Anti- and pro-oxidant factors and endothelial dysfunction in
chronic cigarette smokers with coronary heart disease.Eur
J Intern Med. 2007 Jul;18(4):314-20.
BACKGROUND:
Endothelial dysfunction in cigarette smokers has been ascribed to
increased oxidative damage. The aims of the present study were to
compare the endothelial function of normotensive smokers with that
of non-smokers and to examine its relation to some parameters
representative of oxidative damage and of antioxidant capacity.
METHODS: We investigated 32 chronic smokers (15-30 cigarettes daily)
affected by coronary heart disease, ranging from acute myocardial
infarction to instable angina pectoris, and 28 matched non-smokers
without any definite risk factors. All subjects underwent assessment
of nitric oxide (NO)-dependent endothelial function, measured as
brachial artery vasodilatation in response to reactive ischemia,
using a standardized echographic method. Plasma and urinary levels
of NO were also measured in all subjects, as were urinary
15-isoprostane F(2t), plasma serum lipids, homocysteine (Hcy),
ascorbic acid, retinol, tocopherol, and alpha- and beta-carotene (by
high-performance liquid chromatography). RESULTS: Smokers showed a
significantly lower NO-mediated vasodilatation response (3.50% vs.
6.18%, p<0.001) and higher levels of urinary NO metabolites and
15-isoprostane F(2t). They also had higher levels of Hcy (p<0.001);
these values were significantly and inversely related to NO serum
levels (r=-0.512, p<0.001). Moreover, smokers had a significant and
corresponding reduction in circulating levels of ascorbic acid,
tocopherol, and alpha- and beta-carotene. CONCLUSIONS: The present
study shows a clear relation between endothelial dysfunction (NO
production impairment) and cigarette smoking, especially in the
presence of high levels of LDL-cholesterol. It also defines some
markers of both oxidative damage and antioxidant protective capacity
in this condition. The monitoring of these factors may be advisable
in order to assess the amount of endothelial damage.
Chronic and
acute effects of smoking on left and right ventricular relaxation in
young healthy smokers.Chest.
2007 Apr;131(4):1142-8.
BACKGROUND:
Left ventricular (LV) diastolic dysfunction has been observed in
cigarette smokers with coronary artery disease. The aim of the study
was to assess LV and right ventricular (RV) diastolic function in
healthy, young, and slim smokers before and after smoking one
cigarette. MATERIAL AND METHODS: The participants were 66 healthy
volunteers (age < 40 years; body mass index < 25 kg/m(2)): 33
smokers (study group [HS]) and 33 nonsmokers (control group).
Echocardiographic examination was done in the HS before smoking one
cigarette (HS-1) and after smoking one cigarette (HS-2). To assess
diastolic function of LV and RV mitral valve flow (MVF), pulmonary
venous flow (PVF) and tricuspid valve flow (TVF) were evaluated.
RESULTS: MVF early to late phase ratio (E/A) was significantly lower
in HS-1 and HS-2 than in the control group. The PVF systolic to
diastolic phase ratio (S/D) was significantly higher in HS-1 and
HS-2 than in the control group. These changes suggest LV diastolic
function impairment in the HS, but the MVF pattern remained within
the normal range. PVF S/D showed systolic dominance (S/D > 1)
typical for impaired LV relaxation and abnormal for this age group.
TVF E/A was significantly lower in HS-2 than in HS-1 and control
subjects and suggests RV diastolic dysfunction. CONCLUSIONS: The
following conclusion are made: (1) MVF and PVF demonstrate LV
relaxation impairment in healthy smokers before and after smoking
one cigarette; (2) the assessment of PVF is a good method reflecting
LV diastolic function changes, even when MVF remains normal; and (3)
TVF shows RV relaxation impairment after smoking one cigarette in
healthy smokers.
Tobacco use and risk of myocardial infarction in 52 countries in the
INTERHEART study: a case-control study.Lancet.
