Smoking and Cardiovascular Disease

ICTR in the News: Erectile Dysfunction Means Increased Risk for Heart Disease, Regardless of Other Risk Factors

Smoking and Cardiovascular Disease | Johns Hopkins Medicine

Erectile dysfunction (ED) indicates greater cardiovascular risk, regardless of other risk factors, such as cholesterol, smoking and high blood pressure, according new research published in the American Heart Association’s journal Circulation.

In the study, which followed more than 1,900 men, ages 60 to 78, over 4 years, those who reported ED were twice as ly to experience heart attacks, cardiac arrests, sudden cardiac death and fatal or non-fatal strokes.

Erectile dysfunction (ED) — defined as the inability to achieve or maintain an erection for satisfactory sexual intercourse — affects nearly 20 percent of men over age 20, according to research.

Cardiovascular disease and ED share common risk factors, including obesity, hypertension, smoking, diabetes and metabolic syndrome — a condition marked by a cluster of features such as elevated blood sugar, hypertension and excess abdominal fat.

“Our results reveal that erectile dysfunction is, in and of itself, a potent predictor of cardiovascular risk,” says study senior investigator Michael Blaha, M.D., M.P.H., associate professor of medicine at the Johns Hopkins School of Medicine in Baltimore, Maryland.

“Our findings suggest that clinicians should perform further targeted screening in men with erectile dysfunction, regardless of other cardiac risk factors and should consider managing any other risk factors — such as high blood pressure or cholesterol — that much more aggressively.”

Limited evidence of a link between ED and cardiovascular disease has emerged over the last several years, but results of this latest study provide what researchers say is the strongest indication to date that sexual dysfunction indicates heightened cardiovascular risk.

During the four-year follow-up, there were a total of 115 fatal and non-fatal heart attacks, fatal and non-fatal strokes, cardiac arrests and sudden cardiac deaths. A greater proportion of men who reported ED (6.

3 percent) suffered heart attacks, cardiac arrests or strokes than men who didn’t report ED (2.6 percent).

When the investigators adjusted their analysis to eliminate the potential influence of other risk factors, that risk was somewhat lessened but still markedly higher: Men with ED were nearly twice as ly to suffer cardiovascular events than men without ED.

Participants in the research are part of the ongoing Multi-Ethnic Study of Atherosclerosis, which is following more than 6,000 people of various ethnic and racial backgrounds at several cities across the United States.

Men seeking treatment and evaluation for ED should be a signal to conduct a comprehensive cardiovascular evaluation, said Blaha. Additionally, the researchers say, men should be aware that ED places them at elevated risk for cardiovascular disease.

“The onset of ED should prompt men to seek comprehensive cardiovascular risk evaluation from a preventive cardiologist,” Blaha noted. “It is incredible how many men avoid the doctor and ignore early signs of cardiovascular disease, but present for the first time with a chief complaint of ED.  This is a wonderful opportunity to identify otherwise undetected high-risk cases.”

Co-authors on the study included Iftekhar Uddin, M.B.B.S., M.S.P.H.; Mohammadhassan Mirbolouk, M.D., M.P.H.; Zeina Dardari, M.P.H.; David Feldman, B.S.; Miguel Cainzos, M.D., M.P.H.; Andrew DeFilippis, M.D., M.Sc.; Philip Greenland, M.D.; Ron Blankstein, M.D.

; Kevin Billups, M.D.; Martin Miner, M.D.; and Khurram Nasir, M.D., M.P.H.The work was funded by the National Heart, Lung, and Blood Institute and by the National Center for Research Resources, with additional support by the U.S. Environmental Protection Agency.

–Written by Ekaterina Pesheva for the American Heart Association



Smoking and Cardiovascular Disease | Johns Hopkins Medicine
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Scientists from the Johns Hopkins Medical School reported today that a person who drinks five or more cups of coffee a day is almost three times as ly to develop heart problems as a person who drinks no coffee at all.

The scientists said that a long-term study of more than 1,000 graduating medical students, followed for up to 38 years, found that 51 have so far either died suddenly of heart failure or suffered heart attacks or severe heart pain. Those who drank five or more cups of coffee per day had a 2.8 times greater risk of having the heart problems than those who drank no coffee.

Dr. Thomas A.

Pearson, a co-author of the report, called the findings ''preliminary'' but suggested that an individual who has taken the standard steps to avoid heart disease, such as quitting smoking and having blood pressure and cholesterol levels checked, might additionally want to limit coffee consumption to two cups a day as part of ''a prudent life style.''

However, three other experts who addressed a press conference on the issue called it ''premature'' to make any firm recommendations on the basis of the Hopkins study, because most previous studies, with some exceptions, have found no link between coffee consumption and heart disease. ''The overwhelming preponderance of evidence is reassuring,'' said Dr. Charles Hennekens, associate professor of medicine at the Harvard Medical School, who moderated the press conference.

The coffee study was one of the more provocative reports presented on the opening day of the annual scientific meeting of the American Heart Association, which is being held this year at the District of Columbia Convention Center.

In other papers delivered today, scientists reported that aerobic exercise can control high blood pressure in some individuals, that new synthetic compounds can reduce the absorption of heart-threatening cholesterol in animals, and that cigarette smoke inhaled by nonsmokers whose spouses smoke appears to increase the risk of death.

