Smoking Nicotine and Heart Health
Medical Disclaimer: This content is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Information is based on current medical literature and clinical guidelines but may not apply to your specific situation. Individual responses vary based on personal medical history and concurrent conditions. Always consult qualified healthcare providers for medical decisions. Never delay seeking medical care based on content you’ve read. If experiencing a medical emergency, seek immediate medical attention.
These articles provide education to enhance your healthcare partnership. All treatment decisions should involve your healthcare team. Use this knowledge to have informed discussions, not replace medical care.
In Brief
Every cigarette sends thousands of chemicals into the bloodstream within minutes. They do far more than harm the lungs. They injure the lining of the arteries throughout the body, drive inflammation, make the blood clot more easily, and speed up the plaque buildup behind heart attacks and strokes. The U.S. Surgeon General has concluded that smoking causes these conditions, not just that it is linked to them.⁶ One fact about this damage surprises most people: it is front-loaded. The main ways smoking harms arteries reach nearly full strength at very low doses. That is why even one cigarette a day carries a large share of the heart risk of a full pack, and why for heart attack and stroke there is no safe level.² This article explains how smoke reaches the heart and vessels, what it does to them step by step, and which diseases follow. It focuses on the cardiovascular harm, which people tend to underestimate, while noting that smoking also causes cancer and lung disease. How the body recovers after quitting is the subject of Article 4.
Smoking Is a Leading Cause of Heart Disease, Not Only Lung Disease
Smoking is best known as a cause of lung cancer and chronic lung disease. Those diseases are devastating and important. Less widely appreciated is that smoking is also one of the most powerful causes of cardiovascular disease. It injures arteries throughout the body, speeds up atherosclerosis, promotes clot formation, and drives heart attack, stroke, peripheral artery disease, and aortic aneurysm. Smoking accounts for roughly a third of all cardiovascular deaths in people over 35, which makes cardiovascular disease one of the largest categories of smoking-related death.¹ This article explains how that damage happens, and why even low levels of smoking carry substantial cardiovascular risk.
Cigarette smoke is not one substance. It is a mix of thousands of chemicals released when tobacco burns. It comes in two parts. The gas phase includes carbon monoxide and reactive oxidant gases. The particle phase — the “tar” — carries nicotine, metals, and other harmful compounds into the lungs.¹ From there, it does not stay in the lungs. Within a minute of a puff, these chemicals cross into the blood and travel to arteries all over the body. Because smoking injures the endothelium throughout the circulation, virtually every arterial bed is affected — coronary, cerebral, peripheral, renal, mesenteric, and aortic.¹
People who smoke are roughly two to four times more likely to develop cardiovascular disease than people who never smoked.⁶ This is the first article in a ten-part series on smoking, nicotine, and heart health. It explains how smoke reaches and injures the heart and vessels, and which diseases follow. Later articles cover secondhand smoke, why nicotine makes quitting so hard, what recovers after stopping, and the medications and strategies that help. We start where the damage begins: the lining of the arteries.
The Endothelium: Where the Injury Begins
Every blood vessel is lined by a single layer of cells called the endothelium. It is not just a passive lining. It is an active tissue that runs through the entire circulation and controls how vessels behave.³ A healthy endothelium makes nitric oxide, a molecule that keeps arteries relaxed and open, discourages clotting, and holds inflammation down. When it works, blood flows smoothly, arteries widen when the body needs more blood, and the vessel wall resists plaque.
Smoke injures this lining early and directly. The oxidants in smoke destroy nitric oxide and damage the cells that make it. The endothelium then makes less of it and loses its ability to keep vessels relaxed and clot-resistant.³,⁴ This is measurable in real people, not just in theory. Within minutes of breathing cigarette smoke — including secondhand smoke — the arteries of healthy people widen less than they should on a test called flow-mediated dilation.¹,⁴ That is a sign the endothelium has been impaired. This injury is one of the earliest steps in atherosclerosis, the disease process behind most heart attacks and strokes. How atherosclerosis develops is covered in more detail in the Coronary Artery Disease series.
