scholarly journals An LRP8 Variant Is Associated with Familial and Premature Coronary Artery Disease and Myocardial Infarction

2007 ◽  
Vol 81 (4) ◽  
pp. 780-791 ◽  
Author(s):  
Gong-Qing Shen ◽  
Lin Li ◽  
Domenico Girelli ◽  
Sara B. Seidelmann ◽  
Shaoqi Rao ◽  
...  
2016 ◽  
Vol 9 (4) ◽  
Author(s):  
Ijaz Ahmad ◽  
Qaiser Shafique

Objective: To evaluate risk factors and arteriography findings in young patients under 40 year of age admitted with first acute myocardial infarction (AMI). Design: A prospective descriptive study. Place and Duration of Study: Cardiology Department, Allama Iqbal Medical College/ Jinnah Hospital, Lahore from July 2002 to June 2003. Patients and Methods: During the study period, 274 patients with first AMI were admitted in our coronary care unit and 52 (19%) were under 40 year of age. These 52 patients underwent pre-discharge coronary arteriography. Results: Forty-five (87%) were male and seven (13%) were female. Risk factors in all study patients were smoking in 79%, systemic hypertension in 35%, diabetes mellitus in 31%, hyperlipidemia in 19% and family history of premature coronary artery disease in 17%. Risk factors were distinctly less frequent in patients without coronary atherosclerosis. Cigarette smoking was the main risk factor in male patients while diabetes and hypertension were main risk factors in female patients. Forty-six patients (88%) had significant CAD (greater than 50% diameter narrowing of at least one major coronary artery), 5(10%) had normal coronary arteries and one patient (2%) had marked coronary ectasia. In patients with significant coronary artery disease, the prevalence rate of one, two and three vessel disease was 52, 28 and 20 percent, respectively. No patient had congenital coronary anomaly or significant left main CAD. Conclusion: AMI in persons under the age of 40 years accounts for approximately 19% of AML In this age group, AMI is a disease of men who smoke & single vessel CAD predominates. Approximately half of the young patients have single vessel coronary disease, and in up to 10%, the cause is not related to atherosclerosis. Coronary angiography may be warranted in young patients with AMI to define the anatomy of the disease and to permit optimal management


Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Sheikh Bilal B Khalid ◽  
Javaria Mahmood

Introduction: Cisplatin-based chemotherapeutic regimen (CBCR) is known for increasing risk of venous thromboembolic (TE) disease. We report a unique case of STEMI associated with CBCR which we believe was caused by coronary artery thrombosis. Case description: A 31-yo man with a past history of germ cell tumor presented with chest pain radiating to back and left arm. It started this morning and intensity did not worsen with exertion. He denied any dyspnea, diaphoresis or palpitations. He was non-smoker and non-obese. He denied any family history of premature coronary artery disease. He had undergone unilateral orchiectomy a year ago, and was currently receiving chemotherapy with bleomycin, etoposide and cisplatin; the last dose of his 3 rd cycle was given the day before. EKG showed ST elevation in leads I, aVL, V4 and V5. Troponin I was high to 6.9 ng/ml (ULN 0.045 ng/ml). He received intravenous infusion of thrombolytic. An angiogram done the next day showed moderate mid-LAD disease with residual clot. A CT scan and an echocardiogram later showed left ventricular thrombus (LVT). He was kept on therapeutic enoxaparin along with aspirin. Follow up echocardiogram showed resolution of the thrombus. His chemotherapy was stopped, and he has been kept on active surveillance since then. Discussion: Most cases of CBCR-associated myocardial infarction that have been reported have been seen in the older population with other risk factors for coronary artery disease. Cases where angiographic data was available, coronary artery vasospasm appeared to be the culprit rather than a true plaque rupture. While the presence of LVT raises possibility of thromboembolism to coronaries causing MI, the angiographic findings support accelerated plaque formation to be the cause of infarction. In earlier reports, elevated pre-treatment level of von Willebrand factor has been postulated to have some role in the disease pathogenesis. Other possible mechanisms for pathogenesis include endothelial cell damage, platelet activation, and imbalance between thromboxane-prostacyclin levels. This case emphasizes the need to keep cardiac etiologies of chest pain in the differential when evaluating patients on CBCR as timely intervention is life saving and prevent morbidity.


2009 ◽  
Vol 102 (07) ◽  
pp. 131-136 ◽  
Author(s):  
Claudine Soria ◽  
Claire dit Sollier ◽  
Jeanne-Yvonne Borg ◽  
Mathieu Coudert ◽  
Gilles Montalescot ◽  
...  