The findings on cigarette smoke were the latest results to emerge from a large study, known as the Multiple Risk Factor Intervention Trial, that is testing ways to reduce deaths from coronary heart disease. The findings were presented by scientists from the University of Minnesota, who analyzed how the health status of nonsmoking men was affected by whether or not their wives smoked.

The study focused on 1,245 married men who reported that they had never smoked cigarettes, pipes, cigars, or cigarillos. Of these, 286 were married to women who smoked and were thus presumed to inhale tobacco smoke from their wives regularly, while 959 were married to women who did not smoke.

When the two groups were compared, the men married to smokers had higher levels of carbon monoxide in the blood, performed less well on pulmonary function tests, and died at a higher rate than those married to nonsmokers.

In particular they also suffered more fatal and nonfatal heart problems. The risk of death or heart problems appeared higher for those whose wives smoked 20 or more cigarettes a day than for those whose wives smoked less.

Effects of Aerobic Exercise

The report on aerobic exercise, presented by John E. Martin, a behavioral psychologist with the Veterans Administration Medical Center in Jackson, Miss.

, was described as the first controlled study to compare the effects of aerobic exercise with less strenuous exercises. The study was very small, involving only 19 men, all suffering from mild high blood pressure.

All of the men stopped taking medication during the study and relied solely on exercise.

Ten of the men were given a ''routine aerobic exercise program'' to increase breathing and blood flow to the muscles. They rode stationary bicycles, walked on treadmills, jogged slowly in the laboratory, and walked briskly. The other nine simply did such ''low-level calisthenics'' as toe-touching, arm circling and stretching.

As it turned out, the blood pressure of those doing aerobic exercises dropped to normal within two months and remained there while the exercise program was maintained.

Members of the other group had no change in blood pressure until they, too, were put on aerobic exercises, and then their blood pressures fell to normal. ''In certain individuals,'' Dr.

Martin concluded, ''aerobic exercise may be a viable alternative to medication.''

Another report suggested that new synthetic compounds, similar to natural glycosides found in alfalfa, can reduce the intestinal absorption of cholesterol in rats and monkeys. The compounds seem to bind to the cholesterol and carry it through the intestinal tract to be excreted in feces, according to Dr. Manuel R.

Malinow, professor of medicine at Oregon Health Sciences University in Portland. Dr. Malinow said he doubted that the compounds would ever substitute for a low-cholesterol diet but said they might make it possible to eat high cholesterol foods a little more often.

If such pills are ever developed, he said, they would probably not be available for 5 or 10 years.

Coffee Drinking Habits

The Johns Hopkins coffee study followed 1,130 white male medical students who graduated from the medical school between 1948 and 1964. Information on coffee use and smoking habits was obtained by questionnaires at five-year intervals for up to 25 years. However, the study did not collect information on whether the type of coffee consumed was caffeinated or decaffeinated.

Dr. Pearson said the study was unusual because it started following subjects at an early age, typically about 22 years old, and it tracked changes in coffee drinking habits over the years instead of assuming the consumption remained constant.

The study found that even when other factors associated with heart disease, such as smoking, high blood pressure, cholesterol and age, were taken into account, coffee alone appeared to increase the risk of heart problems, causing 2.

5 times as much heart damage in those who drank five or more cups a day as in those who drank none.

However, Dr. Pearson acknowledged that a study of physicians might not indicate the effects of coffee in the broader population, and he agreed the evidence was too slight to recommmend a national policy on coffee consumption. He said the Hopkins study has not yet been published or reviewed by scientific peers.

Dr. Lynn Rosenberg, an epidemiologist at the Boston University School of Medicine, said that while some studies have raised questions about coffee, her own study and most others have found no link between coffee and heart disease.

She said a possible link has neither been established nor ruled out. Some recent studies suggest that coffee may increase cholesterol levels, she said, providing a plausible mechanism by which coffee might cause heart disease.

But if coffee does increase the risk of heart attacks, she said, the risk is ''ly to be small.''

“,”author”:”Philip M. Boffey, Special To the New York Times”,”date_published”:”1985-11-12T05:00:00.000Z”,”lead_image_url”:””,”dek”:null,”next_page_url”:null,”url”:””,”domain”:””,”excerpt”:”Continue reading the main storyBy Philip M. Boffey, Special To the New York Times”,”word_count”:1197,”direction”:”ltr”,”total_pages”:1,”rendered_pages”:1}


Research News Tip Sheet: Story Ideas From Johns Hopkins

Smoking and Cardiovascular Disease | Johns Hopkins Medicine

Newswise — During the COVID-19 pandemic, Johns Hopkins Medicine Media Relations is focused on disseminating current, accurate and useful information to the public via the media. As part of that effort, we are distributing our “COVID-19 Tip Sheet: Story Ideas from Johns Hopkins” every Tuesday throughout the duration of the outbreak.

We also want you to continue having access to the latest Johns Hopkins Medicine research achievements and clinical advances, so we are issuing a second tip sheet every Thursday, covering topics not related to COVID-19 or the SARS-CoV-2 virus.

Stories associated with journal publications provide a link to the paper. Interviews with the researchers featured may be arranged by contacting the media representatives listed.


Media Contact: Vanessa Wasta, M.B.A.

