scholarly journals High-sensitivity C-reactive Protein, Lipoprotein(a) and Homocysteine are Risk Factors for Coronary Artery Disease in Japanese Patients with Peripheral Arterial Disease

2015 ◽  
Vol 22 (4) ◽  
pp. 344-354 ◽  
Author(s):  
Hisao Kumakura ◽  
Kishu Fujita ◽  
Hiroyoshi Kanai ◽  
Yoshihiro Araki ◽  
Yoshiaki Hojo ◽  
...  
2002 ◽  
Vol 144 (3) ◽  
pp. 449-455 ◽  
Author(s):  
Walter S. Speidl ◽  
Senta Graf ◽  
Stefan Hornykewycz ◽  
Mariam Nikfardjam ◽  
Alexander Niessner ◽  
...  

2017 ◽  
Vol 11 (2) ◽  
pp. 79-84
Author(s):  
Syed Dawood Md Taimur ◽  
Mashhud Zia Chowdhury ◽  
Md Enamul Hakim

Background: Peripheral arterial disease (PAD) is under diagnosed in primary care practices, yet the extent of unrecognized PAD in patients with coronary artery disease (CAD) is unknown.Objective: To assess the prevalence of previously unrecognized PAD in patients undergoing coronary angiogram and to determine the relationship between presence of PAD and severity of CAD. Material &Methods: This five years retrospective study was conducted at invasive lab of the department of Cardiology, Ibrahim Cardiac Hospital & Research Institute, Dhaka, Bangladesh from January 2010 to December 2014. Total 77 patients were included in this study. Study variables were age, sex, risk factors like hypertension, diabetes mellitus, dyslipidaemia, smoking habit and positive family history for ischemic heart disease, severity of coronary artery and peripheral artery disease.Results: Mean age was 56.83±13.64 years, Male mean age was 53.98±15.08 years and female mean age was 54.5±1.73years. Hypertension were detected in 55.8%, diabetes in 87%, dyslipidaemia in 81.8%, smoking habits in 88.3% and 58.4% had positive family history. After catheterization 88.3% had peripheral arterial disease and 71.4% had coronary artery disease. Out of 77 patients 52 had both coronary and peripheral arterial disease which was statistically significant (p<.014). Coronary angiogram revealed 28.6% (22) patients had triple vessel disease, 23.3% (18) had single vessel disease, 19.5% (15) had double vessel disease and 28.6% (22) were normal coronary arteries. Peripheral angiogram revealed 51.9% had superficial femoral artery disease, 24.7% had anterior tibial artery disease, 26% had posterior tibial artery disease, 15.6% had common iliac artery and common femoral artery disease and 2.6% had renal artery disease.Conclusion: There is a strong and definite correlation between coronary and peripheral arterial disease. We found that cardiovascular risk factors were in fact risk factors for both PAD and CAD.University Heart Journal Vol. 11, No. 2, July 2015; 79-84


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Heidi T May ◽  
Jeffrey L Anderson ◽  
Benjamin D Horne ◽  
Robert R Pearson ◽  
Robert L Wolfert ◽  
...  

Background : Inflammation plays a role in the development and progression of coronary artery disease (CAD), with circulating markers of vascular inflammation being used in risk assessment including high sensitivity C-reactive protein (hsCRP) and lipoprotein-associated phospholipase A 2 (LpPLA 2 ). While hsCRP responds to the systemic inflammatory stimulus of acute myocardial infarction (AMI), LpPLA 2 has been proposed to be more vascular-specific and to vary minimally based upon clinical presentation. To test this hypothesis, we evaluated both biomarkers among CAD patients presenting with stable angina (SA), unstable angina (USA) or acute myocardial infarction (AMI). Methods : LpPLA 2 (PLAC TM test, diaDexus, Inc.) and hsCRP were measured from samples donated by consenting patients (N=1,010) enrolled in the registry of the Intermountain Heart Collaborative Study that underwent angiographic evaluation for CAD. Patients were categorized by presentation status (SA=637; USA=205; and AMI=168), stratified according to median levels of LpPLA 2 (350.2 ng/mL) and hsCRP above and below 3 mgl/L and followed for 7.5 ± 2.4 years for CAD death. Results : Age averaged 64 ± 12 years and 70% were male. While median hsCRP (mg/L) levels differed significantly by presentation [2.86, 2.80, and 13.7 for SA, USA, and AMI, respectively (p<0.0001)], median LpPLA 2 (ng/mL) levels [350.2, 353.1, and 348.1 for SA, USA, and AMI, respectively (p=0.67)], did not. LpPLA 2 was not only a better predictor of CAD death among the entire cohort (LpPLA 2 : adjusted Hazard Ratio [HR]= 1.47, p=0.04; hsCRP: adjusted HR=0.95, p=0.81), it was a better predictor among patients presenting with AMI (LpPLA 2 : adjusted HR3 1.80, p=0.30; hsCRP adjusted HR=0.76, p=0.63). Conclusions : Among CAD patients, LpPLA 2 varies minimally among differing presentations compared to hsCRP and is a better a predictor of CAD death among those presenting with AMI. This information supports the hypothesis that LpPLA 2 is a vascular specific marker of inflammation and independent of transient systemic inflammatory effects.


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