Japan Atherosclerosis Society (JAS) Guidelines for Prevention of Atherosclerotic Cardiovascular Diseases 2017

In the paper

“It is also increased in patients who suffer from hypertension, diabetes, metabolic syndromes, sleep apnea syndrome (SAS), smoking, stress caused by disasters, etc., but at the same time, it has been reported that the CAVI improves with treatment of these contributing factors25).”

What the sources say

• Not checked yetcites [25] 25) Saiki A, Sato Y, Watanabe R, Watanabe Y, Imamura H, Yamaguchi T, Ban N, Kawana H, Nagumo A, Nagayama D, Ohira M, Endo K, Tatsuno I. The role of a novel arterial stiffness parameter, cardio-ankle vascular index (CAVI), as a surrogate marker for cardiovascular diseases. J Atheroscler Thromb, 2016; 23: 155-168 source

In the paper

“in comparison with the LDL-C < 80 mg/dL group, the risk was increased by 1.4 times in the 80–99 mg/dL group, 1.7 times in the 100–119 mg/dL group, 2.2 times in the 120–139 mg/dL group, and 2.8 times in the ≥ 140 mg/dL group37).”

What the sources say

• Not checked yetcites [37] 37) Imano H, Noda H, Kitamura A, Sato S, Kiyama M, Sankai T, Ohira T, Nakamura M, Yamagishi K, Ikeda A, Shimamoto T, Iso H. Low-density lipoprotein cholesterol and risk of coronary heart disease among Japanese men and women: The Circulatory Risk in Communities Study (CIRCS). Prev Med, 2011; 52: 381-386 source

In the paper

“When the TC level was ≥ 240 mg/dL, even though the hazard ratio further increased to 1.79 times, the PAF dropped to 11.9%.”

In the paper

“Among the types of stroke, LDL-C has been shown to be positively related to cerebral infarction and negatively related to hemorrhagic stroke”

In the paper

“A 24-year follow-up in NIPPON DATA80 showed that the hazard ratio for CAD death was 1.55 times higher in the TC ≥ 220 mg/dL group than in the TC < 220 mg/dL group, and the population attributable fraction (PAF) was 18.2%54).”

What the sources say

• Not checked yetcites [54] 54) Sugiyama D, Okamura T, Watanabe M, Higashiyama A, Okuda N, Nakamura Y, Hozawa A, Kita Y, Kadota A, Murakami Y, Miyamatsu N, Ohkubo T, Hayakawa T, Miyamoto Y, Miura K, Okayama A, Ueshima H. Risk of hypercholesterolemia for cardiovascular disease and the population attributable fraction in a 24-year Japanese cohort study. J Atheroscler Thromb, 2015; 22: 95-107 source

In the paper

“Regarding stroke, it has been shown that TC is positively related to cerebral infarction and negatively related to hemorrhagic stroke, a result that many studies have in common.”

In the paper

“Elevated LDL-C predicts the CAD incidence and mortality in the future.”

In the paper

“The association between TC and the incidence/mortality rate of CAD is almost linear, but a statistically significant increase in risk with TC levels around 220 mg/dL has been observed in many studies.”

In the paper

“Although a relationship between TC and risk of CAD death was seen in both the men and women, some reports have stated that this relation is attenuated in elderly individuals who are ≥ 65 years old55).”

What the sources say

• Not checked yetcites [55] 55) Nagasawa SY, Okamura T, Iso H, Tamakoshi A, Yamada M, Watanabe M, Murakami Y, Miura K, Ueshima H. Relation between serum total cholesterol level and cardiovascular disease stratified by sex and age group: A pooled analysis of 65 594 individuals from 10 cohort studies in Japan. J Am Heart Assoc, 2012; 1: e001974 source

In the paper

“There are reports saying that the association is unclear51, 67), and there are also those that revealed an increase in risk when non-HDL-C levels were low70).”

What the sources say

• Not checked yetcites [51] 51) Tanabe N, Iso H, Okada K, Nakamura Y, Harada A, Ohashi Y, Ando T, Ueshima H, Japan Arteriosclerosis L. Serum total and non-high-density lipoprotein cholesterol and the risk prediction of cardiovascular events - the JALS-ECC. Circ J, 2010; 74: 1346-1356 source
• Not checked yetcites [67] 67) Imamura T, Doi Y, Ninomiya T, Hata J, Nagata M, Ikeda F, Mukai N, Hirakawa Y, Yoshida D, Fukuhara M, Kitazono T, Kiyohara Y. Non-high-density lipoprotein cholesterol and the development of coronary heart disease and stroke subtypes in a general Japanese population: The Hisayama study. Atherosclerosis, 2014; 233: 343-348 source
• Not checked yetcites [70] 71) Kitamura A, Noda H, Nakamura M, Kiyama M, Okada T, Imano H, Ohira T, Sato S, Yamagishi K, Iso H. Association between non-high-density lipoprotein cholesterol levels and the incidence of coronary heart disease among Japanese: The Circulatory Risk in Communities Study (CIRCS). J Atheroscler Thromb, 2011; 18: 454-463 source

In the paper

“In all of these studies, the risk of onset and risk of death were evidently increased when non-HDL-C levels were ≥ 170–180 mg/dL or more, but there was no fixed trend observed in the women51, 64, 71, 73).”

What the sources say

• Not checked yetcites [51] 51) Tanabe N, Iso H, Okada K, Nakamura Y, Harada A, Ohashi Y, Ando T, Ueshima H, Japan Arteriosclerosis L. Serum total and non-high-density lipoprotein cholesterol and the risk prediction of cardiovascular events - the JALS-ECC. Circ J, 2010; 74: 1346-1356 source
• Not checked yetcites [64] 64) Okamura T, Kokubo Y, Watanabe M, Higashiyama A, Miyamoto Y, Yoshimasa Y, Okayama A. Low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol and the incidence of cardiovascular disease in an urban Japanese cohort study: The Suita study. Atherosclerosis, 2009; 203: 587-592 source
• Not checked yetcites [71] 72) Tanaka F, Makita S, Onoda T, Tanno K, Ohsawa M, Itai K, Sakata K, Omama S, Yoshida Y, Ogasawara K, Ogawa A, Ishibashi Y, Kuribayashi T, Okayama A, Nakamura M. Predictive value of lipoprotein indices for residual risk of acute myocardial infarction and sudden death in men with low-density lipoprotein cholesterol levels <120 mg/dl. Am J Cardiol, 2013; 112: 1063-1068 source

In the paper

“A low HDL-C level is a risk for developing CAD and ischemic stroke. On the contrary, the risk decreases when HDL-C levels are high39, 53, 76–79).”

What the sources say

• Not checked yetcites [39] 39) Yokokawa H, Yasumura S, Tanno K, Ohsawa M, Onoda T, Itai K, Sakata K, Kawamura K, Tanaka F, Yoshida Y, Nakamura M, Terayama Y, Ogawa A, Okayama A. Serum low-density lipoprotein to high-density lipoprotein ratio as a predictor of future acute myocardial infarction among men in a 2.7-year cohort study of a Japanese northern rural population. J Atheroscler Thromb, 2011; 18: 89-98 source
• Not checked yetcites [53] 53) Kitamura A, Iso H, Naito Y, Iida M, Konishi M, Folsom AR, Sato S, Kiyama M, Nakamura M, Sankai T, Shimamoto T, Komachi Y. High-density lipoprotein cholesterol and premature coronary heart disease in urban Japanese men. Circulation, 1994; 89: 2533-2539 source
• Not checked yetcites [76] 77) Soyama Y, Miura K, Morikawa Y, Nishijo M, Nakanishi Y, Naruse Y, Kagamimori S, Nakagawa H. High-density lipoprotein cholesterol and risk of stroke in Japanese men and women: The Oyabe Study. Stroke, 2003; 34: 863-868 source
• Not checked yetcites [77] 78) Iso H, Sato S, Kitamura A, Imano H, Kiyama M, Yamagishi K, Cui R, Tanigawa T, Shimamoto T. Metabolic syndrome and the risk of ischemic heart disease and stroke among Japanese men and women. Stroke, 2007; 38: 1744-1751 source
• Not checked yetcites [78] 79) Satoh H, Tomita K, Fujii S, Kishi R, Tsutsui H. Lower high-density lipoprotein cholesterol is a significant and independent risk for coronary artery disease in Japanese men. J Atheroscler Thromb, 2009; 16: 792-798 source
• Not checked yetcites [79] 80) Okamura T, Hayakawa T, Kadowaki T, Kita Y, Okayama A, Ueshima H, NIPPON DATA90 Research Group. The inverse relationship between serum high-density lipoprotein cholesterol level and all-cause mortality in a 9.6-year follow-up study in the Japanese general population. Atherosclerosis, 2006; 184: 143-150 source

In the paper

“But at the same time, there are reports stating that an association does not exist in regard to stroke.”

In the paper

“Compared to nonsmokers, smokers face a higher risk for CAD and stroke, and there is a dose-response relationship in this association102).”

What the sources say

• Not checked yetcites [102] 103) Kono S, Ikeda M, Tokudome S, Nishizumi M, Kuratsune M. Smoking and mortalities from cancer, coronary heart disease and stroke in male Japanese physicians. J Cancer Res Clin Oncol, 1985; 110: 161-164 source

In the paper

“there have been many reports on hypertriglyceridemia being a risk factor for ischemic stroke, though the association is weaker than that with CAD46, 65, 87, 93–95).”

What the sources say

• Not checked yetcites [46] 46) Noda H, Iso H, Saito I, Konishi M, Inoue M, Tsugane S, JPHC Study Group. The impact of the metabolic syndrome and its components on the incidence of ischemic heart disease and stroke: The Japan Public Health Center-based study. Hypertens Res, 2009; 32: 289-298 source
• Not checked yetcites [65] 65) Okamura T, Kokubo Y, Watanabe M, Higashiyama A, Ono Y, Miyamoto Y, Yoshimasa Y, Okayama A. Triglycerides and non-high-density lipoprotein cholesterol and the incidence of cardiovascular disease in an urban Japanese cohort: The Suita study. Atherosclerosis, 2010; 209: 290-294 source
• Not checked yetcites [87] 88) Iso H, Naito Y, Sato S, Kitamura A, Okamura T, Sankai T, Shimamoto T, Iida M, Komachi Y. Serum triglycerides and risk of coronary heart disease among Japanese men and women. Am J Epidemiol, 2001; 153: 490-499 source

In the paper

“some reports have stated that its ability to predict the risk for cardiovascular events is higher using blood collected in a nonfasting state91).”

