Jessica Monterrosa Mena – The Early Career Voice

The Protective Role of Anti-Hypertension Medication Among Patients with Comorbidities for COVID-19 Outcomes

May 2, 2022May 2, 2022 Jessica Monterrosa Mena

Millions of people around the world take Angiotensin-converting enzyme inhibitors (ACEi) and Angiotensin II receptor blockers (ARB) to manage hypertension, heart failure, and coronary artery disease. Concerns of ACEi and ARB potentially increasing the risk of COVID-19 illness severity and mortality among vulnerable populations heightened once scientists reported that risk factors for developing complications included being older, male, and having cardiovascular comorbidities¹. One comprehensive study using over 17,000 primary care records found that chronic heart disease has a hazard ratio of 1.57 for COVID-19 related death and the hazard ratio remained high at 1.17 even when accounting for confounding variables, suggesting that people with heart disease are at increased risk of mortality². In the same study, high blood pressure or hypertension diagnoses were associated with hazard ratio of 0.89, a lower risk of COVID-19 mortality compared to people with normal blood pressure, but insight into how age, sex, comorbidities, and medications influence outcomes were not directly addressed. Such findings fueled a debate about whether ACEI/ARB should be maintained or withdrawn in patients with COVID-19.

The role of ACEi and ARBS drugs in COVID-19 outcomes among cardiovascular patients also became a point of interest due to their mechanism of action in the human body. ACEi and ARB act on the renin-angiotensin-aldosterone system (RAAS), a hormone system important for regulating blood pressure, fluid balance, and inflammation processes that affect cardiovascular health outcomes. While ACEi and ARB drugs are used as the first line of treatment to manage vasoconstriction, there is a question as to how these medications can alter the RAAS balance. In a previous blog, we discussed how the SARS-CoV-2 virus uses the of angiotensin-converting enzyme 2 (ACE2) receptor to enter host target cells³. This receptor not only acts as the entry point for the virus, but normally acts as a crucial element for regulating RAAS biochemical processes. The inflammatory, tissue damaging, and vasoconstriction effects of Angiotensin II (Ang II) in the body are mitigated by ACE2 activity, and ARB and ACEi drugs also target the Ang II protein⁴. COVID-19 related research has provided a new understanding of how underlying disease states, behavioral habits like smoking, or genetics could influence ACE2 activity in the body. The unique collaboration between clinicians and scientists during the COVID-19 pandemic has provided new mechanistic insight about how the complex RAAS pathway and the factors that influence disease progression.

Ongoing population studies such as The International Study of Inflammation in COVID-19 (ISIC) and The Michigan Medicine COVID-19 Cohort (M2C2) make use of detailed medical records bio-banked human samples, and advanced statistical modeling to evaluate the potential benefits and harms of ACEi and ARB medications. Using stored blood samples and electronic medical records from patients hospitalized specifically for COVID-19, researchers were able to assess for an association between ACEi or ARB use and in-hospital patient outcomes, such as requiring mechanical ventilation or admission into intensive care. The research team overseeing the ISIC and M2C2 studies analyzed the health outcomes of about 1,600 people hospitalized for COVID-19 and reported that patients taking ACEi or ARB had about 10% mortality compared to 14% who were not on those medications⁵. Among those taking medications, 24% of patients required ventilation during hospitalization, compared to 20% of those not any treatment. These results were surprising as people taking medication also had significantly more comorbidities such as diabetes compared with the non-ACEi/ARB group. Knowing that people who use ACE inhibitors or ARB are not more susceptible to severe COVID-19 illness or increased risk of mortality during hospitalization has now led to the widely accepted practice of not discontinuing these drugs in people who are infected with SARS-CoV-2. In fact, people on anti-hypertensive medication had lower levels of inflammation biomarkers during hospital admission compared to those who don’t take ACEi and ARB drugs. This insight suggests that ACEi/ARB drugs could counter the inflammatory effects of COVID-19, which could be an interesting future direction of this research. Large scale studies have been valuable for providing evidence on how to mitigate detrimental outcomes during the COVID-19 pandemic and future findings will continue to influence guidelines for monitoring cardiovascular homeostasis, targeting treatments for vulnerable populations, and managing chronic illnesses.

