Association between 10-Year Atherosclerotic Cardiovascular Disease Risk and Vascular Endothelial Function in Patients with Vasospastic Angina

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.

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.


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.


2020 ◽  
Vol 13 (Suppl_1) ◽  
Author(s):  
Muhammed Atere ◽  
William Lim ◽  
Vishnuveni Leelaruban ◽  
Bhavya Narala ◽  
Stephanie Herrera ◽  
...  

Background: Cardiovascular disease is the leading cause of mortality in the United States. Approximately 25% of total deaths in the United States are attributed to cardiovascular diseases. Modification of risk factors has been shown to reduce mortality and morbidity in people with coronary artery disease. Medications such as statins are well known for reducing risks and recent data has shown that statins are beneficial in the primary prevention of coronary artery disease. The purpose of this study is to assess whether statins are being prescribed on discharge to patients who are identified as intermediate to high risk using the ACC/AHA Pooled Cohort Equations. Methodology: We reviewed and analyzed the charts of hospitalized patient’s ages 40 to 79 years who were discharged under the service of Internal Medicine at Richmond University Medical Center from September 2018 to August 2019. Exclusion criteria included: patients that expired before discharge or were admitted to the intensive or coronary care units, pregnancy, previous diagnosis of coronary/peripheral artery disease or stroke, already on statins or lipid-lowering medications, allergic to statins, discharged on statins for coronary/peripheral artery disease or stroke, and patients with liver disease or elevated liver enzymes. We used the ACC/AHA Pooled Cohort Equations risk to calculate the 10-year coronary artery disease risk for each patient. Results: The 10-year risk is grouped as low risk (<5%), borderline risk (5% to 7.4%), intermediate risk (7.5% to 19.9%) and high risk (≥20%). Among 898 patients, 10% had intermediate and high risk that were not discharged with statins. Among the 10%, about 6.6% were intermediate risk and 3.4% were high risk. Conclusions: A significant number of intermediate and high-risk patients were discharged without statins, although a CT coronary calcium may be helpful in further classifying the risk in some of them. We believe that a lipid profile should be checked in all hospitalized patients 40 years and older in order to calculate their atherosclerosis cardiovascular disease risk score and to possibly initiate statins after discussing the benefits and side effects, particularly in the intermediate risk group. The continuation of statins would be followed up by their primary care physicians. We plan to liaise with the information technology department in our facility to provide a link to the risk calculator in the electronic medical record so that the risk can be calculated and statins initiated as necessary. We will conduct a follow up review to assess for effectiveness.


Circulation ◽  
2021 ◽  
Author(s):  
Tiffany M. Powell-Wiley ◽  
Paul Poirier ◽  
Lora E. Burke ◽  
Jean-Pierre Després ◽  
Penny Gordon-Larsen ◽  
...  

The global obesity epidemic is well established, with increases in obesity prevalence for most countries since the 1980s. Obesity contributes directly to incident cardiovascular risk factors, including dyslipidemia, type 2 diabetes, hypertension, and sleep disorders. Obesity also leads to the development of cardiovascular disease and cardiovascular disease mortality independently of other cardiovascular risk factors. More recent data highlight abdominal obesity, as determined by waist circumference, as a cardiovascular disease risk marker that is independent of body mass index. There have also been significant advances in imaging modalities for characterizing body composition, including visceral adiposity. Studies that quantify fat depots, including ectopic fat, support excess visceral adiposity as an independent indicator of poor cardiovascular outcomes. Lifestyle modification and subsequent weight loss improve both metabolic syndrome and associated systemic inflammation and endothelial dysfunction. However, clinical trials of medical weight loss have not demonstrated a reduction in coronary artery disease rates. In contrast, prospective studies comparing patients undergoing bariatric surgery with nonsurgical patients with obesity have shown reduced coronary artery disease risk with surgery. In this statement, we summarize the impact of obesity on the diagnosis, clinical management, and outcomes of atherosclerotic cardiovascular disease, heart failure, and arrhythmias, especially sudden cardiac death and atrial fibrillation. In particular, we examine the influence of obesity on noninvasive and invasive diagnostic procedures for coronary artery disease. Moreover, we review the impact of obesity on cardiac function and outcomes related to heart failure with reduced and preserved ejection fraction. Finally, we describe the effects of lifestyle and surgical weight loss interventions on outcomes related to coronary artery disease, heart failure, and atrial fibrillation.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Iulia Iatan ◽  
Zari Dastani ◽  
Ron Do ◽  
Swneke D. Bailey ◽  
Isabelle Ruel ◽  
...  

Low plasma HDL-C is a well-established risk factor for coronary artery disease. The role of endothelial lipase (EL) in HDL metabolism has been recently characterized. The proprotein convertase subtilisin/kexin 5 (PC5/6 or PCSK5) is known to inactivate both EL and lipoprotein lipase (LPL) ex vivo , enzymes critical in modulating plasma levels of HDL-C. In the present study, we investigated the role of human PCSK5 genetic variants on HDL-C; in addition, we characterized lipoprotein fractions in Pcsk5 +/− mice, compared with wild type. Sequencing of the PCSK5 gene was performed in 12 probands with low HDL-C (<5 th percentile) and 7 novel non-coding genetic variants were found. We genotyped these SNPs along with 163 tag SNPs and 12 additional SNPs (n=182 total) selected from the HapMap Project, in 457 individuals with documented coronary artery disease. We identified 10 SNPs associated with HDL-C (p<0.05), with the strongest result being rs11144782 (minor allele frequency: 0.164, p=0.002). In an analysis of HDL-C as a dichotomous trait, 3 of the 10 SNPs were also associated with low HDL-C at either the 5 th or the 10 th percentile (p<0.05). The rare allele of rs111447782 decreased HDL by 0.076 mmol/L in a gene dosage-dependent fashion. We further investigated the effect of this SNP on other lipoprotein levels and identified an association with very low density lipoprotein (p=0.039), triglycerides (p=0.049) and total ApoB (p=0.022) levels. Furthermore, in conditional regression analysis, we identified 3 additional SNPs contributing to HDL-C (p<0.05), all independent of the effect of rs11144782. In addition, we characterized serum from Pcsk5 KO mice. Serum from Pcsk5 +/− mice ( Pcsk5 −/− is embryonic lethal) showed reduction in HDL-C by gel permeation chromatography on HPLC and size redistribution of HDL species by 1D and 2D PAGGE. These results, and the rs11144782 SNP result presented above, are consistent with the concept that PCSK5 modulates HDL, likely upstream of EL and LPL. We conclude that variability at the PCSK5 gene locus influences HDL-C levels and consequently, atherosclerotic cardiovascular disease risk.


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