scholarly journals Prevalence of elevated lipoprotein (a) in atherosclerotic cardiovascular disease and its relation to severity of coronary artery disease

2021 ◽  
Vol 73 ◽  
pp. S80
Author(s):  
Abhijeet Kumar ◽  
Kavita Tyagi ◽  
Kushal Madan ◽  
Ashwani Mehta
Author(s):  
Kazuomi Kario ◽  
Satoshi Hoshide ◽  
Keisuke Narita ◽  
Yukie Okawara ◽  
Hiroshi Kanegae ◽  
...  

Resistant hypertension is an important cardiovascular risk factor. This analysis of the JAMP study (Japan Ambulatory Blood Pressure Monitoring Prospective) data investigated the effects of uncontrolled resistant hypertension diagnosed using ambulatory blood pressure (BP) monitoring on the risk of heart failure (HF) and overall cardiovascular events. The JAMP study patients with hypertension and no HF history were included. They had true resistant hypertension (24-hour BP ≥130/80 mm Hg), pseudoresistant hypertension (24-hour BP <130/80 mm Hg), well-controlled nonresistant hypertension (24-hour BP <130/80 mm Hg), or uncontrolled nonresistant hypertension (24-hour BP ≥130/80 mm Hg). The primary end point was total cardiovascular events, including atherosclerotic cardiovascular disease (fatal/nonfatal stroke and fatal/nonfatal coronary artery disease), and HF. During 4.5±2.4 years of follow-up the overall incidence per 1000 person-years was 10.1 for total cardiovascular disease, 4.1 for stroke, 3.5 for coronary artery disease, and 2.6 for HF. The adjusted risk of total cardiovascular and HF events was significantly increased in patients with true resistant versus controlled nonresistant hypertension (hazard ratio, 1.66 [95% CI, 1.12–2.48]; P =0.012 and 2.24 [95% CI, 1.17–4.30]; P =0.015, respectively) and versus uncontrolled nonresistant hypertension (1.51 [1.03–2.20]; P =0.034 and 3.03 [1.58–5.83]; P <0.001, respectively). The findings were robust in a sensitivity analysis using a slightly different definition of resistant hypertension. True resistant hypertension diagnosed using ambulatory BP monitoring is a significant independent risk factor for cardiovascular disease events, especially for HF. This highlights the importance of diagnosing and effectively treating resistant hypertension. Registration: URL: https://www.umin.ac.jp/ctr ; Unique identifier: UMIN000020377.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Pao-Hsien Chu

Background and aims: Elevated lipoprotein(a) is an independent risk factor for atherosclerotic cardiovascular disease especially in familial hypercholesterolemia. The association of elevated lipoprotein(a) within non-familial hypercholesterolemia or healthy population however, is not known. Therefore, we investigated the associations between elevated lipoprotein(a) and the risk of cardiovascular disease in a non-familial hypercholesterolemia clinically healthy young age cohort. Methods: In this retrospective cohort study, we reviewed medical records of 3,427 participants with lipoprotein(a) levels from a tertiary healthcare center in Taiwan. We further classified lipoprotein(a) level into four groups and analyzed cardiovascular events. Results: Our study population had a mean age 46 years old that were 78% male. Mean total cholesterol and low-density lipoprotein level were 195 mg/dL and 118 mg/dL respectively. Overall, 12.9% of the participants had an elevated lipoprotein(a) level (>30 mg/dL), and 2.7% had a very high level (>70 mg/dL). Thirty-three events including 6 participants with stroke and 27 with coronary artery disease were identified. A lipoprotein(a) level >70 mg/dL was associated with a higher risk of coronary artery disease events in Kaplan-Meier analysis. Aging was associated with a higher lipoprotein(a) value in the male participants but not in the female participants. However, the severity of fatty liver was not positively associated with lipoprotein(a) value. Conclusions: Elevated lipoprotein(a) was associated with coronary events but not the severity of fatty liver disease in non-familial hypercholesterolemia clinically healthy population. Aging may be associated with a higher lipoprotein(a) level in males but not females.


