scholarly journals A Resuscitated Case of Acute Myocardial Infarction with both Familial Hypercholesterolemia Phenotype Caused by Possibly Oligogenic Variants of the PCSK9 and ABCG5 Genes and Type I CD36 Deficiency

Author(s):  
Ryo Nishikawa ◽  
Masato Furuhashi ◽  
Mika Hori ◽  
Masatsune Ogura ◽  
Mariko Harada-Shiba ◽  
...  
2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Svendsen ◽  
H.W Krogh ◽  
J Igland ◽  
G.S Tell ◽  
L.J Mundal ◽  
...  

Abstract Background and aim We have previously reported that individuals with familial hypercholesterolemia (FH) have a two-fold increased risk of acute myocardial infarction (AMI) compared with the general population. The consequences of having an AMI on re-hospitalization and mortality are however less known. The aim of the present study was to compare the risk of re-hospitalization with AMI and CHD and risk of mortality after incident (first) AMI-hospitalization between persons with and without FH (controls). Methods The original study population comprised 5691 persons diagnosed with FH during 1992–2014 and 119511 age and sex matched controls randomly selected from the general Norwegian population. We identified 221 individuals with FH and 1947 controls with an incident AMI registered in the Norwegian Patient Registry (NPR) or the Cardiovascular Disease in Norway Project during 2001–2017. Persons with incident AMI were followed until December 31st 2017 for re-hospitalization with AMI or coronary heart disease (CHD) registered in the NPR, and for mortality through linkage to the Norwegian Cause of Death Registry. Risk of re-hospitalization was compared with sub-hazard ratios (SHR) from competing risk regression with death as competing event, and mortality was compared using hazard ratios (HR) from Cox regression. All models were adjusted for age. Results Risk of re-hospitalization was 2-fold increased both for AMI [SHR=2.53 (95% CI: 1.88–3.41)] and CHD [SHR=1.82 (95% CI: 1.44–2.28)]. However, persons with FH did not have increased 28-day mortality following an incident AMI (HR=1.05 (95% CI: 0.62–1.78), but the longer-term (>28 days) mortality after first AMI was increased in FH [HR=1.45 (95% CI: 1.07–1.95]. Conclusion This study yields the important finding that persons with FH have increased risk of re-hospitalization of both AMI and CHD after incident AMI. These findings call for more intensive follow-up of individuals with FH after an AMI. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): University of Oslo and Oslo University Hospital


Author(s):  
Karianne Svendsen ◽  
Henriette W. Krogh ◽  
Jannicke Igland ◽  
Grethe S. Tell ◽  
Liv J. Mundal ◽  
...  

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.


Cases Journal ◽  
2008 ◽  
Vol 1 (1) ◽  
pp. 71 ◽  
Author(s):  
Anita A Kumar ◽  
Ghanshyam Shantha ◽  
Yadav Srinivasan ◽  
N Senthil ◽  
K Rajkumar ◽  
...  

2016 ◽  
Vol 10 (1) ◽  
pp. 117-121
Author(s):  
Zulkuf Karahan ◽  
Murat Ugurlu ◽  
Berzal Ucaman ◽  
Ali Veysel Ulug ◽  
Ilyas Kaya ◽  
...  

Background: Angiotensin converting enzyme (ACE) gene polymorphism is associated with high renin-angiotensin system causing myocardial fibrosis and ventricular repolarization abnormality. Based on these findings, this study was designed to determine the association between ACE gene insertion/deletion (I/D) polymorphism and QT dispersion after acute myocardial infarction (MI). Objective and Methods: The study included 108 patients with acute MI. Blood samples were obtained from all the patients for genomic DNA analysis. ECGs were recorded at baseline and at the end of a 6-month follow up. The OT dispersion was manually calculated. Results: The mean age of the patients was 57.5 ±9.9 years (ranging from 36 to 70). The patients with DD genotype showed longer QT dispersion than patients with II or DI genotype at the baseline, while at the end of the six-month follow up the patients with DI genotype showed longer QT dispersion than patients with DD or II genotypes. However, the magnitude of the QT dispersion prolongation was higher in patients carrying the ACE D allele than patients who were not carrying it, at baseline and at the end of six-month follow up (52.5 ±2.6 msn vs. 47.5±2.1 msn at baseline, 57±3.2 msn vs. 53±2.6 msn in months, P: 0.428 and P: 0.613, respectively). Conclusion: Carriers of the D allele of ACE gene I/D polymorphism may be associated with QT dispersion prolongation in patients with MI.An interaction of QT dispersion and ACE gene polymorphism may be associated with an elevation of serum type I-C terminal pro-collagen concentration, possibly leading to myocardial fibrosis, and increased action potential duration.


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