References:

Patel AB, & Verma A. (2020). COVID-19 and Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: What Is the Evidence? JAMA. https://doi.org/10.1001/jama.2020.4812
Williamson EJ, Walker AJ, Bhaskaran K, et al. (2020). Factors associated with COVID-19-related death using OpenSAFELY. Nature. 2020;584(7821):430-436. doi:1038/s41586-020-2521-4
Raizada MK, & Ferreira AJ, (2007). ACE2: A New Target for Cardiovascular Disease Therapeutics. Journal of Cardiovascular Pharmacology, 50(2), 112–119. https://doi.org/10.1097/FJC.0b013e3180986219
Monterrosa Mena, J. ACE-2 and Immune System Changes in Smokers May Underlie COVID-19 Vulnerability. https://earlycareervoice.professional.heart.org/ace-2-and-immune-system-changes-in-smokers-may-underlie-covid-19-vulnerability/
Pan N, Hayek S, the ISIC Group, et al. (2021). Angiotensin‐Converting Enzyme Inhibitors, Angiotensin II Receptor Blockers, and Outcomes in Patients Hospitalized for COVID‐ Journal of the American Heart Association, 10(24), e023535. https://doi.org/10.1161/JAHA.121.023535

“The views, opinions, and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness, and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions, or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your health matters. If you think you are having a heart attack, stroke, or another emergency, please call 911 immediately.”

ACE-2 and Immune System Changes in Smokers May Underlie COVID-19 Vulnerability

April 13, 2022April 6, 2022 Jessica Monterrosa Mena

Clinicians report that people with pre-existing conditions such as cardiac disease, hypertension, and diabetes are at higher risk of mortality from COVID-19. With tobacco smoking being the leading cause of preventable death worldwide, it is surprising that smokers are underrepresented in hospital records¹. While hospital record data gives insight into the risk factors that influence COVID-19 outcomes, tobacco studies provide a further understanding of how smoking compromises the immune system. In fact, many human and rodent studies show that smoking increases the expression of angiotensin-converting enzyme 2, also known as the ACE-2 receptor and entry point for the SARS-CoV-2 virus². Normally, ACE-2 has a protective role in the cardiovascular system by regulating vasoconstriction, inflammation, and tissue damage. These protective functions are inhibited once the SARS-CoV-2 virus binds to ACE-2, and receptors levels then decrease following infection³, thereby allowing disease-causing biochemical processes to develop. ACE-2 levels are also known to vary among individuals, and people with cardiopulmonary diseases and those who take medications that help lower blood pressure also have high expression of the receptor ⁴. Therefore, human and animal studies focusing on the role of ACE-2 in cardiopulmonary disease and immune defenses provide insight that may be helpful for establishing biomarkers of COVID-19 disease progression and developing medication strategies for susceptible populations

Recent studies provide evidence that both traditional cigarettes and electronic cigarette (eCig) devices alter ACE-2 activity. One study assessed the levels of ACE-2 and transmembrane serine protease-2, which also facilitates viral entry, in peripheral blood mononuclear cell samples of young smokers collected before the pandemic². These young smokers had elevated levels of ACE-2 compared to non-smokers, and the effects were stronger in traditional cigarette smokers than in eCig users. Interestingly, the plasma cotinine levels (a measure of tobacco smoke exposure) were comparable between cigarette and eCig smokers, suggesting that non-nicotine components of traditional cigarettes may play a significant role in altering the immune system. While the study demonstrates that changes in ACE-2 could potentially increase susceptibility to viral entry and promote COVID-19 complications even among young healthy smokers, this study does not suggest that eCigs can be used as an effective harm-reduction strategy.

