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2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure

The 2022 American College of Cardiology (ACC) meeting was held in Washington DC. It was the first ACC meeting offering both in-person and virtual participation. After two years of uncertainty about the future of scientific meetings, hopefully, the COVID-19 pandemic was under control, and the cardiovascular community had the opportunity to meet colleagues, friends, and mentors/mentees once again. A day before the conference, the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure was released. A year ago, the 2021 Expert Decision Pathway for heart failure Treatment Optimization was released; however, the emerging new therapies available for heart failure necessitate the early update of heart failure (HF) guideline.

Guideline directed medical therapy (GDMT) for heart failure with reduced ejection fraction (HFrEF: LVEF EF≤ 40%) and heart failure with mildly reduced ejection fraction (HFmrEF: LVEF 41%–49%) now includes four-pillar medications: sodium-glucose cotransporter 2 inhibitor (SGLT-2i), angiotensin receptor neprilysin inhibitor (ARNI)/ angiotensin-converting enzyme inhibitor (ACEi)/angiotensin receptor blocker (ARB), beta-blockers and mineralocorticoid receptor antagonist (MRA). New recommendations for patients with heart failure with preserved ejection fraction (HFpEF: LVEF ≥ 50%) were made for the first time. SGLT2i (Class of Recommendation 2a), MRAs (Class of Recommendation 2b), ARNIs (Class of Recommendation 2b), and ARB (Class of Recommendation 2b) are now the cornerstone of HF therapies in patients with HFpEF. Avoidance of routine use of nitrates or phosphodiesterase-5 inhibitors (Class of Recommendation 3: No Benefit) was endorsed in this patient population. Health care professionals also need to understand drugs that may worsen HF. In patients with HFrEF, non-dihydropyridine calcium channel-blocking, class IC antiarrhythmic medications and dronedarone, thiazolidinediones, dipeptidyl peptidase-4 (DPP-4) inhibitors (Saxagliptin and Alogliptin) and Non-steroidal anti-inflammatory drugs should be avoided (Class of Recommendation 3: Harm). In patients with HFrEF without a specific indication, such as atrial fibrillation, or venous thromboembolism, anticoagulation is not indicated (Class of Recommendation 3: No Benefit).

The new guideline also revised the definition for HF stages. Stage A (At risk for HF) was defined as patients with hypertension, cardiovascular disease, diabetes mellitus, obesity, exposure to cardiotoxic agents, or a family history of cardiomyopathy. Stage B (Pre-HF) was defined as patients without current or previous HF symptoms/signs but evidence of structural heart disease, increased filling pressures or elevated stress cardiac biomarker (persistent elevated cardiac troponin or natriuretic peptide). Stage C: patients with current or previous symptoms/signs of HF, and stage D (advanced HF): patients with marked HF symptoms that interfere with daily activity with recurrent hospitalization despite optimized GDMT. The guideline provides therapies for patients at each stage of HF to prevent the progression of HF.

Moreover, the 2022 HF guideline endorsed five additional therapies once GDMT has been optimized. Ivabradine (Class of Recommendation 2a) was recommended for patients with HFrEF, New York Heart Association (NYHA) I-III, in normal sinus rhythm, heart rate ≥70 beats per minute on a maximally tolerated beta-blocker. Vericiguat (Class of Recommendation 2a) for patients with LVEF <45%. Digoxin (Class of Recommendation 2b) for symptomatic HFrEF. Polyunsaturated fatty acids (Class of Recommendation 2b) for HF NYHA II-IV and potassium binders (Class of Recommendation 2b) for patients with HF with hyperkalemia while taking renin-angiotensin-aldosterone system inhibitors. Further recommendations were provided for select patients with HF and anemia, iron deficiency, hypertension, atrial fibrillation, malignancy, sleep disorder, and mitral regurgitation. I would highly recommend my blog readers to review this enlightening just-released HF guideline: https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063

“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.”

 

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

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.

  1. 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/
  2. 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
  3. 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.
  4. 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
  5. 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

“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.”