What the sources say

• Not checked yetcites [91] 92) Castelli WP. Lipids, risk factors and ischaemic heart disease. Atherosclerosis, 1996; 124 Suppl: S1-9 source

In the paper

“Passive smoking is a risk factor for CAD and stroke.”

In the paper

“Smoking is a risk factor for CAD, stroke, abdominal aortic aneurysm and peripheral artery disease (PAD).”

In the paper

“A comparison between subjects with hypertension and those without hypertension in the lipid intervention study J-LIT showed that the relative risk for CAD in primary prevention subjects was 2.05 times higher in women and 2.15 times in men124).”

What the sources say

• Not checked yetcites [124] 125) Kannel WB, McGee DL. Diabetes and glucose tolerance as risk factors for cardiovascular disease: The Framing-ham study. Diabetes Care, 1979; 2: 120-126 source

In the paper

“Silent myocardial ischemia often coexists in diabetic patients, and this may result in delayed diagnosis132).”

What the sources say

• Not checked yetcites [132] 133) Goraya TY, Leibson CL, Palumbo PJ, Weston SA, Killian JM, Pfeifer EA, Jacobsen SJ, Frye RL, Roger VL. Coronary atherosclerosis in diabetes mellitus: A population-based autopsy study. J Am Coll Cardiol, 2002; 40: 946-953 source

In the paper

“the incidence rate of CAD was 5.0/1,000 person-years for diabetic patients and 1.6/1,000 person-years for subjects with normal glucose tolerance (NGT).”

What the sources say

• Not checked yetcites [128] 129) Iso H, Imano H, Kitamura A, Sato S, Naito Y, Tanigawa T, Ohira T, Yamagishi K, Iida M, Shimamoto T. Type 2 diabetes and risk of non-embolic ischaemic stroke in Japanese men and women. Diabetologia, 2004; 47: 2137-2144 source

In the paper

“it has been revealed in a meta-analysis that the relative risks for CAD and stroke are 1.31115) and 1.25116), respectively.”

What the sources say

• Not checked yetcites [115] 116) Oono IP, Mackay DF, Pell JP. Meta-analysis of the association between secondhand smoke exposure and stroke. J Public Health (Oxf), 2011; 33: 496-502 source
• Not checked yetcites [116] 117) Pan A, Wang Y, Talaei M, Hu FB, Wu T. Relation of active, passive, and quitting smoking with incident type 2 diabetes: a systematic review and meta-analysis. Lancet Diabetes Endocrinol, 2015; 3: 958-967 source

In the paper

“The estimation by EPOCH-JAPAN showed a death rate of 50% from all forms of cerebro- and CVD, 52% from stroke and 59% from CAD. They were all assessed to be caused by high BPs that exceed the optimum level.”

What the sources say

• Not checked yetcites [123] 124) Sasaki J, Kita T, Mabuchi H, Matsuzaki M, Matsuzawa Y, Nakaya N, Oikawa S, Saito Y, Shimamoto K, Kono S, Itakura H; J-LIT Study Group. Gender difference in coronary events in relation to risk factors in Japanese hypercholesterolemic patients treated with low-dose simvastatin. Circ J, 2006; 70: 810-814 source

In the paper

“the incidence rate of cerebral infarction was 6.5/1,000 person-years in diabetic subjects, that significantly higher than the 1.9/1,000 personyears in subjects with NGT128).”

What the sources say

• Not checked yetcites [128] 129) Iso H, Imano H, Kitamura A, Sato S, Naito Y, Tanigawa T, Ohira T, Yamagishi K, Iida M, Shimamoto T. Type 2 diabetes and risk of non-embolic ischaemic stroke in Japanese men and women. Diabetologia, 2004; 47: 2137-2144 source

In the paper

“the relative risk of getting stroke and stroke-related death was 1.41 times higher for those who smoke ≤ 20 cigarettes a day and 1.56 times for those who exceed 20 sticks112).”

What the sources say

• Not checked yetcites [112] 113) Katanoda K, Marugame T, Saika K, Satoh H, Tajima K, Suzuki T, Tamakoshi A, Tsugane S, Sobue T. Population attributable fraction of mortality associated with tobacco smoking in Japan: A pooled analysis of three large-scale cohort studies. J Epidemiol, 2008; 18: 251-264 source

In the paper

“Even in cross-sectional studies conducted in Japan, the proportion of PAD, as determined using the ABI, was shown to be 3.7 times higher in current smokers (4.2 times for those with ≥ 45 pack-years) and 3.7 times in ex-smokers.”

What the sources say

• Not checked yetcites [114] 115) Barnoya J, Glantz SA. Cardiovascular effects of secondhand smoke: Nearly as large as smoking. Circulation, 2005; 111: 2684-2698 source

In the paper

“A meta-analysis has shown that smokers have lower HDL-C levels and higher LDL-C and TG levels, and the dose-response relationship has again been observed119).”

What the sources say

• Not checked yetcites [119] 120) Ministry of Health, Labour and Welfare of Japan. Review conference on the health impacts of smoking. Segment 5 health impacts of smoke-free tobacco and electronic cigarettes. http://www.mhlw.go.jp/file/05-Shingikai-10901000Kenkoukyoku-Soumuka/0000172687.pdf

In the paper

“Compared to lifetime nonsmokers, the relative risk for developing CAD and death from it was 2.15 times higher for those who smoke ≤ 20 cigarettes a day and 3.28 times for those who smoke > 20 sticks in a meta-analysis.”

In the paper

“the hazard ratio for cerebro- and cardiovascular disease-related death increases progressively with an elevation of BP levels that exceed the optimal level (< 120/80 mmHg). This association was stronger in the middle-aged adults than in the elderly123).”

What the sources say

• Not checked yetcites [123] 124) Sasaki J, Kita T, Mabuchi H, Matsuzaki M, Matsuzawa Y, Nakaya N, Oikawa S, Saito Y, Shimamoto K, Kono S, Itakura H; J-LIT Study Group. Gender difference in coronary events in relation to risk factors in Japanese hypercholesterolemic patients treated with low-dose simvastatin. Circ J, 2006; 70: 810-814 source

In the paper

“It has been estimated that 13% adults in Japan have CKD155)”

What the sources say

• Not checked yetcites [155] 156) Joint Committee for Comprehensive Risk Management Chart for the Prevention of Cerebro- Cardiovascular Diseases, Comprehensive risk management for the prevention of cerebro- cardiovascular diseases in Japan. J Atheroscler Thromb, 2017; 24: 749-764 source

In the paper

“As the risk of these composite outcomes differs greatly depending on the cause, GFR and amount of proteinuria (albuminuria), the severity of CKD is classified (CGA classification)153, 154) using these three primary factors.”

What the sources say

• Not checked yetcites [153] 154) Japanese Society of Nephrology. Health guidance for the examinees of kidney medical checkup and suggestions to the referral criteria to medical institutions. 2017; 59: 38-42 (in Japanese)
• Not checked yetcites [154] 155) Imai E, Horio M, Watanabe T, Iseki K, Yamagata K, Hara S, Ura N, Kiyohara Y, Moriyama T, Ando Y, Fujimoto S, Konta T, Yokoyama H, Makino H, Hishida A, Matsuo S. Prevalence of chronic kidney disease in the Japanese general population. Clin Exp Nephrol, 2009; 13: 621-630 source

In the paper

“Features of coronary lesions in diabetic patients include (1) multiple-vessel disease, (2) highly complicated and diffuse133, 134) and (3) multiple calcified lesions135).”

What the sources say

• Not checked yetcites [133] 134) Kataoka Y, Yasuda S, Morii I, Otsuka Y, Kawamura A, Miyazaki S. Quantitative coronary angiographic studies of patients with angina pectoris and impaired glucose tolerance. Diabetes Care, 2005; 28: 2217-2222 source
• Not checked yetcites [134] 135) Hoff JA, Quinn L, Sevrukov A, Lipton RB, Daviglus M, Garside DB, Ajmere NK, Gandhi S, Kondos GT. The prevalence of coronary artery calcium among diabetic individuals without known coronary artery disease. J Am Coll Cardiol, 2003; 41: 1008-1012 source
• Not checked yetcites [135] 136) Cui R, Iso H, Yamagishi K, Saito I, Kokubo Y, Inoue M, Tsugane S. Diabetes mellitus and risk of stroke and its subtypes among Japanese: The Japan public health center study. Stroke, 2011; 42: 2611-2614 source

In the paper

“But in diabetic patients, it has been reported that the increase in relative risk of CAD was higher in women than men, resulting in reduced gender differences149, 150).”

What the sources say

• Not checked yetcites [149] 150) Peters SA, Huxley RR, Woodward M. Diabetes as a risk factor for stroke in women compared with men: A systematic review and meta-analysis of 64 cohorts, including 775,385 individuals and 12,539 strokes. Lancet, 2014; 383: 1973-1980 source
• Not checked yetcites [150] 151) Fujihara K, Igarashi R, Yamamoto M, Ishizawa M, Matsubayasi Y, Matsunaga S, Kato K, Ito C, Koishi M, Yamanaka N, Kodama S, Sone H. Impact of glucose tolerance status on the development of coronary artery disease among working-age men. Diabetes Metab, 2017; 43: 261-264 source

In the paper

“according to the vital statistics of 2014, the (approximate) rate of mortality due to ischemic heart disease in a target population of 100,000 is 49.8 for men and 36.6 for women.”

In the paper

“Women have a lower risk for MI and MI-related death than men, but the gender difference decreases with aging.”

In the paper

“According to a large-scale cohort study in Canada157), the association between LDL-C and ASCVD is lower when eGFR is lower, and the association was no longer significant when eGFR was < 15 mL/min/1.73 m2.”

What the sources say

• Not checked yetcites [157] 158) Wanner C, Krane V, Marz W, Olschewski M, Mann JF, Ruf G, Ritz E, German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med, 2005; 353: 238-248 source

In the paper

“In the Hisayama study, the incidence rate of CAD in patients with IGT is 1.9 times higher than that of subjects with NGT, even though it was lower than the level of 2.6 times in diabetics128).”

