Low-Grade Inflammation, Thrombogenicity, and Atherogenic Lipid Profile in Cigarette Smokers

Yasue, Hirofumi; Hirai, Nobumitsu; Mizuno, Yuji; Harada, Eisaku; Itoh, Teruhiko; Yoshimura, Michihiro; Kugiyama, Kiyotaka; Ogawa, Hisao

doi:10.1253/circj.70.8

Cited by 101 publications

(86 citation statements)

References 52 publications

(89 reference statements)

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“…Previous studies have shown three mechanisms by which smoking causes CI: atheromatous atherosclerosis of arterial wall (Prati et al 2006), platelets agglutination in small vessels (Yasue et al 2006), and cardiogenic thrombosis due to arrhythmia or cardiage dysfunction such as myocardial infarction (Cirillo et al 2006). Using the panoramic dental radiographs, only the result of the atherosclerotic mechanism can be seen as the presence of carotid artery calcification, as shown in this study.…”

Section: Discussionsupporting

confidence: 59%

Long-Term Cigarette Smoking Increases the Prevalence of Carotid Artery Calcification Seen on Panoramic Dental Radiographs in Male Patients

Kumagai

Yamagishi

Fukui

et al. 2007

Tohoku J. Exp. Med.

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Panoramic dental radiographs are commonly used in general dentistry and oral and maxillofacial surgery to examine upper and lower teeth, maxilla, mandible and the surroundings simultaneously. Carotid artery calcification, a specific indicator of atherosclerotic change of the carotid arteries, can be seen on the radiographs. Many studies have suggested that cigarette smoking is a risk factor of atherosclerotic change as well as cerebral infarction. We hypothesized that smoking could increase the prevalence of carotid artery calcification, and compared the radiographs of smokers and non-smokers aged 50 years and over: 146 male smokers, 165 male non-smokers, 42 female smokers and 422 female non-smokers. This is the first study to focus on carotid artery calcification seen on panoramic dental radiographs to show the connection between smoking and atherosclerotic change. In male patients, carotid artery calcification was seen in 18 (14.1%) of the smokers, and in 8 (4.8%) of the non-smokers, which clearly shows that male patients aged 50 years old or over are more likely to develop carotid artery calcification if they smoke. However, there is no significant difference between female smokers and female non-smokers in the same age group. Dentists are in a good position to find carotid artery calcification on radiographs. When this is found on a radiograph, the patient should be advised to stop smoking and be referred to a physician for further tests. Clinicians should be aware that this radiographic finding indicates the presence of atherosclerotic change of the carotid arteries. carotid artery calcification; panoramic dental radiograph; cerebral infarction; cigarette smoking; atherosclerosis

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Section: Discussionsupporting

confidence: 59%

Long-Term Cigarette Smoking Increases the Prevalence of Carotid Artery Calcification Seen on Panoramic Dental Radiographs in Male Patients

Kumagai

Yamagishi

Fukui

et al. 2007

Tohoku J. Exp. Med.

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“…Yasue, et al showed that inflammation markers, such as the blood levels of CRP, fibrinogen, and leukocytes, which are a manifestation of chronic inflammation, are elevated in current smokers compared with subjects who have never smoked. 19) Furthermore, it was also reported that smokers have increased levels of several inflammatory biomarkers. 20,21) It is thus quite probable that smoking induces inflammation, an atherogenic lipid profile, and a propensity to thrombosis, thereby promoting the development of coronary atherothrombosis.…”

Section: Discussionmentioning

confidence: 99%

<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

Katayama¹,

Iwasaki²,

Sakoda³

et al. 2008

Int. Heart J.