There is good news built into this. Endothelial function is not lost for good. It begins to recover within weeks of stopping, which is where Article 4 picks up.⁴
The same injury shows up in other parts of the circulation. The arteries supplying the penis are smaller than the coronary arteries, so the endothelial dysfunction that smoking causes often reduces blood flow there first. This is why erectile dysfunction can appear years before heart disease is diagnosed, and why it can be an early warning sign of arterial disease.¹⁷
From this first injury, several kinds of damage follow. They are worth taking one at a time, because each one adds something different.
The Mechanisms of Cardiovascular Injury
Loss of nitric oxide and poor vessel function
Nitric oxide does more than prevent clots and inflammation. It is also how arteries widen to meet demand — during exercise, for example, when the heart and muscles need more blood. Smoke floods the vessel with oxidants, a state called oxidative stress. This uses up nitric oxide. Arteries then widen less and constrict more easily.³,⁴ Over years, the artery settles into a tighter, stiffer, more reactive state. Much of what follows starts here.
Chronic inflammation
Smoking keeps the whole circulation in a low-grade state of inflammation. Inflammatory cells rise, and inflammatory markers such as C-reactive protein and fibrinogen go up in smokers.¹,³ Inflammation is now understood to be one of the driving forces of atherosclerosis, not just a consequence of it.³ Inflammatory cells push into the injured artery wall, soak up cholesterol, and become the foam cells at the core of an early plaque. The same inflammation later thins the cap over a plaque, which is what makes it likely to rupture.³,⁴ So smoking does two things to plaque: it makes it grow faster, and it makes it more unstable and prone to rupture.³,⁴ Smoking feeds this process without a break.
Blood that clots too easily
This one deserves extra attention, because it explains why smoking causes sudden events and why even small amounts are dangerous. Most heart attacks happen not because an artery slowly closes, but because a vulnerable plaque suddenly ruptures and a clot forms on it within minutes, cutting off blood flow. Smoking drives both sides of that event: it makes plaques more likely to rupture, and it makes the blood more likely to clot. It makes platelets — the cell fragments that start clots — more likely to activate and clump. It raises fibrinogen and other clotting factors. And it impairs the body’s ability to break clots down.¹,⁵ So when a plaque ruptures, the clot that forms is bigger, forms faster, and is more likely to block the vessel completely.⁵ Many strokes work the same way. Not all do — some strokes come from a clot that forms in a fibrillating heart and travels to the brain, or from disease of the brain’s smallest vessels. But across these routes, smoking makes the clotting step more likely and more severe. When smoking stops, much of this begins to reverse: the blood becomes less prone to clotting, and the inflammatory drive on the plaque eases. Article 4 covers how quickly.
Worse cholesterol
Smoking also worsens the cholesterol picture. It lowers HDL, the protective cholesterol, and changes LDL so it is more easily oxidized. Oxidized LDL does more damage to the artery wall and is taken up more readily by inflammatory cells.³,⁴ So the same amount of cholesterol in the blood does more harm in a smoker.
Nicotine’s effect on heart rate, blood pressure, and rhythm
Nicotine is the addictive part of tobacco, and it also acts directly on the heart. It triggers the release of adrenaline and related stress hormones. These raise heart rate and blood pressure, increase the heart’s demand for oxygen, and can tighten the coronary arteries.¹,⁷ A healthy person handles these short surges. But in someone with narrowed coronary arteries, more oxygen demand plus less supply can cause ischemia — not enough blood flow to the heart muscle. Nicotine’s role in addiction, and why quitting is genuinely hard, is the subject of Article 3.