What the sources say

• Not checked yetcites [128] 129) Iso H, Imano H, Kitamura A, Sato S, Naito Y, Tanigawa T, Ohira T, Yamagishi K, Iida M, Shimamoto T. Type 2 diabetes and risk of non-embolic ischaemic stroke in Japanese men and women. Diabetologia, 2004; 47: 2137-2144 source

In the paper

“CKD is not merely a highrisk condition for end-stage kidney disease but also for ASCVD.”

In the paper

“Women generally have a lower risk for CAD than men.”

In the paper

“compared to male subjects with NGT male diabetic patients increased the risk of CAD by 17 times higher at ages 31–40 years, and by 2 to 3 times higher at ages 41 to 61 years”

What the sources say

• Not checked yetcites [151] 152) Nakamura J, Kamiya H, Haneda M, Inagaki N, Tanizawa Y, Araki E, Ueki K, Nakayama T. Causes of death in Japanese patients with diabetes based on the results of a survey of 45,708 cases during 2001-2010: Report of the committee on causes of death in diabetes mellitus. J Diabetes Investig, 2017; 8: 397-410 source

In the paper

“The JPHC study showed that the risk for CAD was 1.65 times higher in the borderline glucose tolerance group and 3.05 times higher in the diabetic group as compared to subjects with NGT, indicating the risk increases before the incidence of diabetes146).”

What the sources say

• Not checked yetcites [146] 147) Nakagami T. Hyperglycaemia and mortality from all causes and from cardiovascular disease in five populations of Asian origin. Diabetologia, 2004; 47: 385-394 source

In the paper

“In the J-LIT study, the incidence rate in primary prevention patients was 0.9/1,000 person-years 180) and 4.5/1,000 person-years in CAD patients173).”

What the sources say

• Not checked yetcites [180] 181) Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y, Oikawa S, Sasaki J, Hishida H, Itakura H, Kita T, Kitabatake A, Nakaya N, Sakata T, Shimada K, Shirato K, for the Japan EPA lipid intervention study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised openlabel, blinded endpoint analysis. Lancet, 2007; 369: 1090-1098 source
• Not checked yetcites [173] 174) Furukawa Y, Ehara N, Taniguchi R, Haruna Y, Ozasa N, Saito N, Doi T, Hoshino K, Tamura T, Shizuta S, Abe M, Toma M, Morimoto T, Teramukai S, Fukushima M, Kita T, Kimura T, CREDO-Kyoto Investigators. Coronary risk factor profile and prognostic factors for young Japanese patients undergoing coronary revascularization. Circ J, 2009; 73: 1459-1465 source

In the paper

“There was almost no difference between the mortality rates of cerebral infarction for men and women (target population of 100,000), which were 25.4 and 28.8, respectively.”

In the paper

“Traditional risk factors (high LDL-C, low HDL-C, hypertension, diabetes, and smoking) are associated with genetic predisposition and are influenced by habits within the family.”

In the paper

“a family history of CAD is considered to also include genetic and environmental risk factors, a fact that is already known.”

In the paper

“In JELIS, primary prevention patients had an incidence rate of 1.6/1,000 person-years while the rate was 6.8/1,000 person-years in patients with CAD181).”

What the sources say

• Not checked yetcites [181] 182) The Japanese Coronary Artery Disease (JCAD) Study Investigators. Current status of the background of patients with coronary artery disease in Japan. Circ J, 2006; 70: 1256-1262 source

In the paper

“A family history of CAD, especially in first-degree close relatives (parents, children, brothers and sisters), and a family history of premature CAD (age of incidence: < 55 years for men and < 65 years for women) are strong risk factors for CAD.”

In the paper

“Up to the 90s age group, the mortality rate of cerebral infarction was lower in women than men.”

In the paper

“The incidence of CAD differs in the various regions and populations in Japan, and is higher in cities than in rural areas98)”

What the sources say

• Not checked yetcites [98] 99) Takii T, Yasuda S, Takahashi J, Ito K, Shiba N, Shirato K, Shimokawa H. Trends in acute myocardial infarction incidence and mortality over 30 years in Japan: Report from the Miyagi-AMI Registry Study. Circ J, 2010; 74: 93-100 source

In the paper

“because diabetic patients who are complicated with conditions shown in Table 3b had a high risk for recurrence of CAD”

In the paper

“As patients with FH are difficult to treat, and their risk of CAD in the future is extremely high”

In the paper

“In both scores, the fasting LDL-C value is calculated using the Friedewald formula.”

In the paper

“the fact that the baseline year is 1980, and when this baseline hazard is applied to more recent cohort populations, the estimated mortality of the high-risk group is higher than the actual measured mortality of recent populations341).”

What the sources say

• Not checked yetcites [341] 342) Tanaka T, Okamura T. Blood cholesterol level and risk of stroke in community-based or worksite cohort studies: A review of Japanese cohort studies in the past 20 years. Keio J Med, 2012; 61: 79-88 source

In the paper

“An LDL-C level of ≥ 180 mg/dL has always indicated a high risk for CAD, and may also suggest the presence of familial hypercholesterolemia (FH).”

In the paper

“The currently available risk scoring tools can be used even if the patient is on medication, but the actual risks of cerebro- and cardiovascular diseases differ in patients with or without antihypertensive drug treatment.”

In the paper

“Stroke comprises a large proportion of the cases of cerebro- and cardiovascular disease in Japan.”

In the paper

“Few available medications are effective for increasing low HDL-C, and some reports have found that CAD risk is low if a low HDL level is not accompanied by other lipid abnormalities351).”

What the sources say

• Not checked yetcites [351] 352) Tan CE, Glantz SA. Association between smoke-free legislation and hospitalizations for cardiac, cerebrovascular, and respiratory diseases: a meta-analysis. Circulation, 2012; 126: 2177-2183 source

In the paper

“The NIPPON DATA80 had various advantages, including the fact that groups were selected from all over Japan by random sampling, the chart was based on a baseline survey conducted before statins were available and its high suitability for the observation of the natural course of disease, making it very useful for the assessment of absolute risk.”

In the paper

“Obesity, especially excess visceral fat accumulation, is considered to be an independent risk factor for CVD and promotes atherosclerosis directly or indirectly via dyslipidemia, impaired glucose tolerance, hypertension and the dysregulated production of adipocytokine362–365).”

What the sources say

• Not checked yetcites [362] 363) Larsson B, Svardsudd K, Welin L, Wilhelmsen L, Bjorntorp P, Tibblin G. Abdominal adipose tissue distribution, obesity, and risk of cardiovascular disease and death: 13 year follow up of participants in the study of men born in 1913. Br Med J (Clin Res Ed), 1984; 288: 1401-1404 source
• Not checked yetcites [363] 364) Carr DB, Utzschneider KM, Hull RL, Kodama K, Retzlaff BM, Brunzell JD, Shofer JB, Fish BE, Knopp RH, Kahn SE. Intra-abdominal fat is a major determinant of the national cholesterol education program adult treatment panel III criteria for the metabolic syndrome. Diabetes, 2004; 53: 2087-2094 source
• Not checked yetcites [364] 365) Matsuzawa Y. The metabolic syndrome and adipocytokines. FEBS Lett, 2006; 580: 2917-2921 source
• Not checked yetcites [365] 366) Japan Society for the Study of Obesity, ed.: 2011 Diagnostic guidelines for obesity. J Jpn Soc Study of Obesity, 2011; 17: 1-78 (in Japanese)

In the paper

“Although the expectation of weight gain hinders the start of smoking cessation and causes resumption of smoking”

In the paper

“The 2016 medical fee revision expanded coverage to qualifying minors.”

In the paper

“a recent meta-analysis reported a 4–5 kg increase in body weight 1 year after quitting smoking, with the increase quite pronounced within the first 3 months after cessation358).”

What the sources say

• Not checked yetcites [358] 359) Gepner AD, Piper ME, Johnson HM, Fiore MC, Baker TB, Stein JH. Effects of smoking and smoking cessation on lipids and lipoproteins: outcomes from a randomized clinical trial. Am Heart J, 2011; 161: 145-151 source

In the paper

“In ASCVD patients, the benefits of smoking cessation are apparent soon after quitting, and the longer the duration of abstinence from smoking, the greater is the decrease of risk107).”

What the sources say

• Not checked yetcites [107] 108) Higashiyama A, Okamura T, Ono Y, Watanabe M, Kokubo Y, Okayama A. Risk of smoking and metabolic syndrome for incidence of cardiovascular disease--comparison of relative contribution in urban Japanese population: The Suita study. Circ J, 2009; 73: 2258-2263 source

In the paper

“Short-term worsening of blood glucose and lipid levels may be observed during that interval, but improvement in insulin resistance117), increase in HDL-C359) and reduction in oxidized LDL360) have been reported regardless of weight gain.”

What the sources say

• Not checked yetcites [117] 118) Ishizaka N, Ishizaka Y, Toda E, Hashimoto H, Nagai R, Yamakado M. Association between cigarette smoking, metabolic syndrome, and carotid arteriosclerosis in Japanese individuals. Atherosclerosis, 2005; 181: 381-388 source
• Not checked yetcites [359] 360) Komiyama M, Shimada S, Wada H, Yamakage H, Satoh-Asahara N, Shimatsu A, Akao M, Morimoto T, Takahashi Y, Hasegawa K. Time-dependent changes of atherosclerotic LDL complexes after smoking cessation. J Atheroscler Thromb, 2016; 23: 1270-1275 source
• Not checked yetcites [360] 361) Clair C, Rigotti NA, Porneala B, Fox CS, D’Agostino RB, Pencina MJ, Meigs JB. Association of smoking cessation and weight change with cardiovascular disease among adults with and without diabetes. JAMA, 2013; 309: 1014-1021 source

In the paper

“Passive smoking also increases CAD and stroke risk115, 116)”

What the sources say

• Not checked yetcites [115] 116) Oono IP, Mackay DF, Pell JP. Meta-analysis of the association between secondhand smoke exposure and stroke. J Public Health (Oxf), 2011; 33: 496-502 source
• Not checked yetcites [116] 117) Pan A, Wang Y, Talaei M, Hu FB, Wu T. Relation of active, passive, and quitting smoking with incident type 2 diabetes: a systematic review and meta-analysis. Lancet Diabetes Endocrinol, 2015; 3: 958-967 source

In the paper

“As with other drug dependencies, symptoms of nicotine withdrawal appear soon after quitting, and that makes it difficult for many smokers to quit.”