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SUMMARYDespite increased risk for coronary artery disease and acute myocardial infarction (AMI), prior studies have found that smokers with AMI have lower mortality rates than nonsmokers, a phenomenon often termed 'smoker's paradox'. The present study was designed to examine the etiology of 'smoker's paradox', especially with respect to the association with inflammation.The subjects included 528 consecutive AMI patients who were admitted within 24 hours of onset and underwent successful coronary intervention. Of the 528 subjects, 232 (44%) were smokers.The cardiac mortality rates over a 6 month period was significantly lower in the smoking group than the nonsmoking group (3% versus 9%, P = 0.01). There were significantly more male patients in the smoking group, and the smoking group was significantly younger than the nonsmoking group (P < 0.0001). The value of high sensitivity C-reactive protein (hs-CRP) on admission and 24 hours after onset, and serum amyloid A protein (SAA) were significantly higher, and acute phase BNP was significantly lower (hs-CRP on admission 1.36 ± 1.03 mg/dL versus 0.75 ± 0.82 mg/dL, P = 0.02, hs-CRP at 24 hours 3.86 ± 4.32 mg/dL versus 2.90 ± 3.46 mg/dL, P = 0.008, SAA; 288 ± 392 µg/dL versus 176 ± 206 µg/dL, P < 0.05, BNP; 248 ± 342 pg/mL versus 444 ± 496 pg/mL, P = 0.0002) in the smoking group than in the nonsmoking group. The early ST-segment resolution rate was higher in the smoking group compared with the nonsmoking group (80% versus 66%, P = 0.003).The reason why smokers with AMI have lower mortality rates than nonsmokers, the so-called 'smoker's paradox', is believed to be because smoking induces inflammation and smokers may have less damage to microvascular function after primary percutaneous coronary intervention. (Int Heart J 2008; 49: 13-24) Key words: Myocardial infarction, Smoking, Inflammation EVEN though many epidemiologic studies have shown that cigarette smoking is associated with higher rates of myocardial infarction and death from coronary From the

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“…4 The mechanism by which cigarette smoking causes atherosclerosis remains unknown, only cigarette smoking have been ground to change the level of lipoproteins. [5][6][7][8][9] Plasma lipoprotein abnormalities are said to be the major underlying risk factors and may even be essential for the common occurrence of atherosclerotic vascular diseases. 10 Nicotine stimulates sympathetic adrenal system, leading to increased secretion of catecholamine resulting in increased lipolysis and increased concentration of plasma free fatty acids (FFA) which further result in increased secretion of hepatic FFAs and hepatic triglycerides along with VLDL-C in the blood stream.…”

Section: Introductionmentioning

confidence: 99%

To study the hypotensive and hypolipidemic effects of garlic in smokers in the North Indian population

Sanagapati

Vujhini

2015

Int J Res Med Sci

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Low-Grade Inflammation, Thrombogenicity, and Atherogenic Lipid Profile in Cigarette Smokers

Cited by 101 publications

References 52 publications

Long-Term Cigarette Smoking Increases the Prevalence of Carotid Artery Calcification Seen on Panoramic Dental Radiographs in Male Patients

Long-Term Cigarette Smoking Increases the Prevalence of Carotid Artery Calcification Seen on Panoramic Dental Radiographs in Male Patients

<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

To study the hypotensive and hypolipidemic effects of garlic in smokers in the North Indian population

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Low-Grade Inflammation, Thrombogenicity, and Atherogenic Lipid Profile in Cigarette Smokers

Cited by 101 publications

References 52 publications

Long-Term Cigarette Smoking Increases the Prevalence of Carotid Artery Calcification Seen on Panoramic Dental Radiographs in Male Patients

Long-Term Cigarette Smoking Increases the Prevalence of Carotid Artery Calcification Seen on Panoramic Dental Radiographs in Male Patients

<b>The Etiology of &lsquo;Smoker&rsquo;s Paradox&rsquo; in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>

To study the hypotensive and hypolipidemic effects of garlic in smokers in the North Indian population

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<b>The Etiology of ‘Smoker’s Paradox’ in Acute Myocardial Infarction With Special Emphasis on the Association With Inflammation</b>