SummaryProtein Z (PZ) is the cofactor of PZ dependent inhibitor (ZPI) that inhibits activated coagulation factor X. PZ was expected to play a role in coronary artery disease (CAD) but with inconsistent clinical findings. We therefore evaluated whether PZ plasma level and/or three genetic variants encoding for low PZ plasma level were associated with premature CAD in stable young post-myocardial infarction (MI) patients. PZ plasma level and three polymorphisms A-13G, G-103A and G79A were determined in 176 young stable post-MI patients and in 176 sex- and age-matched controls (FITE-NAT population). Moreover the genotypes, resulting from the combination of the three polymorphisms (A-13G/G-103A/G79A), were studied. PZ plasma level and the number of patients disclosing a PZ deficiency did not differ between post-MI patients and controls. The presence of the mutated allele for each polymorphism was associated with a significantly reduced level of PZ. The A-13G polymorphism was associated with premature CAD only in univariate analysis. Whereas, the presence of rare genotypes of PZ gene was an independent risk factor for premature CAD. In conclusion, PZ plasma level is not a key player in the pathophysiology of premature coronary artery disease. But, rare genotypes of PZ gene were found to be associated with premature CAD.


1998 ◽  
Vol 80 (12) ◽  
pp. 878-880 ◽  
Author(s):  
J. W. Eikelboom ◽  
R. Parsons ◽  
R. R. Taylor ◽  
F. M. van Bockxmeer ◽  
R. I. Baker

SummaryThe 20210 G/A prothrombin gene mutation is associated with an increased risk of venous thrombosis but whether there is an association of the mutation with premature coronary artery disease and acute myocardial infarction remains unclear.To further assess the role of the G/A genotype as a risk factor for arterial vascular disease, we performed a case-control study of 644 patients aged less than 50 years with angiographically proven coronary artery disease, 402 of whom had myocardial infarction, and 679 unrelated healthy control subjects aged less than 50 years, randomly selected from the electoral roll.The prevalence of the G/A genotype was 2.5% in patients with coronary artery disease, and 3.2% in control subjects (odds ratio 0.8; 95% confidence interval 0.35 to 1.83). The mutation was not more frequent among patients with a history of myocardial infarction (2.2%, odds ratio 0.7; 95% confidence interval 0.27 to 2.05), and there was no evidence of an interaction between the prothrombin mutation and conventional cardiovascular disease risk factors. There was no association between genotype and extent of angiographic coronary artery disease (p = 0.73).We conclude that the 20210 G/A prothrombin gene mutation is not a major risk factor for premature coronary artery disease in our predominantly Caucasian Australian population.


2021 ◽  
Vol 54 (3) ◽  
pp. 268-272
Author(s):  
Ayaz Mir ◽  
Syed Zia Ullah ◽  
Atif Sher Muhammad ◽  
Faiza Farooq ◽  
Ali Ammar ◽  
...  

Objectives: Premature coronary artery disease (CAD) is on the rise in our population, and multivessel disease (MVD) is no longer an uncommon finding in young patients. Therefore, aim of this study was to determine the predictors of MVD in young patients who presented with ST-Segment Elevation Myocardial Infarction (STEMI). Methodology: For this study, we enrolled 294 young adult (18-40 years) patients with STEMI. MVD was diagnosed based on angiography. Demographic characteristics and baseline risk profiles were considered for the univariate and multivariate analyses to determine the predictors of MVD. Results: Out of 294 patients, 90.5% (266) were males, and the mean age was 35.45 ± 4.07 years. Our 24.1% (71) patients were hypertensive (HTN), and 36.1% (106) were smokers. A total of 94 patients had MVD. Patients with MVD were older and more likely to have diabetes (DM) and HTN than their counterparts. Only age and DM were found to be significant independent predictors of MVD. The risk of developing MVD was higher in diabetics, with adjusted odds ratios (ORs) [95% CI] of 2.47 [1.23-4.97; p=0.011]. Conclusion: In conclusion, we showed that age and DM are independent predictors of MVD in a young Pakistani adult population presenting with STEMI. However, none of the other risk factors, such as obesity, male gender or smoking, were found to be significantly associated with MVD in Pakistani adults with premature CAD. Although significantly associated, HTN does not prove to be an independent predictor of multivessel CAD in young adults.


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