Carbon monoxide and less oxygen
Carbon monoxide in smoke binds to hemoglobin, the protein in red blood cells that carries oxygen. It binds far more tightly than oxygen does, forming carboxyhemoglobin and lowering how much oxygen the blood can carry.¹ Smokers carry clearly higher carboxyhemoglobin levels than nonsmokers.¹ This is one reason smokers often have reduced exercise capacity. And for a heart already getting less blood through narrowed arteries, blood that also carries less oxygen makes the problem worse.
Stiffer arteries and faster plaque
Sustained over years, these mechanisms change the artery’s structure. Arteries in long-term smokers grow stiffer and build plaque faster than they otherwise would.³ In many ways, smoking makes arteries behave as though they are much older than the person’s actual age. Stiffer arteries make the heart work harder and push blood pressure up. Faster plaque buildup is the thread connecting smoking to coronary disease, stroke, and peripheral artery disease.
The table below summarizes these mechanisms, splitting the immediate effect from the long-term consequence.
| Mechanism | Immediate effect | Long-term consequence |
| Endothelial dysfunction | Nitric oxide falls; arteries dilate poorly and turn clot-prone¹,³,⁴ | Early atherosclerosis; arteries stiffen and age³,⁴ |
| Inflammation | Inflammatory cells and markers rise¹,³ | Plaque growth and destabilization³ |
| Prothrombotic shift | Platelets activate; clotting factors rise¹,⁵ | Faster, larger clots; heart attack and ischemic stroke⁵ |
| Lipid changes | HDL falls; LDL oxidizes more readily³,⁴ | More efficient plaque buildup³,⁴ |
| Nicotine (autonomic) | Heart rate and blood pressure rise; coronary arteries constrict¹,⁷ | Higher cardiac workload; ischemia in narrowed arteries¹,⁷ |
| Carbon monoxide | Carboxyhemoglobin rises; blood carries less oxygen¹ | Reduced exercise capacity; added strain on an ischemic heart¹ |
| Arterial stiffening | Vessels lose elasticity³ | Higher blood pressure and cardiac workload³ |
These mechanisms do not occur independently. Endothelial injury promotes inflammation. Inflammation accelerates plaque formation. Plaque becomes vulnerable to rupture. And blood that clots too easily turns a plaque rupture into an acute heart attack or stroke. Smoking injures the cardiovascular system through several complementary pathways acting at once, not through one isolated mechanism. That is why its effects are so broad.
Timing matters too. Cardiovascular injury reflects both how much and how long a person smokes. Some effects appear within minutes, but continued smoking keeps the endothelium injured, the blood inflamed, and clotting elevated year after year — so the damage accumulates over time.¹
Why There Is No Safe Level
It is natural to assume the risk rises in step with how much you smoke — that one cigarette a day would carry about one-twentieth the danger of a pack. The evidence shows that is wrong, and the reason is in the biology.
A large meta-analysis pooled 141 cohort studies. It found that someone smoking about one cigarette a day carries a big share of the extra coronary heart disease risk of someone smoking twenty a day — roughly half of it in men, and about a third in women.² That is far more than the one-twentieth that proportional thinking predicts. For stroke the pattern was nearly identical: about 41% of the extra risk in men, and 34% in women.² The authors concluded that for coronary heart disease and stroke, there is no safe level of smoking.² The risk does not build up gradually with each cigarette. Much of it is already there at very low exposure.
The mechanisms explain why. The Surgeon General’s review describes a curve that rises steeply at low doses — including secondhand smoke and occasional smoking — and then flattens as the number of cigarettes climbs.¹ The effects that trigger sudden events — blood tipped toward clotting and a disrupted endothelium — are largely switched on by small amounts of smoke. They do not need heavy exposure to reach nearly full force.¹,⁵ Once platelets are primed and the endothelium has lost its protection, smoking more does not add much, because much of the damage that causes a sudden event is already done.
The heart risk of smoking is front-loaded, not proportional. For the heart and vessels, there is no safe number of cigarettes. The ways smoking damages arteries reach nearly full strength at very low doses. This is why “cutting down” does not protect the heart the way people expect, and why the goal that matters is stopping, not reducing. It also means occasional and social smoking are not the safe middle ground they are often assumed to be.