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Preparing for the AHA Predoctoral Fellowship Application

In the second year of my Ph.D., I began applying for predoctoral fellowships. There are only a limited number of fellowship programs that I am eligible for as an international student, as I was ineligible for most federally funded research fellowships. My advisor suggested that I apply to the American Heart Association predoctoral fellowship, which is open to any full-time student enrolled in a doctoral degree program (Ph.D., MD, DO, DVM, PharmD, DDS, DrPH, PhD in nursing or equivalent health science doctoral degrees) without any restriction on residence or citizenship. The AHA predoctoral fellowship awards one or two years of NIH-rate predoctoral fellow stipend, funds for health insurance, and an additional $2,000 for project support.

In addition to being a great opportunity to obtain funding support for my research, applying for predoctoral fellowships also helped me polish my grantsmanship and clarify my research directions.  In my fourth year, I was awarded a two-year AHA predoctoral fellowship. Here are some of my tips for preparing for the AHA Predoctoral Fellowship:

  1. Enroll in a grant writing course in your program if your institution has one. Before applying for predoctoral fellowships, I took the grant writing course that was taught by one of the professors in my department. In the course, I was able to obtain feedback on my research grant, not only from experienced professors but also from my peers. Since I had limited experience in grant writing, taking an organized course really helped me navigate the process and build a solid draft. In addition, this experience gave me an opportunity to think deeply and incorporate others’ feedback on my research directions.
  2. Connect with individuals who can write you a stellar recommendation. The AHA predoctoral fellowship application requires three letters of reference, but the proposal sponsor (likely your principal advisor), co-sponsor, collaborator, or consultant cannot serve as a referent. Therefore, you will likely have to reach out to other faculty members, previous research mentors, or other individuals. Staying in touch with these individuals is a great way to ensure their support of your application.
  3. Think of how to convey your research to a broad audience. One of my favorite aspects of the AHA application is thinking about how my work could achieve AHA’s mission to achieve a world of longer, healthier lives. To communicate the value of my research, I wrote a non-scientist summary of my project and outline how my work supports AHA’s mission in my proposal. In fact, this summary to a non-scientist audience is one of the key peer review criteria of the award. Attending courses and workshops on science communication really helped me clarify my writing and avoid scientific jargons.
  4. Update your resume. Like other predoctoral fellowship applications, you will have to document your academic record as well as your prior research experience and/or publications. Don’t forget to update your resume from time to time to make sure you are presenting the best version of yourself.
  5. Don’t give up. I missed the funding mark in my first AHA fellowship application and was only awarded after resubmission. The reviewers’ comments on my first application, which I addressed in my resubmitted application, improved my proposal and research directions in general. Needless to say, resilience is a necessary quality in research!

The deadline for the 2023 AHA predoctoral fellowship is Wednesday, September 7, 2022. Mark your calendar and don’t miss this excellent opportunity!

“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.”

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Bypass Surgery – Reducing Risk for Stroke in Moyamoya Patients

In our previous blog, we discussed the diagnosis of Moyamoya disease using medical imaging such as CT and MRI. Patients with Moyamoya disease often have a higher risk for stroke due to their abnormal blood vessels in the brain. Once the diagnosis is confirmed, several treatment strategies are available to prevent strokes from happening. One of the most effective ways is bypass surgery.

In essence, a bypass surgery connects a blood vessel from outside the brain to a vessel inside the brain to redirect blood flow around a blocked artery. The figure in this blog illustrates the bypass procedure for Moyamoya patients. In this case, the superficial temporal artery (STA) outside the brain is connect to the middle cerebral artery (MCA) inside the brain to restore cerebral blood flow (CBF). It is a very complicated procedure that often requires more than 6 hours to perform by well-trained neurosurgeons. If the patient has blocked vessels on both sides of the brain, the neurosurgeon often has to perform two procedures to treat each side separately. After the surgery, the patient will recover in the ICU before being discharged. The patient will also need to have regular imaging exams such as MRI or CT after the surgery. The images can help doctors monitor the recovery from the surgery and identify any new vessel occlusions and risk for strokes.