1998 ◽  
Vol 44 (8) ◽  
pp. 1827-1832 ◽  
Author(s):  
Ishwarlal Jialal

Abstract Cardiovascular disease is the leading cause of morbidity and mortality in Westernized populations. Evolving lipoprotein risk factors include LDL oxidation and lipoprotein(a) [lp(a)]. Several lines of evidence support a role for oxidatively modified LDL in atherogenesis and its in vivo existence. There are both direct and indirect measures of oxidative stress. The most relevant direct measure of lipid peroxidation is urinary F2 isoprostanes. The most common indirect measure of LDL oxidation is quantifying the lag phase of copper-catalyzed LDL oxidation by assaying conjugated diene formation. Lp(a) is increased in patients with cardiovascular and cerebrovascular disease. However, not all prospective studies have confirmed a positive relationship between Lp(a) and cardiovascular events. Lp(a) appears to present three major problems: standardization of the assay, establishing its role in atherogenesis, and the lack of an effective therapy that can substantially lower Lp(a) concentrations. Thus, at the present time, Lp(a) concentrations should not be recommended for the general population but be reserved for patients with coronary artery disease without established risk factors, young patients with coronary artery disease or cerebrovascular disease, or a family history of premature atherosclerosis and family members of an index patient with increased concentrations of Lp(a). Although both LDL oxidation and Lp(a) are evolving risk factors for cardiovascular disease, more data are needed before they become part of the established lipoprotein repertoire.


2020 ◽  
Vol 126 (9) ◽  
pp. 1159-1177 ◽  
Author(s):  
Krishna G. Aragam ◽  
Pradeep Natarajan

An individual’s susceptibility to atherosclerotic cardiovascular disease is influenced by numerous clinical and lifestyle factors, motivating the multifaceted approaches currently endorsed for primary and secondary cardiovascular disease prevention. With growing knowledge of the genetic basis of atherosclerotic cardiovascular disease—in particular, coronary artery disease—and its contribution to disease pathogenesis, there is increased interest in understanding the potential clinical utility of a genetic predictor that might further refine the assessment and management of atherosclerotic cardiovascular disease risk. Rapid scientific and technological advances have enabled widespread genotyping efforts and dynamic research in the field of coronary artery disease genetic risk prediction. In this review, we describe how genomic analyses of coronary artery disease have been leveraged to create polygenic risk scores. We then discuss evaluations of the clinical utility of these scores, pertinent mechanistic insights gleaned, and practical considerations relevant to the implementation of polygenic risk scores in the health care setting.


2021 ◽  
Vol 15 ◽  
pp. 175394472110512
Author(s):  
Ahmed M. Shafter ◽  
Kashif Shaikh ◽  
Amit Johanis ◽  
Matthew J. Budoff

Atherosclerotic cardiovascular disease (ASCVD) is a common disease among the general population, and includes four major areas: (1) coronary heart disease (CHD), manifested by stable angina, unstable angina, myocardial infarction (MI), heart failure, and coronary death; (2) cerebrovascular disease, manifested by transient ischemia attack and stroke; (3) peripheral vascular disease, manifested by claudication and critical limb ischemia; and (4) aortic atherosclerosis and aortic aneurysm (thoracic and abdominal). CHD remains the leading cause of death for both men and women in the United States. So, it is imperative to identify people at risk of CHD and provide appropriate medical treatment or intervention to prevent serious complications and outcomes including sudden cardiac death. Coronary artery calcification (CAC) is a marker of subclinical coronary artery disease. Therefore, coronary artery calcium score is an important screening method for Coronary artery disease (CAD). In this article, we performed a comprehensive review of current literatures and studies assessing the prognostic value of CAC for future cardiovascular disease (CVD) events. We searched PubMed, MEDLINE, Google Scholar, and Cochrane library. We also reviewed the 2018 American College of Cardiology (ACC)/American Heart Association (AHA) guideline on the assessment of CVD risk. A CAC score of zero corresponds to very low CVD event rates (∼1% per year) and hence a potent negative risk marker. This has been referred to as the ‘power of zero’ and affords the lowest risk of any method of risk calculation. It is now indicated in the 2018 ACC/AHA Cholesterol guidelines to be used to avoid statins for 5–10 years after a score of zero, and then re-assess the patient.