The Diseases That Follow
These mechanisms come together in a set of well-defined diseases. Different cardiovascular diseases emphasize different mechanisms, but all arise from the same underlying vascular injury. In each one, the link to smoking is strong, dose-dependent, and — in the Surgeon General’s judgment — causal. The 2014 report concluded the evidence is enough to say smoking causes coronary heart disease, stroke, atherosclerotic aortic aneurysm, and death.⁶
The numbers that follow are large, and they add up to a real-world toll. In the 50-year follow-up of British doctors, men who smoked their whole lives died about ten years younger than lifelong nonsmokers — a gap driven substantially by cardiovascular and other smoking-caused disease.¹²
Coronary heart disease and heart attack. Smoking accelerates coronary plaque and, by tipping the blood toward clotting, triggers the clot that causes most heart attacks. In INTERHEART, a study across 52 countries, current smoking was linked to nearly a tripling of the odds of a first heart attack (odds ratio 2.87 versus never smokers). The risk climbed as the number of cigarettes rose.⁸,¹¹ Smoking is consistently one of the most important preventable causes of coronary disease worldwide.⁸
Ischemic stroke. The same injury that hits the coronary arteries hits the arteries to the brain. Smoking roughly doubles the risk of ischemic stroke, and the risk rises with the amount smoked.⁶ The mechanism is the familiar one: faster plaque in the arteries feeding the brain, plus blood primed to form the clot that blocks them.
Peripheral artery disease. Smoking is the single strongest preventable risk factor for peripheral artery disease — plaque in the arteries to the legs. It is more strongly linked to peripheral artery disease than to almost any other cardiovascular condition.⁶ It causes pain with walking, slows wound healing, and in advanced cases threatens the limb.
Abdominal aortic aneurysm. Smoking is the dominant preventable risk factor for an abdominal aortic aneurysm — a weakening and ballooning of the body’s largest artery that can be fatal if it bursts.⁶ Smoking both promotes aneurysm formation and speeds its growth.⁹ The link is strong enough that the U.S. Preventive Services Task Force recommends a one-time screening ultrasound for men aged 65 to 75 who have ever smoked.⁹ This is one of the few places in medicine where a smoking history, on its own, changes what screening a person should get.
Sudden cardiac death and atrial fibrillation. Smoking is an established cause of sudden cardiac death. In a meta-analysis of prospective studies, current smokers had roughly three times the risk of nonsmokers, rising with the amount smoked.¹³ Smoking is also linked to atrial fibrillation, the most common sustained heart-rhythm problem — current smokers carry about a 32% higher risk in pooled data, again dose-dependent.¹⁴
One more point belongs here, because it is easy to miss when risk factors are listed one by one. Smoking rarely acts alone. It compounds the effects of high blood pressure, diabetes, high LDL cholesterol, and obesity, speeding up vascular injury through overlapping mechanisms. In INTERHEART, the major risk factors combined to multiply risk, so a smoker who also has high blood pressure, poor cholesterol, or diabetes faces a risk far greater than adding each one up.⁸ This reflects one of the central ideas in cardiovascular medicine: long-term risk usually comes from several interacting factors, not one number in isolation. Smoking is also a cause of type 2 diabetes and raises insulin resistance, and it worsens the vascular complications of diabetes once it is present — connections developed in the Diabetes series.⁶ That is why smoking is one of the highest-impact risk factors there is: it injures arteries directly and amplifies every other risk at the same time.