Red blood cells not only carry oxygen from one part of the body to another, they also act as sponges in the circulatory system, soaking up toxins such as poisons shed from infections. The more red blood cells available in the blood system, the faster the recovery from toxin-related threats to the body.

Johns Hopkins biomedical engineer Jordan Green, Ph.D., and his colleagues have developed a nanoparticle that has the shape and “skin” of red blood cells. The red blood cell mimics can be injected into the bloodstream and circulate within vessels for long periods to absorb toxic substances.

A report on the work appears in the April 15, 2020, issue of the journal Science Advances.

Green says that other research groups have developed sphere-shaped nanoparticles as toxic sponges, but his team found that more closely matching the shape of the oxygen-carrying cells is a critical step forward.

“Most nanoparticles are spheres, but we hypothesized that mimicking the elongated shape of red blood cells may work better — in part because it has more surface area — to absorb toxins,” says Green, professor of biomedical engineering, ophthalmology, oncology, neurosurgery, materials science and engineering, and chemical and biomolecular engineering at the Johns Hopkins University School of Medicine and a member of the Johns Hopkins Kimmel Cancer Center.

First author Elana Ben-Akiva, Green and the Johns Hopkins team used biodegradable plastic-coated nanoparticles and stretched them to create elongated shapes. Then, they wrapped the lengthened nanoparticles in the membranes, or outer coating, of mouse red blood cells.

Next, the team injected the newly created nanoparticles into mice that had a lethal dose of alpha-toxin from the Staphylococcus aureus bacteria to evaluate the ability of the nanoparticles to serve as a sepsis detoxification therapy. Sepsis is a fatal condition caused by the release of toxins from bacteria into the bloodstream.

Compared with uncoated, spherical nanoparticles, Green and his team found that their red blood cell-mimicking nanoparticles stayed approximately 600% longer in the bloodstream of mice before being engulfed by immune system cells. Half of the toxin-laden mice survived long term — meaning more than one week after being treated — with the newly created nanoparticles, compared with a survival time of only several hours for mice in the control group.

“The more we learn about biology, the more we can engineer treatments to match it, and the better our treatments work,” says Green.


Media Contact: Brian Waters

Smoking a cigarette can have long-term damaging effects on not only the smoker’s lungs, but the lungs of people surrounding the smoker as well.

Although there are many reported instances of vaping-induced lung injuries from electronic cigarettes, secondhand vaping smoke injuries have yet to be documented. That is, until now. In the Feb.

19, 2020, issue of the journal BMJ Case Reports, Johns Hopkins Medicine researchers report identifying a patient they believe developed an inflammatory lung condition from secondhand e-cigarette smoke.

The researchers diagnosed a 37-year-old woman with hypersensitivity pneumonitis, a rare immune system disorder that can be caused by exposure to allergens in the environment such as animal dander, household mold or chemicals.

The condition causes inflammation in the tissues surrounding the air sacs of the lungs, leading to scarring and possible permanent damage.

In this specific case, the researchers noted that the woman’s lungs are somewhat weak as she was born prematurely and that her husband is a frequent e-cigarette user.

In 2016, the patient was diagnosed with asthma but continued to wheeze after treatment. A bronchoscopy failed to determine an underlying cause for her respiratory problem.

Johns Hopkins physicians, including Panagis Galiatsatos, M.D., M.H.S., first saw the woman two years later.

Galiatsatos, assistant professor of pulmonary and critical care medicine at the Johns Hopkins University School of Medicine, and his colleagues reviewed the patient’s medical history, conducted tests and concluded that she had hypersensitivity pneumonitis. They could only point to one possible source for the responsible irritant: the smoke from her husband’s e-cigarettes.

“This is the first case that we are aware of that reports a dire health consequence of secondhand smoke from vaping,” Galiatsatos says. “Now that we know people with more sensitive lungs may be more at risk for complications due to someone else’s vaping, we will ly document more of these cases in the future.”

Galiatsatos has recommended that the woman avoid any firsthand or secondhand exposure to traditional or e-cigarettes. The researchers say that future studies should focus on whether or not secondhand smoke from e-cigarettes can lead to lung damage in healthy people, even if they do not show outward symptoms.


Media Contact: Michael E. Newman

a parent of teenagers at a party, Mother Nature depends on chaperones to keep one of her charges, the immune system, in line so that it doesn’t mistakenly attack normal cells, tissues and organs in our bodies.

A recent study by Johns Hopkins Medicine researchers has demonstrated that in mice — and probably humans as well — one biological chaperone may play a key role in protection against such attacks, known as autoimmune responses, which are a hallmark of diseases such as multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus and type 1 diabetes.

The researchers detailed their study in the Feb. 18, 2020, issue of the journal PLOS Biology (see news release for more details).

“Short protein fragments that come from bacteria, viruses and other pathogens act as antigens to trigger our immune system to remove the invaders, a process that depends on other proteins acting and interacting in a specific sequence of events,” says Scheherazade Sadegh-Nasseri, Ph.D., professor of pathology at the Johns Hopkins University School of Medicine. “In our mouse study, we have shown that a specific disruption in this regimen can redirect the immune system to turn against a healthy body — something that we believe also is ly occurring in humans.”

In their effort to identify this “chaperone disruption,” the researchers relied on the fact that for a mammal’s immune system to trigger a response, antigenic proteins must be exposed, or “presented,” to immune cells known as T lymphocytes, or T cells.