In the paper

“Rapid weight loss resulting from extensive calorie restriction may lead to rapid rebound weight gain.”

In the paper

“Metabolic syndrome has been proposed as a high-risk condition for ASCVD independent of hyper-LDL cholesterolemia.”

In the paper

“regardless a history of ASCVD, smoking cessation decreases the development and subsequent progression of ASCVD, and the risk of death due to ASCVD.”

In the paper

“Hyper-LDL cholesterolemia is a major risk factor for ASCVD, and its management protocol has been established.”

In the paper

“In Japan, when both medical facilities and patients satisfy certain requirements, health insurance coverage is applied for smoking cessation treatment for 12 weeks355).”

What the sources say

• Not checked yetcites [355] 356) Stead LF, Perera R, Bullen C, Mant D, Hartmann-Boyce J, Cahill K, Lancaster T. Nicotine replacement therapy for smoking cessation. Cochrane Database Syst Rev, 2012; 11: CD000146 source

In the paper

“For screening of obesity disease in daily clinical practice, a waist circumference at the umbilical level of ≥ 85 cm for men and ≥ 90 cm for women is used as the criteria of visceral fat accumulation368).”

What the sources say

• Not checked yetcites [368] 369) Muramoto A, Matsushita M, Kato A, Yamamoto N, Koike G, Nakamura M, Numata T, Tamakoshi A, Tsushita K. Three percent weight reduction is the minimum requirement to improve health hazards in obese and overweight people in Japan. Obes Res Clin Pract.,2014; 8: e466-475 source

In the paper

“Therefore, the diagnostic criteria of metabolic syndrome include no criterion concerning the LDL-C level.”

In the paper

“As decreasing the number of cigarettes smoked or switching to low-nicotine or low-tar tobacco does not lead to a reduction in risk”

In the paper

“In Japan, the ideal body weight is defined to be a BMI of 22, which has the lowest morbidity, and a BMI ≥ 25 is diagnosed as obesity366).”

What the sources say

• Not checked yetcites [366] 367) The Examination Committee of Criteria for Obesity Disease in Japan (2002) Japan Society for the Study of Obesity: New criteria for obesity disease in Japan. Circ J, 2002; 66: 987-992 source

In the paper

“In Japan, active support of lifestyle modification resulted in a weight loss of ≥ 3% in obese individuals within 1 year, could reduce LDL-C, TG, uric acid, and blood pressure levels, improve blood glucose control, and increase HDL-C levels significantly320, 372).”

What the sources say

• Not checked yetcites [320] 321) Nakamura T, Tokunaga K, Shimomura I, Nishida M, Yoshida S, Kotani K, Islam AH, Keno Y, Kobatake T, Nagai Y. Contribution of visceral fat accumulation to the development of coronary artery disease in non-obese men. Atherosclerosis, 1994; 107: 239-246 source
• Not checked yetcites [372] 373) Svendsen OL, Hassager C, Christiansen C. Effect of an energy-restrictive diet, with or without exercise, on lean tissue mass, resting metabolic rate, cardiovascular risk factors, and bone in overweight postmenopausal women. Am J Med, 1993; 95: 131-140 source

In the paper

“An RCT comparing an energy-restrictive diet with an energy-restrictive diet+exercise in overweight postmenopausal women found decreases in body weight and amount of body fat; decreased TG, TC, LDL-C, and the LDL-C/HDL-C ratio; and a decrease in SBP in both groups373).”

What the sources say

• Not checked yetcites [373] 374) Kuller LH, Simkin-Silverman LR, Wing RR, Meilahn EN, Ives DG. Women’s healthy lifestyle project: A randomized clinical trial: Results at 54 months. Circulation, 2001; 103: 32-37 source

In the paper

“The increase in HDL-C was positively correlation with the duration of exercise, and exercising for ≥ 121 minutes/week significantly increased the levels.”

What the sources say

• Not checked yetcites [612] 614) Kelley GA, Kelley KS. Aerobic exercise and lipids and lipoproteins in men: A meta-analysis of randomized controlled trials. J Mens Health Gend, 2006; 3: 61-70 source

In the paper

“Among 8 reports of systematic review and metaanalysis of RCTs with comparison of exercise and non-exercise control including Japanese participants and were published after 2,000, significant decreases in LDL-C and TG levels were reported in two articles, respectively.”

What the sources say

• Not checked yetcites [577] 579) Aune D, Norat T, Leitzmann M, Tonstad S, Vatten LJ. Physical activity and the risk of type 2 diabetes: A systematic review and dose-response meta-analysis. Eur J Epidemiol, 2015; 30: 529-542 source
• Not checked yetcites [607] 609) Kelley GA, Kelley KS, Tran ZV. Walking, lipids, and lipoproteins: A meta-analysis of randomized controlled trials. Prev Med, 2004; 38: 651-661 source
• Not checked yetcites [608] 610) Kelley GA, Kelley KS, Tran ZV. Aerobic exercise and lipids and lipoproteins in women: A meta-analysis of randomized controlled trials. J Womens Health (Larchmt), 2004; 13: 1148-1164 source
• Not checked yetcites [609] 611) Kelley GA, Kelley KS, Tran ZV. Exercise, lipids, and lipoproteins in older adults: A meta-analysis. Prev Cardiol, 2005; 8: 206-214 source
• Not checked yetcites [610] 612) Kodama S, Tanaka S, Saito K, Shu M, Sone Y, Onitake F, Suzuki E, Shimano H, Yamamoto S, Kondo K, Ohashi Y, Yamada N, Sone H. Effect of aerobic exercise training on serum levels of high-density lipoprotein cholesterol: A meta-analysis. Arch Intern Med, 2007; 167: 999-1008 source
• Not checked yetcites [611] 613) Kuhle CL, Steffen MW, Anderson PJ, Murad MH. Effect of exercise on anthropometric measures and serum lipids in older individuals: A systematic review and meta-analysis. BMJ Open, 2014; 4: e005283 source
• Not checked yetcites [612] 614) Kelley GA, Kelley KS. Aerobic exercise and lipids and lipoproteins in men: A meta-analysis of randomized controlled trials. J Mens Health Gend, 2006; 3: 61-70 source
• Not checked yetcites [613] 615) Kelley GA, Kelley KS. Impact of progressive resistance training on lipids and lipoproteins in adults: Another look at a meta-analysis using prediction intervals. Prev Med, 2009; 49: 473-475 source

In the paper

“Even in secondary prevention, the incidence of cardiovascular events is clearly high if FH, ACS, DM, noncardiogenic cerebral infarction, PAD, CKD, and metabolic syndrome are also present, or if there is an overlap of the major risk factors or continued smoking (Table 3) (refer to Chapter 3, 1–8: History of CAD).”

In the paper

“A recent survey in Japan, found that 65% patients with ACS, and 55% for other secondary prevention patients, achieved an LDL-C management target of < 100 mg/dL.”

What the sources say

• Not checked yetcites [626] 628) Ford I, Murray H, McCowan C, Packard CJ. Long-term safety and efficacy of lowering low-density lipoprotein cholesterol with statin therapy: 20-year follow-up of West of Scotland Coronary Prevention Study. Circulation, 2016; 133: 1073-1080 source

In the paper

“Although the absolute risk of CAD is lower in the Japanese population than in Western countries, the relative risk of LDL-C and CAD is similar.”

In the paper

“Statins competitively inhibit HMG-CoA reductase, which is a rate-limiting enzyme of cholesterol synthesis, in turn suppressing cholesterol biosynthesis657).”

What the sources say

• Not checked yetcites [657] 659) Bakker-Arkema RG, Davidson MH, Goldstein RJ, Davignon J, Isaacsohn JL, Weiss SR, Keilson LM, Brown WV, Miller VT, Shurzinske LJ, Black DM. Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia. JAMA, 1996; 275: 128-133 source

In the paper

“Myopathy-like symptoms, such as hepatic disorders, an increased creatine kinase (CK) level, and muscular weakness, have been reported as adverse reactions to statins.”

In the paper

“It also increased the HDL-C level by 8–9% while decreasing the TG level by 20–30%.”

In the paper

“Rhabdomyolysis, characterized by an increased myoglobin level in the blood and urine, has also been reported, though this complication is very rare.”

In the paper

“A review performed outside of Japan reported that larger suppressive effects on cardiovascular events can be achieved by maintaining the LDL-C level at < 50 mg/dL646).”

What the sources say

• Not checked yetcites [646] 648) Frick MH, Elo O, Haapa K, Heinonen OP, Heinsalmi P, Helo P, Huttunen JK, Kaitaniemi P, Koskinen P, Manninen V. Helsinki Heart Study: Primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease. N Engl J Med, 1987; 317: 1237-1245 source

In the paper

“The subsequent activation of SREBP2 promotes LDL receptor synthesis and results in a reduction in the blood LDL-C level658).”

What the sources say

• Not checked yetcites [658] 660) Pharmaceuticals and Medical Devices Agency. Revisions to the “Precautions of use” of HMG-CoA reducatase inhibitor-containing pharmaceutical drugs. 2016 https://www.pmda.go.jp/files/000214541.pdf (in Japanese)

In the paper

“Therefore, the combined use of ezetimibe with statins is ideal and provides a synergistic effect: combination therapy with 10 mg of ezetimibe and a statin at the usual dose decreases the LDL-C level by approximately 35–50%664–666), which is equivalent to the effects achieved using a maximum statin dose alone.”