2006 Aug 19;368(9536):647-58.
BACKGROUND:
Tobacco use is one of the major avoidable causes of cardiovascular
diseases. We aimed to assess the risks associated with tobacco use
(both smoking and non-smoking) and second hand tobacco smoke (SHS)
worldwide. METHODS: We did a standardised case-control study of
acute myocardial infarction (AMI) with 27,089 participants in 52
countries (12,461 cases, 14,637 controls). We assessed relation
between risk of AMI and current or former smoking, type of tobacco,
amount smoked, effect of smokeless tobacco, and exposure to SHS. We
controlled for confounders such as differences in lifestyles between
smokers and non-smokers. FINDINGS: Current smoking was associated
with a greater risk of non-fatal AMI (odds ratio [OR] 2.95, 95% CI
2.77-3.14, p<0.0001) compared with never smoking; risk increased by
5.6% for every additional cigarette smoked. The OR associated with
former smoking fell to 1.87 (95% CI 1.55-2.24) within 3 years of
quitting. A residual excess risk remained 20 or more years after
quitting (1.22, 1.09-1.37). Exclusion of individuals exposed to SHS
in the never smoker reference group raised the risk in former
smokers by about 10%. Smoking beedies alone (indigenous to South
Asia) was associated with increased risk (2.89, 2.11-3.96) similar
to that associated with cigarette smoking. Chewing tobacco alone was
associated with OR 2.23 (1.41-3.52), and smokers who also chewed
tobacco had the highest increase in risk (4.09, 2.98-5.61). SHS was
associated with a graded increase in risk related to exposure; OR
was 1.24 (1.17-1.32) in individuals who were least exposed (1-7 h
per week) and 1.62 (1.45-1.81) in people who were most exposed (>21
h per week). Young male current smokers had the highest population
attributable risk (58.3%; 95% CI 55.0-61.6) and older women the
lowest (6.2%, 4.1-9.2). Population attributable risk for exposure to
SHS for more than 1 h per week in never smokers was 15.4%
(12.1-19.3). CONCLUSION: Tobacco use is one of the most important
causes of AMI globally, especially in men. All forms of tobacco use,
including different types of smoking and chewing tobacco and
inhalation of SHS, should be discouraged to prevent cardiovascular
diseases.
Does the impact of smoking on coronary heart disease
differ by low-density lipoprotein cholesterol level?: the
Atherosclerosis Risk in Communities (ARIC) Study.
Circ J. 2006 Sep;70(9):1105-10.
BACKGROUND: The
association of smoking with coronary heart disease (CHD) occurrence
has been reported to be weaker for populations with lower plasma
cholesterol levels. Recent studies suggest that low-density
lipoprotein cholesterol (LDL-C) and smoking contribute to different
stages of atherosclerosis, so the present study was designed to test
the hypothesis that smoking is a stronger risk factor for CHD when
LDL-C is high. METHODS AND RESULTS: The study group of 13,410
middle-aged adults who were initially free of stroke and CHD were
followed and over 13.3 years there were 932 incident CHD events.
Tests for multiplicative interaction were performed using
proportional hazards models. Both smoking and increased LDL-C were
risk factors for CHD incidence. The relative hazard (RH) of CHD in
relation to smoking tended to be larger among higher LDL-C
categories compared with lower LDL-C categories. For example, when
the participants were dichotomized into 4 categories, using smoking
>or=15 cigarettes per day and LDL-C >or=130 mg/dl as cutoffs, those
with high LDL-C and heavier cigarette smoking showed a very high RH
of CHD (RH =2.81) compared with that expected from the product of
the RHs of high LDL-C (RH =1.15) only x heavy smoking only (RH
=1.71) (p for interaction =0.04). CONCLUSIONS: These results suggest
positive multiplicative interactions between smoking and LDL-C for
CHD incidence.
Cardiovascular risks associated with smoking: a review for
clinicians.Eur
J Cardiovasc Prev Rehabil. 2006 Aug;13(4):507-14.
The
cardiovascular consequences of cigarette smoking may not be as
readily recognized as the adverse respiratory consequences. Smoking
results in sudden death, myocardial infarction, coronary heart
disease, worsened outcomes after angioplasty or bypass surgery,
cerebrovascular disease, aortic aneurysm, peripheral vascular
disease, increased risk of complications of hypertension and
impotence. Physicians should encourage and help all their smoking
patients to quit. Pharmacotherapy for smoking cessation is one of
the most cost-effective healthcare interventions and should be
offered to all dependent smokers. Both nicotine replacement and
bupropion have been shown to be well tolerated in populations with
cardiovascular disease.
Smoking cessation for patients with cardiovascular disease: what is
the best approach?
Am J Cardiovasc Drugs. 2003;3(5):339-49.
Tobacco use
remains the major preventable cause of early mortality and morbidity
in the US and is a major risk factor for cardiovascular disease (CVD).
Quitting smoking rapidly reduces the risk of cardiovascular events.