At Stanford Moyamoya center, Dr. Gary Steinberg is an eminent neurosurgeon who has performed hundreds of such bypass surgeries for Moyamoya patients all over the world. The center offers a highly experienced group of professionals who see several new patients every week, making Stanford the largest Moyamoya referral center in the world. The bypass procedures require approximately three days of hospitalization at Stanford Hospital or Lucile Packard Children’s Hospital Stanford. Post-operatively, patients experience some minor scalp pain from the incision while some patients may get mild headaches. Patients with Moyamoya have minimal restrictions after surgery. The Moyamoya center also has a team to support international patients who want to receive care and treatment in the US.

Source: Stroke https://www.ahajournals.org/doi/10.1161/strokeaha.117.018563

References:

https://www.ahajournals.org/doi/10.1161/strokeaha.117.018563

“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.”

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How Poster Presentations Are Vital to the Conference

The poster presentation provides an excellent platform to communicate research findings and promote networking visually. Poster presentation helps make clever use of time and space for scientific discussion among conference attendees, thus are beneficially for both presenter and the conference organizer1,2. The outbreak of COVID-19 dramatically changed our lives, especially traveling and gatherings. With most scientific conferences online or hybrid, we now have an option of “e-posters”. Instead of printing your poster, you can submit a PDF version and insert a 2 to 5 minutes long video discussing your poster. In my opinion, e-posters are more beneficial as they allow you to share your work from the comfort of your home. Besides, speaking from personal experience, you can present your work at more conferences and across the borders without worrying about funding.

What are the benefits of poster/e-poster presentation, and why should you consider doing it?1

  1. Posters offer the opportunity to network and communicate with other attendees from your field, leading to collaborations and job offers. My own postdoctoral offer results from a conversation during a poster session.
  2. Due to time constraints and limited slot availability, not every trainee receives a chance for oral presentation. However, poster session allows a vast majority of trainees to share their work. Besides, question & answer session for oral presentation is typically 5 to 10 minutes and does not allow in-depth conversations. Conversely, poster sessions usually last a couple of hours, thus providing a platform for more extended discussion without time constraints.
  3. You can discuss specific aspects of your research receive detailed critiques, and impartial discussion/review by peers that can help you improve your work, ideas, or potential manuscripts. It can even provide you a new direction for your project.
  4. Poster presentations are an excellent platform to improve your presentation skills. One advantage is that those poster sessions allow you to explain your research differently. You can present as short as 3 minutes but can go up to 15-20 minutes. You also learn to communicate your work visually and verbally to a broader audience.
  5. In my opinion, abstracts and poster presentations are one of the ways to show your potential employees that you are active in the scientific community and participate in the meeting. Besides, almost all the conferences have poster awards thus, you have an opportunity to keep a feather in your cap or, should I say, resume.

What are some of the things to keep in mind for poster/e-poster presentation? 

Remember, the poster’s purpose is to visually communicate the latest research in a quick, efficient, and effective manner2. One should design your poster considering the readers and venue, especially doing an e-poster. Most people will view e-poster from their laptop screen; therefore, font size needs to be adjusted so that they don’t have trouble reading. Besides, a person might stop on your poster for less than a minute before deciding whether to engage in in-depth conversation or not. Therefore, I cannot emphasize enough the inclusion of graphical abstract, and your overall poster should synchronize as an illustrated abstract of your work. For more tips for designing a poster, please read a detailed article by Dr. Adam M. Persky2.

Two personal tips, something I learned over the year, are that:

  1. Don’t hesitate to invite people to your poster, especially when doing an e-poster. I have had valuable input to my projects from every person I invited to my e-poster. It helped me build my network too.
  2. Prepare your talk based on your audience. Suppose you attend a general regional conference, where people from all fields of science like engineering and biology are coming. In that case, you should be ready with a layman summary of your work so that people from other fields can understand your work. However, if you are going to conferences focused on your area of research, then you can include detailed results.

What are Vascular Discovery 2022 abstract submission categories?

