An ultrasound activated oxygen generation nanosystem specifically alleviates myocardial hypoxemia and promotes cell survival following acute myocardial infarction

2020 ◽  
Vol 8 (28) ◽  
pp. 6059-6068
Author(s):  
Huini Fu ◽  
Jingke Fu ◽  
Sicong Ma ◽  
Hui Wang ◽  
Shuzhi Lv ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cell Survival ◽  
Cardiac Cells ◽  
Oxygen Generation ◽  
Infarction Size ◽  
Activated Oxygen ◽  
Myocardial Infarction Size ◽  
Cell Survival And Proliferation

An ultrasound-activated oxygen generation nanosystem was developed to significantly reduce the myocardial infarction size as well as promote the cell survival and proliferation of cardiac cells after acute myocardial infarction.

2230Results from the CAMI1 Study: selective CRP apheresis as a new treatment option in acute myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Garlichs ◽  
J Torzewski ◽  
A Sheriff ◽  
C Pfluecke ◽  
H Darius ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Plasma Levels ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Study Endpoint ◽  
Infarction Size ◽  
Myocardial Infarction Size

Abstract Background Inflammation is increasingly recognized as an important pathogenic feature in cardiovascular disease. In patients with STEMI, C-reactive protein (CRP), the prototype human acute phase protein, is a marker of poor prognosis and independently predicts 30-day mortality. In STEMI, CRP may indeed be intimately involved in myocardial damage by activating the complement system in the ischemic tissue. In animal experiments, CRP removal after STEMI reduces infarct size and results in a significantly better left ventricular ejection fraction (LVEF). Recently, in the multi-center matched-control pilot study on CRP apheresis in Acute Myocardial Infarction (CAMI1), a newly designed CRP adsorber has been demonstrated to efficiently and selectively lower CRP plasma levels in humans. Here, we present preliminary data of the ongoing trial. Methods Up to the present day, 67 STEMI patients were enrolled in the study following complete coronary revascularization. 32 patients received CRP apheresis, whereas 35 patients treated by standard protocols served as controls. CRP apheresis started 24±12 h and 48±12 h after onset of symptoms. In case of a rapid increase in CRP plasma levels following the 2nd session, a 3rd session was carried out another 24 h later. In each apheresis session, 6000 ml plasma was treated via peripheral venous access. Primary study endpoint was myocardial infarction size as determined by Cardiac Magnetic Resonance Imaging (MRI) 5±3 days after STEMI. Results Apheresis sessions were well tolerated with no relevant side effects. Peak CRP plasma levels after STEMI ranged from 12 mg/l to 279 mg/l. The peak CRP level after AMI can be calculated precisely with at 2–3 CRP quantifications during the first 24 h after the onset of symptoms. The regression coefficient for this analysis is 0.95. This mathematical step allows for the comparison of the CRP-apheresis group and the controls on the basis of their individual CRP peak levels. The statistical evaluation shows that the apheresis patients no longer correlate with the control with regard to the endpoints infarct size, LVEF, longitudinal strain and circumferential strain. They perform significantly better at all endpoints. The CRP apheresis reduced the development of myocardial damage. Conclusions Here, an unequivocal association between infarct size and CRP is demonstrated for the first time. CRP apheresis following STEMI is feasible and safe. Our preliminary results in a small cohort show a significant beneficial effect of CRP apheresis on myocardial infarction size and wall motion. Selective CRP apheresis may emerge as a new therapeutic approach in the treatment of acute myocardial infarction.

Late prognostic value of scintigraphic parameters of acute myocardial infarction size in complicated myocardial infarction without heart failure

1983 ◽  
Vol 51 (7) ◽  
pp. 1045-1051 ◽  
Author(s):  
Elias H. Botvinick ◽  
Juan F. Perez-Gonzalez ◽  
Richard Dunn ◽  
Thomas Ports ◽  
Kanu Chatterjee ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Prognostic Value ◽  
Infarction Size ◽  
Myocardial Infarction Size

scholarly journals 1078-92 Human umbilical cord mononuclear cells limit acute myocardial infarction size

2004 ◽  
Vol 43 (5) ◽  
pp. A269-A270 ◽  
Author(s):  
Robert J Henning ◽  
Hamdi Abu-Ali ◽  
John Randolph ◽  
Michael Morgan ◽  
John Balis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Umbilical Cord ◽  
Mononuclear Cells ◽  
Human Umbilical Cord ◽  
Infarction Size ◽  
Myocardial Infarction Size

scholarly journals Acute Myocardial Infarction Size and Myoglobin Release into Serum

1992 ◽  
Vol 30 (12) ◽  
Author(s):  
J. R. Delanghe ◽  
M. L. De Buyzere ◽  
L. P. Cluyse ◽  
H. M. Thierens ◽  
D. L. Clement
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarction Size ◽  
Myocardial Infarction Size

scholarly journals C-reactive protein increases myocardial damage after STEMI

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C.D Garlichs ◽  
W Ries ◽  
J Torzewski ◽  
C Pfluecke ◽  
F Heigl ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Plasma Levels ◽  
Circumferential Strain ◽  
Myocardial Damage ◽  
Study Endpoint ◽  
Funding Source ◽  
Infarction Size ◽  
Myocardial Infarction Size

Abstract Background The CAMI-1 study dealt with the depletion of CRP by apheresis in patients with acute myocardial infarction (AMI). CRP, the prototype human acute phase protein, has been known as a marker of poor prognosis in AMI and independently predicts 30-day mortality. Methods 66 STEMI patients were enrolled in the study following complete coronary revascularization (2–12 h after the onset of symptoms). 32 patients received CRP apheresis, whereas 34 patients treated by standard protocols served as controls. CRP apheresis started 24±12 h and 48±12 h after onset of symptoms. In case of a rapid increase in CRP plasma levels following the 2nd session, a 3rd session was carried out another 24 h later. A specific CRP adsorber removed up to 79% of the original CRP. In each apheresis session, 6000 ml of plasma was treated via peripheral venous access. Primary study endpoint was myocardial infarction size as determined by Cardiac Magnetic Resonance Imaging (CMR) 2–9 days after STEMI. Results Aphereses sessions were well tolerated with no relevant side effects. Peak CRP plasma levels after STEMI ranged from 9 to 279 mg/l. The expected peak CRP level after AMI can be calculated precisely with 2–3 CRP quantifications during the first 24 h after the onset of symptoms. The regression coefficient for this analysis is 0.91. This mathematical step allows for the comparison of the CRP-apheresis group and the controls on the basis of their individual CRP peak levels. The statistical evaluation shows that the CRP concentration is significantly associated with the damage (infarct size, LVEF, circumferential strain) in the controls. This association was lost in the aphereses patients: they performed significantly better at all endpoints (infarct size, LVEF, circumferential strain) than the controls. The CRP apheresis significantly reduced myocardial damage. To our surprise, two apheresis patients had an infarct size of 0%. Conclusions For the first time we find an unequivocal association between myocardial infarct size and the CRP concentration. This is in some respects a surprise, since the basic assumption in AMI is that the vascular occlusion leads to primary damage and the reperfusion to secondary damage, which would not have led one to expect such a clear dose-response relationship as that observed here. In addition, our results show a significant beneficial effect of CRP apheresis on myocardial infarction size and wall motion. Selective CRP apheresis is now being further evaluated as a therapeutic approach in the treatment of acute myocardial infarction in a registry (CAMI registry). Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Pentracor GmbH

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