ACUTE MYOCARDIAL INFARCTION AFTER THE USE OF AMOXICILLIN/CLAVULANIC ACID: TYPE I KOUNIS SYNDROME

Author(s):  
Kadriye Orta Kilickesmez ◽  
Okay Abaci ◽  
Omer Ezzat ◽  
Ugur Coskun ◽  
Serdar Kucukoglu
2009 ◽  
Vol 136 (1) ◽  
pp. e3-e5 ◽  
Author(s):  
Murat Biteker ◽  
Nilüfer Ekşi Duran ◽  
Funda Sungur Biteker ◽  
Emre Ertürk ◽  
Ahmet Çağrı Aykan ◽  
...  

2017 ◽  
Vol 36 (5) ◽  
pp. 391.e1-391.e5
Author(s):  
Rita Marinheiro ◽  
Pedro Amador ◽  
Filipa Semedo ◽  
Catarina Sá ◽  
Tatiana Duarte ◽  
...  

2004 ◽  
Vol 96 (4) ◽  
pp. 1306-1311 ◽  
Author(s):  
Jarkko Magga ◽  
Mikko Puhakka ◽  
Seppo Hietakorpi ◽  
Kari Punnonen ◽  
Paavo Uusimaa ◽  
...  

Experimental data suggest that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) act locally as antifibrotic factors in heart. We investigated the interrelationships of natriuretic peptides and collagen markers in 93 patients receiving thrombolytic treatment for their first acute myocardial infarction (AMI). Collagen formation following AMI, evaluated as serum levels of amino terminal propeptide of type III procollagen, correlated with NH2-terminal proANP ( r = 0.45, P < 0.001), BNP ( r = 0.55, P < 0.001) and NH2-terminal proBNP ( r = 0.50, P < 0.01) on day 4 after thrombolysis. Levels of intact amino terminal propeptide of type I procollagen decreased by 34% ( P < 0.001), and levels of carboxy terminal cross-linked telopeptide of type I collagen (ICTP) increased by 65% ( P < 0.001). ICTP levels correlated with NH2-terminal proBNP ( r = 0.25, P < 0.05) and BNP ( r = 0.28, P < 0.05) on day 4. Our results suggest that ANP and BNP may act as regulators of collagen scar formation and left ventricular remodeling after AMI in humans. Furthermore, degradation of type I collagen is increased after AMI and may be regulated by BNP.


2019 ◽  
Vol 12 (12) ◽  
pp. e232472
Author(s):  
Luca Conti ◽  
Kelly Gatt ◽  
Christopher Zammit ◽  
Karen Cassar

Acute coronary syndrome occurring during the course of a type I hypersensitivity reaction constitutes Kounis syndrome. We report a case of a 64-year-old man who presented with a non-ST elevation myocardial infarction and peripheral blood eosinophilia. He had rhinitis and constitutional symptoms for several days prior to presentation. Blood investigations revealed moderate eosinophilia and elevated IgE levels. A cardiac MRI showed generalised oedema with a subtle wall motion abnormality in basal inferior/inferolateral wall, and subendocardial high signal on late gadolinium enhancement suggesting a localised myocardial infarction. A coronary angiogram then revealed triple vessel disease. A diagnosis of Kounis syndrome was made. Within days of starting appropriate treatment, the patient’s eosinophil count returned to normal with improvement of clinical picture.


2010 ◽  
Vol 142 (2) ◽  
pp. e20-e22 ◽  
Author(s):  
Salvatore Patanè ◽  
Filippo Marte ◽  
Alessio Currò ◽  
Claudia Cimino

2008 ◽  
Vol 124 (1) ◽  
pp. e4-e7 ◽  
Author(s):  
Yusuf Tavil ◽  
Murat Turfan ◽  
Sedat Türkoğlu ◽  
Adnan Abacı

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