  • Aortic Aneurysm Disease
  • Apolipoproteins and Lipid Metabolism
  • Blood Coagulation, Platelet Function and Antithrombotic Therapy
  • Cardiovascular Precision Medicine
  • COVID-19
  • Functional Genomics and Epigenetics in Vascular Disease
  • Immune Mechanisms of Atherosclerosis
  • Immunity and Inflammation in Vascular Biology
  • Metabolic Disorders and Atherosclerosis
  • Molecular and Cellular Mechanisms of Atherosclerosis
  • Molecular, Developmental and Cellular Biology of Vessel Wall
  • Peripheral Artery Disease, Carotid Artery Disease and Stroke
  • Population Science and Genetics in Vascular Discovery
  • Sex Differences in Cardiovascular Disease
  • Therapeutic Targets in Atherosclerosis
  • Venous Thromboembolism and Lymphatic Disease

What are the Vascular Discovery 2022 poster award categories?

  • Kenneth M. Brinkhous Young Investigator Prize in Thrombosis and the Irvine H. Page Young Investigator Research Award: Finalists will receive a chance to present oral abstracts during the meeting, and winners will be announced during council dinner. The Brinkhaus Prize recognizes outstanding endeavors in thrombosis, whereas the Page Award encourages investigators to continue careers in arteriosclerosis and vascular biology. Both awards are aimed to recognize new investigators.
  • ATVB Emerging Scientist Award for Women is sponsored by the ATVB Women’s Leadership Committee and recognizes excellent research conducted by women in the field of arteriosclerosis, thrombosis, and vascular biology. The finalists will present their abstracts during the poster session, give a 2-minute rapid-fire presentation during the Mentor of Women Award Luncheon, and the winner will be announced during the Council Dinner.
  • ATVB Investigators in Training Award recognizes pre-doctoral and postdoctoral in arteriosclerosis, thrombosis, and vascular biology who are members of the ATVB Council. The finalists will present their poster abstracts, and the winner will be announced at the Council Dinner.
  • ATVB Diversity Outreach Travel Grants encourages minority, early career investigators and students, to participate in the Vascular Discovery: From Genes to Medicine Scientific Sessions
  • 2 awards sponsored by the PVD Council (these are not competitions, and the winners will be recognized during the Council Dinner):
    • The Alan T. Hirsch, MD Mid-Career Award in Vascular Medicine supports mid-career level investigators studying the peripheral vascular disease. This award encourages participation in the PVD Council and AHA activities by providing travel funds to attend the Vascular Discovery: From Genes to Medicine Scientific Sessions, present research in oral or poster format, and engage in discussion with senior investigators.
    • The Robert W. Hobson, II, MD Early Career Investigator Award recognizes excellence in basic or clinical science in early career investigators in vascular and endovascular medicine, vascular surgery, or vascular biology.

Registration for the Vascular Discovery Conference is now open. Advance pricing opens on 4/1.  Register now for the best price!

REFERENCE

  1. Lab O. 7 reasons why you should present posters at a conference. Accessed March 20, 2022. https://people.clas.ufl.edu/oppenhe/2014/06/09/7-reasons-why-you-should-present-posters-at-a-conference/
  2. Persky AM. Scientific Posters: A Plea from a Conference Attendee. Am J Pharm Educ. Dec 25 2016;80(10):162. doi:10.5688/ajpe8010162

“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.”

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Blood Pressure and Hypertension Control Matter for Young Adults

Many young adults (18-39 year-olds) view themselves as physically healthy and may wonder why their doctor is concerned about their blood pressure. However, being young does not prevent you from developing elevated or high blood pressure. Uncontrolled blood pressure in young adults is a significant public health concern. In the U.S., 1 in 5 young men and 1 in 6 young women have hypertension. Hypertension control also varies by age group, with only 39% of U.S. young adults with hypertension having achieved control (blood pressure < 140/90 mmHg) compared with 58% of middle-aged adults (40-59 year-olds) and 54% of older adults (≥60 year-olds). Importantly, given that young adults with hypertension have more prolonged exposure to high blood pressure, they ultimately have a higher lifetime risk for cardiovascular disease. Early monitoring, diagnosis, and managed treatment are important to reduce the risk of serious medical conditions associated with uncontrolled hypertension.

