Coronary artery disease and myocardial infarction

2020 ◽  
pp. 349-354
Author(s):  
Perry Elliott ◽  
Pier D. Lambiase ◽  
Dhavendra Kumar

This chapter covers coronary artery disease (CAD) and myocardial infarction, starting with an introduction to the main causal and treatable risk factors for CAD and myocardial infarction, then goes on to discuss the Mendelian disorders associated with CAD (e.g. Tangier disease, sitosterolaemia, etc.) Association studies based on the candidate gene approach are discussed along with genomic studies, e.g. polygenic risk scores.

2017 ◽  
Vol 10 (1) ◽  
pp. 45-51
Author(s):  
Sharadindu Shekhar Roy ◽  
STM Abu Azam ◽  
Md Khalequzzaman ◽  
Mohammad Ullah ◽  
Samir Kumar Kundu ◽  
...  

Background: The superiority of the GRACE and TIMI risk scores in predicting the angiographic severity of coronary artery disease in patients with non ST-elevation myocardial infarction (NSTEMI) has not yet been established. This study was done to compare the GRACE and TIMI risk scores in predicting the angiographic severity of coronary artery disease in this group of patients.Method: The cross sectional study done in the Department of Cardiology, NICVD, Dhaka. The patients admitted with NSTEMI were evaluated to calculate the GRACE and TIMI risk score from April, 2015 to April, 2016.Coronary angiogram was done during index hospitalization and the severity of the coronary artery disease was assessed by vessel score and Gensini score.Results: Of 115 patients assessed, a positive correlation of the vessel score and Gensini score was observed with both the GRACE and TIMI risk scores (p=<0.001) and the GRACE score (r=0.59) correlated better than the TIMI score (r=0.52). The GRACE score presented area under the Receiver Operating Characteristic (ROC) curve of 0.844(95% CI = 0.774 – 0.914) significantly superior to the area under the ROC curve of 0.752(95% CI =0.658– 0.846) of the TIMI score for the difference between the two scores.Conclusion: Both the GRACE and TIMI scores had good predictive value in predicting the severity of coronary artery disease in the patients with NSTEMI but when both the scores were compared, the GRACE score was found to be superior and correlated better with the severity of coronary artery disease.Cardiovasc. j. 2017; 10(1): 45-51


2020 ◽  
Vol 29 (8) ◽  
pp. 1388-1395
Author(s):  
Laurence J Howe ◽  
Frank Dudbridge ◽  
Amand F Schmidt ◽  
Chris Finan ◽  
Spiros Denaxas ◽  
...  

Abstract Background There is growing evidence that polygenic risk scores (PRSs) can identify individuals with elevated lifetime risk of coronary artery disease (CAD). Whether they can also be used to stratify the risk of subsequent events among those surviving a first CAD event remain uncertain, with possible biological differences between CAD onset and progression, and the potential for index event bias. Methods Using two baseline subsamples of UK Biobank: prevalent CAD cases (N = 10 287) and individuals without CAD (N = 393 108), we evaluated associations between a CAD PRS and incident cardiovascular and fatal outcomes. Results A 1 SD higher PRS was associated with an increased risk of incident myocardial infarction (MI) in participants without CAD (OR 1.33; 95% CI 1.29, 1.38), but the effect estimate was markedly attenuated in those with prevalent CAD (OR 1.15; 95% CI 1.06, 1.25) and heterogeneity P = 0.0012. Additionally, among prevalent CAD cases, we found an evidence of an inverse association between the CAD PRS and risk of all-cause death (OR 0.91; 95% CI 0.85, 0.98) compared with those without CAD (OR 1.01; 95% CI 0.99, 1.03) and heterogeneity P = 0.0041. A similar inverse association was found for ischaemic stroke [prevalent CAD (OR 0.78; 95% CI 0.67, 0.90); without CAD (OR 1.09; 95% CI 1.04, 1.15), heterogeneity P &lt; 0.001]. Conclusions Bias induced by case stratification and survival into UK Biobank may distort the associations of PRS derived from case-control studies or populations initially free of disease. Differentiating between effects of possible biases and genuine biological heterogeneity is a major challenge in disease progression research.


2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Naomi Ogawa ◽  
Yasushi Imai ◽  
Hiroyuki Morita ◽  
Ryozo Nagai

Coronary artery disease (CAD) is a multifactorial disease with environmental and genetic determinants. The genetic determinants of CAD have previously been explored by the candidate gene approach. Recently, the data from the International HapMap Project and the development of dense genotyping chips have enabled us to perform genome-wide association studies (GWAS) on a large number of subjects without bias towards any particular candidate genes. In 2007, three chip-based GWAS simultaneously revealed the significant association between common variants on chromosome 9p21 and CAD. This association was replicated among other ethnic groups and also in a meta-analysis. Further investigations have detected several other candidate loci associated with CAD. The chip-based GWAS approach has identified novel and unbiased genetic determinants of CAD and these insights provide the important direction to better understand the pathogenesis of CAD and to develop new and improved preventive measures and treatments for CAD.


2019 ◽  
Author(s):  
Florian Wünnemann ◽  
Ken Sin Lo ◽  
Alexandra Langford-Avelar ◽  
David Busseuil ◽  
Marie-Pierre Dubé ◽  
...  

AbstractCoronary artery disease (CAD) represents one of the leading causes of morbidity and mortality worldwide. Given the healthcare risks and societal impacts associated with CAD, their clinical management would benefit from improved prevention and prediction tools. Polygenic risk scores (PRS) based on an individual’s genome sequence are emerging as potentially powerful biomarkers to predict the risk to develop CAD. Two recently derived genome-wide PRS have shown high specificity and sensitivity to identify CAD cases in European-ancestry participants from the UK Biobank. However, validation of the PRS predictive power and transferability in other populations is now required to support their clinical utility. We calculated both PRS (GPSCAD and metaGRSCAD) in French-Canadian individuals from three cohorts totaling 3639 prevalent CAD cases and 7382 controls, and tested their power to predict prevalent, incident and recurrent CAD. We also estimated the impact of the founder French-Canadian familial hypercholesterolemia deletion (LDLR delta > 15kb deletion) on CAD risk in one of these cohorts and used this estimate to calibrate the impact of the PRS. Our results confirm the ability of both PRS to predict prevalent CAD comparable to the original reports (area under the curve (AUC) = 0.72-0.84). Furthermore, the PRS identified about 6-7% of individuals at CAD risk similar to carriers of the LDLR delta > 15kb mutation, consistent with previous estimates. However, the PRS did not perform as well in predicting incident (AUC= 0.56 - 0.60) or recurrent (AUC= 0.56 - 0.60) CAD. This result suggests that additional work is warranted to better understand how ascertainment biases and study design impact PRS for CAD. Collectively, our results confirm that novel, genome-wide PRS are able to predict CAD in French-Canadians; with further improvements, this is likely to pave the way towards more targeted strategies to predict and prevent CAD-related adverse events.


2020 ◽  
Vol 29 (4) ◽  
pp. 634-640 ◽  
Author(s):  
Patrick A. Gladding ◽  
Malcolm Legget ◽  
Diane Fatkin ◽  
Peter Larsen ◽  
Robert Doughty

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