scholarly journals Assessment of Small Dense Low-Density Lipoprotein and Apolipoprotein B/Apolipoprotein A-I Ratio to Predict the Peripheral Arterial Disease in Patients with Hypertension

Author(s):  
Kurniawan Prihutomo ◽  
MID. Pramudianti ◽  
Amiroh Kurniati

Small Dense Low-Density Lipoprotein (sdLDL) and the ApoB/ApoA-I ratio has greater atherogenic potential and is a better marker to predict atherosclerotic blood vessel disease. The purpose of this study was to determine the relationship between the sdLDL and ApoB/ApoA-I ratio to assess the prevalence risk of Peripheral Arterial Disease (PAD) in hypertensive patients. A cross-sectional observational analytic study was performed in 51 hypertension patients with age> 18 years old in Dr. Moewardi Hospital Surakarta from May until June 2018. Patients have measured ABI scores, BMI, blood pressure, lipid profile, ApoB, and ApoA levels. Data were statistically analyzed was using bivariate analysis and multivariate analysis. P-value <0.05 was statistically significant. The prevalence of PAD was 54.90%. Bivariate analysis of age variables (PR: 3.15; 95%Cl: 1.128-8.811; p=0.005), sdLDL (PR: 2; 95%Cl: 0.997-4.013; p=0.03), the ratio of ApoB/ApoA-I (PR: 5.786; 95%Cl: 0.899-37.224; p=0.007), and smoking (PR: 1.896; 95%Cl: 1.210-2.971; p=0.015) was significantly related with PAD. After adjustment of age, smoking, and dyslipidemia variables using multivariate logistic regression analysis, PAD was still related with sdLDL (PR: 10.55; 95%CI: 1.80-61.73; p=0.009), age (PR: 11. 61; 95%CI: 1.83-61.73; p=0.009), and smoking (PR: 11.96; 95%CI: 1.71-83.81; p= 0.013). sdLDL and ApoB/ApoA-I ratio were related to PAD. However, sdLDL, age, and smoking are independent variables of PAD in hypertension patients.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M.R Poudel ◽  
S Kirana ◽  
D Stoyanova ◽  
K.P Mellwig ◽  
D Hinse ◽  
...  

Abstract Background Elevated lipoprotein (a) [LP (a)] levels are an independent, genetic, and causal factor for cardiovascular disease and associated with myocardial infarction (MI). Although the association between circulating levels of lipoprotein(a) [Lp(a)] and risk of coronary artery disease (CAD) is well established, its role in risk of peripheral arterial disease (PAD) remains unclear. PAD affects over 236 million individuals and follows ischaemic heart disease (IHD) and cerebrovascular disease (CVD) as the third leading cause of atherosclerotic cardiovascular morbidity worldwide. LP (a) is genetically determined, stable throughout life and yet refractory to drug therapy. While 30 mg/dl is considered the upper normal value for LP (a) in central Europe, extremely high LP (a) levels (&gt;150mg/dl) are rare in the general population. The aim of our study was to analyse the correlation between lipoprotein (a) [LP (a)] levels and an incidence of PAD in high-risk patients. Patients and methods We reviewed the LP (a) concentrations of 52.898 consecutive patients admitted to our cardiovascular center between January 2004 and December 2014. Of these, 579 patients had LP (a) levels above 150 mg/dl (mean 181.45±33.1mg/dl). In the control collective LP (a) was &lt;30mg/dl (n=350). Other atherogenic risk factors in this group were HbA1c 6.58±1.65%, low density lipoprotein (LDL) 141.99±43.76 mg/dl, and body mass index 27.81±5.61. 54.40% were male, 26.07% were smokers, 93.2% had hypertension, and 24% had a family history of cardiovascular diseases. More than 82.6% were under statins. The mean glomerular filtration rate (GFR) was 69.13±24.8 ml/min [MDRD (Modification of Diet in Renal Disease)]. Results 45.00% (n=261) of the patients with LP (a) &gt;150mg/dl had PAD. The prevalence of PAD in patients with LP (a) &lt;30mg/dl in our control collective was 15.8%. (P- Value 0.001). Patients with LP (a) &gt;150mg/dl had a significantly increased risk for PAD (Odds ratio 4.36, 95% CI 2.94–6.72, p: 0.001). 19.1% of patients were re-vascularized by percutaneous angioplasty (PTA) and 7.09% of patients had to undergo peripheral vascular bypass (PVB). Mean LP (a) level in patients with PAD was 182.6±31.61. Conclusion Elevated LP (a) levels above 150 mg/dl are associated with a significantly increased risk of PAD in our collective and it confirms our hypothesis. Over one fourth of these patients had severe PAD and requiring revascularization therapy. We need more prospective studies to confirm our findings. Funding Acknowledgement Type of funding source: None


2002 ◽  
Vol 6 (6) ◽  
pp. 467-470 ◽  
Author(s):  
Motohiro Kamimura ◽  
Masaki Matsuo ◽  
Takashi Miyahara ◽  
Karue Kimura ◽  
Kimiyo Matsumoto ◽  
...  

Clinics ◽  
2010 ◽  
Vol 65 (4) ◽  
pp. 383-387 ◽  
Author(s):  
Ruben Miguel Ayzin Rosoky ◽  
Nelson Wolosker ◽  
Michel Nasser ◽  
Antonio Eduardo Zerati ◽  
Magnus Gidlund ◽  
...  

Vascular ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 193-200 ◽  
Author(s):  
Ralph G. DePalma ◽  
Virginia W. Hayes ◽  
Patricia E. May ◽  
H. Treat Cafferata ◽  
Hamid A. Mohammadpour ◽  
...  

This exploratory substudy of The Iron (Fe) and Atherosclerosis Study (FeAST) compared baseline inflammatory markers, including cytokines, C-reactive protein (CRP), and ferritin, in subjects with peripheral arterial disease (PAD) taking statins with subjects with PAD who were not taking statins. Inflammatory markers in the serum of 47 subjects with PAD not taking statins and a healthy cohort of 21 medication-free men were compared with 53 PAD subjects taking statins at entry to the FeAST. Healthy subjects demonstrated lower levels of tumor necrosis factor (TNF)-R1, interleukin-6 (IL-6), and CRP. TNF-α R1 averaged 2.28 ng/mL versus 3.52 ng/mL, p  =  .0025; IL-6 averaged 4.24 pg/mL versus16.61 pg/mL, p  =  .0008; and CRP averaged 0.58 mg/dL versus 0.92 mg/dL, p  =  .0192. A higher level of IL-6 was observed in PAD statin takers versus PAD subjects not taking statins: 19.47 pg/mL versus 13.24 pg/mL, p  =  .0455. As expected, total cholesterol and low-density lipoprotein levels were lower in the statin-treated group, p  =  .0006 and p  =  .0001, respectively. No significant differences in inflammatory cytokines were detected for varying doses of simvastatin. Additionally, no significant differences in inflammatory biomedical markers were found in subjects with PAD alone compared with those with concomitant coronary artery disease (CAD). Unexpectedly, serum inflammatory cytokine IL-6 levels were significantly higher in PAD subjects receiving statins. There was no difference in measured inflammatory markers in PAD subjects with concomitant CAD.


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