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"documento" => "article" "crossmark" => 1 "subdocumento" => "rev" "cita" => "Med Clin. 2019;152:147-53" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "Disease of the holobiont, the example of multiple sclerosis" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "147" "paginaFinal" => "153" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "El holobionte enfermo, el ejemplo de la esclerosis múltiple" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Federico Castillo-Álvarez, María Eugenia Marzo-Sola" "autores" => array:2 [ 0 => array:2 [ "nombre" => "Federico" "apellidos" => "Castillo-Álvarez" ] 1 => array:2 [ "nombre" => "María Eugenia" "apellidos" => "Marzo-Sola" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0025775318305682" "doi" => "10.1016/j.medcli.2018.08.019" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775318305682?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020618305898?idApp=UINPBA00004N" "url" => "/23870206/0000015200000004/v1_201902100719/S2387020618305898/v1_201902100719/en/main.assets" ] "en" => array:15 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Special article</span>" "titulo" => "Tobacco consumption, the forgotten factor in the calculation and approach of cardiovascular risk" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "154" "paginaFinal" => "158" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "César Minué-Lorenzo, Eduardo Olano-Espinosa" "autores" => array:2 [ 0 => array:4 [ "nombre" => "César" "apellidos" => "Minué-Lorenzo" "email" => array:2 [ 0 => "cminue@hotmail.com" 1 => "cesaraugustominue@salud.madrid.org" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "Eduardo" "apellidos" => "Olano-Espinosa" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Centro de Salud Perales del Río, DAC, Servicio Madrileño de Salud, Getafe (Madrid), Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Centro de Salud Los Castillos, DAO, Servicio Madrileño de Salud, Alcorcón (Madrid), Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Tabaquismo, el gran olvidado en el cálculo y abordaje del riesgo cardiovascular" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">On May 31 of each year, the World Health Organization celebrates <span class="elsevierStyleItalic">World No Tobacco Day</span> in order to highlight the risks associated with smoking. The slogan for 2018 was: “Tobacco and heart disease”. It was chosen deliberately.</p><p id="par0010" class="elsevierStylePara elsevierViewall">The role of smoking as a cardiovascular risk factor (CVRF) is significant, and its study and treatment should be a priority in both primary and secondary prevention of cardiovascular disease (CVD). However, this is not always the case: patients are usually warned about hypertension, diabetes or dyslipidaemia, accompanied by a weak “you should stop smoking”.</p><p id="par0015" class="elsevierStylePara elsevierViewall">This is due to several reasons: a lack in training for most doctors and nurses in smoking; poor interest and support from the health system (which currently does not finance first-line treatments to stop smoking), and the pressure by the pharmaceutical industry, which emphasises the treatment of other CVRF in promotional and training activities they finance.</p><p id="par0020" class="elsevierStylePara elsevierViewall">The truth is that CVD is closely associated with known and modifiable CVRF, and its prevention must be based on multifactorial interventions that differ among the general population (promotion of healthy habits, opportunistic detection of CVRF in males aged >40 and in females >50 or postmenopausal females), patients with known CVRF (calculation of CVR) and patients with high CVR, in which a priority intervention<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">1</span></a> should be carried out, given that the preventive profitability is greater as subjects’ risk increase.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Smoking as a cardiovascular risk factor. Pathogeny</span><p id="par0025" class="elsevierStylePara elsevierViewall">We know that smoking greatly increases the risk of coronary, cerebrovascular, peripheral arterial and aortic aneurysm.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a> Results from the INTERHEART study, that used cases and controls with 30,000 patients, showed that the risk of suffering an acute myocardial infarction was multiplied by almost three. It was calculated that the attributable population fraction (percentage of acute myocardial infarction attributable to smoking) was 35%.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">3</span></a> With differences according to studies, smoking triples the risk of sudden death<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a> and doubles that of stroke. Of great interest is the fact that epidemiological data indicate <span class="elsevierStyleItalic">a non-linear relationship</span> between the intensity of tobacco smoke and ischaemic heart disease. Although the dose of active smokers is 100 times that of passive smoking, the relative risk of coronary disease is 1.78 and 1.31, respectively.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">4</span></a> The results of a variety of meta-analysis in different populations, genders and geographical areas<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a> confirm the causal relationship between involuntary exposure to tobacco smoke and CVD mortality. The excess risk of cerebrovascular disease due to exposure to environmental tobacco smoke has also been established.