Here’s a quick primer on blood pressure values and meanings and the effect of elevated blood pressure on cardiac structure and functioning:

Blood pressure is the force that blood applies to the walls of arteries as it’s pumped throughout the body.

Generally, your arteries can withstand some pressure, but there are limits to what the arteries can handle. For this reason, blood pressure is measured and monitored, and the values are categorized based on how the level of pressure affects our health. The four blood pressure categories are:

  • Normal: systolic less than 120, and diastolic less than 80
  • Elevated: 120 – 129, and less than 80
  • Hypertension (stage 1): 130 – 139, or 80 – 89
  • Hypertension (stage 2): 140 or higher, or 90 or higher
  • Hypertensive crisis: higher than 180, and/or higher than 120

Only normal blood pressure is considered healthy, while elevated or high blood pressure is associated with damaging the heart and arteries by forcing the heart to pump harder. When the heart works harder to pump blood, this can cause the heart muscles to thicken (altering the structure of the heart) and make it harder for the heart to fill with and pump blood (altering the functioning of the heart). The body’s arteries will also begin to narrow and harden, limiting the normal flow of blood.

Fortunately, high blood pressure is treatable and preventable. But uncontrolled hypertension affects nearly half of adults in the U.S., with many people unaware they even have the condition. The CDC recommends that knowing key facts about hypertension, getting your blood pressure checked regularly, and taking action to control your blood pressure if it is high is key to lowering your risk.

Source: “6 Facts About High Blood Pressure.” Venngage. https://venngage.net/pl/bVswgLzcpM

Since hypertension does not cause noticeable symptoms, it mustn’t be ignored. Over time, high blood pressure quietly damages the circulatory system and increases one’s risk of developing adverse health conditions – thus, hypertension is known as a silent killer. Additionally, high blood pressure is associated with poorer outcomes with COVID.

Steps to lower your blood pressure are often considered manageable and include common lifestyle modifications:

  • Smoking cessation
  • Maintaining a healthy weight
  • Consuming low levels of salt
  • Getting plenty of exercise
  • Limiting alcohol
  • Eating healthy

However, the patient experience among young adults with hypertension suggests significant barriers to receiving adequate blood pressure control management exist for this population. In a multi-center qualitative study, Johnson et al. (2016) identified unique emergent themes among young adults with hypertension that differed from prior hypertension qualitative studies in older age groups. Young adults voiced that the chronic disease diagnosis and the recommended lifestyle modifications made them feel older than their biological age. The participants also mentioned ongoing adverse psychological effects associated with their diagnosis and feeling a sense of self-blame and shame. This may be a critical point of intervention for healthcare teams to understand and address the negative emotional and mental health effects that a hypertension diagnosis has on young adults. Other emergent themes identified in the focus groups included the cost-benefit analysis performed by young adults when determining the necessity of recommended blood pressure treatment plan (e.g., lifestyle modifications, medication) and concern about experiencing negative social stigma based on their behavior choices reflecting new lifestyle modifications. Finally, most participants reported discarding hypertension education materials after leaving the clinic, citing that the materials were not tailored to young adults and their lifestyles.

These themes identified important barriers to young adult patients’ education on hypertension awareness and risks and opportunities for hypertension treatment non-adherence related to both medication and lifestyle modifications. Young adults with hypertension represent a unique population that could benefit from targeted interventions to improve hypertension control and cardiovascular disease prevention.

