Protective Effects of IRFI-016, a New Antioxidant Agent, in Myocardial Damage, following Coronary Artery Occlusion and Reperfusion in the Rat

Pharmacology ◽  
1994 ◽  
Vol 48 (3) ◽  
pp. 157-166 ◽  
Author(s):  
G.M. Campo ◽  
F. Squadrito ◽  
M. Ioculano ◽  
D. Altavilla ◽  
B. Zingarelli ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Damage ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Protective Effects ◽  
Antioxidant Agent

Effects of propranolol on myocardial damage resulting from coronary artery occlusion followed by reperfusion

1986 ◽  
Vol 111 (3) ◽  
pp. 519-524 ◽  
Author(s):  
Kozui Miyazawa ◽  
Haru Fukuyama ◽  
Eiichi Komatsu ◽  
Ichiro Yamaguchi
Keyword(s):  
Coronary Artery ◽  
Myocardial Damage ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion

Protective effects of hypothermia on ischemic stressed myocardium during short-term, repeated coronary artery occlusion

1982 ◽  
Vol 394 (S1) ◽  
pp. R14-R14
Author(s):  
H. Korb ◽  
A. Hoeft ◽  
D. Baller ◽  
R. Schräder ◽  
H. G. Wolpers ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Protective Effects ◽  
Short Term

The reduction of myocardial damage and leukocyte polymorphonuclear accumulation following coronary artery occlusion by the tyrosine kinase inhibitor tyrphostin AG 556

Life Sciences ◽  
2000 ◽  
Vol 67 (21) ◽  
pp. 2615-2629 ◽  
Author(s):  
Domenica Altavilla ◽  
Francesco Squadrito ◽  
Giuseppe M. Campo ◽  
Antonino Saitta ◽  
Giovanni Squadrito ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Myocardial Damage ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion

Failure of Captopril to Attenuate Myocardial Damage, Neutrophil Accumulation, and Mortality Following Coronary Artery Occlusion and Reperfusion in Rat

Angiology ◽  
1994 ◽  
Vol 45 (8) ◽  
pp. 717-724 ◽  
Author(s):  
Jonathan Leor ◽  
Nira Varda-Bloom ◽  
David Hasdai ◽  
Zehava Ovadia ◽  
Alexander Battler
Keyword(s):  
Coronary Artery ◽  
Myocardial Damage ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Neutrophil Accumulation

Cardiac involvement in patients with sorafenib or sunitinib treatment for metastatic renal cell carcinoma

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 5110-5110 ◽  
Author(s):  
M. Schmidinger ◽  
U. M. Vogl ◽  
C. Schukro ◽  
A. Bojic ◽  
M. Bojic ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Coronary Artery ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Biochemical Markers ◽  
Myocardial Damage ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Gene Products ◽  
Tki Treatment

5110 Background: Tyrosine-kinase inhibitors (TKI) of the VEGF and PDGF-receptor have significant clinical activity in patients with renal cell carcinoma (RCC). These agents target the VHL-hypoxia-inducible gene pathway and lead to inhibition of hypoxia- inducible factor (HIF)-induced gene products. Physiologically, HIF-1 related gene products are important mediators of myocardial response to ischemia, myocardial remodeling, peri-infarct vascularisation and vascular permeability. The aim of this prospective observational study was to investigate clinical and biochemical signs of myocardial damage in patients undergoing TKI-treatment for RCC. Methods: 73 consecutive patients (median age 65, range 44–68) intended for TKI treatment were analyzed for medical history of coronary artery disease (CAD) and risk-factors. Measurements of biochemical markers of cardiac damage (creatine kinase MB -CK-MB- and cardiac troponin T -cTNT-) and electrocardiogram (ECG) were performed before treatment. In patients developing cardiac symptoms during TKI treatment and/or at occurrence of CK-MB or TNT elevations, changes in ECG were analyzed and patients underwent echocardiography. Results: All patients had normal CK-MB and TNT levels at baseline. 17 patients (23%) developed (week 2–32 of treatment) significant CK-MB elevation, (TNT n=5), with clinical symptoms in 7 patients. No patient had uncontrolled hypertension. Detailed ECG’s comparison before and during treatment revealed significant changes in 10 out of 17 patients, such as ST-segment depression or elevation, T-wave changes and symptomatic AV-conduction disturbance, requiring pacemaker-implantation. 3 patients underwent coronary angiography with one patient showing acute coronary artery occlusion and myocardial infarction. 6 out of 17 patients had abnormal findings on echocardiography, such as reduced left ventricular function Conclusions: TKI-induced HIF-inhibition may be associated with severe myocardial damage. The underlying mechanism may not necessarily be caused by overt coronary artery occlusion. ECG-changes and biochemical markers are the most important indicators in the preclinical stage. Therefore, careful cardiac monitoring during TKI-treatment is strongly recommended. No significant financial relationships to disclose.

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