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">In the ARIC study,<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">5</span></a> the atherosclerotic plaque in smokers progressed 50% more after three years than in non-smokers (20% more in the case of passive smoking). The components and mechanisms responsible are not completely clear.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Tobacco smoke increases inflammation and thrombosis, and decreases the availability of nitric oxide, which is involved in endothelial vasodilation and in the regulation of inflammation, leucocyte adhesion, platelet activation and thrombosis. It also modifies the lipid profile (increasing total cholesterol, triglycerides and LDL and decreasing HDL) and facilitates insulin resistance. All this favours arteriosclerosis.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">But in addition to the slower arteriosclerotic effect, smoking promotes acute rupture of the plaque and thrombosis through platelet dysfunction, action on prothrombotic factors and alteration of fibrinolysis. Small exposures, as in the case of passive smoking, can induce acute arterial and haemodynamic changes.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a> This mechanism probably explains the decrease in the number of admissions for acute myocardial infarction that follows the implementation of smoke-free policies,<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">6</span></a> why the relationship between smoking and CVD is not linear and why smoking little or exposure to passive smoke increases CVR by 30%.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">The management of cardiovascular risk factors</span><p id="par0045" class="elsevierStylePara elsevierViewall">The calculation of individual CVR, a key point of the main clinical practice guidelines for the prevention of arteriosclerosis, represents a qualitative leap from the isolated assessment of CVRF and is based on the gradual and continuous increase in risk according to a personal conjunction of factors. Its fundamental objective is to <span class="elsevierStyleItalic">help us make decisions</span> when we intervene, although it can also serve to motivate patients to comply with pharmacological and behavioural measures by graphically explaining how risk is reduced by controlling their CVRF.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Therefore, the practical management of CVRFs is not only to calculate the population risk, but also to pursue the objective of treating specific patients and thereby preventing excessive medicalisation, on one hand, and CVD, on the other. To do this we must prioritise our interventions, while considering: the ‘intensity’ of the factor, its ‘weight’ in CVR, its vulnerability to the intervention of choice, scientific evidence that supports this intervention, the risk/benefit balance, its cost/effectiveness, its possible interactions, side effects and contraindications and the values, beliefs and preferences of our patients, whom we must inform as much as possible, encourage to improve their health and, in addition to all this, empathetically and respectfully suggest recommendations and support all positive achievements no matter how small. Quite an odyssey.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Smoking as a cardiovascular risk factor to prioritise</span><p id="par0055" class="elsevierStylePara elsevierViewall">If the patient is a smoker, regardless of any other circumstance, CVRF well be the highest absolute risk and the lowest number needed to harm (NNH). The reader can calculate that.</p><p id="par0060" class="elsevierStylePara elsevierViewall">For various reasons (broad consensus, adapted cohorts, clinical guide, the HEARTSCORE programme, patient material and data recording), we recommend using the SCORE tables for these calculations (<a id="intr0010" class="elsevierStyleInterRef" href="http://www.heartscore.org/">www.heartscore.org</a>). This helps us to graphically show and share with the patient how, in the vast majority of cases, quitting smoking can reduce risks, control blood pressure and reduce cholesterol levels by 40% with statins. We will explore this further with an example later.</p><p id="par0065" class="elsevierStylePara elsevierViewall">In the hypothetical case of having to prioritise the treatment of a patient's risk factor, we should assess CVRF criteria – its ‘weight’, vulnerability to intervention, etc. – or of the intervention itself – its effectiveness, benefit/risk, cost/effectiveness, etc. All these paths lead us to preferentially intervene in the smoking habit.</p><p id="par0070" class="elsevierStylePara elsevierViewall">If we add to this that a nicotine dependence treatment is considered the gold standard in terms of effectiveness and efficiency due to the large quantity and quality of the evidence supporting it,<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">7</span></a> that the use of first line pharmacological treatments is very limited in time and that a large number of smokers spontaneously express their desire to stop smoking, we can conclude that, far from including it in ‘lifestyle recommendations’, we should seriously consider incorporating it into our usual clinical routine, with all the professional consequences that would entail.