Two chaperone proteins in humans, DO and DM, work together to assist this presentation so that the immune system correctly determines that the protein fragments are foreign and not from normal, healthy components of the body. While previous research has provided a good understanding of DM’s role in this process, the function of DO has remained unclear until now.

To better define DO’s involvement in immunity and autoimmunity, Sadegh-Nasseri and her colleagues focused on H2-O, the chaperone protein in mice that is comparable to DO in humans.

The researchers found that H2-O in mice, and ly DO in humans, may be helping select the stronger binding protein fragments — the ones targeted as being from antigens — for presentation, ensuring that the immune response is highly specific.

Using two different laboratory-induced autoimmune responses in mice, they also discovered that the absence of H2-O disrupts normal helper T cell function and allows full-blown autoimmune disorders — similar to rheumatoid arthritis and multiple sclerosis in humans — to occur.

By linking the absence of a key chaperone protein, H2-O, with two experimental autoimmune disorders in mice, the researchers say this points to a similar impact in humans if DO is not present to keep the immune system focused on true invaders.

“We know that DO evolved later than DM in warm-blooded mammals, so perhaps DO’s chaperoning role was nature’s solution for preventing autoimmune disorders,” Sadegh-Nasseri says. “Better understanding of this role could lead to improved diagnostic techniques and therapies for such diseases.”


Media Contact: Vanessa McMains, Ph.D.

The genetic condition arrhythmogenic right ventricular cardiomyopathy (ARVC) causes fat to build up in heart tissue, which can lead to irregular heartbeats and sudden cardiac death.

By following the structural changes in the hearts in people with the disorder over time, Johns Hopkins Medicine researchers believe they may have found a biomarker that could predict the progression of the disease and predict who would need aggressive treatment sooner to prevent death.

In their new study, published in the Journal of the American Heart Association on April 9, 2020, the researchers reported that monitoring the increasing stiffness of the right ventricular chamber of the heart was linked to structural changes indicating worsening of disease.

“If we can confirm these structural changes are linked with actual cardiovascular events, such as irregular heartbeat, heart failure or sudden death, then we can see if using this measurement can predict who would most benefit from earlier intervention,” says Allison Hays, M.D., associate professor of medicine at the Johns Hopkins University School of Medicine. “The ultimate goal would be to save more lives.”

Their study used images from echocardiograms repeated on average of 3.5 years apart in 40 patients with ARVC.

In the study, the researchers found that those patients with abnormal function in the right ventricle (measured using a technique called strain imaging) were 18 times more ly to have worsening of their heart disease over time, defined by a progressive increase in size of the right ventricle and reduced ability to pump blood the heart.


Media Contact: Valerie Mehl

A low-dose, two-drug epigenetic (the addition of chemical compounds to genes to regulate their activity) therapy used for more than a decade to attack tumor cells also appears to target certain tumor-promoting immune system cells, limits the suppression of other cancer-fighting cells, and reduces the spread and recurrence of three human cancer types. That’s according to new research in mice from the Johns Hopkins Kimmel Cancer Center and Peking University Cancer Hospital and Institute in China.

If confirmed in further studies, the findings, described in the Feb. 26, 2020, online issue of Nature, could advance efforts to stem postoperative and other metastases — the migration of cancer cells to sites beyond a tumor’s original location and the process responsible for the vast majority of cancer deaths.

The drugs studied, 5-azacitidine and entinostat, target epigenetic factors, chemical changes to DNA and the packaging of DNA in the nucleus of cells that, in the case of cancers, shut down tumor suppressor genes.

In the new study, the drugs also blocked the activity of cells in the immune system called myeloid-derived suppressor cells (MDSCs), which are known to suppress another immune system component, cancer-killing T cells.

A team led by Malcolm Brock, M.D.

, director of the Kimmel Cancer Center’s clinical and translational research in thoracic surgery, found that in mice, the treatment — especially when given after surgery to remove a tumor — significantly decreased the migration of MDSCs to the lung. It also significantly limited the growth and formation of metastatic tumors in the animals’ lungs as compared with untreated mice.

The medications stopped cells from setting up a cancer-welcoming environment, called a premetastatic niche, which sometimes occurs after surgical removal of a cancerous tumor. Chemically reprogrammed by the drugs, MDSCs were less successful at accumulating in distant organs and at paving the way for the spread of lung, esophageal and breast cancer tissue implanted in the mice.

Mice implanted with non-small cell lung cancer, esophageal squamous cell carcinoma or breast cancer tumors had significantly longer periods of disease remission and overall survival when they received the drugs after their implanted tumors were removed. Low-dose therapy with the two drugs has been demonstrated in other cancer types to be well-tolerated in humans.


Smoking and Respiratory Diseases

Smoking and Cardiovascular Disease | Johns Hopkins Medicine

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According to the Centers for Disease Control and Prevention (CDC), diseases caused by smoking kill more than 480,000 people in the U.S. each year.

In fact, smoking is directly responsible for almost 90% of lung cancer and COPD deaths. Even with antismoking campaigns and health warnings, many people continue to smoke or start to smoke every year.

About 8% of kids under age 18 are current tobacco users.

What are the risks linked to smoking?