References:

  1. Centers for Disease Control and Prevention. Hypertension Cascade: Hypertension Prevalence, Treatment and Control Estimates Among US Adults Aged 18 Years and Older Applying the Criteria From the American College of Cardiology and American Heart Association’s 2017 Hypertension Guideline—NHANES 2013–2016. Atlanta, GA: US Department of Health and Human Services; 2019.
  2. Virani SS, Alonso A, Benjamin EJ, Bittencourt MS, Callaway CW, Carson AP, et al. Heart disease and stroke statistics-2020 update: a report from the American Heart Association. Circulation 2020;141:e139-596.
  3. Wall HK, Hannan JA, Wright JS. Patients with undiagnosed hypertension: Hiding in plain sight. JAMA2014;312(19):1973–1974.
  4. Parcha V, Patel N, Kalra R, Arora G, Arora P. Prevalence, Awareness, Treatment, and Poor Control of Hypertension Among Young American Adults: Race-Stratified Analysis of the National Health and Nutrition Examination Survey. Mayo Clin Proc. 2020 Jul;95(7):1390-1403. doi: 10.1016/j.mayocp.2020.01.041. PMID: 32622447.
  5. Johnson HM, Warner RC, LaMantia JN, Bowers BJ. “I have to live like I’m old.” Young adults’ perspectives on managing hypertension: a multi-center qualitative study. BMC Family Practice. 2016 Dec;17(1):1-9.
  6. https://www.houstonmethodist.org/blog/articles/2020/jan/why-your-blood-pressure-matters-even-in-your-20s-and-30s/
  7. https://www.cdc.gov/bloodpressure/5_surprising_facts.htm
  8. “6 Facts About High Blood Pressure.” Venngage. https://venngage.net/pl/bVswgLzcpM

“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.”

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Atherosclerosis in Prehistorical Times

Since some of the risk factors for atherosclerosis such as eating fast food, lacking physical activity, and developing diabetes appeared with the modernization of our societies, it is natural to think that atherosclerosis is a disease of the modern world.

However, atherosclerosis also existed in the ancient civilizations of Egypt, Peru, the American Southwest, and the Aleutian Islands who were all pre-agricultural hunter-gatherers. These observations were pioneered by Czermak in 1852 and taken further by the Horus study published by The Lancet in 2013 where vessel calcification was detected in 34% of the 137 mummies examined. The location of atherosclerosis was very similar to what we see nowadays. The aorta, as well as the femoral, tibial and carotid arteries, were affected, and in older mummies, atherosclerosis was detected in more than one vascular bed. The mummies who were 43 years old at the age of death were more likely to have atherosclerosis compared to those who were 32, highlighting the importance of advanced age in the development of the disease, which we also see nowadays. William Murphy and his colleagues also found carotid calcific atherosclerosis in the Otzi iceman from 3300 BCE.

Since ancient people had a very different lifestyle compared to modern humans, what were the reasons that lead to the development of atherosclerosis back then?

Genetic contribution

Humans have an innate predisposition to atherosclerosis. We now know how important this genetic link is to the disease as the discovery of novel genes involved in atherosclerosis is allowing the development of novel therapies (PCSK9 for example).

Gain of function mutations in lipid-related genes (LDLR, APOB, PCSK9 etc.) cause increased life-long exposure to LDL-C which could not be treated in ancient times. Not to mention the additive contribution of polymorphisms in different genes to atherosclerosis development which we have only started to understand recently (polygenic risk scores).

Inflammation

We now know the major contribution of inflammation to atherosclerosis and how chronic inflammation, which we see in diseases such as rheumatoid arthritis or systemic lupus erythematosus, increases the risk of developing atherosclerosis.

Ancient people had a high exposure to infections, such as tuberculosis and syphilis, against which they had no antimicrobial or vaccines. Chronic inflammation as a result of recurrent untreated infections may have contributed to atherosclerosis development.

Close proximity of these ancient populations to contaminated waters rich in microbes and parasites (such as Schistosoma species, Trichinella spiralis, Taenia species (tapeworm), Plasmodium falciparum (malaria) could have also increased the risk. Systemic inflammation caused by chronic infections in ancient populations could very well have accelerated the development of other inflammatory diseases, such as atherosclerosis. Throughout the years, constant exposure to infections could have led to the selection of genes that provide a strong and effective inflammatory response to Homo sapiens which is only showing to be deleterious nowadays as heightened inflammatory reactions accelerate atherosclerosis and other diseases associated with aging.