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Some special considerations</span><p id="par0075" class="elsevierStylePara elsevierViewall">Although it is becoming less frequent, the advice to ‘reduce’ smoking can still be seen in clinical reports. In addition to the great difficulty of reducing the number of cigarettes and, above all, to maintain that lower number (it is, in a large number of cases, an addiction), this reduction would not reduce the risk of CVD due to the aforementioned lack of proportionality in the relationship between the intensity of exposure to tobacco and CVD. This is confirmed at the population level. A Norwegian cohort study that monitored 50,000 people for 30 years, showed that halving the number of cigarettes did not decrease the risk of total death, or of death or CVD.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">8</span></a> We should not confuse this purported permanent decrease in consumption – that has no validity as a harm reduction strategy – with a progressive reduction in the number of cigarettes as a strategy to quit smoking altogether, to which we will refer later.</p><p id="par0080" class="elsevierStylePara elsevierViewall">When talking about the mechanisms by which smoking increases CVR, we have seen how small exposures to tobacco smoke trigger the possibilities of suffering a cardiovascular event, but some doctors and many smokers who smoke only a few cigarettes a day are often not aware of risk. Is this so?</p><p id="par0085" class="elsevierStylePara elsevierViewall">A recent meta-analysis confirms this data: when analysing data from 141 cohorts, it was calculated that the excess risk of smoking <span class="elsevierStyleItalic">one cigarette per day</span> was 74% in males and 57% in females for ischaemic heart disease and 30% in males and 46% in females for stroke.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">9</span></a> The advice is clear: there is no safe minimum consumption.</p><p id="par0090" class="elsevierStylePara elsevierViewall">In terms of the gender, a popular trend, do we know whether the role of smoking in CVRF is similar in males and females? In addition to the peculiarities of CVD in females, little represented in clinical trials, we know from population studies that females are especially susceptible to the action of smoking in their CVD genesis, 25% more than men<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">10</span></a> (relative risk of infarction in female smokers of 2.24 and in male smokers of 1.43), so that 50% of coronary events in females are attributable to smoking.</p><p id="par0095" class="elsevierStylePara elsevierViewall">A frequent concern when quitting smoking is weight gain. In most cases, this is less than 4<span class="elsevierStyleHsp" style=""></span>kg and is preventable, it has a much lower incidence than smoking does on health, finances and quality of life and we know that it does not influence the decrease in cardiovascular events.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">11</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">On the other hand, smoking is associated, according to a meta-analysis by the Surgeon General of 46 studies, with a 37% higher risk of suffering from diabetes,<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a> with a dose-response relationship. Quitting smoking reduces risk and improves insulin sensitivity. In addition, diabetic non-smokers have a more favourable lipid profile, a controlled glycated haemoglobin and lower mortality.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">In diabetic patients, actions with fewer NNT and, therefore, that are most efficient, are, in order: to quit smoking, tensional control, the use of metformin, lipid reduction and, finally, adequate glycaemic control.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">12</span></a></p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Tobacco and secondary prevention</span><p id="par0110" class="elsevierStylePara elsevierViewall">Quitting smoking after a heart attack reduces the risk of mortality by 36%,<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">13</span></a> according to a Cochrane review. Many other measures considered essential, such as the use of statins, antiaggregation or beta-blockers, reduce the risk in a much smaller proportion.<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">1</span></a> However, patients recently discharged from hospital due to an acute coronary syndrome are not always given the option to attend programmes to stop smoking, rather they are simply recommended them.</p><p id="par0115" class="elsevierStylePara elsevierViewall">Despite all these data, around 50% of patients continue to smoke after a cardiovascular event.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">13</span></a> Even though intensive anti-smoking interventions targeting patients hospitalised for acute CVD have shown that these programmes increase the chances of abandonment and can reduce mortality,<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">14</span></a> only a minority of patients admitted for heart attacks receive pharmacological treatment to stop smoking at discharge. On the other hand, relapses, common in dependencies, also occur. We should not assume that the enormous emotional impact of an acute coronary syndrome is enough to stop patients smoking, and to stay smoke-free.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Health advice to quit smoking</span><p id="par0120" class="elsevierStylePara elsevierViewall">It is not difficult to give good health advice to patients and encourage them to quit smoking, as the reasons are many and powerful: effectiveness, efficiency, absence of side effects and interactions, the synergistic effect of the intervention from different professionals, and the reach it would have on the population, as it is considered a public health issue.