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      Acute electrocardiographic changes during smoking: an observational study

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          Abstract

          Objective

          To study the temporal relationship of smoking with electrophysiological changes.

          Design

          Prospective observational study.

          Setting

          Tertiary cardiac center.

          Participants

          Male smokers with atypical chest pain were screened with a treadmill exercise test (TMT). A total of 31 such patients aged 49.8±10.5 years, in whom TMT was either negative or mildly positive were included. Heart rate variability (HRV) parameters of smokers were compared to those of 15 healthy non-smoking participants.

          Interventions

          All patients underwent a 24 h Holter monitoring to assess ECG changes during smoking periods.

          Results

          Heart rate increased acutely during smoking. Mean heart rate increased from 83.8±13.7 bpm 10 min before smoking, to 90.5±16.4 bpm during smoking, (p<0.0001) and returned to baseline after 30 min. Smoking was also associated with increased ectopic beats (mean of 5.3/h prior to smoking to 9.8/h during smoking to 11.3/h during the hour after smoking; p<0.001). Three patients (9.7%) had significant ST–T changes after smoking. HRV index significantly decreased in smokers (15.2±5.3) as compared to non-smoking controls participants (19.4±3.6; p=0.02), but the other spectral HRV parameters were comparable.

          Conclusions

          Heart rate and ectopic beats increase acutely following smoking. Ischaemic ST–T changes were also detected during smoking. Spectral parameters of HRV analysis of smokers remained in normal limits, but more importantly geometrical parameter—HRV index—showed significant abnormality.

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          Most cited references18

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          Low heart rate variability in a 2-minute rhythm strip predicts risk of coronary heart disease and mortality from several causes: the ARIC Study. Atherosclerosis Risk In Communities.

          Low heart rate variability (HRV) is associated with a higher risk of death in patients with heart disease and in elderly subjects and with a higher incidence of coronary heart disease (CHD) in the general population. We studied the predictive value of HRV for CHD and death from several causes in a population study of 14 672 men and women without CHD, aged 45 to 65, by using the case-cohort design. At baseline, in 1987 to 1989, 2-minute rhythm strips were recorded. Time-domain measures of HRV were determined in a random sample of 900 subjects, for all subjects with incident CHD (395 subjects), and for all deaths (443 subjects) that occurred through 1993. Relative rates of incident CHD and cause-specific death in tertiles of HRV were computed with Poisson regression for the case-cohort design. Subjects with low HRV had an adverse cardiovascular risk profile and an elevated risk of incident CHD and death. The increased risk of death could not be attributed to a specific cause and could not be explained by other risk factors. Low HRV was associated with increased risk of CHD and death from several causes. It is hypothesized that low HRV is a marker of less favorable health.
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            Assessment of autonomic function in cardiovascular disease: physiological basis and prognostic implications.

            Certain abnormalities of autonomic function in the setting of structural cardiovascular disease have been associated with an adverse prognosis. Various markers of autonomic activity have received increased attention as methods for identifying patients at risk for sudden death. Both the sympathetic and the parasympathetic limbs can be characterized by tonic levels of activity, which are modulated by, and respond reflexively to, physiological changes. Heart rate provides an index of the net effects of autonomic tone on the sinus node, and carries prognostic significance. Heart rate variability, though related to heart rate, assesses modulation of autonomic control of heart rate and carries additional prognostic information, which in some cases is more powerful than heart rate alone. Heart rate recovery after exercise represents the changes in autonomic tone that occur immediately after cessation of exercise. This index has also been shown to have prognostic significance. Autonomic evaluation during exercise and recovery may be important prognostically, because these are high-risk periods for sudden death, and the autonomic changes that occur with exercise could modulate this high risk. These markers provide related, but not redundant information about different aspects of autonomic effects on the sinus node.
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              Role of smoking in global and regional cardiovascular mortality.

              Smoking is a major cause of cardiovascular disease mortality. There is little information on how it contributes to global and regional cause-specific mortality from cardiovascular diseases for which background risk varies because of other risks. We used data from the American Cancer Society's Cancer Prevention Study II (CPS II) and the World Health Organization Global Burden of Disease mortality database to estimate smoking-attributable deaths from ischemic heart disease, cerebrovascular disease, and a cluster of other cardiovascular diseases for 14 epidemiological subregions of the world by age and sex. We used lung cancer mortality as an indirect marker for accumulated smoking hazard. CPS-II hazards were adjusted for important covariates. In the year 2000, an estimated 1.62 (95% CI, 1.27 to 2.04) million cardiovascular deaths in the world, 11% of total global cardiovascular deaths, were due to smoking. Of these, 1.17 million deaths were among men and 450,000 among women. There were 670,000 (95% CI, 440,000 to 920,000) smoking-attributable cardiovascular deaths in the developing world and 960,000 (95% CI, 770,000 to 1,200,000) in industrialized regions. Ischemic heart disease accounted for 54% of smoking-attributable cardiovascular mortality, followed by cerebrovascular disease (25%). There was variability across regions in the role of smoking as a cause of various cardiovascular diseases. More than 1 in every 10 cardiovascular deaths in the world in the year 2000 were attributable to smoking, demonstrating that it is an important preventable cause of cardiovascular mortality.
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                Author and article information

                Journal
                BMJ Open
                BMJ Open
                bmjopen
                bmjopen
                BMJ Open
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                2044-6055
                2013
                5 April 2013
                : 3
                : 4
                : e002486
                Affiliations
                Department of Cardiology, All India Institute of Medical Sciences , New Delhi, India
                Author notes
                [Correspondence to ] Dr Balram Bhargava; balrambhargava@ 123456yahoo.com
                Article
                bmjopen-2012-002486
                10.1136/bmjopen-2012-002486
                3641479
                23562816
                4045d725-183d-424c-ae1d-5b1ba065b7dc
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/3.0/ and http://creativecommons.org/licenses/by-nc/3.0/legalcode

                History
                : 12 December 2012
                : 5 February 2013
                : 7 March 2013
                Categories
                Cardiovascular Medicine
                Research
                1506
                1683
                1683
                1734

                Medicine
                clinical physiology
                Medicine
                clinical physiology

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