Why Smoking Hits Younger Than People Expect
Many people picture heart disease as a problem for old age. Smoking changes that. The endothelial injury described earlier starts with the first exposures, not after decades.¹,⁴ Atherosclerosis is a slow process that begins quietly, years before symptoms — and smoking speeds it up, so it tends to bring disease forward rather than simply making it more likely. Heart attacks in the 30s and 40s are not rare among smokers. In one registry of people who had a heart attack at age 50 or younger, about half were smokers at the time.¹⁵ The exposure also adds up: the longer and heavier the smoking, the more injury accumulates. For a younger smoker, quitting now removes years of future exposure — which is exactly why quitting early matters, rather than putting it off.
Common Beliefs vs What the Evidence Shows
Several widely held beliefs about smoking and the heart run counter to what the evidence shows. Clearing them away is part of understanding the biology.
| Common Belief | What the Evidence Shows |
| “Cutting down to a few a day removes most of the danger to my heart.” | About one cigarette a day carries a large share — roughly a third to a half — of the excess coronary and stroke risk of a pack a day, not the one-twentieth intuition suggests; for these diseases there is no safe level.² |
| “The real danger of smoking is cancer; the heart is a lesser concern.” | Cardiovascular disease is one of the largest categories of smoking-caused death, not a secondary one; people who smoke face two to four times the risk of developing it.⁶ |
| “Light, low-tar, or filtered cigarettes are easier on the heart.” | These do not meaningfully lower cardiovascular risk; the vascular injury comes from mechanisms that filters and lower tar ratings do not address.¹ |
| “My grandfather smoked until 90, so it can’t be that dangerous.” | Individual anecdotes do not change population risk. For every long-lived smoker, many others died years early from smoking-related disease.¹² |
| “I’ve smoked for decades, so the damage is already done.” | Quitting lowers cardiovascular risk at any age; among people with established coronary disease, cessation is linked to a substantial drop in mortality.¹⁰ Some clotting effects begin to reverse within days (Article 4). |
What This Means
The biology here points to a few practical conclusions, and they are worth saying plainly.
For the heart, the goal is stopping, not cutting down. Because the harm is front-loaded, going from a pack to a few a day leaves much of the heart risk in place.² This is not an argument against cutting down on the way to quitting — many people do — but a low daily count is not close to safe.
Occasional, social, and “light” smoking are not exempt. The same mechanisms that make one cigarette a day matter apply to intermittent use.
None of this makes quitting easy. Smoking is a real addiction, and stopping is hard — hard enough that even a heart attack is often not enough to end it. Among people who had a heart attack at age 50 or younger, 62% were still smoking a year later.¹⁵ Most people who smoke want to quit, and about half try each year, but fewer than one in ten succeed in a given year without help.¹⁶ That difficulty is real, and it is the reason the rest of this series exists — to explain why quitting is so hard, and to lay out the treatments and strategies that make it far more achievable. Nicotine dependence is the subject of Article 3, and the medications and methods that work are covered in Articles 5 and 6.
The effort is worth it. The clotting and endothelial effects that drive sudden events are among the first to recover after stopping, and quitting lowers heart risk at any age. When you quit changes how much you regain: in the British doctors study, stopping around age 30 avoided almost the entire decade of lost life, and even stopping at 50 or 60 recovered several years.¹² In the young heart-attack study above, the patients who did quit cut their risk of dying by roughly two-thirds.¹⁵ The recovery timeline is the subject of Article 4, and quitting after heart disease has already developed is the subject of Article 10.
What This Means for You
- There is no safe level of smoking for the heart. Even about one cigarette a day carries a large share of the coronary and stroke risk of a full pack.²
- Cutting down helps mainly as a step toward quitting. It does not remove the cardiovascular risk. For the heart, stopping is the goal, not reducing.²
- Smoking damages arteries throughout the body — the heart, brain, legs, and aorta — not just the lungs.¹,⁶
- Smoking multiplies your other risks. It matters even more if you also have high blood pressure, high cholesterol, or diabetes.⁸
- Quitting starts to help sooner than most people expect. Endothelial function begins to improve within weeks, and quitting lowers cardiovascular risk at any age.⁴,¹⁰
When cardiovascular symptoms are an emergency. Because this article concerns diseases that can strike suddenly, one safety point belongs here. Sudden chest pain, pressure, or tightness; pain spreading to the arm, jaw, or back; sudden shortness of breath; sudden weakness, numbness, difficulty speaking, or facial drooping; sudden vision loss; a sudden severe headache; or loss of consciousness or near-fainting can be emergency signs of a heart attack or stroke. Call emergency services immediately. These are not reasons to wait and see.