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">7</span></a> There are excellent monographs and teaching programmes that can train professionals in the elementary techniques of motivational speaking, but all of them will be useless unless health professionals realise that our attitude must be determined and <span class="elsevierStyleItalic">unanimous</span>, we must our lead by example and offer to help patients to quit smoking - this is essential to improving our interventions in CVR.</p><p id="par0125" class="elsevierStylePara elsevierViewall">A frequent perception is that patients smoke because they want to: everyone knows the risks. Apart from dealing with the concept of dependence, this is a false assumption. Many smokers think they do not have a higher-than-average risk of heart attack. A French study found that almost half of smokers considered that the risk of cancer only began when smoking more than when they did.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">15</span></a></p><p id="par0130" class="elsevierStylePara elsevierViewall">On the other hand, studying other aspects is of interest. If the patient thinks they have a high risk (50%, for example) and we tell them that they only have an 8% risk, they will be relieved (“it's not that bad”). Concerns about CVD and their personal or environmental experiences can also shape their response. When communicating risk, mathematical functions can often be difficult to understand, such as the NNT, useful from a clinical perspective but complex to understand. Some options may be to offer information in terms of ‘vascular age’ (the age which a patient's CVR would be if it they did not have CVRF: for example, if a 50-year-old male has a score of 4% (this score corresponds to being a smoking, having a systolic blood pressure of 160<span class="elsevierStyleHsp" style=""></span>mmHg and a total cholesterol of 280<span class="elsevierStyleHsp" style=""></span>mg/dl) their ‘vascular age’ is 70. If we reduce cholesterol by 5<span class="elsevierStyleHsp" style=""></span>mmol/l (to about 200<span class="elsevierStyleHsp" style=""></span>mg/dl), the vascular age is reduced to 66 (the patient ‘recovers’ four years). If we reduce their blood pressure to 140<span class="elsevierStyleHsp" style=""></span>mmHg, their vascular age is reduced to 65 years (they ‘recover’ five years). If they stop smoking, their vascular age is reduced to 60 years (they ‘recover’ 10 years).<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">16</span></a> When transmitting information, it is also advisable to avoid small percentages, information overload or excessive statistics. To make shared decisions with the patient, it is essential that they understand their priorities, the perceived risk and personal previous experiences; they must be informed of the scientific evidence, benefits, risks and alternatives.</p><p id="par0135" class="elsevierStylePara elsevierViewall">But, in addition to using rational processes, we also use our emotions to make decisions. We all tend to assume that risks are lower when associated with the things we like (and vice versa). The risks of an accident in a house where there is a weapon, are lower than in a house with a pool, although most of us would be much more concerned if our child was to spend the afternoon with their friend in the first house. The reality is that people stop smoking less than we think, even after a heart attack.</p><p id="par0140" class="elsevierStylePara elsevierViewall">So, what arguments can we use to correctly advise our patients to stop smoking or to refute their erroneous beliefs from the perspective of CVR? Let's take a look at a series of frequent clinical situations that use high quality evidence.</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">The benefits of quitting smoking in terms of cardiovascular disease</span><p id="par0145" class="elsevierStylePara elsevierViewall">We have seen that the <span class="elsevierStyleItalic">RCV Score</span> tables allow us to prioritise actions and graphically simulate risk reductions according to type of CVRF, and that the measure that almost always have the greatest impact in primary prevention is to simply stop smoking, which also has the added benefit of reducing risk in other non-cardiovascular diseases and for non-smokers.</p><p id="par0150" class="elsevierStylePara elsevierViewall">Under real conditions, the MRFIT study<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">17</span></a> in which patients initially without heart disease participated, smokers who quit had a 37% lower risk of coronary mortality after one year, and 62% after three years.</p><p id="par0155" class="elsevierStylePara elsevierViewall">We know from the results of the follow-up of the cohort by British doctors<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">18</span></a> that the survival curve of those who quit smoking before 35 years of age is superimposable over that of those who have never smoked, and that the sooner the habit of smoking is stopped, the better the results obtained. Although the follow-ups of a variety of cohorts tell us that to quit smoking is beneficial at any age, since, although survival is not comparable to that of those who have never smoked, it is better than that of those who continue to do so. The results of a meta-analysis by Mons et al.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">19</span></a> carried out in people older than 60, showed that the CVR of the person who stops smoking is never fully equal to the CVR of those who have never smoked, although it is almost superimposable after not having smoked for 10 years.