Smokers increase their risk of lung disease, including lung cancer. But they also increase their risk of other illnesses such as heart disease, stroke, and mouth (oral) cancer. Risks from smoking, as they relate to lung disease, include the following:

Chronic obstructive pulmonary disease (COPD). This includes:

  • Chronic bronchitis. This is a long-term (chronic) inflammation of the large airways (bronchi). Symptoms include coughing mucus over a long period.
  • Emphysema. This chronic lung condition affects the air sacs (alveoli) in the lungs. Symptoms include shortness of breath, coughing, fatigue, sleep and heart problems, weight loss, and depression.

Lung cancer. This is an abnormal growth of cells that can result in lumps, masses, or tumors. It may start in the lining of the bronchi, or other areas of the respiratory system. Smoking, including secondhand smoke, is the leading cause of lung cancer. Symptoms of lung cancer include:

  • Cough
  • Chest pain
  • Shortness of breath
  • Wheezing
  • Recurring lung infections
  • Bloody or rust-colored sputum
  • Hoarseness
  • Swelling of the neck and face
  • Pain and weakness in the shoulders, arms, or hands
  • Unexplained fever

Other cancers. Smoking increases the risk of lung and oral cancer. But it also increases the risk of other respiratory system cancers. These include cancer of the nose, sinuses, voice box, and throat. Smoking also increases the risk of many other cancers of GI (gastrointestinal), urinary, and female reproductive systems.

The symptoms of smoking-related lung diseases may look other lung conditions or health problems. If you have any symptoms of lung disease, see your healthcare provider as soon as possible.

How dangerous is secondhand smoke?

Secondhand smoke is smoke that is exhaled by smokers and smoke emitted from the burning end of a lit cigarette, cigar, or pipe. It causes more than 7,000 lung cancer deaths each year in people who don’t smoke. It can also lead to lung conditions and heart disease. Symptoms linked to secondhand smoke exposure may include:

  • Eye, nose, and throat irritation
  • Coughing
  • Too much mucus in the airways
  • Chest discomfort or pain

Children and infants exposed to tobacco smoke are more ly to experience ear infections, and asthma. They are also at a higher risk for sudden infant death syndrome (SIDS) than children and infants not exposed to secondhand smoke.

What are the benefits of quitting smoking?

People who quit smoking can actually reverse some of the lung damage. Other benefits of quitting smoking may include the following:

  • Decreased risk for lung disease
  • Decreased risk for heart disease
  • Decreased risk for cancer
  • Reduced cigarette stains on fingers and teeth
  • Reduced occurrence of cough
  • Elimination of stale cigarettes smell on clothing and hair
  • Improved smell and taste
  • Saving money by not buying cigarettes

How does cigar smoking affect a person's risk of lung cancer and other types of cancer?

Cigars actually pose the same, if not greater, risk as cigarettes for oral cancer. Although many cigar smokers do not inhale, their risk for oral, throat, and esophageal cancers is the same as for cigarette smokers. Consider these facts from the CDC:

  • Compared with nonsmokers, cigar smokers who inhale are more ly to develop oral cancer, esophageal cancer, and laryngeal cancer.
  • Cigar smokers who inhale and smoke 5cigars a day may have a lung cancer risk similar to one-pack-a-day cigarette smokers.
  • Secondhand smoke from cigars contains toxins and cancer-causing agents (carcinogens) similar to secondhand cigarette smoke, but in higher concentrations.

How do people stop smoking? 

Quitting smoking is very difficult. The following tips can help you quit using tobacco products:

  • Think about why you want to quit. Make a list of the reasons.
  • Set a quit date.
  • Try to pick a time when you have as little stress as possible. 
  • Ask for support and encouragement from family, friends, and coworkers.
  • If you don't already exercise, start to increase your physical activity to improve your health.
  • Try to get enough sleep each night and eat healthy. Along with exercise, healthy sleeping and eating habits will help you cope with quitting.
  • Join a smoking cessation program or support group. These programs are available in most communities. There are also programs available by phone and online:
    • Try the website.
    • Try your state's quitline. Call 800-QUIT-NOW (800-784-8669).

Medicines to help you stop smoking

There are both prescription and over-the-counter medicines that can help you stop smoking. Talk with your healthcare provider about these medicines and whether or not any of them are right for you.

Over-the-counter medicines:

  • Nicotine patch. Nicotine is delivered through the skin.
  • Nicotine gum. Gum delivers nicotine quickly.
  • Nicotine lozenge. Lozenges are hard candy.

Prescription medicines:

  • Nicotine nasal spray. Nicotine is also delivered quickly.
  • Nicotine inhaler. Using an inhaler is smoking cigarettes.
  • Antidepressant medicine (bupropion). It helps to lessen cravings for nicotine.
  • Varenicline tartrate. It helps to lessen the discomfort of quitting. It also lessens the pleasure you get from smoking.


Secondhand Smoke Exposure and Subclinical Cardiovascular Disease: The Multi‐Ethnic Study of Atherosclerosis

Smoking and Cardiovascular Disease | Johns Hopkins Medicine

Few studies have evaluated the association between secondhand smoke (SHS) and subclinical cardiovascular disease among ethnically diverse populations. This study assesses the impact of SHS on inflammation and atherosclerosis (carotid intima‐media thickness, coronary artery calcification, and peripheral arterial disease).