What the sources say

• Not checked yetcites [664] 666) Ballantyne CM, Houri J, Notarbartolo A, Melani L, Lipka LJ, Suresh R, Sun S, LeBeaut AP, Sager PT, Veltri EP, Ezetimibe Study Group. Effect of ezetimibe coadministered with atorvastatin in 628 patients with primary hypercholesterolemia: A prospective, randomized, double-blind trial. Circulation, 2003; 107: 2409-2415 source
• Not checked yetcites [665] 667) Thomopoulos C, Skalis G, Michalopoulou H, Tsioufis C, Makris T. Effect of low-density lipoprotein cholesterol lowering by ezetimibe/simvastatin on outcome incidence: Overview, meta-analyses, and meta-regression analyses of randomized trials. Clin Cardiol, 2015; 38: 763-769 source
• Not checked yetcites [666] 668) Takada T, Yamanashi Y, Konishi K, Yamamoto T, Toyoda Y, Masuo Y, Yamamoto H, Suzuki H. NPC1L1 is a key regulator of intestinal vitamin k absorption and a modulator of warfarin therapy. Sci Transl Med, 2015; 7: 275ra223 source

In the paper

“A meta-analysis of large-scale clinical trials involving combination therapy with ezetimibe and statins in patients with high-risk conditions such as FH, ACS, and PAD, confirmed the safety of combination therapy and cardiovascular event suppression resulting from its LDL-C-lowering effects667).”

What the sources say

• Not checked yetcites [667] 669) The lipid research clinics coronary primary prevention trial results. I. Reduction in incidence of coronary heart disease. JAMA, 1984; 251: 351-364 source

In the paper

“PCSK9 inhibitors decrease TG levels by 20–25% and increases HDL-C levels by 10–15%.”

In the paper

“Resin administration results in a decreased LDL-C level, as well as VLDL synthesis and an increased blood TG level because of bile acid absorption.”

In the paper

“In addition to decreasing the LDL-C level, this drug also decreases the HDL-C level.”

In the paper

“These drugs bind specifically to and inhibit the actions of the PCSK9 (proprotein convertase subtilisin/kexin type 9) protein, which is involved in the degradation of LDL receptors in the liver. In doing so, it increases the recycling of LDL receptors, thereby showing a blood LDL-C-lowering effect681).”

What the sources say

• Not checked yetcites [681] 683) Teramoto T, Kobayashi M, Tasaki H, Yagyu H, Higashikata T, Takagi Y, Uno K, Baccara-Dinet MT, Nohara A. Efficacy and safety of alirocumab in Japanese patients with heterozygous familial hypercholesterolemia or at high cardiovascular risk with hypercholesterolemia not adequately controlled with statins . ODESSEY JAPAN Randomized Controlled Trial. Circ J, 2016; 80: 19801987 source

In the paper

“These inhibitors also decrease the Lp(a) level, on which statins do not show a lowering effect.”

In the paper

“It is also used to reflect the degree of systemic arteriosclerosis or as an alternative assessment factor for predicting the risk of co-existence or onset of ASCVD (e.g., CAD, PAD, cerebrovascular diseases, etc.)5–8).”

What the sources say

• Not checked yetcites [5] 5) Nezu T, Hosomi N, Aoki S, Matsumoto M. Carotid intima-media thickness for atherosclerosis. J Atheroscler Thromb, 2016; 23: 18-31 source
• Not checked yetcites [6] 6) O’Leary DH, Polak JF, Kronmal RA, Manolio TA, Burke GL, Wolfson SK. Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. Cardiovascular health study collaborative research group. N Engl J Med, 1999; 340: 14-22 source
• Not checked yetcites [7] 7) del Sol AI, Moons KG, Hollander M, Hofman A, Koudstaal PJ, Grobbee DE, Breteler MM, Witteman JC, Bots ML. Is carotid intima-media thickness useful in cardiovascular disease risk assessment? The Rotterdam Study. Stroke, 2001; 32: 1532-1538 source
• Not checked yetcites [8] 8) Lorenz MW, Markus HS, Bots ML, Rosvall M, Sitzer M. Prediction of clinical cardiovascular events with carotid intima-media thickness: A systematic review and metaanalysis. Circulation, 2007; 115: 459-467 source

In the paper

“using death instead of disease onset as the outcome and the absence of information on LDL-C and HDL-C are major issues”

In the paper

“FMD starts decreasing from early stages of arteriosclerosis31, 32), and it is therefore useful for the initial assessment of ASCVD.”

What the sources say

• Not checked yetcites [31] 31) Corretti MC, Anderson TJ, Benjamin EJ, Celermajer D, Charbonneau F, Creager MA, Deanfield J, Drexler H, Gerhard-Herman M, Herrington D, Vallance P, Vita J, Vogel R, Force International Brachial Artery Reactivity Task Force. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery: A report of the international brachial artery reactivity task force. J Am Coll Cardiol, 2002; 39: 257-265 source
• Not checked yetcites [32] 32) Celermajer DS, Sorensen KE, Bull C, Robinson J, Dean-field JE. Endothelium-dependent dilation in the systemic arteries of asymptomatic subjects relates to coronary risk factors and their interaction. J Am Coll Cardiol, 1994; 24: 1468-1474 source

In the paper

“A feature of CAVI is its nondependence on BP during measurement28).”

What the sources say

• Not checked yetcites [28] 28) Shirai K, Hiruta N, Song M, Kurosu T, Suzuki J, Tomaru T, Miyashita Y, Saiki A, Takahashi M, Suzuki K, Takata M. Cardio-ankle vascular index (CAVI) as a novel indicator of arterial stiffness: Theory, evidence and perspectives. J Atheroscler Thromb, 2011; 18: 924-938 source

In the paper

“SR indicated that the Suita study, which used CAD as its outcome, is most suitable for risk calculation in this set of guidelines.”

In the paper

“a conflict of interest (COI) statement has been obtained from each member of the committee involved in drafting the Guidelines for Prevention of Atherosclerotic Cardiovascular Diseases 2017.”

In the paper

“It has excellent specificity14–17), and organic coronary stenosis can almost be ruled out if no abnormalities are detected using this technique.”

What the sources say

• Not checked yetcites [14] 14) Vanhoenacker PK, Heijenbrok-Kal MH, Van Heste R, Decramer I, Van Hoe LR, Wijns W, Hunink MG. Diagnostic performance of multidetector CT angiography for assessment of coronary artery disease: Meta-analysis. Radiology, 2007; 244: 419-428 source
• Not checked yetcites [15] 15) Schroeder S, Achenbach S, Bengel F, Burgstahler C, Cademartiri F, de Feyter P, George R, Kaufmann P, Kopp AF, Knuuti J, Ropers D, Schuijf J, Tops LF, Bax JJ, Working Group Nuclear Cardiology and Cardiac CT; European Society of Cardiology; European Council of Nuclear Cardiology. Cardiac computed tomography: Indications, applications, limitations, and training requirements: Report of a writing group deployed by the working group nuclear cardiology and cardiac CT of the European society of cardiology and the European council of nuclear cardiology. Eur Heart J, 2008; 29: 531-556 source
• Not checked yetcites [16] 16) Budoff MJ, Dowe D, Jollis JG, Gitter M, Sutherland J, Halamert E, Scherer M, Bellinger R, Martin A, Benton R, Delago A, Min JK. Diagnostic performance of 64-multidetector row coronary computed tomographic angiography for evaluation of coronary artery stenosis in individuals without known coronary artery disease: Results from the prospective multicenter accuracy (assessment by coronary computed tomographic angiography of individuals undergoing invasive coronary angiography) trial. J Am Coll Cardiol, 2008; 52: 1724-1732 source
• Not checked yetcites [17] 17) Miller JM, Rochitte CE, Dewey M, Arbab-Zadeh A, Niinuma H, Gottlieb I, Paul N, Clouse ME, Shapiro EP, Hoe J, Lardo AC, Bush DE, de Roos A, Cox C, Brinker J, Lima JA. Diagnostic performance of coronary angiography by 64-row CT. N Engl J Med, 2008; 359: 2324-2336 source

In the paper

“Aging22), hypertension23), diabetes24), and pulse rate22) are CVD risk factors that have been reported to cause increased baPWV, and they show a good correlation with the Framingham Risk Score.”

What the sources say

• Not checked yetcites [22] 22) Tomiyama H, Yamashina A, Arai T, Hirose K, Koji Y, Chikamori T, Hori S, Yamamoto Y, Doba N, Hinohara S. Influences of age and gender on results of noninvasive brachial-ankle pulse wave velocity measurement--a survey of 12517 subjects. Atherosclerosis, 2003; 166: 303 source
• Not checked yetcites [23] 23) Yamashina A, Tomiyama H, Arai T, Koji Y, Yambe M, Motobe H, Glunizia Z, Yamamoto Y, Hori S. Nomogram of the relation of brachial-ankle pulse wave velocity with blood pressure. Hypertens Res, 2003; 26: 801-806 source
• Not checked yetcites [24] 24) Ohnishi H, Saitoh S, Takagi S, Ohata J, Isobe T, Kikuchi Y, Takeuchi H, Shimamoto K. Pulse wave velocity as an indicator of atherosclerosis in impaired fasting glucose: The Tanno and Sobetsu study. Diabetes Care, 2003; 26: 437-440 source

In the paper

“IMT is assessed as the thickness adjusted by age4).”

What the sources say

• Not checked yetcites [4] 4) Homma S, Hirose N, Ishida H, Ishii T, Araki G. Carotid plaque and intima-media thickness assessed by b-mode ultrasonography in subjects ranging from young adults to centenarians. Stroke, 2001; 32: 830-835 source

In the paper

“Specifically, we formulated the CQ, “Does an assessment method that predicts the incidence of or death due to ASCVD in the Japanese exist?”, and performed an SR.”

In the paper

“We believe that the determination of the incidence rate of CAD instead of the overall risk assessment has enabled a clearer demonstration of the importance of each risk.”

In the paper

“TC therefore predicts the occurrence of and death from stroke.”

In the paper

“However, the accuracy of the direct method and the non-HDL-C calculation cannot be guaranteed when the TG level is ≥ 1000 mg/dL101) and ≥ 600 mg/dL, respectively.”

What the sources say

• Not checked yetcites [101] 102) National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. Atlanta (GA). Centers for Disease Control and Prevention (US). Chapter 8. The health consequences of smoking-50 years of progress: A report of the Surgeon General, 2014: 411-457

In the paper

“It also increases the risk for diabetes, dyslipidemia and metabolic syndrome, in turn contributing to an added risk for ASCVD.”

In the paper

“This finding is consistent with the results of randomized controlled trials revealing that the use of statin did not decrease the risk for ASCVD significantly in dialysis patients158, 159), suggesting the importance of implementing effective measures on patients with earlier stages of CKD.”