</p><p id="par0160" class="elsevierStylePara elsevierViewall">Furthermore, although the relative risk of smoking for heart disease is greater at younger ages,<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a> being a more frequent disease with age, the absolute benefit in terms of quitting is enormous. Smoking doubles cardiovascular mortality risk even at older ages, such as those older than 60.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">2</span></a></p><p id="par0165" class="elsevierStylePara elsevierViewall">The decrease in <span class="elsevierStyleItalic">populational</span> mortality from ischaemic heart disease in recent decades is due to several reasons. Different models indicate that, initially, the main cause was an improvement in the control of the CVRF, especially the decrease in the prevalence of smoking. More recently, the appearance of new treatments has also contributed to this decline. Despite the fact that the role of each varies according to the models used and countries studied,<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">20</span></a> the importance of encouraging measures to reduce smoking – responsible for most of the decline and a reference for the modification of other lifestyles – is a constant. Even the implementation of smoke-free policies decreases hospitalisation and mortality of coronary and probably cerebrovascular disease.<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">2,6</span></a></p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">My patient wants to stop smoking: how can I help them?</span><p id="par0170" class="elsevierStylePara elsevierViewall">A combination of cognitive-behavioural and pharmacological treatment is the treatment of choice for smokers who would like to quit smoking.<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">21</span></a> Both types of treatment have shown their efficacy in cardiac patients.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a></p><p id="par0175" class="elsevierStylePara elsevierViewall">The most commonly used strategy to address the problem of smoking is the ‘five As’: find out (<span class="elsevierStyleItalic">ask</span>), give advice (<span class="elsevierStyleItalic">advise</span>), assess whether the patient is ready to quit (<span class="elsevierStyleItalic">assess</span>), refer (<span class="elsevierStyleItalic">assist</span>) and agree a follow-up (<span class="elsevierStyleItalic">arrange</span>). Advice should be given to all smokers and they should be asked whether they are willing to try to quit, a question that condenses the classic phases of change (precontemplation, contemplation, preparation, action, maintenance, relapse). Those who do not want to make an attempt to stop should receive a motivational intervention and those who express their willingness to quit should be given help.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">23</span></a> Should they want to quit, a progressive reduction of the number of cigarettes is an option as long as the main aim is to completely stop, and a date to do so has been set; this option has results similar to those of an abrupt cessation, depending on the characteristics and preferences of the smoker.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">24</span></a></p><p id="par0180" class="elsevierStylePara elsevierViewall">Regarding pharmacological resources, we know that the use of nicotine replacement therapy (NRT) increases the likelihood of quitting smoking.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">25</span></a> The combination of more than one type of NRT is more effective than the use of only one, and could be valid for patients with more intense dependence.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">26</span></a> TSN lacks the thrombotic and proaggregative effects of smoking cigarettes, generates less sympathetic stimulation and is not associated with an increased risk of cardiovascular effects. In general, caution of its use is recommended in the immediate period following a heart attack because some clinical trials have excluded its use two weeks later.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">26</span></a> The use of patches after an acute coronary episode is safe in the short and long term. Although there are other more complex profiles which vary according to, for example, the Fagerström test for nicotine dependency, guidelines recommend: 21<span class="elsevierStyleHsp" style=""></span>mg patches for 24<span class="elsevierStyleHsp" style=""></span>h (15<span class="elsevierStyleHsp" style=""></span>mg for 16<span class="elsevierStyleHsp" style=""></span>h) for four weeks, 14<span class="elsevierStyleHsp" style=""></span>mg (10<span class="elsevierStyleHsp" style=""></span>mg for 16<span class="elsevierStyleHsp" style=""></span>h) for two weeks and 7<span class="elsevierStyleHsp" style=""></span>mg (5<span class="elsevierStyleHsp" style=""></span>mg for 16<span class="elsevierStyleHsp" style=""></span>h) for the following two weeks, for those who smoke more than 10 cigarettes per day.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">27</span></a></p><p id="par0185" class="elsevierStylePara elsevierViewall">Bupropion, which doubles the possibilities of quitting smoking, is considered safe for patients with heart disease.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a> It is used for eight weeks at doses of between 150 and 300<span class="elsevierStyleHsp" style=""></span>mg/d, and treatment is started one week prior to the set withdrawal date. The other useful first-line drug to help quit smoking is varenicline. This medication has demonstrated its greater efficacy versus placebo, bupropion and TSN.