Animal models allow researchers to study biological effects in a controlled environment, in which animals are exposed to identical conditions. Studies using rodent models also confirm that the molecular players involved in SARS-CoV-2 infection are modulated by smoking. In one study, mice were exposed to eCigs with and without nicotine for 21 days and developed airway inflammation and immune cell infiltration in the lung⁵. Interestingly, ACE-2 protein levels were also increased in eCig exposed animals, but the effect was stronger in male mice as compared to female mice. There was also a greater effect as male mice exposed to eCig vapor and co-exposed to nicotine, which suggests that changes in ACE-2 protein are influenced by nicotine in a dose-dependent manner and sex-based differences may also be relevant to infection. While replicating such a study in humans to determine whether smoking directly influences viral entry may not be realistic, rodent studies provide valuable insights into sex-specific effects in animals exposed to controlled levels of toxicants.

While it is well established that smoking can promote immune dysregulation and COVID-19 complications, many questions remain as to how nicotine dosage, non-nicotine components, and pollutants unique to eCig devices also influence health outcomes. Processes like genetic heterogeneity of human populations and human expression of proteins that promote viral entry may also underlie susceptibility to COVID-19 mortality, which remains an exciting area of research. Scientific efforts across many fields of discipline continue to uncover the relationship between smoking and ACE-2, and novel findings continue to inform developing clinical trials to study the efficacy of medication for COVID-19 among smokers and patients with cardiopulmonary diseases.

References.

Monterrosa Mena, J. Insights About COVID-19 Health Outcomes in Smokers from Hospital Records, https://earlycareervoice.professional.heart.org/insights-about-covid-19-health-outcomes-in-smokers-from-hospital-records/
Kelesidis, T., Zhang, Y., Tran, E., Sosa, G., & Middlekauff, H. R. (2021). Instigators of COVID-19 in Immune Cells Are Increased in Tobacco Cigarette Smokers and Electronic Cigarette Vapers Compared With Nonsmokers. Nicotine & Tobacco Research, ntab168. https://doi.org/10.1093/ntr/ntab168
Kuba K, Imai Y, Rao S, Gao H, Guo F, Guan B, Huan Y, Yang P, Zhang Y, Deng W, Bao L, Zhang B, Liu G, Wang Z, Chappell M, Liu Y, Zheng D, Leibbrandt A, Wada T, Slutsky AS, Liu D, Qin C, Jiang C, Penninger JM. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nat Med. 2005 Aug;11(8):875-9. doi: 10.1038/nm1267.
Igase, M., Kohara, K., Nagai, T. et al. Increased Expression of Angiotensin Converting Enzyme 2 in Conjunction with Reduction of Neointima by Angiotensin II Type 1 Receptor Blockade. Hypertens Res 31, 553–559 (2008). https://doi.org/10.1291/hypres.31.553
Naidu, V., Zeki, A. A., & Sharma, P. (2021). Sex differences in the induction of angiotensin converting enzyme 2 (ACE-2) in mouse lungs after e-cigarette vapor exposure and its relevance to COVID-19. Journal of Investigative Medicine, 69(5), 954–961. https://doi.org/10.1136/jim-2020-001768

