GIPS IV

Preservation of myocardial function after myocardial infarction

3 Current vacancy for GIPS IV

Physician-Scientist (Ischemic and Valvular Disease)

Project: GIPS IV, Early Synergy Research line: Ischemic Heart Diseases

More about this vacancy

MD/PhD students

Project: BIOSTAT-CHF, Early Synergy, GIPS IV, iPHORECAST, KETONE-HF, PLN cardiomyopathy, RACE V, RACE‐8‐HF, RED-CVD, SECRETE-HF, STOP-HF, APAF-CRT, AF RISK, Adiposity in Heart Failure with Preserved Ejection Fraction, RASTA AF, RACE 9, Selenium and Heart Failure Research line: Heart Failure, Ischemic Heart Diseases, Experimental Cardiology, Atrial Fibrillation

More about this vacancy

Bachelor and Master students

Project: BIOSTAT-CHF, Early Synergy, GIPS IV, Adiposity in Heart Failure with Preserved Ejection Fraction, iPHORECAST, KETONE-HF, RACE V, RACE‐8‐HF, RED-CVD, SECRETE-HF, Selenium and Heart Failure, STOP-HF, PLN cardiomyopathy, AF RISK, APAF-CRT, RACE 9, RASTA AF Research line: Heart Failure, Ischemic Heart Diseases, Experimental Cardiology, Atrial Fibrillation

More about this vacancy

In the past decades, as a result of advances in pharmacological, reperfusion and preventive strategies, prognosis of patients with ST-elevated myocardial infarction has substantially improved and mortality has decreased.  However, permanent myocardial injury related to the ischemia and subsequent reperfusion is still observed in the vast majority (88%) of patients and harbors a risk of heart failure development. Although many advances have been made, there is no specific treatment that targets myocardial reperfusion injury, which is considered to be a paradoxical form of myocardial damage that occurs as a result of the restoration of vessel patency. Reducing myocardial reperfusion injury is expected to further decrease infarct size, decreasing adverse cardiac remodeling and improving cardiac function as well as clinical outcome.

Currently, H2S has been shown to protect from (myocardial) ischemia reperfusion injury in various experimental animal models. It reduces infarct size and apoptosis and attenuates cardiac function. Inhibition of leukocyte endothelial cell interactions, neutralization of reactive oxygen species (ROS) and the reduction of apoptotic signaling are the suggested as additional mechanisms underlying the cardioprotective effect of H2S. An intermediate of H2S, sodium thiosulfate (STS), which acts as a H2S donor, can safely be administered intravenously to humans. STS has an orphan drug registration in the treatment of cyanide poisoning, prevention of ototoxicity in children receiving cisplatinum chemotherapy and in the treatment of calciphylaxis.

The GIPS-IV study designed by our group will be the first study to determine the efficacy of a H2S-donor to reduce myocardial infarct size in patient with ST-elevated myocardial infarction and is currently recruiting.

“We are good at restoring the coronary blood flow via percutaneous interventions. However, usually the oxygen shortage has already caused damage to the cardiac muscle. In our hospital we are testing new strategies to improve the response of the heart to oxygen shortages.”

People involved

Principal investigator

Pim van der Harst

Cardiologist
Team

Erik Lipsic

Cardiologist

Gabija Pundziute-Do Prado

Cardiologist

Marie-Sophie de Koning

Physician-scientist

Press & publications

A Genotype-Guided Strategy for Oral P2Y12 Inhibitors in Primary PCI.

Claassens DMF, Vos GJA, Bergmeijer TO, Hermanides RS, van 't Hof AWJ, van der Harst P, Barbato E, Morisco C, Tjon Joe Gin RM, Asselbergs FW, Mosterd A, Herrman JR, Dewilde WJM, Janssen PWA, Kelder JC, Postma MJ, de Boer A, Boersma C, Deneer VHM, Ten Berg JM. N Engl J Med. 2019

view on publisher site

Coronary Angiography after Cardiac Arrest without ST-Segment Elevation.

Lemkes JS, Janssens GN, van der Hoeven NW, Jewbali LSD, Dubois EA, Meuwissen M, Rijpstra TA, Bosker HA, Blans MJ, Bleeker GB, Baak R, Vlachojannis GJ, Eikemans BJW, van der Harst P, van der Horst ICC, Voskuil M, van der Heijden JJ, Beishuizen A, Stoel M, Camaro C, van der Hoeven H, Henriques JP, Vlaar APJ, Vink MA, van den Bogaard B, Heestermans TACM, de Ruijter W, Delnoij TSR, Crijns HJGM, Jessurun GAJ, Oemrawsingh PV, Gosselink MTM, Plomp K, Magro M, Elbers PWG, van de Ven PM, Oudemans-van Straaten HM, van Royen N. N Engl J Med. 2019

view on publisher site

Computational quantitative flow ratio to assess functional severity of coronary artery stenosis.

Ties D, van Dijk R, Pundziute G, Lipsic E, Vonck TE, van den Heuvel AFM, Vliegenthart R, Oudkerk M, van der Harst P. Int J Cardiol. 2018

view on publisher site

Enhancing cardiovascular artificial intelligence (AI) research in the Netherlands: CVON-AI consortium.

Benjamins JW, van Leeuwen K, Hofstra L, Rienstra M, Appelman Y, Nijhof W, Verlaat B, Everts I, den Ruijter HM, Isgum I, Leiner T, Vliegenthart R, Asselbergs FW, Juarez-Orozco LE, van der Harst P. Neth Heart J. 2019

view on publisher site

Effect of metformin on left ventricular function after acute myocardial infarction in patients without diabetes: the GIPS-III randomized clinical trial.

Lexis CP, van der Horst IC, Lipsic E, Wieringa WG, de Boer RA, van den Heuvel AF, van der Werf HW, Schurer RA, Pundziute G, Tan ES, Nieuwland W, Willemsen HM, Dorhout B, Molmans BH, van der Horst-Schrivers AN, Wolffenbuttel BH, ter Horst GJ, van Rossum AC, Tijssen JG, Hillege HL, de Smet BJ, van der Harst P, van Veldhuisen DJ; GIPS-III Investigators. JAMA. 2014

view on publisher site

External links