Methods and Results

We examined 5032 nonsmoking adults aged 45 to 84 years without prior cardiovascular disease participating in the Multi‐Ethnic Study of Atherosclerosis (MESA) from 2000 to 2002. SHS exposure was determined by self‐report, and urinary cotinine was measured in a representative subset (n=2893).

The multi‐adjusted geometric mean ratios (95% CIs) for high‐sensitivity C‐reactive protein and interleukin‐6 comparing 407 participants with SHS ≥12 h/wk versus 3035 unexposed participants were 1.13 (1.02–1.26) and 1.04 (0.98–1.11), respectively. The multi‐adjusted geometric mean ratio for carotid intima‐media thickness was 1.02 (0.

97–1.07). Fibrinogen and coronary artery calcification were not associated with SHS. The prevalence of peripheral arterial disease (ankle‐brachial index ≤0.9 or ≥1.4) was associated with detectable urinary cotinine (odds ratio, 2.10; 95% CI, 1.09–4.04) but not with self‐reported SHS.

Urinary cotinine was not associated with inflammation or carotid intima‐media thickness.


Despite limited exposure assessment, this study supports the association of SHS exposure with inflammation and peripheral arterial disease.

Secondhand smoke (SHS) exposure is a global cause of morbidity and mortality.1 A third of nonsmoking adults are exposed to SHS worldwide.1 In the United States, 25% of the population remains exposed to SHS, disproportionately affecting communities with low income.

2 SHS is an established cardiovascular disease (CVD) risk factor.3, 4 Meta‐analyses have estimated that SHS exposure is associated with a 31% increased risk of coronary heart disease3 and 20% to 30% increased risk of stroke.

5, 6, 7 The enactment of indoor smoke‐free policies have been followed by important reductions in coronary heart disease hospitalizations,8 providing additional support for the potential cardiovascular benefits of reducing SHS exposure.

The 2014 Surgeon General Report, however, estimated that around 33 000 nonsmokers continue to die every year from SHS‐related coronary heart disease in the United States.6

Possible mechanisms for SHS‐related cardiovascular toxicity include increased platelet aggregability, endothelial dysfunction, inflammation, oxidative stress, arterial stiffness, and atherosclerosis.

9, 10 Relatively few studies have evaluated the association between SHS exposure and subclinical CVD among ethnically diverse populations at current levels of exposure.

Self‐reported SHS exposure has been associated with carotid intima‐media thickness (cIMT) and coronary artery calcification (CAC) in studies from the United States11, 12, 13, 14, 15 and Europe,16, 17 although most studies were conducted more than 1 to 2 decades ago, when SHS exposure was much higher than it is today.

Few studies have evaluated the association between SHS and peripheral arterial disease (PAD), with inconsistent findings.

18, 19, 20 With mostly supportive findings, a larger body of evidence is available for the association between SHS exposure and high‐sensitivity C‐reactive protein (hsCRP), including studies among adolescents,21, 22, 23, 24 pregnant women,25 and adults.26, 27, 28, 29, 30, 31, 32, 33, 34 Studies evaluating the association between self‐reported or biomarker‐based SHS exposure and fibrinogen have generally shown consistent positive associations.28, 30, 31, 32, 33, 35 For interleukin‐6 (IL‐6), the evidence is largely null, although most studies are small.26, 27, 30

The Multi‐Ethnic Study of Atherosclerosis (MESA) was specifically designed to assess subclinical CVD and its risk factors among an ethnically diverse cohort from 6 urban communities around the United States.

MESA provides a unique opportunity to inform our understanding of mechanistic pathways for CVD at relevant levels of SHS exposure, which can better inform tobacco product regulation.

The objective of this study is to examine the cross‐sectional association of SHS exposure with markers of inflammation, subclinical atherosclerosis, and PAD in nonsmoking MESA participants.

Study Population

MESA is a community‐based prospective cohort study of 6814 white, black, Hispanic, or Chinese American men and women aged 45 to 84 years free of clinically apparent CVD at baseline (2000–2002). Study details have been previously published.

36 Participants were enrolled from Forsyth County, NC; New York City, NY; Baltimore, MD; St. Paul, MN; Chicago, IL; and Los Angeles, CA. The race/ethnicity distribution was as follows: 39% non‐Hispanic whites, 28% black, 22% Hispanics, and 12% Chinese Americans.

The institutional review boards from all field centers approved the study and all participants provided written informed consent.

SHS exposure was assessed by self‐report in the overall population as well as by urinary cotinine in a random subset. This study was restricted to the baseline visit (2000–2002).

We excluded 887 participants who were current smokers self‐report, 107 participants with urinary cotinine concentrations above concentrations ≥200 ng/mL (ly current smokers),37 149 participants missing data on self‐reported SHS exposure, and 639 participants missing other variables of interest, leaving 5032 participants for this analysis (Figure 1). Among them, 2983 participants had urinary cotinine available. Urinary cotinine, a specific biomarker of recent SHS exposure,38 was analyzed in a random subsample of MESA participants who were enrolled in the MESA lung substudy (n=3965). Sociodemographic characteristics in our study sample for analyses self‐reported SHS exposure (n=5032) and urinary cotinine (n=2982) were similar to the overall noncurrent smoking MESA population (Table S1).

Figure 1. Definition of study population, Multi‐Ethnic Study of Atherosclerosis (MESA), United States, 2000–2002. SHS indicates secondhand smoke.