Smoke inhalation

Indoor smoke is a risk factor for coronary heart disease and cancer. Ancient people used firewood for the majority of their activities (heating, cooking, and lighting) and their home structures, which were mostly subterranean, had little access to ventilation. Soot deposits were identified in the inner surface of the ribs from burials in southern Turkey suggestive of anthracosis. It was also shown that tobacco was also commonly used in ancient civilizations (especially the Peruvians) which, we now know, contributes to increased inflammation and accelerate atherosclerosis development.

Ancient vs modern atherosclerotic plaque

It remains unclear how the features of the atherosclerotic plaque evolved over the years. Calcifications, which are the ends-stage of atherosclerosis, is what is observed in the remains of the ancient plaques seen in some mummies who were probably important people in their communities. However, we have no clue about the composition of these plaques back then since most of the cellular components would have degraded.

Ancient people who developed atherosclerosis might have not lived long enough to die as a result of their plaque rupturing because their life ended in a tragic fight, a deadly infection or they were poisoned by their enemies. This makes it harder for us to understand if the exposure of ancient people to atherosclerotic risk factors was important enough for them to die from this disease or whether this disease evolved to become more deadly during our modern times. Did the features of what we now call ‘vulnerable plaque’ (high lipid content, thin fibrous cap and presence of intraplaque hemorrhage) exist back then or did the plaque display more stable features?

It may be that since infections, wars and famines are less common in our modern world, people now live long enough to die from the consequences of atherosclerosis which has certainly evolved with our modern lifestyles. However, regardless of the era, atherosclerosis has always been lurking in the shadows throughout the evolution of Homo sapiens, displaying a different face as the years pass by.

References

  1. Thompson RC, Allam AH, Lombardi GP, Wann LS, Sutherland ML, Sutherland JD, et al. Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations. The Lancet. 2013 Apr 6;381(9873):1211–22.
  2. Walker EG. Evidence for prehistoric cardiovascular disease of syphilitic origin on the Northern Plains. Am J Phys Anthropol. 1983;60(4):499–503.
  3. Thomas GS, Wann LS, Allam AH, Thompson RC, Michalik DE, Sutherland ML, et al. Why Did Ancient People Have Atherosclerosis?: From Autopsies to Computed Tomography to Potential Causes. Glob Heart. 2014 Jun 1;9(2):229–37.
  4. Murphy WA, Nedden D zur, Gostner P, Knapp R, Recheis W, Seidler H. The Iceman: Discovery and Imaging. Radiology. 2003 Mar;226(3):614–29.
  5. Clarke EM, Thompson RC, Allam AH, Wann LS, Lombardi GP, Sutherland ML, et al. Is atherosclerosis fundamental to human aging? Lessons from ancient mummies. J Cardiol. 2014 May 1;63(5):329–34.
  6. Marchant J. Mummies reveal that clogged arteries plagued the ancient world. Nature [Internet]. 2013 Mar 11 [cited 2022 Mar 20]; Available from: https://www.nature.com/articles/nature.2013.12568

“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.”

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Gender Disparity in the Guideline Authorship, More Work Needs to Be Done on the International Level

Women have been widely underrepresented in cardiology over the past decades. Lately, over the last decade, the American College of Cardiology/American Heart Association (ACC/AHA) has made active efforts to bridge this gap. Other international societies such as the European Society of Cardiology (ESC) and the Canadian Cardiovascular Society (CCS) have also made similar efforts. However, the fruition of these efforts remains questionable. Although there is closure parity in the number of men and women entering medical school, the percentage of women continues to decrease as they advance in their career from medical school to residency and further to fellowship. This phenomenon has been called a “leaky pipeline,” which continues to drop down further going into academics and progressing to leadership.1

