Impact of Smoking Status on Long-Term Mortality in Patients With Acute Myocardial Infarction

Kinjo, Kunihiro; Sato, Hiroshi; Sakata, Yasuhiko; Nakatani, Daisaku; Mizuno, Hiroya; Shimizu, Masahiko; Sasaki, Tatsuya; Kijima, Yoshiyuki; Nishino, Masami; Uematsu, Masaaki; Tanouchi, Jun; Nanto, Shinsuke; Otsu, Kinya; Hori, Masatsugu

doi:10.1253/circj.69.7

Cited by 50 publications

(53 citation statements)

References 38 publications

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“…It has been shown that cardiac events and mortality are lower in subjects who have given up smoking than in subjects who continued to smoke. [41][42][43][44] However, in contrast to many studies, 6,7) our study showed that there was no change in the plasma concentration of norepinephrine or epinephrine between before and after cigarette smoking in either group. The reasons for this result are that it is too short a time to take a sample, and it is too short a time to smoke, because it has been shown that the plasma concentration of catecholamine begins to rise 10 minutes after starting to smoke a cigarette.…”

Section: Discussioncontrasting

confidence: 98%

Cigarette Smoking Augments Sympathetic Nerve Activity in Patients With Coronary Heart Disease

2008

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SUMMARYIt has been shown that cigarette smoking increases blood pressure (BP) and heart rate (HR), and decreases muscle sympathetic nerve activity (MSNA) in healthy young smokers. The decrease in MSNA might be secondary to baroreflex responses to the pressor effect. We tested the hypothesis that cigarette smoking increases MSNA in smokers with impaired baroreflex function.The effects of cigarette smoking on BP, HR, forearm blood flow (FBF), forearm vascular resistance (FVR), and MSNA were examined in 14 patients with stable effort angina (59 ± 3 years, group CAD) and 10 healthy smokers (23 ± 1 years, group C). In group CAD, the arterial baroreflex sensitivity (BRS) was significantly lower than in group C (4.7 ± 0.8 versus 15.1 ± 2.2 msec/mmHg, P < 0.01). In both groups, cigarette smoking increased the plasma concentration of nicotine, systolic and diastolic BP, HR, and FVR significantly (P < 0.01), but decreased FBF significantly (P < 0.01). After smoking, MSNA was decreased significantly in group C (from 35.2 ± 3.5 to 23.5 ± 3.2 bursts/100 beats, P < 0.01), but increased significantly in group CAD (from 48.8 ± 5.4 to 57.3 ± 5.5 bursts/100 beats, P < 0.01). There was significant correlation between BRS and changes in MSNA (r = -0.62, P < 0.01).Cigarette smoking increased MSNA in smokers with impaired baroreflex function. This demonstrates that cigarette smoking stimulates sympathetic nerve activity by both a direct peripheral effect and a centrally mediated effect. (Int Heart J 2008; 49: 261-272)

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Section: Discussioncontrasting

confidence: 98%

Cigarette Smoking Augments Sympathetic Nerve Activity in Patients With Coronary Heart Disease

2008

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“…For example, continued smoking in CAD patients is associated with non-fatal myocardial infarctions, recurrent coronary events, the lowering of high-density lipoprotein cholesterol, restenosis and all-cause mortality (Critchley and Capewell, 2004;Rea et al, 2002;Johansson et al, 1985;Ronnevik et al, 1985;Salonen et al, 1980;Wilson et al, 2000;Perkins and Dick, 1985;Kinjo et al, 2005;Serrano et al, 2003;Kwiterovich et al, 1998). Previous studies show that approximately 14-37% of the cardiac population are current smokers (Attebring et al, 2004;Hasdai et al, 1997;Huijbrechts et al, 1996;Kronish et al, 2006;Taira et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

The association among depressive symptoms, smoking status and antidepressant use in cardiac outpatients

et al. 2009

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Both depression and smoking are highly prevalent and related to poorer outcomes in cardiac patients. In this study, the authors examined the association between depressive symptoms and smoking status, described the frequency and type of antidepressant use, and prospectively tested the effects of antidepressant use in smokers on smoking status and psychosocial outcomes. Participants comprised 1498 coronary artery disease (CAD) outpatients who completed a baseline survey which assessed depressive symptoms, current medications, and smoking status. A second survey was mailed 9 months later that assessed depressive symptoms, anxiety, insomnia, current medications and smoking status. Results showed that current and former-smokers had significantly greater depressive symptoms than non-smokers. Ten percent of patients were taking antidepressants, most frequently SSRIs, with significantly more smokers on antidepressants than former and non-smokers. At follow-up, smokers on antidepressants were less likely to have quit, had greater anxiety, depressive symptoms and insomnia than smokers not using antidepressants. This study demonstrated that smokers and quitters with CAD had greater depressive symptoms and use of antidepressants than non-smokers, but that the antidepressants utilized may not be optimizing outcomes.

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“…They are thought to have responded better to the thrombolytic drugs because of that, and to have had a higher clot lysis rate, which may have had a favorable effect on their rate of TIMI-3 flow acquisition before PCI. 12,13) Nevertheless, this finding does not negate the adverse effect of smoking or the benefit of smoking cessation on the development and outcome of myocardial infarction [14][15][16] and ischemic heart disease. 17,18) It is particularly noteworthy that the rate of occurrence of coronary artery spasm is known to be higher in Japanese than in Westerners, 19) and there is no question about the need for smoking cessation from the standpoint of preventing myocardial infarction due to spasm.…”

Section: Discussionmentioning

confidence: 88%

Predictive Factors of TIMI-3 Flow Before Percutaneous Coronary Intervention in Facilitated Percutaneous Coronary Intervention for Acute Myocardial Infarction Analysis Based on the Fibrinolysis and Subsequent Transluminal Trial (FAST)

et al. 2006

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SUMMARYThe outcome for facilitated percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is known to be more favorable in cases in which TIMI-3 flow is obtained before PCI. We investigated factors that affect the acquisition of TIMI-3 flow before PCI.Facilitated PCI was performed on 178 patients divided into two groups, a group in which TIMI-3 flow was acquired before conducting PCI and another in which it was not, and their background factors and short-term outcomes were investigated. The hemoglobin concentrations, white blood cell (WBC) counts, and HbA1c values were significantly lower in the group in which TIMI-3 flow was acquired before PCI and significantly more had a history of past smoking. According to the results of logistic analysis, WBC count (odds ratio [OR], 0.865, P = 0.0077), hemoglobin concentration (OR, 0.77, P = 0.0257), and smoking history (OR, 0.266, P = 0.0021) were independent factors that predicted acquisition of TIMI-3 flow.The WBC count and hemoglobin value on arrival at the emergency room and history of smoking were shown to be independent factors for acquisition of TIMI-3 flow before PCI in facilitated PCI. (Int Heart J 2006; 47: 29-35)

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Impact of Smoking Status on Long-Term Mortality in Patients With Acute Myocardial Infarction

Cited by 50 publications

References 38 publications

Cigarette Smoking Augments Sympathetic Nerve Activity in Patients With Coronary Heart Disease

Cigarette Smoking Augments Sympathetic Nerve Activity in Patients With Coronary Heart Disease

The association among depressive symptoms, smoking status and antidepressant use in cardiac outpatients

Predictive Factors of TIMI-3 Flow Before Percutaneous Coronary Intervention in Facilitated Percutaneous Coronary Intervention for Acute Myocardial Infarction Analysis Based on the Fibrinolysis and Subsequent Transluminal Trial (FAST)

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