PiCSO® Therapy


Acute Myocardial Infarction

During a myocardial infarction one or several of the heart’s coronary arteries are occluded due to a build-up of plaque in the vessel (Figure 1, left). This limits the flow of oxygenated blood to the myocardium, causing ischemia and necrosis of the muscle, as shown in the heart’s cross section in Figure 1.

Figure 1: Myocardial Infarction*

Myocardial infarctions can be divided into two types, according to their severity.

Non ST-segment Elevated Myocardial Infarction (NSTEMI) is the less severe type. In an NSTEMI, the blood clot only partly occludes the coronary artery, and, as a result only a portion of the heart muscle being supplied by the affected artery dies. ST-Segment Elevation Myocardial Infarction (STEMI) is the most severe type of myocardial infarction, where the coronary artery is completely blocked off by a plaque, and, as a result virtually all the heart muscle being supplied by the affected artery starts to become necrotic.

Restoration of Blood Flow alone does not ensure sufficient microvascular Perfusion

Timely restoration of epicardial blood flow through Primary Percutaneous Coronary Intervention (PCI/ Angioplasty, Stenting) remains the gold standard in the treatment of acute myocardial infarction. The rate of restoration of epicardial blood flow after PCI can be assessed by the angiographic Thrombolysis in Myocardial Infarction Flow (TIMI Flow). TIMI 3 Flow indicates excellent epicardial coronary blood flow after PCI and is achieved in the vast majority of STEMI patients (Figure 2).1

Figure 2: TIMI Flow after PCI in STEMI1


Despite successful PCI, 1-year mortality in STEMI patients remains high, estimated to be between 6% and 14% after PCI. This is a consequence of impaired perfusion at the microvascular level, measured by Myocardial Blush Grade. Figure 3 shows that excellent microvascular perfusion is achieved in only less than 30% of patients, leading to larger infarct size after PCI which has shown to be directly associated with adverse remodeling and decreased left ventricular (LV) function, leading to heart failure and long-term morbidity following STEMI.1

Figure 3: Myocardial Blush Grade (MBG) after PCI in STEMI1

Figure 4 shows the impact of poor microcirculation, measured as Myocardial Blush Grade on 1-year mortality rates in patients with TIMI 3 Flow. 16.7% and 9.8% of patients who have excellent epicardial flow, but poor MBG, 0 or 1 respectively, die within one year.2

Figure 4: 1-year all-cause mortality in patients with TIMI Flow 3 and Myocardial Blush Grade 0-32

Reperfusion Injury contributes to an increased Infarct Size

Impaired microvascular perfusion with subsequent large final infarct size after PCI is in parts attributed to a phenomenon called Reperfusion Injury.

Reperfusion injury is damage of myocardium caused by oxygenated blood returning to the tissue after a period of ischemia. The absence of oxygen and nutrients during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative cell damage in the affected tissue.

Literature shows that reperfusion injury accounts for up to 50% of the final infarct size after STEMI. Figure 5 schematically illustrates that timely reperfusion through PCI may save only up to 50% of the tissue affected by a blocked coronary artery (area at risk, AAR). Up to 50% of the remaining infarct size is due to reperfusion injury which could potentially be saved in the presence of a therapeutic intervention preventing reperfusion injury and thereby promoting microvascular perfusion.

So far, there has not been an effective therapy for preventing myocardial reperfusion injury in reperfused STEMI patients and new technologies may unlock these clinical benefits for the first time.3

Figure 5: The benefits of timely Reperfusion and the Addition of a therapeutic Intervention for preventing myocardial Reperfusion Injury3

This scheme illustrates the benefits of timely reperfusion and the addition of a therapeutic intervention for preventing myocardial reperfusion injury (RI) on myocardial infarct size and myocardial salvage. Nearly 50% of the final myocardial infarct size is due to myocardial RI and can therefore be reduced, thereby maximizing the benefits of myocardial reperfusion.3

Realizing the full Benefits of myocardial Reperfusion

Pressure-controlled Intermittent Coronary Sinus Occlusion (PiCSO®) aims to improve microvascular reperfusion, reduce reperfusion injury, and thereby reduce final Infarct Size and improve cardiac function after PCI in patients with acute myocardial infarction.

  • [1] Stone et al. J Am Coll Cardiol. 2002 Feb 20;39(4):591-7
  • [2] Kampinga et al . Circ Cardiovasc Interv. 2010;3
  • [3] Fröhlich G., Hausenloy D., et al. Eur Heart J (2013) 34 (23): 1714-1722
  • “Blausen 0463 HeartAttack” by Blausen Medical Communications, Inc.; “Heart ant wall infarction” by Patrick J. Lynch, medical illustrator.