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Researchers have found that patients with peripheral artery disease or stroke were less likely to receive recommended treatments to prevent heart attack than those with coronary artery disease. All three are types of atherosclerotic cardiovascular disease.

Depending on the location of the blockage, atherosclerosis increases the risk for three serious conditions: coronary artery disease, stroke and peripheral artery disease.

"Our study highlights the need for public health campaigns to direct equal attention to all three major forms of atherosclerotic cardiovascular disease," said senior study author Erin Michos from the Johns Hopkins University in the US.

"We need to generate awareness among both clinicians and patients that all of these diseases should be treated with aggressive secondary preventive medications, including aspirin and statins, regardless of whether people have heart disease or not," Michos added.

Since atherosclerosis can affect arteries in more than one part of the body, medical guidelines are to treat coronary artery disease, stroke and peripheral artery disease similarly with lifestyle changes and medication, including statins to lower cholesterol levels and aspirin to prevent blood clots.

Lifestyle changes include eating a healthy diet, being physically active, quitting smoking, controlling high cholesterol, controlling high blood pressure, treating high blood sugar and losing weight.

What was unclear was if people with stroke and peripheral artery disease received the same treatments prescribed for those with coronary artery disease.

This study compared more than 14,000 US adults enrolled in the 2006-2015 Medical Expenditure Panel Survey, a national survey of patient-reported health outcomes and conditions, and health care use and expenses.

Slightly more than half of the patients were men, the average age was 65, and all had either coronary artery disease, stroke or peripheral artery disease.

These individuals were the representative of nearly 16 million US adults living with one of the three forms of atherosclerotic cardiovascular disease.

Compared to participants with coronary artery disease, participants with peripheral artery disease were twice more likely to report no statin use and three times more likely to report no aspirin use.

Additionally, people with peripheral artery disease had the highest, annual, total out-of-pocket expenditures among the three atherosclerotic conditions.

The findings showed that participants with stroke were more than twice as likely to report no statin or aspirin use.

Moreover, those with stroke were more likely to report poor patient-provider communication, poor health care satisfaction and more emergency room visits.

"Our study highlights a missed opportunity for implementing life-saving preventive medications among these high-risk individuals," Michos said.

The study was presented in the virtual conference at the American Heart Association's Quality of Care & Outcomes Research Scientific Sessions 2020.

New York, May 19: Cigarette smoke spurs the lungs to make more of the receptor protein which the novel coronavirus uses to enter human cells, according to a study which suggests that quitting smoking might reduce the risk of a severe coronavirus infection.

The findings, published in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to severe COVID-19 disease.

"Our results provide a clue as to why smokers who develop COVID-19 tend to have poor clinical outcomes," said study senior author Jason Sheltzer, a cancer geneticist at Cold Spring Harbor Laboratory in the US.

"We found that smoking caused a significant increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells," Sheltzer said.

According to the scientists, quitting smoking might reduce the risk of a severe coronavirus infection.

They said most individuals infected with the virus suffer only mild illness, if they experience any at all.

However, some require intensive care when the sometimes-fatal virus attacks, the researchers said.

In particular, they said three groups have been significantly more likely than others to develop severe illness -- men, the elderly, and smokers.

Turning to previously published data for possible explanations for these disparities, the scientists assessed if vulnerable groups share some key features related to the human proteins that the coronavirus relies on for infection.

First, they said, they focused on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers.

The scientists said both mice that had been exposed to smoke in a laboratory, and humans who were current smokers had significant upregulation of ACE2.

According to Sheltzer, smokers produced 30-55 per cent more ACE2 than their non-smoking counterparts.

While the researchers found no evidence that age or sex impacts ACE2 levels in the lungs, they said the influence of smoke exposure was surprisingly strong.

However, they said, the change seemed to be temporary.

According to the data, the level of the receptors ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.

The study noted that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells.

Smoking is known to increase the prevalence of such cells, the scientists said.

"Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers' lungs could be a byproduct of smoking-induced secretory cell hyperplasia," Sheltzer explained.

However, Sheltzer said other studies on the effects of cigarette smoke have shown mixed results.

"Cigarette smoke contains hundreds of different chemicals. It's possible that certain ingredients like nicotine have a different effect than whole smoke does," he said.

The researchers cautioned that the actual ACE2 protein may be regulated in ways not addressed in the current study.

"One could imagine that having more cells that express ACE2 could make it easier for SARS-CoV-2 to spread in someone's lungs, but there is still a lot more we need to explore," Sheltzer said.