Insights About COVID-19 Health Outcomes in Smokers from Hospital Records

March 2, 2022February 21, 2022 Jessica Monterrosa Mena

Early in the COVID-19 pandemic, clinicians noticed that some patients with pre-existing medical conditions were at higher risk of severe illness and death. Since then, many observational studies confirmed that people with diabetes, asthma, or cardiovascular disease had a substantially higher risk of COVID-19-related complications and death^1,2. Such studies typically use hospital patient records to study relationships between individual risk factors, like age and sex, and long-term health outcomes. However, studies using hospital record data revealed that smokers may be underrepresented among patients with COVID-19, as highlighted by a recent review study of publications reporting smoking prevalence and clinical outcomes in patients diagnosed with COVID-19³. The review highlights that only a single study out of 15 research articles examined had reported a prevalence of smokers among patients with COVID-19 that resembles the smoking prevalence of the general population. Such findings, raises the question of whether a smoker’s paradox exists with the COVID-19 pandemic. The smoker’s paradox refers to the observational phenomenon of smokers exhibiting improved prognosis and decreased short-term mortality, following cardiovascular events. This idea has been mostly debunked now as a bias in the analysis of observational data and smoking is not considered to be a causative factor that improves health outcomes⁴. So, what considerations should be taken when interpreting health records of patients in order understand whether smokers fare worse COVID-19 outcomes than non-smokers?

Questioning Data Quality and Biases in Patient Record Data

Smoking is associated with many immediate and long-term health consequences, and initiates disease promoting mechanism in cardiopulmonary tissues. A low representation of smokers in hospitalized COVID-19 patients may be due to biases in patient record data collection. A small percentage of people who perceive stigma associated with smoker status may actually conceal smoker status during a primary care visit⁵. Furthermore, smoker screening often does not include questions about smokeless tobacco, electronic cigarette use, and second-hand smoke use, despite the rise in popularity in electronic nicotine delivery systems and cigarette alternatives⁶. Standardization and improved tobacco-related electronic health record questionnaires may begin to address the question of how much tobacco smoke a person is exposed to by including questions that cover sources of exposure, quantity of use, and duration of exposure. Collecting patient data that covers a larger range of exposure possibilities including having someone else in the home that smokers, or individual behaviors of switching from traditional cigarettes to electronic cigarettes, smoking cessation patterns, and years of use may provide better insight into how smoking behaviors influence health outcomes. In the context of the COVID-19 pandemic, smokers’ status is difficult to ascertain in patients who are intubated, sedated, and unresponsive. Closely tracking individual smoker status over time is helpful in those situations when a patient’s care plan should include tobacco withdrawal symptom management.

Smoking directly influences cardiovascular and respiratory health outcomes and using hospital data to derive associations with COVID-19 health outcomes is prone to confounding bias, reverse causation, and inappropriate adjustments in analysis models. In the future, it be possible to use human biomarkers to uncover the specific health effects from smoking. This might include correlating urinary levels of nicotine and cotinine to understand the burden of different tobacco products. For now, research using animal models to assess the health effects of traditional smoking and electronic cigarettes provide insight into the short- and long-term consequences of smoking and elucidates the biochemical processes that exacerbate disease including tissue repair processes, inflammation, and oxidative stress. Understanding the mechanistic processes involved in the exacerbation of COVID-19 disease among smokers may ultimately help identify biomarkers of disease progression and pharmacological treatments for vulnerable populations.

References:

Williamson EJ, Walker AJ, Bhaskaran K, et al. Factors associated with COVID-19-related death using OpenSAFELY. Nature. 2020;584(7821):430-436. doi:1038/s41586-020-2521-4
Why lighting up and COVID-19 don’t mix. American Heart Association News. https://www.heart.org/en/news/2020/05/05/why-lighting-up-and-covid-19-dont-mix#:~:text=Studies%20from%20Wuhan%2C%20China%2C%20where,%2C%20compared%20to%20non%2Dsmokers.
Usman MS, Siddiqi TJ, Khan MS, et al. Is there a smoker’s paradox in COVID-19? BMJ EBM. 2021;26(6):279-284. doi:1136/bmjebm-2020-111492
Doi SA, Islam N, Sulaiman K, et al. Demystifying Smoker’s Paradox: A Propensity Score–Weighted Analysis in Patients Hospitalized With Acute Heart Failure. JAHA. 2019;8(23). https://www.ahajournals.org/doi/10.1161/JAHA.119.013056
Stuber J, Galea S. Who conceals their smoking status from their health care provider? Nicotine & Tobacco Research. 2009;11(3):303-307. doi:1093/ntr/ntn024
LeLaurin JH, Theis RP, Thompson LA, et al. Tobacco-Related Counseling and Documentation in Adolescent Primary Care Practice: Challenges and Opportunities. Nicotine & Tobacco Research. 2020;22(6):1023-1029. doi:1093/ntr/ntz076

Electronic Cigarette Customization Matters.