What the sources say

• Not checked yetcites [158] 159) Fellstrom BC, Jardine AG, Schmieder RE, Holdaas H, Bannister K, Beutler J, Chae DW, Chevaile A, Cobbe SM, Gronhagen-Riska C, De Lima JJ, Lins R, Mayer G, McMahon AW, Parving HH, Remuzzi G, Samuelsson O, Sonkodi S, Sci D, Suleymanlar G, Tsakiris D, Tesar V, Todorov V, Wiecek A, Wuthrich RP, Gottlow M, Johns-son E, Zannad F, AURORA Study Group. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med, 2009; 360: 1395-1407 source
• Not checked yetcites [159] 160) Wilson PW, D’Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation, 1998; 97: 1837-1847 source

In the paper

“Women in the 70s have a mortality rate that is almost the same as men in the 60s, which goes to show that the risk for ASCVD is not low for elderly women164).”

What the sources say

• Not checked yetcites [164] 165) Silberberg JS, Wlodarczyk J, Fryer J, Robertson R, Hens-ley MJ. Risk associated with various definitions of family history of coronary heart disease. The Newcastle Family History Study II. Am J Epidemiol, 1998; 147: 1133-1139 source

In the paper

“However, it was reported in the results of a meta-analysis that both CVD and stroke were not seen to be significantly correlated with the progress of IMT189).”

What the sources say

• Not checked yetcites [189] 190) Olin JW, Allie DE, Belkin M, Bonow RO, Casey DE Jr, Creager MA, Gerber TC, Hirsch AT, Jaff MR, Kaufman JA, Lewis CA, Martin ET, Martin LG, Sheehan P, Stewart KJ, Treat-Jacobson D, White CJ, Zheng ZJ; American Association of Cardiovascular and Pulmonary Rehabilitation; American Diabetes Association; Society for Atherosclerosis Imaging and Prevention; Society for Cardiovascular Magnetic Resonance; Society of Cardiovascular Computed Tomography; PAD Coalition; American Academy of Podiatric Practice Management; ACCF/ AHA Task Force on Performance Measures, Masoudi FA, Bonow RO, DeLong E, Erwin source

In the paper

“Patients in Japan who have a history of stroke are considered to be at a high risk for developing CAD, especially those with noncardiogenic cerebral infarction originating from arteriosclerotic lesions.”

What the sources say

• Not checked yetcites [184] 185) Goto S, Ikeda Y, Shimada K, Uchiyama S, Origasa H, Kobayashi H, J-TRACE Investigators. One-year cardiovascular event rates in Japanese outpatients with myocardial infarction, stroke, and atrial fibrillation. -results from the Japan Thrombosis Registry for Atrial Fibrillation, Coronary, or Cerebrovascular Events (J-TRACE). Circ J, 2011; 75: 2598-2604 source
• Not checked yetcites [185] 186) Kitagawa K, Hougaku H, Yamagami H, Hashimoto H, Itoh T, Shimizu Y, Takahashi D, Murata S, Seike Y, Kondo K, Hoshi T, Furukado S, Abe Y, Yagita Y, Sakaguchi M, Tagaya M, Etani H, Fukunaga R, Nagai Y, Matsumoto M, Hori M, OSACA2 Study Group. Carotid intima-media thickness and risk of cardiovascular events in high-risk patients. Results of the osaka follow-up study for carotid atherosclerosis 2 (OSACA2 Study). Cerebrovasc Dis, 2007; 24: 35-42 source

In the paper

“Even though coronary artery lesions are found at high rates when RAS is present and RAS is an important high-risk condition in CVD, there is insufficient evidence showing that it is a direct primary risk factor for ASCVD.”

In the paper

“Among the causes of death, they reported that cardiovascular-related causes made up 37% and MI made up 22%198).”

What the sources say

• Not checked yetcites [198] 199) Kioka Y, Tanabe A, Kotani Y, Yamada N, Nakahama M, Ueda T, Seitou T, Maruyama M. Review of coronary artery disease in patients with infrarenal abdominal aortic aneurysm. Circ J, 2002; 66: 1110-1112 source

In the paper

“The resulting incidence rates were generally high - 1.25% for all deaths, 0.55% for cardiovascular death, 0.77% for nonfatal MI, and 1.56% for nonfatal stroke184).”

What the sources say

• Not checked yetcites [184] 185) Goto S, Ikeda Y, Shimada K, Uchiyama S, Origasa H, Kobayashi H, J-TRACE Investigators. One-year cardiovascular event rates in Japanese outpatients with myocardial infarction, stroke, and atrial fibrillation. -results from the Japan Thrombosis Registry for Atrial Fibrillation, Coronary, or Cerebrovascular Events (J-TRACE). Circ J, 2011; 75: 2598-2604 source

In the paper

“It was observed in the study that the three-year incidence rate was 6.3% for cardiovascular death, 11.3% for heart disease, 7.0% for cerebrovascular disease and 16.9% for events in the lower extremities193).”

What the sources say

• Not checked yetcites [193] 194) Hobbs SD, Claridge MW, Quick CR, Day NE, Brad-bury AW, Wilmink AB. LDL cholesterol is associated with small abdominal aortic aneurysms. Eur J Vasc Endovasc Surg, 2003; 26: 618-622 source

In the paper

“From these results, even though there are no longitudinal studies demonstrating AAA as a risk factor for ASCVD, there are some cross-sectional studies showing the association between AAA and ASCVD.”

In the paper

“High LDL-C194), high TC195), hypertension196), and smoking are the factors that contribute to the development of AAA, and this is a commonality with ASCVD.”

What the sources say

• Not checked yetcites [194] 195) Tornwall ME, Virtamo J, Haukka JK, Albanes D, Huttunen JK. Life-style factors and risk for abdominal aortic aneurysm in a cohort of Finnish male smokers. Epidemiology, 2001; 12: 94-100 source
• Not checked yetcites [195] 196) Bhak RH, Wininger M, Johnson GR, Lederle FA, Messina LM, Ballard DJ, Wilson SE, Aneurysm Detection and Management (ADAM) Study Group. Factors associated with small abdominal aortic aneurysm expansion rate. JAMA Surg, 2015; 150: 44-50 source
• Not checked yetcites [196] 197) Akai A, Watanabe Y, Hoshina K, Obitsu Y, Deguchi J, Sato O, Shigematsu K, Miyata T. Family history of aortic aneurysm is an independent risk factor for more rapid growth of small abdominal aortic aneurysms in Japan. J Vasc Surg, 2015; 61: 287-290 source

In the paper

“According to subsequent reports, including a meta-analysis, it has been revealed that uric acid level is an independent risk factor for the development of hypertension, stroke, and coronary events206–208).”

What the sources say

• Not checked yetcites [206] 207) Kim SY, Guevara JP, Kim KM, Choi HK, Heitjan DF, Albert DA. Hyperuricemia and risk of stroke: A systematic review and meta-analysis. Arthritis Rheum, 2009; 61: 885-892 source
• Not checked yetcites [207] 208) Kim SY, Guevara JP, Kim KM, Choi HK, Heitjan DF, Albert DA. Hyperuricemia and coronary heart disease: A systematic review and meta-analysis. Arthritis Care Res (Hoboken), 2010; 62: 170-180 source
• Not checked yetcites [208] 209) Zhang W, Iso H, Murakami Y, Miura K, Nagai M, Sugiyama D, Ueshima H, Okamura T, EPOCH-JAPAN GROUP. Serum uric acid and mortality form cardiovascular disease: EPOCH-JAPAN Study. J Atheroscler Thromb, 2016; 23: 692-703 source

In the paper

“it was mentioned that serum uric acid levels (1) can be regarded as an independent predictive factor for the development of hypertension”

What the sources say

• Not checked yetcites [205] 206) Wang J, Qin T, Chen J, Li Y, Wang L, Huang H, Li J. Hyperuricemia and risk of incident hypertension: A systematic review and meta-analysis of observational studies. PLoS One, 2014; 9: e114259 source

In the paper

“RAS is a progressive condition, and individuals with RAS have a tendency for worsened renal function.”

In the paper

“At the same time, it was mentioned in the guideline that conflicting reports on whether serum uric acid level is an independent risk factor for CVD have been produced205).”

What the sources say

• Not checked yetcites [205] 206) Wang J, Qin T, Chen J, Li Y, Wang L, Huang H, Li J. Hyperuricemia and risk of incident hypertension: A systematic review and meta-analysis of observational studies. PLoS One, 2014; 9: e114259 source

In the paper

“As a result, myocardial ischemia was seen in 37% the patients with AAA, 55% patients with PAD and 77% patients with both200).”

What the sources say

• Not checked yetcites [200] 201) Tollefson DF, Ernst CB. Natural history of atherosclerotic renal artery stenosis associated with aortic disease. J Vasc Surg, 1991; 14: 327-331 source

In the paper

“and (2) it can possibly be a predictive factor for the risk of incipient stroke and recurrence, as well as for the re-hospitalization and prognosis caused by heart failure.”

What the sources say

• Not checked yetcites [205] 206) Wang J, Qin T, Chen J, Li Y, Wang L, Huang H, Li J. Hyperuricemia and risk of incident hypertension: A systematic review and meta-analysis of observational studies. PLoS One, 2014; 9: e114259 source

In the paper

“Ninety five percent of renal artery stenosis (RAS) is caused by arteriosclerosis and it coexists with other forms of ASCVD at a high rate.”

In the paper

“As mentioned above, other forms of ASCVD, such as CAD and cerebrovascular disease, easily occur in PAD patients at high incidence rates, and this has also been clearly shown in Japan.”

In the paper

“and that the survival rate decreases with higher degrees of RAS204).”

What the sources say

• Not checked yetcites [204] 205) Yamanaka H, Japanese Society of Gout and Nucleic Acid Metabolism. Japanese guideline for the management of hyperuricemia and gout: Second edition. Nucleosides Nucleotides Nucleic Acids, 2011; 30: 1018-1029 source

In the paper

“A meta-regression analysis has clearly shown that patients with OSA have lower endothelial function than those without OSA, in addition to increased stiffness of the blood vessels and high-sensitivity C-reactive protein level212).”

What the sources say

• Not checked yetcites [212] 213) Zhou M, Guo B, Wang Y, Yan D, Lin C, Shi Z. The association between obstructive sleep apnea and carotid intima-media thickness: A systematic review and metaanalysis. Angiology, 2017; 68: 575-583 source

In the paper

“OSA is on the other hand, seen as a common disease that is closely related to lifestyle habits and is strongly associated with ASCVD.”