<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">28</span></a> Over the last few years there has been much debate about the possible adverse cardiovascular effects of varenicline. A large clinical trial was recently published that used a sample of 8000 patients, promoted by the FDA and carried out by the varenicline and bupropion laboratories, supporting the neuropsychiatric safety of these drugs (the main concern regarding their safety).<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">29</span></a> The results of cardiovascular safety found in this same sample were also published, which concluded that pharmacological treatments to quit smoking do not increase the risk of serious cardiovascular events.<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">30</span></a></p><p id="par0190" class="elsevierStylePara elsevierViewall">A large proportion of the population consult their family doctor throughout the year, which is a great opportunity to intervene in smoking, in the same way that other CVRFs are addressed. However, every and all health professionals must be involved in the management and treatment of the patients who smoke.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">23</span></a> In highly dependent patients who have already attempted to quit or who have certain characteristics (pregnant patients, psychiatric illness or very high CVR), referral to specific smoking units may be appropriate, depending on the available resources.</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Conclusions</span><p id="par0195" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1.</span><p id="par0200" class="elsevierStylePara elsevierViewall">The role of smoking as a CVRF is essential, and its approach and treatment should be a priority in the prevention of CVD.</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2.</span><p id="par0205" class="elsevierStylePara elsevierViewall">In primary prevention, the measure that almost always has the greatest impact on CVR is to stop smoking, which also has the added benefit of reducing the risk of other non-cardiovascular diseases and for non-smokers. At the population level, a decrease in smoking is responsible for most of the decline in mortality from ischaemic heart disease, much more than other measures.</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3.</span><p id="par0210" class="elsevierStylePara elsevierViewall">It is not difficult to give health advice to patients and encourage them to quit smoking, and the reasons to do so are many and powerful.</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">4.</span><p id="par0215" class="elsevierStylePara elsevierViewall">It is always beneficial to stop smoking in terms of survival, but the sooner smoking is stopped, the more benefits obtained.</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">5.</span><p id="par0220" class="elsevierStylePara elsevierViewall">In addition to the great difficulty of reducing the number of cigarettes and maintaining that lower number, this reduction would not reduce the risk of CVD. A non-linear relationship between the intensity of tobacco smoke and ischaemic heart disease is confirmed at the population level. Smoking little results in much CVR.</p></li><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">6.</span><p id="par0225" class="elsevierStylePara elsevierViewall">Women are especially susceptible to the effects of smoking on CVD.</p></li><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">7.</span><p id="par0230" class="elsevierStylePara elsevierViewall">The weight gain that can occur when quitting does not affect the risk of CVD.</p></li><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">8.</span><p id="par0235" class="elsevierStylePara elsevierViewall">In secondary prevention, stopping smoking after a heart attack decreases the risk of mortality in a greater proportion than statins, antiaggregation and beta-blockers.</p></li></ul></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Conflict of interest</span><p id="par0240" class="elsevierStylePara elsevierViewall">The authors declare no conflict of interest.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:12 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Smoking as a cardiovascular risk factor. Pathogeny" ] 2 => array:2 [ "identificador" => "sec0015" "titulo" => "The management of cardiovascular risk factors" ] 3 => array:2 [ "identificador" => "sec0020" "titulo" => "Smoking as a cardiovascular risk factor to prioritise" ] 4 => array:2 [ "identificador" => "sec0025" "titulo" => "Some special considerations" ] 5 => array:2 [ "identificador" => "sec0030" "titulo" => "Tobacco and secondary prevention" ] 6 => array:2 [ "identificador" => "sec0035" "titulo" => "Health advice to quit smoking" ] 7 => array:2 [ "identificador" => "sec0040" "titulo" => "The benefits of quitting smoking in terms of cardiovascular disease" ] 8 => array:2 [ "identificador" => "sec0045" "titulo" => "My patient wants to stop smoking: how can I help them?" ] 9 => array:2 [ "identificador" => "sec0050" "titulo" => "Conclusions" ] 10 => array:2 [ "identificador" => "sec0055" "titulo" => "Conflict of interest" ] 11 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2018-06-05" "fechaAceptado" => "2018-07-16" "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Minué-Lorenzo C, Olano-Espinosa E. 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