January 31, 2022January 28, 2022 Jessica Monterrosa Mena

Electronic nicotine delivery systems (ENDS) are increasingly popular as an alternative to standard ‘combustion’ cigarettes. ENDS come in a large variety of forms and offer adulterant choices that enhance the user’s experience, such as flavors, humectants, and nicotine in different concentrations. There is a common perception that vaping is a safer alternative to traditional tobacco cigarettes as the ‘smoke’ lacks tars and other toxicants found in cigarette smoke⁽¹⁾. That may be true to some extent, however the ability of users to modify ENDS, like adjusting the power wattage, changing the type of heating element, and use of e-liquids with different flavor and nicotine concentrations, will influence the amounts of toxic chemicals in the inhaled aerosol. Under normal circumstances, the vapor contains, contrary to popular opinion, some of the same toxic compounds (formaldehyde, acetaldehyde, acrolein…) that are found in CCs ⁽²⁾. The ability to add custom adulterants to the vape fluid can add to the complexity of assessing potential risks. How modifications, or customizations might contribute to health effects and the generation of harmful chemicals is a topic that deserves more attention.

Devices are usually composed of a heating element, often a disposable metal heating coil, and atomizer tanks which directly produce the vapor. The most common heating coils and atomizer units can be comprised of different metals, such as stainless teel, nickel-chromium or nichrome, Kanthal nickel, or titanium. At usual setting these all work well, however they degrade with extended use. In some devices, users can set temperatures sufficiently high that degradation products of the device hardware such as metals are aerosolized and inhaled along with the vaporized e-liquid containing nicotine, flavoring, and solvents ⁽³⁾. Environmental metal contaminants are known risk factors for cardiovascular disease. Users of eC devices could inadvertently select vaping profiles that promote chemical reactions with the normally low-toxicity e-liquid to generate harmful chemicals in the aerosol they are inhaling at levels even exceeding traditional cigarettes.

Many studies have already brought insight into how device settings can generate levels of metals in inhaled aerosol that are unique to the modifiable aspects of eC devices. One study found increased concentrations of metals such as arsenic (As), chromium (Cr), copper (Cu), iron (Fe), manganese (Mn), nickel (Ni), lead (Pb), antimony (Sb), tin (Sn), and zinc (Zn) concentrations in eC aerosols when the device power is increased from low (20 Watts) to intermediate (40 Watts) settings ⁽⁴⁾. These exposure levels to metals like Ni from ENDS could exceed those of traditional reference cigarettes. It is interesting to note that ENDS from different manufactures emit different concentrations of metals, suggesting that heating and cooling patterns of individual devices could influence the amount of metals released. A similar study also found higher metal levels in aerosol and e-liquid after it comes in contact with the metal heating coil, compared to the original e-liquid in the dispenser vial ⁽⁵⁾. Elevated levels of metal biomarkers such as Cu, Cr, Sn, and Pb were found in the urine of electronic cigarette users. These studies highlight the need to further study how the unique customizable aspects of ENDS technology contribute to the formation of varying levels of contaminants in the inhaled aerosol. There is no question that smoking is a risk factor for cardiovascular disease and can increase blood pressure, heart rate, among other health outcomes. Educating the public about the health burden that ENDS pose and informing users about the potential dangers of vaping at elevated temperatures or using degraded heating components can be a step towards reducing use of new tobacco products.