In this review, we identify and discuss best approaches to assist
smoking cessation among patients with CVD. Establishing office
systems that reliably identify smokers to healthcare providers is an
essential first step. Once the patient is identified as a smoker,
providers should inquire about their willingness to quit and advise
them to quit or provide motivation to get ready to make a quit
attempt. Behavioral (counseling) and pharmacologic (nicotine
replacement and non-nicotine medications) treatments double or
triple long-term cessation rates and should be offered in
combination to all patients with CVD who use tobacco. More intensive
behavioral therapy is more effective and should be delivered when
possible. The choice of pharmacotherapy will depend upon the
clinical history of the patient and patient preference. Nicotine
replacement and sustained release bupropion (bupropion SR) are
first-line treatments for smoking cessation. Nicotine patches have
been studied extensively in patients with stable CVD and have been
shown to be safe. Bupropion SR has relatively few cardiovascular
adverse effects and may be especially useful for patients with CVD;
its safety is currently being studied. Special consideration is
needed for hospitalized patients with acute coronary syndromes (e.g.
myocardial infarction and unstable angina). The safety of
pharmacotherapy in the acute setting is not yet established.
Behavioral interventions, however, are very effective and should be
delivered to all hospitalized smokers. Finally, it is important to
create a clinical environment that is supportive of treating
patients with tobacco dependence. Simple changes in office and
hospital routines and procedures (routine screening to identify
smokers, prompts to encourage intervention and links to more
intensive tobacco dependence treatment programs) will substantially
improve the identification, treatment, and outcomes of patients with
CVD who use tobacco.
Epidemiology of smoking-induced cardiovascular disease.Prog
Cardiovasc Dis. 2003 Jul-Aug;46(1):11-29.
Cigarette
smoking is a major cause of coronary heart disease, stroke, aortic
aneurysm, and peripheral vascular disease. The risk is manifest both
as an increased risk for thrombosis of narrowed vessels and as an
increased degree of atherosclerosis in those vessels. The
cardiovascular risks owing to cigarette smoking increase with the
amount smoked and with the duration of smoking. Risks are not
reduced by smoking cigarettes with lower machine-measured yields of
tar and nicotine, but those who have only smoked pipes or cigars
seem to have a lower risk for cardiovascular diseases. Cessation of
cigarette smoking reduces disease risks, although risks may remain
elevated for a decade or more after cessation.
Tobacco Smoking in Patients with Cardiovascular Disease.Curr
Treat Options Cardiovasc Med. 2001 Aug;3(4):313-322.
Smoking tobacco
is a major risk factor for patients with cardiovascular disease (CVD).
Quitting smoking rapidly reduces the risk for cardiovascular events.
The majority of patients who smoke express a desire to stop, and
cost-effective interventions are available. Behavioral (counseling)
and pharmacologic (nicotine replacement and non-nicotine
medications) treatments double or triple the rate of long-term
cessation and should be offered in combination to all patients with
CVD who use tobacco. Behavioral therapy can be effectively delivered
by a variety of health care providers and means (in person,
telephone, mail). For patients with CVD, more intensive and
sustained interventions should be encouraged. Nicotine patches have
been studied extensively in patients with stable CVD and are safe.
Bupropion (a non-nicotine aid) also may be especially useful for
patients with CVD. Special consideration is needed for patients with
acute coronary syndromes (ie, myocardial infarction and unstable
angina). It is important to create a clinical environment that
supports treatment of patients with nicotine addiction. Simple
changes in office and hospital routines and procedures (establishing
routine screening to identify users of tobacco, prompts to encourage
intervention, establishing links to more intensive
nicotine-dependence treatment programs) can substantially improve
the identification, treatment, and outcomes for patients with CVD
who use tobacco.
Cigarette smoking and coronary heart disease: risks and management.Cardiol
Clin. 1996 Feb;14(1):51-68.
Tobacco smoking
is the leading preventable cause of death in the United States and
an important cause of CHD. The effect of smoking on the
cardiovascular system and coronary risk factors is pervasive.
Unfavorable effects include acute increases in blood pressure and
coronary vascular resistance, reduction in oxygen delivery,
enhancement of platelet aggregation, increased fibrinogen, and
depression of HDL cholesterol. Smoking cessation reduces
cardiovascular morbidity and mortality rates relatively rapidly,
even among individuals who stop smoking only after the age of 65 or
after developing the clinical manifestations of CHD including
myocardial infarction. Behavioral smoking-cessation programs and
nicotine-replacement therapy each have been demonstrated to be
effective for the treatment of smoking. The most effective treatment
currently available is to combine the two. Nicotine-replacement
therapy is safe and effective in patients with stable coronary heart
disease. Although the threat or diagnosis of CHD is a powerful
stimulus to spontaneous smoking cessation, many smokers continue to
smoke after events such as myocardial infarction or CABG surgery.
Studies have demonstrated that physician advice to stop smoking,
supplemented by brief counseling by a nurse and follow-up,
dramatically increases the smoking-cessation rate of patients
hospitalized with myocardial infarction and is highly cost
effective. In the outpatient setting, physician advice and
counseling is also effective in helping smokers with or without CHD
to stop smoking. This article outlines a simple protocol that has
been demonstrated to be effective for counseling smokers.
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