How Strong Is the Evidence?
Not all of the conclusions in this article rest on equally certain evidence, and knowing the difference is part of using it well. The table below summarizes how confident the current evidence is in each main conclusion.
| Conclusion | Strength of evidence |
| Smoking causes coronary heart disease, stroke, peripheral artery disease, and aortic aneurysm | Very high — Surgeon General causal conclusion⁶ |
| The cardiovascular harm is front-loaded — large even at low daily amounts | High — large meta-analysis² |
| Smoking injures the artery lining and pushes the blood toward clotting | High³,⁴,⁵ |
| Smoking multiplies the effect of other cardiovascular risk factors | High⁸ |
| Quitting lowers cardiovascular risk at any age | High¹⁰ |
Clinical Bottom Line
Smoking is thought of as a lung disease, but one of its largest tolls — by some analyses the largest — is cardiovascular. It injures the endothelium, inflames and stiffens arteries, tips the blood toward clotting, worsens cholesterol biology, and accelerates the atherosclerosis behind heart attacks, strokes, peripheral artery disease, and aortic aneurysms — relationships the Surgeon General has judged causal.⁶ The single most important fact is that this harm is front-loaded. Because the clotting and endothelial mechanisms reach nearly full strength at very low doses, even one cigarette a day carries a large share of the risk of a pack, and for coronary disease and stroke there is no safe level.² The practical consequence is that the goal for the heart is stopping, not cutting down. The damage is substantial, but much of it is not fixed in place — many of these processes begin to improve soon after the last cigarette, which is where the rest of this series turns. Smoking is not one risk factor among many; it injures the arteries directly and multiplies every other cardiovascular risk at the same time. Every cigarette matters — but so does every day without one.
What Comes Next
This article covered what smoking does to the cardiovascular system and why even small amounts matter. Article 2 turns to the people around the smoker: how secondhand smoke reaches the blood vessels of nonsmokers — including children, partners, and coworkers — and why cardiovascular effects can occur even with limited exposure. Article 3 then examines nicotine and the brain, and why quitting is a genuine physical challenge rather than a test of character.
Key Terms
Atherosclerosis: The disease process in which cholesterol, inflammation, and injury build up plaque within the artery wall over years; the underlying cause of most heart attacks and strokes.
Atrial fibrillation: The most common sustained heart-rhythm disturbance, in which the heart’s upper chambers beat irregularly; associated with smoking and a major risk factor for stroke.
Carbon monoxide: A gas in tobacco smoke that binds hemoglobin more tightly than oxygen, reducing the blood’s oxygen-carrying capacity.
Carboxyhemoglobin: Hemoglobin bound to carbon monoxide rather than oxygen; elevated in smokers.
Catecholamines: Stress hormones (including adrenaline) that raise heart rate and blood pressure; released in response to nicotine.
Endothelium: The single-cell layer lining every blood vessel; regulates vessel tone, clotting, and inflammation, and produces nitric oxide.
Fibrinogen: A clotting protein in the blood; elevated levels favor clot formation and are raised by smoking.
Flow-mediated dilation: A test of how well an artery widens in response to increased blood flow; a measure of endothelial function.
Ischemia: Inadequate blood flow to a tissue, depriving it of oxygen; in the heart, the cause of angina and heart attack.
Nicotine: The primary addictive component of tobacco; also has direct cardiovascular effects through catecholamine release.
Nitric oxide: A molecule produced by healthy endothelium that keeps vessels relaxed and resistant to clotting; depleted by tobacco smoke.