2021 ◽  
Author(s):  
Venexia Walker ◽  
Marijana Vujkovic ◽  
Alice R Carter ◽  
Neil M Davies ◽  
Miriam Udler ◽  
...  

Background: Type 2 diabetes and atherosclerotic cardiovascular disease share several risk factors. However, it is unclear whether the effect of these risk factors on liability to atherosclerotic cardiovascular disease is independent of their effect on liability to type 2 diabetes. Methods: We performed univariate Mendelian randomization to quantify the effects of continuous risk factors from the IEU OpenGWAS database on liability to three outcomes: type 2 diabetes, coronary artery disease, and peripheral artery disease, as well as the effects of liability to type 2 diabetes on the risk factors. We also performed two-step Mendelian randomization for mediation to estimate the mediating pathways between the risk factors, liability to type 2 diabetes, and liability to the atherosclerotic cardiovascular disease outcomes where possible. Results: We found evidence for 53 risk factors as causes of liability to coronary artery disease, including eight which were causes of liability to type 2 diabetes only and four which were consequences only. Except for fasting insulin and hip circumference, the direct and total effects from the two-step Mendelian randomization were similar. This suggests that the combination of these risk factors with liability to type 2 diabetes was unlikely to alter liability to coronary artery disease beyond their individual effects. We also found 13 risk factors that were causes of liability peripheral artery disease, including six which were causes of liability to type 2 diabetes only and four which were consequences only. Again, the direct and total effects were similar for these ten risk factors apart from fasting insulin. Conclusions: Most risk factors were likely to affect liability to atherosclerotic cardiovascular disease independently of their relationship with liability to type 2 diabetes. Control of modifiable risk factors therefore remains important for reducing atherosclerotic cardiovascular disease risk regardless of patient liability to type 2 diabetes.


Cardiology ◽  
2021 ◽  
pp. 1-7
Author(s):  
Kyoung-Ha Park ◽  
Woo Jung Park ◽  
Hyun-Sook Kim ◽  
Sang Ho Jo ◽  
Sung-Ai Kim ◽  
...  

<b><i>Background:</i></b> Endothelial dysfunction is a predictor of atherosclerotic cardiovascular disease (ASCVD) and plays an important role in vasospastic angina (VA). <b><i>Objectives:</i></b> This study evaluated whether flow-mediated dilation (FMD) is also a good marker of 10-year ASCVD risk (10Y-ASCVDR) in patients with VA. <b><i>Methods:</i></b> Based on their clinical history and coronary artery diameter stenosis (DS), patients were retrospectively enrolled into VA (DS &#x3c;50% and positive ergonovine provocation), minor coronary artery disease (mCAD, DS &#x3c;30%), and significant coronary artery disease (sCAD, DS ≥50%) groups. Endothelial function was evaluated by FMD. <b><i>Results:</i></b> Each group contained 50 patients. The 10Y-ASCVDR was significantly higher in the sCAD group than in the VA and mCAD groups (10.86 ± 7.30, 4.71 ± 4.04, and 4.77 ± 4.30, respectively, <i>p</i> &#x3c; 0.001). The FMD was significantly higher in the mCAD group than in the VA and sCAD groups (6.37 ± 4.25, 3.10 ± 2.23, and 3.07 ± 1.89, respectively, <i>p</i> &#x3c; 0.001). A significant correlation was found between the FMD and 10Y-ASCVD in the mCAD group (<i>r</i> = −0.622, <i>p</i> &#x3c; 0.001) and the sCAD group (<i>r</i> = −0.557, <i>p</i> &#x3c; 0.001) but not in the VA group (<i>r</i> = −0.193, <i>p</i> = 0.179). After adjusting for potential confounders such as BMI, C-reactive protein, maximal coronary stenosis, and brachial-ankle pulse wave velocity, multivariate analysis showed that FMD was independently associated with 10Y-ASCVDR in all patients. However, when looking only at the VA group, FMD did not correlate independently with 10Y-ASCVDR. <b><i>Conclusions:</i></b> Unlike mCAD and sCAD, we found no correlation between 10Y-ASCVDR and endothelial function in VA. Thus, our results support that FMD is not a good marker of atherosclerotic cardiovascular risk in VA.


2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.


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