In the paper

“The TC/HDL-C ratio, non-HDL-C/HDL-C ratio, LDL-C/HDL-C ratio, and apo B/AI ratio are markers for ASCVD. (Evidence level: E-1a)”

What the sources say

• Not checked yetcites [268] 269) Sniderman AD, Williams K, Contois JH, Monroe HM, McQueen MJ, de Graaf J, Furberg CD. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein b as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes, 2011; 4: 337-345 source
• Not checked yetcites [273] 274) Kastelein JJ, van der Steeg WA, Holme I, Gaffney M, Cater NB, Barter P, Deedwania P, Olsson AG, Boekholdt SM, Demicco DA, Szarek M, LaRosa JC, Pedersen TR, Grundy SM, TNT Study Group; IDEAL Study Group. Lipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment. Circulation, 2008; 117: 3002-3009 source
• Not checked yetcites [274] 275) Ray KK, Cannon CP, Cairns R, Morrow DA, Ridker PM, Braunwald E. Prognostic utility of apoB/AI, total cholesterol/HDL, non-HDL cholesterol, or hs-CRP as predictors of clinical risk in patients receiving statin therapy after acute coronary syndromes: Results from PROVE IT-TIMI 22. Arterioscler Thromb Vasc Biol, 2009; 29: 424-430 source
• Not checked yetcites [275] 276) Hong LF, Yan XN, Fan Y, Wu Q, Luo SH, Yang B, Li JJ. Is the ratio of apoB/apoA-1 the best predictor for the severity of coronary artery lesions in chinese diabetics with stable angina pectoris? An assessment based on gensini scores. J Geriatr Cardiol, 2015; 12: 402-409

In the paper

“In the sub-analysis of MRFIT, the nonfasting TG level was as useful as, or even more useful than, the fasting TG level for the risk for CAD; a nonfasting TG level of ≥ 200 mg/dL indicates a high risk246).”

What the sources say

• Not checked yetcites [246] 247) Nordestgaard BG, Langsted A, Mora S, Kolovou G, Baum H, Bruckert E, Watts GF, Sypniewska G, Wiklund O, Boren J, Chapman MJ, Cobbaert C, Des-camps OS, von Eckardstein A, Kamstrup PR, Pulkki K, Kronenberg F, Remaley AT, Rifai N, Ros E, Langlois M, European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) Joint Consensus Initiative. Author information. Fasting is not routinely required for determination of a lipid profile: Clinical and laboratory implications including flagging at desirable concentration cut-points-a joint consens source

In the paper

“The association between the levels of small dense LDL and CAD has been reported in numerous sources251–256), and its relationship with PAD and aneurysms has also been demonstrated257, 258).”

What the sources say

• Not checked yetcites [251] 252) St-Pierre AC, Cantin B, Dagenais GR, Mauriege P, Bernard PM, Despres JP, Lamarche B. Low-density lipoprotein subfractions and the long-term risk of ischemic heart disease in men: 13-year follow-up data from the Quebec Cardiovascular study. Arterioscler Thromb Vasc Biol, 2005; 25: 553-559 source
• Not checked yetcites [252] 253) Arsenault BJ, Lemieux I, Despres JP, Wareham NJ, Luben R, Kastelein JJ, Khaw KT, Boekholdt SM. Cholesterol levels in small LDL particles predict the risk of coronary heart disease in the epic-norfolk prospective population study. Eur Heart J, 2007; 28: 2770-2777 source
• Not checked yetcites [253] 254) El Harchaoui K, van der Steeg WA, Stroes ES, Kuivenhoven JA, Otvos JD, Wareham NJ, Hutten BA, Kastelein JJ, Khaw KT, Boekholdt SM. Value of lowdensity lipoprotein particle number and size as predictors of coronary artery disease in apparently healthy men and women: The EPIC…Norfolk prospective population study. J Am Coll Cardiol, 2007; 49: 547-553 source
• Not checked yetcites [254] 255) Austin MA, Rodriguez BL, McKnight B, McNeely MJ, Edwards KL, Curb JD, Sharp DS. Low-density lipoprotein particle size, triglycerides, and high-density lipoprotein cholesterol as risk factors for coronary heart disease in older Japanese-American men. Am J Cardiol, 2000; 86: 412-416 source
• Not checked yetcites [255] 256) Koba S, Hirano T, Ito Y, Tsunoda F, Yokota Y, Ban Y, Iso Y, Suzuki H, Katagiri T. Significance of small dense low-density lipoprotein-cholesterol concentrations in relation to the severity of coronary heart diseases. Atherosclerosis, 2006; 189: 206-214 source
• Not checked yetcites [256] 257) Rizzo M, Pernice V, Frasheri A, Berneis K. Atherogenic lipoprotein phenotype and LDL size and subclasses in patients with peripheral arterial disease. Atherosclerosis, 2008; 197: 237-241 source
• Not checked yetcites [257] 258) Rizzo M, Krayenbuhl PA, Pernice V, Frasheri A, Battista Rini G, Berneis K. LDL size and subclasses in patients with abdominal aortic aneurysm. Int J Cardiol, 2009; 134: 406-408 source
• Not checked yetcites [258] 259) Hirano T, Ito Y, Koba S, Toyoda M, Ikejiri A, Saegusa H, Yamazaki J, Yoshino G. Clinical significance of small dense low-density lipoprotein cholesterol levels determined by the simple precipitation method. Arterioscler Thromb Vasc Biol, 2004; 24: 558-563 source

In the paper

“The risk starts increasing when the nonfasting TG level reaches 115 mg/dL, and at ≥ 167 mg/dL, the risk increases by ≥ 3 times.”

What the sources say

• Not checked yetcites [88] 89) Satoh H, Nishino T, Tomita K, Tsutsui H. Fasting triglyceride is a significant risk factor for coronary artery disease in middle-aged Japanese men. Circ J, 2006; 70: 227-231 source

In the paper

“Lp(a) is an independent risk factor for CAD and stroke.”

What the sources say

• Not checked yetcites [221] 222) Kronenberg F, Utermann G. Lipoprotein (a): Resurrected by genetics. J Intern Med, 2013; 273: 6-30 source
• Not checked yetcites [222] 223) Dube JB, Boffa MB, Hegele RA, Koschinsky ML. Lipoprotein (a): More interesting than ever after 50 years. Curr Opin Lipidol, 2012; 23: 133-140 source
• Not checked yetcites [223] 224) Schaefer EJ, Lamon-Fava S, Jenner JL, McNamara JR, Ordovas JM, Davis CE, Abolafia JM, Lippel K, Levy RI. Lipoprotein (a) levels and risk of coronary heart disease in men. The lipid research clinics coronary primary prevention trial. JAMA, 1994; 271: 999-1003 source
• Not checked yetcites [224] 225) Bennet A, Di Angelantonio E, Erqou S, Eiriksdottir G, Sigurdsson G, Woodward M, Rumley A, Lowe GD, Danesh J, Gudnason V. Lipoprotein (a) levels and risk of future coronary heart disease: Large-scale prospective data. Arch Intern Med, 2008; 168: 598-608 source
• Not checked yetcites [225] 226) Erqou S, Kaptoge S, Perry PL, Di Angelantonio E, Thompson A, White IR, Marcovina SM, Collins R, Thompson SG, Danesh J, Emerging Risk Factors Collaboration. Lipoprotein (a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 2009; 302: 412-423 source
• Not checked yetcites [226] 227) Marcovina SM, Koschinsky ML. Evaluation of lipoprotein (a) as a prothrombotic factor: Progress from bench to bedside. Curr Opin Lipidol, 2003; 14: 361-366 source
• Not checked yetcites [227] 228) Clarke R, Peden JF, Hopewell JC, Kyriakou T, Goel A, Heath SC, Parish S, Barlera S, Franzosi MG, Rust S, Bennett D, Silveira A, Malarstig A, Green FR, Lathrop M, Gigante B, Leander K, de Faire U, Seedorf U, Hamsten A, Collins R, Watkins H, Farrall M, Consortium P. Genetic variants associated with lp (a) lipoprotein level and coronary disease. N Engl J Med, 2009; 361: 2518-2528 source
• Not checked yetcites [228] 229) Boffa MB, Koschinsky ML. Lipoprotein (a): Truly a direct prothrombotic factor in cardiovascular disease? J Lipid Res, 2016; 57: 745-757 source

In the paper

“High Lp(a) concentrations are found in patients with FH, and it is presumed that hyper-Lp (a)-lipoproteinemia further increases the risk for CVD in patients with FH222).”

What the sources say

• Not checked yetcites [222] 223) Dube JB, Boffa MB, Hegele RA, Koschinsky ML. Lipoprotein (a): More interesting than ever after 50 years. Curr Opin Lipidol, 2012; 23: 133-140 source

In the paper

“When the size of apolipoprotein (a) [apo(a)] is small, the concentration of Lp(a) is high, and there is a high risk of CVD.”