References:

Benowitz, N. L., & Burbank, A. D. (2016). Cardiovascular toxicity of nicotine: Implications for electronic cigarette use. Trends in cardiovascular medicine, 26(6), 515–523. https://doi.org/10.1016/j.tcm.2016.03.001
Perraud, V., M.J. Lawler, K.T. Malecha, R.M. Johnson, D.A. Herman, N. Staimer et al.: Chemical characterization of nanoparticles and volatiles present in mainstream hookah smoke. Aerosol Science and Technology 53(9): 1023-1039 (2019)
Wylie, B. J., Hauptman, M., Hacker, M. R., & Hawkins, S. S. (2021). Understanding Rising Electronic Cigarette Use. Obstetrics and gynecology, 137(3), 521–527. https://doi.org/10.1097/AOG.0000000000004282
Zhao, D., Navas-Acien, A., Ilievski, V., Slavkovich, V., Olmedo, P., Adria-Mora, B., Domingo-Relloso, A., Aherrera, A., Kleiman, N. J., Rule, A. M., & Hilpert, M. (2019). Metal concentrations in electronic cigarette aerosol: Effect of open-system and closed-system devices and power settings. Environmental research, 174, 125–134. https://doi.org/10.1016/j.envres.2019.04.003
Olmedo, P., Rodrigo, L., Grau-Pérez, M., Hilpert, M., Navas-Acién, A., Téllez-Plaza, M., Pla, A., & Gil, F. (2021). Metal exposure and biomarker levels among e-cigarette users in Spain. Environmental research, 202, 111667. Advance online publication. https://doi.org/10.1016/j.envres.2021.111667
Bhatnagar A, Whitsel LP, Blaha MJ, Huffman MD, Krishan-Sarin S, Maa J, Rigotti N, Robertson RM, Warner JJ; on behalf of the American Heart Association. New and emerging tobacco products and the nicotine endgame: the role of robust regulation and comprehensive tobacco control and prevention: a presidential advisory from the American Heart Association. 2019;139:e937–e958. doi: 10.1161/CIR.0000000000000669.

“The views, opinions and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your personal health matters. If you think you are having a heart attack, stroke or another emergency, please call 911 immediately.”

Mental Health at the Forefront of Cardiovascular Health Discussions at AHA21

December 30, 2021December 17, 2021 Jessica Monterrosa Mena

Mental health was a big topic of conversation at AHA21, a fitting topic when pandemic related stress, clinician burn out, and depression seem to be at an all-time high. As a graduate student myself, I was interested in attending sessions that touched on depression, wellness, and work-life balance topics. A Health and Tech panel session titled, “Mental Health and Cardiovascular Disease,” addressed how depression and languishing mental health can heighten the risk of cardiovascular diseases and cardiovascular events. This is because chronic stress activates our sympathetic nervous system and promotes changes in heart rate, blood pressure, and stress hormone levels. While there is a diverse array of known factors that influence depression, clinicians are now taking on the challenging task to measure how mental health contributes and modulates cardiovascular health outcomes.

Clinicians often connect patients with resources and educate patients about chronic disease self-management. However, when patients are coping with chronic physical conditions, mental health conditions can go unrecognized and may further impact health outcomes. As stated in the panel conversation, an astonishing 22% of people with heart disease struggle with depression as well. Properly identifying patients with depression is particularly important as mental health challenges that accompany traumatic health crises can interfere with cardiovascular disease treatments, often managed with lifestyle changes and adherence to strict medication regiments. Clinicians who are willing to attain mental health training to recognize mental health symptoms may provide more useful resources to patients. For example, routine mental health screening during visits were discussed to be a powerful tool that can help clinicians assess depression and anxiety symptoms and facilitate patients getting comprehensive assessment and specific resources that may improve overall health outcomes.