SHS Exposure

Information on current SHS exposure was obtained during the study visit by asking noncurrent smoking participants the following question: “During the past year about how many hours per week were you in close contact with people when they were smoking? (eg, in your home, in a car, at work or other close quarters).” SHS exposure was categorized as unexposed and as approximate quartiles of hours of SHS exposure per week among the exposed (1, 2–3, 4–11, and 12 or more hours per week).

Urinary cotinine (ng/mL) was measured by immunoassay LLD (lower detection limit) (Immulite 2000 Nicotine Metabolite Assay; Diagnostic Products Corp., Los Angeles, CA) as part of the MESA Lung Study.

37 The average half‐life of urinary cotinine is 16 hours.38 The limit of detection for urinary cotinine was 10 ng/mL.

In our study sample (which excluded participants with cotinine >200 ng/mL), 10% (n=299) of participants had detectable urinary cotinine measurements.

Inflammation Markers

Serum hsCRP was measured using a high‐sensitivity assay (N‐High‐Sensitivity CRP; Dade Behring, Deerfield, IL) (intra‐assay coefficient of variation [CV] ranged from 2.3% to 4.4% and the interassay CV ranged from 2.1% to 5.7%).

IL‐6 was measured by ultrasensitive enzyme‐linked immunosorbent assay (Quantikine HS Human IL‐6 Immunoassay; R&D Systems, Minneapolis, MN) (analytical CV 6.3%).39 Serum fibrinogen was measured by immunoprecipitation using the BNII nephelometer (N‐Antiserum to Human Fibrinogen; Dade Behring) (intra‐assay and interassay CV as 2.7% and 2.6%, respectively).

We evaluated inflammation markers as continuous. We also categorized hsCRP ≥2 mg/L as suggested in a previous study.40

cIMT and CAC

The right and left common and internal carotid arteries and the near and far walls were imaged according to a scanning protocol using high‐resolution B‐mode ultrasound with a Logiq 700 machine (General Electric Medical Systems, Waukesha, WI).

Images were digitized and analyzed centrally at the MESA ultrasound reading center (Tufts Medical Center).

We defined internal and common cIMT as the mean of the maximum cIMT of the near and far walls on the right and left sides as in previous MESA studies.

CAC was measured using an electron‐beam computed tomography scanner (Imatron C‐150XL; GE‐Imatron, San Francisco, CA) (Imatron C‐150XL; GE‐Imatron, San Francisco, CA) in 3 sites (Chicago, IL; Los Angeles, CA; and New York, NY) and by a multidetector row computed tomography system (Lightspeed, General Electric Medical Systems, Waukesha, WI; or Volume Zoom, Siemens, Erlanger, Germany) in 3 sites (Baltimore, MD; Winston‐Salem, NC; and St. Paul, MN).41 Images were centrally read at the MESA CT reading center (Harbor–University of California, Los Angeles). The scanning protocol for MESA has been previously published.42 For each scan, the total phantom‐adjusted Agatston score, defined as the sum of calcium measures from the left anterior descending, circumflex, and left and right coronary arteries, was calculated; the mean score was used in these analyses. We analyzed CAC as two binary measures: (1) present (CAC >0) versus absent, or (2) 75th percentile for the entire MESA population.

Peripheral Arterial Disease

Ankle‐brachial index (ABI) measurements were obtained after the patient rested in the supine position for 5 minutes using a specific protocol to measure systolic blood pressure in each posterior tibial and dorsalis pedis artery in both legs and in the brachial artery in both arms with a continuous‐wave Doppler ultrasound probe. For each leg, the ABI was calculated as the higher of the posterior tibial or dorsalis pedis systolic pressures in each leg divided by the higher of the 2 systolic blood pressure measurements in both arms. For this study, we analyzed ABI as 3 binary measurements: (1) ABI ≤0.9 (excluding participants with ABI ≥1.4), (2) ABI ≥1.4 (excluding participants with ABI ≤0.9), and (3) ABI ≤0.9 or ABI ≥1.4 in accordance with previous MESA studies showing both low and high ABIs were associated with CVD events.43

Other Variables

Standardized questionnaires were used to obtain sociodemographic information (education, family income), current alcohol and tobacco use, medical history, medication use, and family history of CVD.

Body mass index (BMI) was calculated as measured weight in kilograms divided by measured height in meters squared. Systolic and diastolic resting blood pressures were measured in the seated position using the Critikon Dinamap Pro 100 monitor (Critikon, Tampa, FL).

Hypertension was defined as a systolic blood pressure ≥140 mm Hg, a diastolic blood pressure ≥90 mm Hg, or the use of medications for hypertension.44

Lipids including total and high‐density lipoprotein cholesterol, triglycerides, and glucose levels were measured from fasting plasma samples in a central laboratory (University of Vermont, Burlington, VT).

45 Low‐density lipoprotein cholesterol (LDL‐C) was calculated by the Friedewald equation among participants with a triglyceride value 0, CAC >75th percentile, ABI ≤0.9, ABI ≥1.4, and ABI ≤0.9 or ABI ≥1.4), we calculated prevalence odds ratios (ORs) by SHS exposure using multivariate logistic regression.

Hours of SHS exposure per week were modeled as categorical with 5 categories and 0 hours of self‐reported SHS exposure per week as the reference category. Models were adjusted for covariates in a progressive manner.