Oxidative stress: Damage caused by an excess of reactive oxidant molecules; abundant in tobacco smoke and a driver of endothelial injury.
Peripheral artery disease (PAD): Atherosclerosis in the arteries supplying the limbs, most often the legs; smoking is its strongest modifiable risk factor.
Abdominal aortic aneurysm (AAA): A weakening and ballooning of the abdominal aorta, the body’s largest artery; smoking is its dominant modifiable risk factor.
Platelets: Cell fragments in the blood that initiate clotting; made more reactive by smoking.
Prothrombotic: Favoring the formation of blood clots.
Sudden cardiac death: Unexpected death from a sudden loss of heart function, usually caused by a life-threatening rhythm disturbance; risk is markedly increased by smoking.
References
- U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease. A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control and Prevention; 2010. https://www.ncbi.nlm.nih.gov/books/NBK53017/
- Hackshaw A, Morris JK, Boniface S, Tang JL, Milenković D. Low cigarette consumption and risk of coronary heart disease and stroke: meta-analysis of 141 cohort studies in 55 study reports. BMJ. 2018;360:j5855. https://doi.org/10.1136/bmj.j5855
- Messner B, Bernhard D. Smoking and cardiovascular disease: mechanisms of endothelial dysfunction and early atherogenesis. Arterioscler Thromb Vasc Biol. 2014;34(3):509–515. https://doi.org/10.1161/ATVBAHA.113.300156
- Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004;43(10):1731–1737. https://doi.org/10.1016/j.jacc.2003.12.047
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- U.S. Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control and Prevention; 2014. https://www.ncbi.nlm.nih.gov/books/NBK179276/
- Benowitz NL. Nicotine addiction. N Engl J Med. 2010;362(24):2295–2303. https://doi.org/10.1056/NEJMra0809890
- Yusuf S, Hawken S, Ôunpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364(9438):937–952. https://doi.org/10.1016/S0140-6736(04)17018-9
- US Preventive Services Task Force. Screening for abdominal aortic aneurysm: US Preventive Services Task Force recommendation statement. JAMA. 2019;322(22):2211–2218. https://doi.org/10.1001/jama.2019.18928
- Critchley JA, Capewell S. Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review. JAMA. 2003;290(1):86–97. https://doi.org/10.1001/jama.290.1.86
- Teo KK, Ounpuu S, Hawken S, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet. 2006;368(9536):647–658. https://doi.org/10.1016/S0140-6736(06)69249-0
- Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ. 2004;328(7455):1519. https://doi.org/10.1136/bmj.38142.554479.AE
- Aune D, Schlesinger S, Norat T, Riboli E. Tobacco smoking and the risk of sudden cardiac death: a systematic review and meta-analysis of prospective studies. Eur J Epidemiol. 2018;33(6):509–521. https://doi.org/10.1007/s10654-017-0351-y
- Aune D, Schlesinger S, Norat T, Riboli E. Tobacco smoking and the risk of atrial fibrillation: a systematic review and meta-analysis of prospective studies. Eur J Prev Cardiol. 2018;25(13):1437–1451. https://doi.org/10.1177/2047487318780435
- Biery DW, Berman AN, Singh A, et al. Association of smoking cessation and survival among young adults with myocardial infarction in the Partners YOUNG-MI Registry. JAMA Netw Open. 2020;3(7):e209649. https://doi.org/10.1001/jamanetworkopen.2020.9649
- Centers for Disease Control and Prevention. Smoking Cessation: Fast Facts. Atlanta, GA: U.S. Department of Health and Human Services, CDC; 2024. https://www.cdc.gov/tobacco/php/data-statistics/smoking-cessation/index.html
- Cortese F, Costantino MF, Luzi G. Can we consider erectile dysfunction as an early marker of cardiovascular disease? JACC Adv. 2023;2(4):100384. https://doi.org/10.1016/j.jacadv.2023.100384
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