Digital solutions may also be effective tools for managing mental health and heart-healthy behaviors in the future. There is biotechnology in the works that may help patients track physiological reactions to daily stressful experiences, and individual step count and heart rate variability data may one day help clinicians make better informed decisions. One digital intervention program in the works in the works is Happify Heart and Mind, tailored to address lifestyle changes that would benefit individuals with heart disease risk factors. Clinical trial data presented at this session showed that depression, anxiety, and overall wellbeing was improved in patients who used Happify compared to traditional psychoeducation. The take-away question to walk away with after this session is to reflect on who would benefit the most from digital solutions. While scientists can leverage technology to touch on the complex relationship between mental health and cardiovascular health, these solutions need to be adapted to cross the digital literacy divide. Patients who face social inequities would stand to benefit most from personalized and adaptable comprehensive interventions, and clinicians can help connect the most underserved patients with digital resources and support programs.

Resources:

https://www.heart.org/en/healthy-living/healthy-lifestyle/mental-health-and-wellbeing/how-does-depression-affect-the-heart

Social Media Advice for Early and Mid-Career Professionals from #AHA21

November 15, 2021November 15, 2021 Jessica Monterrosa Mena

The schedule of events as a first-time attendee to AHA Scientific Sessions can be overwhelming! As an early career blogger, I decided to attend sessions to get advice from professionals on managing social media presence in “Social Media in Cardiology- Managing Misinformation as Fellows in Training”. It was reassuring to take part in a lively discussion with many participants asking questions ranging from, “How do I start developing my social media presence” to “How do I deal with mansplaining?” We were lucky enough to have experienced panelist give their insights.

There are many benefits to taking part in social media as an early career professional. It can be used as a platform to find role models and mentorship or start project and publication collaborations. These connections can be established by simply joining broad dialogues, tagging experts in a conversation, or sending a direct message to interesting people. Establishing a social media persona can also include creating a place to ask questions, sharing expert consensus, and guiding dialogue in a specific discipline. As field experts and early career scientists, we are uniquely positioned to gather cutting edge information and share our knowledge with broader audiences. In order to be successful in these endeavors, choose your social media platform carefully. Understanding the age-group audience predominating that specific platform can inform the type of content you decide to post and will influence how you frame your ideas.

While participating in an environment that is not curated can allow you the freedom of sharing pictures of your dogs along with scientific news, panel experts also reminded us that everything on social media lives forever. The downsides of social media include hostility, mansplaining, and being discredited and turned into a meme. Not everything you post can be edited, and typos can be an annoyance for yourself and others when conversations are picking up speed. However, when your post turns out to be factually wrong or misguided, a public apology might ensue. Being transparent about how you gathered information and why you are sharing it with others can help establish and maintain trust in quickly developing online discussions.

Things can also get tricky when dealing with misinformation or with patients asking for medical advice. Many patients seek to educate themselves by seeking information online, and practitioners have a responsibility to educate and be effective leaders in this online space. In fact, social media training is becoming a desirable and valuable skills set for many early and mid-career professionals. Professionals can use social media to spread scientific evidence for the greater good but will also need to develop an approach for responding to misinformation. When engaging in difficult conversations, be explicit about the limits of what you are offering and avoid driving more traffic to misinformation pages. Be cautious when engaging with misinformation posts; give others the benefit of the doubt but stay concise in your responses and only provide the correct information. If you are unable to engage in a meaningful discourse you can move on, or if you are so inclined you can call out, block, ignore, or mute hostile people. There is a balance between the benefits you gain from social media and the time you spend online. Overall, to make social media a positive part of your career, make sure to set boundaries, build trust, and be accurate about what you post. Social media can be an effective way to build your professional persona, make meaningful connections, and communicate science if you develop the right approach.

This program is part of the FIT Program at #AHA21. The panelists Danielle Belardo MD, Amir Goyal MD MAS, Martha Gulati MD MS FAHA, Virginia Bartlett, and was moderated by Christina Rodrigues Ruiz, MS and Sasha Prisco MD, PhD.