Model 1 adjusted for age, sex, race/ethnicity, study site, education (high school or less, some college but no degree/technical school certificate, associate's degree/bachelor's degree/graduate degree), and income (


Johns Hopkins Gazette | September 26, 2005

Smoking and Cardiovascular Disease | Johns Hopkins Medicine
Performing cardiac stress tests that measure exercise capacity and heart rate recovery can improve dramatically on existing techniques that predict who is most ly to suffer a heart attack or die from coronary heart disease, the leading cause of death in the United States, a team of cardiologists at Johns Hopkins reports.

In the Sept. 13 edition of the journal Circulation, the Johns Hopkins team reports that 90 percent of men and women with no early signs of coronary heart disease, or CHD, who, nevertheless, died from it had had below average results from their cardiac stress tests conducted 10 to 20 years earlier.

The team's analysis showed these asymptomatic people were two to four times more ly to die from CHD within 10 to 20 years than people with average or better-than-average stress test results, even though traditional scoring for major risk factors for the disease, such as age, blood pressure, blood cholesterol levels and smoking status, had determined the asymptomatic people to be at low or intermediate risk of having heart problems.

According to the cardiologists, these exercise stress tests are easy to perform, lasting less than 20 minutes and requiring only that a person walk on a treadmill at progressively higher speeds and inclines every three minutes until they become markedly fatigued. During the test, people are hooked up to a heart monitor.

“This is the strongest evidence to date that selective use of cardiac stress testing improves prediction of who is really at high risk of suffering a fatal heart attack when traditional risk assessment suggests they are not at high risk of a heart attack within the next 10 years,” said senior study author and cardiologist Roger S. Blumenthal, an associate professor and director of the Ciccarone Preventive Cardiology Center at the School of Medicine and its Heart Institute. The traditional risk factors combine to give a score called the Framingham Risk Score, or FRS, that was developed in the last 20 years. Considered the gold standard, the FRS is a summary estimate of the major risk factors for heart disease: age, blood pressure, blood cholesterol levels and smoking status. It consists of a percentage range of how ly a person is to suffer a fatal or nonfatal heart attack within 10 years.

However, Blumenthal says that many people, especially women, with cardiovascular problems go undetected despite use of the Framingham score, which does not factor in a person's family history, weight or exercise habits. Blumenthal is also a spokesman for the American Heart Association, which estimates that 656,000 Americans died from CHD in 2002, the last year for which statistics are available.

More than 6,100 people took part in the study, conducted from 1972 to 1995 and part of a larger project known as the Lipid Research Clinics Prevalence Study. All participants in this smaller Johns Hopkins study were age 30 to 70. None had early signs of heart disease, but every participant did have at least one major risk factor for it.

At 10 medical centers across the United States, study participants were given a physical examination, had blood tests performed and were scored on the FRS.

Each participant also underwent cardiac stress testing, which included stress testing for exercise capacity and heart rate recovery plus any changes in the heart's electrical signaling that are typical of decreased blood flow to the heart muscle.

Those with a Framingham score of less than 10 percent were gauged to be at low risk for future CHD, while participants with a score between 10 percent and 20 percent were ranked at intermediate risk for future CHD, and those with a score higher than 20 percent were judged to be at high risk of CHD.

Once participants were ranked by Framingham score, the researchers monitored their health every six months until death or the end of the study to find out who did or did not die from a heart attack or CHD.

Cardiac stress testing is used to gauge how well the heart works when it has to pump harder and use more oxygen, for example, while walking on a treadmill. The exercise, sustained for five to 10 minutes, mimics the strain placed on the heart when arteries are blocked or narrowed.

The researchers' goal, however, was to determine if more accurate prediction of whether or not a person will die from a heart attack could be made by adding exercise capacity and heart rate recovery to current assessment techniques that relied mostly on monitoring the heart's electrical signaling.

During stress testing, a person's breathing, blood pressure and heart rate are monitored while the intensity of their exercising is slowly increased to see how their heart responds. The amount, in number of beats per minute, that the heart rate drops two minutes after exercise stops is also recorded to determine heart rate recovery.

Using tables that take into account a person's age, gender and weight, the results can be compared against average scores to see if a person is below, at or above the norm. There is very little risk of harm associated with the testing because participants are closely monitored.

The researchers report that 246 participants died from CHD even though they had initially been categorized by their FRS as at either low or intermediate risk of the disease. However, 225 of those who died also had below average test scores for exercise capacity and heart rate recovery.

“Our best means of preventing coronary heart disease is to identify those most ly to develop the condition and intervene before symptoms appear,” said the study's lead author, cardiologist Samia Mora, then a research fellow at Johns Hopkins. “Cardiac stress testing could significantly improve our abilities to find and aggressively treat these people so that they are much less ly to suffer a heart attack.”

According to the researchers, these latest results support conclusions from earlier this year that traditional risk assessment with the FRS can be improved with selective use of cardiac CT scans to measure calcium scores in individuals with more than one risk factor, such as obesity, smoking, sedentary lifestyle or a family history of heart disease.

Funding for the study was provided by the Maryland Athletic Club Charitable Foundation.

Other researchers involved were Rita Redberg, of the University of California, San Francisco; and A. Richey Sharrett, of Johns Hopkins.