What the sources say

• Not checked yetcites [221] 222) Kronenberg F, Utermann G. Lipoprotein (a): Resurrected by genetics. J Intern Med, 2013; 273: 6-30 source
• Not checked yetcites [222] 223) Dube JB, Boffa MB, Hegele RA, Koschinsky ML. Lipoprotein (a): More interesting than ever after 50 years. Curr Opin Lipidol, 2012; 23: 133-140 source
• Not checked yetcites [223] 224) Schaefer EJ, Lamon-Fava S, Jenner JL, McNamara JR, Ordovas JM, Davis CE, Abolafia JM, Lippel K, Levy RI. Lipoprotein (a) levels and risk of coronary heart disease in men. The lipid research clinics coronary primary prevention trial. JAMA, 1994; 271: 999-1003 source
• Not checked yetcites [224] 225) Bennet A, Di Angelantonio E, Erqou S, Eiriksdottir G, Sigurdsson G, Woodward M, Rumley A, Lowe GD, Danesh J, Gudnason V. Lipoprotein (a) levels and risk of future coronary heart disease: Large-scale prospective data. Arch Intern Med, 2008; 168: 598-608 source
• Not checked yetcites [225] 226) Erqou S, Kaptoge S, Perry PL, Di Angelantonio E, Thompson A, White IR, Marcovina SM, Collins R, Thompson SG, Danesh J, Emerging Risk Factors Collaboration. Lipoprotein (a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 2009; 302: 412-423 source
• Not checked yetcites [226] 227) Marcovina SM, Koschinsky ML. Evaluation of lipoprotein (a) as a prothrombotic factor: Progress from bench to bedside. Curr Opin Lipidol, 2003; 14: 361-366 source
• Not checked yetcites [227] 228) Clarke R, Peden JF, Hopewell JC, Kyriakou T, Goel A, Heath SC, Parish S, Barlera S, Franzosi MG, Rust S, Bennett D, Silveira A, Malarstig A, Green FR, Lathrop M, Gigante B, Leander K, de Faire U, Seedorf U, Hamsten A, Collins R, Watkins H, Farrall M, Consortium P. Genetic variants associated with lp (a) lipoprotein level and coronary disease. N Engl J Med, 2009; 361: 2518-2528 source
• Not checked yetcites [228] 229) Boffa MB, Koschinsky ML. Lipoprotein (a): Truly a direct prothrombotic factor in cardiovascular disease? J Lipid Res, 2016; 57: 745-757 source

In the paper

“MDALDL is useful for prognostic prediction of the incidence of CAD and the recurrence of stenosis after percutaneous coronary intervention (PCI) in diabetic patients with a history of CAD236).”

What the sources say

• Not checked yetcites [236] 237) Ito T, Fujita H, Tani T, Ohte N. Malondialdehyde-modified low-density lipoprotein is a predictor of cardiac events in patients with stable angina on lipid-lowering therapy after percutaneous coronary intervention using drug-eluting stent. Atherosclerosis, 2015; 239: 311-317 source

In the paper

“PTX-3 is expected to serve as a specific marker reflecting CVD in the future283–286).”

What the sources say

• Not checked yetcites [283] 284) Iwata A, Miura S, Tanaka T, Ike A, Sugihara M, Nishikawa H, Kawamura A, Saku K. Plasma pentraxin-3 levels are associated with coronary plaque vulnerability and are decreased by statin. Coron Artery Dis, 2012; 23: 315-321 source
• Not checked yetcites [284] 285) Hollan I, Nebuloni M, Bottazzi B, Mikkelsen K, Forre OT, Almdahl SM, Mantovani A, Fagerland MW, Auk-rust P, Meroni PL, Feiring Heart Biopsy Study Group. Pentraxin 3, a novel cardiovascular biomarker, is expressed in aortic specimens of patients with coronary artery disease with and without rheumatoid arthritis. Cardiovasc Pathol, 2013; 22: 324-331 source
• Not checked yetcites [285] 286) Yasunaga T, Ikeda S, Koga S, Nakata T, Yoshida T, Masuda N, Kohno S, Maemura K. Plasma pentraxin 3 is a more potent predictor of endothelial dysfunction than high-sensitive c-reactive protein. Int Heart J, 2014; 55: 160-164 source
• Not checked yetcites [286] 287) Gerhard GT, Duell PB. Homocysteine and atherosclerosis. Curr Opin Lipidol, 1999; 10: 417-428 source

In the paper

“Recent reports have suggested that the association of CRP and PTX-3 in coronary artery plaques in pathological autopsies shows that both CRP and PTX-3 reflect unstable plaques.”

What the sources say

• Not checked yetcites [283] 284) Iwata A, Miura S, Tanaka T, Ike A, Sugihara M, Nishikawa H, Kawamura A, Saku K. Plasma pentraxin-3 levels are associated with coronary plaque vulnerability and are decreased by statin. Coron Artery Dis, 2012; 23: 315-321 source
• Not checked yetcites [284] 285) Hollan I, Nebuloni M, Bottazzi B, Mikkelsen K, Forre OT, Almdahl SM, Mantovani A, Fagerland MW, Auk-rust P, Meroni PL, Feiring Heart Biopsy Study Group. Pentraxin 3, a novel cardiovascular biomarker, is expressed in aortic specimens of patients with coronary artery disease with and without rheumatoid arthritis. Cardiovasc Pathol, 2013; 22: 324-331 source
• Not checked yetcites [285] 286) Yasunaga T, Ikeda S, Koga S, Nakata T, Yoshida T, Masuda N, Kohno S, Maemura K. Plasma pentraxin 3 is a more potent predictor of endothelial dysfunction than high-sensitive c-reactive protein. Int Heart J, 2014; 55: 160-164 source
• Not checked yetcites [286] 287) Gerhard GT, Duell PB. Homocysteine and atherosclerosis. Curr Opin Lipidol, 1999; 10: 417-428 source

In the paper

“hs-CRP has also been associated with the onset risk of MI and stroke, of which the association is particularly strong in MI281).”

What the sources say

• Not checked yetcites [281] 282) Wensley F, Gao P, Burgess S, Kaptoge S, Di Angelantonio E, Shah T, Engert JC, Clarke R, Davey-Smith G, Nordestgaard BG, Saleheen D, Samani NJ, Sandhu M, Anand S, Pepys MB, Smeeth L, Whittaker J, Casas JP, Thompson SG, Hingorani AD, Danesh J, C Reactive Protein Coronary Heart Disease Genetics Collaboration (CCGC). Association between c reactive protein and coronary heart disease: Mendelian randomisation analysis based on individual participant data. BMJ, 2011; 342: d548 source

In the paper

“The apo B/AI ratio, in particular, was strongly involved in the coronary atherosclerosis; however, the significance disappeared after adjustment for confounding factors276).”

What the sources say

• Not checked yetcites [276] 277) Hisamatsu T, Fujiyoshi A, Miura K, Ohkubo T, Kadota A, Kadowaki S, Kadowaki T, Yamamoto T, Miyagawa N, Zaid M, Torii S, Takashima N, Murakami Y, Okamura T, Horie M, Ueshima H, SESSA Research Group. Lipoprotein particle profiles compared with standard lipids in association with coronary artery calcification in the general Japanese population. Atherosclerosis, 2014; 236: 237-243 source

In the paper

“In addition, small dense LDL is more strongly associated with the risk for CAD259), the severity of coronary atherosclerosis256, 260), and the incidence of ASCVD in secondary prevention261) than is LDL-C among Japanese populations.”

What the sources say

• Not checked yetcites [259] 260) Koba S, Yokota Y, Hirano T, Ito Y, Ban Y, Tsunoda F, Sato T, Shoji M, Suzuki H, Geshi E, Kobayashi Y, Katagiri T. Small LDL-cholesterol is superior to LDL-cholesterol for determining severe coronary atherosclerosis. J Atheroscler Thromb, 2008; 15: 250-260 source
• Not checked yetcites [256] 257) Rizzo M, Pernice V, Frasheri A, Berneis K. Atherogenic lipoprotein phenotype and LDL size and subclasses in patients with peripheral arterial disease. Atherosclerosis, 2008; 197: 237-241 source
• Not checked yetcites [260] 261) Nishikura T, Koba S, Yokota Y, Hirano T, Tsunoda F, Shoji M, Hamazaki Y, Suzuki H, Itoh Y, Katagiri T, Kobayashi Y. Elevated small dense low-density lipoprotein cholesterol as a predictor for future cardiovascular events in patients with stable coronary artery disease. J Atheroscler Thromb, 2014; 21: 755-767 source

In the paper

“However, the distributions of CRP and PTX-3 in the plaques are not the same, and there is a possibility that they play different roles.”

What the sources say

• Not checked yetcites [283] 284) Iwata A, Miura S, Tanaka T, Ike A, Sugihara M, Nishikawa H, Kawamura A, Saku K. Plasma pentraxin-3 levels are associated with coronary plaque vulnerability and are decreased by statin. Coron Artery Dis, 2012; 23: 315-321 source
• Not checked yetcites [284] 285) Hollan I, Nebuloni M, Bottazzi B, Mikkelsen K, Forre OT, Almdahl SM, Mantovani A, Fagerland MW, Auk-rust P, Meroni PL, Feiring Heart Biopsy Study Group. Pentraxin 3, a novel cardiovascular biomarker, is expressed in aortic specimens of patients with coronary artery disease with and without rheumatoid arthritis. Cardiovasc Pathol, 2013; 22: 324-331 source
• Not checked yetcites [285] 286) Yasunaga T, Ikeda S, Koga S, Nakata T, Yoshida T, Masuda N, Kohno S, Maemura K. Plasma pentraxin 3 is a more potent predictor of endothelial dysfunction than high-sensitive c-reactive protein. Int Heart J, 2014; 55: 160-164 source
• Not checked yetcites [286] 287) Gerhard GT, Duell PB. Homocysteine and atherosclerosis. Curr Opin Lipidol, 1999; 10: 417-428 source

In the paper

“However, rather than the levels of these lipids and apolipoproteins, the ratio of different cholesterols and the ratio of different apolipoproteins contained in each lipoprotein are risk factors for ASCVD.”

What the sources say

• Not checked yetcites [268] 269) Sniderman AD, Williams K, Contois JH, Monroe HM, McQueen MJ, de Graaf J, Furberg CD. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein b as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes, 2011; 4: 337-345 source
• Not checked yetcites [273] 274) Kastelein JJ, van der Steeg WA, Holme I, Gaffney M, Cater NB, Barter P, Deedwania P, Olsson AG, Boekholdt SM, Demicco DA, Szarek M, LaRosa JC, Pedersen TR, Grundy SM, TNT Study Group; IDEAL Study Group. Lipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment. Circulation, 2008; 117: 3002-3009 source
• Not checked yetcites [274] 275) Ray KK, Cannon CP, Cairns R, Morrow DA, Ridker PM, Braunwald E. Prognostic utility of apoB/AI, total cholesterol/HDL, non-HDL cholesterol, or hs-CRP as predictors of clinical risk in patients receiving statin therapy after acute coronary syndromes: Results from PROVE IT-TIMI 22. Arterioscler Thromb Vasc Biol, 2009; 29: 424-430 source
• Not checked yetcites [275] 276) Hong LF, Yan XN, Fan Y, Wu Q, Luo SH, Yang B, Li JJ. Is the ratio of apoB/apoA-1 the best predictor for the severity of coronary artery lesions in chinese diabetics with stable angina pectoris? An assessment based on gensini scores. J Geriatr Cardiol, 2015; 12: 402-409