action. The intermittent coronary sinus pressure increase leads to:
- Redistribution of blood to the border zone of the deprived myocardium2
- Enhanced washout of deleterious agents from the microcirculation3
- Increased expression of vascular endothelial growth factor in the myocardium4,5
It could be shown that myocardial salvage is related to increase in coronary artery pressure and coronary sinus pressure amplitude.6
Figure 4 shows a schematic view of the main modes of action of PiCSO: The redistribution of blood and the washout of deleterious agents.
Figure 5: Improved Microvascular Reperfusion
-  Zaman, A.G. et al.: PiCSO to Improve Myocardial Salvage and Reduce Infarct Size in STEMI: Emerging Data; TCT 2016
-  Ido A, et al., am J Physiol. Heart Cir Physiol 2110;280:H1361-7
-  Beatt KJ, et al., Br Heart J 1988;59:159-67
-  Weigel G, et al., J Thorac Surg 2007;133
-  Mohl W, et al., Nat Clin Pract Cardiovasc Med 2008;5:528-0
-  Mohl W, et al., Am J Cardiol 1984 Mar 15;53(7):923-8