As per recent original research published in the Journal of American Heart Association, there is persistent disparity in including women in the guideline authorships from the ACC/AHA, ESC, and CCS guidelines from 2006-2020.2 The authors extracted all published guidelines from 2006-2020, reporting 80 ACC/AHA (1288 authors, 28% women), 64 CCS (988 authors, 26% women), 59 ESC (1157 authors, 16% women) guidelines suggesting vast underrepresentation of women in the leadership. There is a positive trend towards inclusion of women in the ACC/AHA guidelines, from11 (12.6%) in 2006 to 63 (42.6%) in 2020 (average annual percentage change, 6.6% [2.3% to 11.1%];P=0.005).2 There was a similar increase in the inclusion of women in the ESC guidelines as well, from 1 (7.1%) in 2006 to 23 (25.8%) in 2020 (average annual percentage change, 6.6% [0.2% to 13.5%]; P=0.04). Interestingly, the inclusion of women in CCS guidelines remained similar over the years.

In recent years, there has been a comparatively higher inclusion of women in ACC/AHA than CCS and ESC. This could be reflective of earlier efforts initiated by ACC/AHA back in 1995 by setting up nationwide and statewide women in cardiology chapters to promote women in cardiology. The study reported a higher inclusion of women in the guideline writing group when a woman was a chair or at least one of the chairs was women in the ACC(48% versus 30% versus 21%; P<0.0001) and ESC (43% versus 34% versus 14%; P<0.0001) guidelines; however, a similar trend was not seen in the CCS guidelines. These results are intriguing, as guideline writing committees are chosen independently by the task force group without direct input from the chairs. These results suggest inherent bias in the selection of writing group members.2

The authors also report women authors’ inclusion in general cardiology and subspecialties, reporting a higher inclusion of women in pediatric cardiology and heart failure followed by general cardiology and lowest in interventional and electrophysiology guidelines. The lower inclusion of women in the intervention and electrophysiology guidelines is likely secondary to fewer women in these fields; this has been likely attributed to the procedure-oriented areas and women shying away from these fields due to potential radiation exposure. Currently, professional societies like Women as One SCAI have put special efforts to promote women in the procedure-oriented fields and decrease overall radiation exposure.3-6

Another interesting aspect of this study was the repetition of the unique authors (the same authors being included in multiple guidelines) revealed 31.9% of women authors were repeat authors, which was similar to 32.9% of men authors. However, the highest frequency of inclusion of repeated men authors was higher than women. The authors propose limiting the number of times an author can be included on guidelines as a potential way to encourage more women in cardiology in the leadership.

It is important to achieve parity in the guideline authorship group as this group should reflect the population we serve. Prior studies have also supported that having a diverse physician group or patient treated by physicians of similar racial and ethnic backgrounds has better clinical outcomes. Thus, concerted efforts to plug the leaky pipeline at every step can help achieve gender parity in cardiology and promote leadership among women in cardiology.1

Prominent researcher and senior author Dr. Martha Gulati says: “This work was led by fellow-in-training Dr. Devesh Rai. He was particularly interested in the need for the inclusion of women in cardiology. I was honored to serve as the senior author and mentor of Dr. Rai and am grateful that the upcoming generation of cardiologists, regardless of whether male or female, are interested in seeing a change in our cardiology community in terms of diversity, equity, and inclusion.

Our work demonstrated that there is a significant disparity in the inclusion of women on all national guideline committees within AHA/ACC, ESC, and the CCS. Additionally, women are less likely to serve as a chair of cardiology guidelines. Further advocacy is required to promote equity, diversity, and inclusion in our cardiology guidelines globally.”

Reference

  1. Arnett DK. Plugging the Leaking Pipeline. Circulation: Cardiovascular Quality and Outcomes. 2015;8:S63-S64.
  2. Rai D, Kumar A, Waheed SH, Pandey R, Guerriero M, Kapoor A, Tahir MW, Zahid S, Hajra A, Balmer‐Swain M, Castelletti S, Maas AHEM, Grapsa J, Mulvagh S, Zieroth S, Kalra A, Michos ED and Gulati M. Gender Differences in International Cardiology Guideline Authorship: A Comparison of the US, Canadian, and European Cardiology Guidelines From 2006 to 2020. Journal of the American Heart Association. 2022;11:e024249.
  3. Cardiology ACo. Welcome to the Women in Cardiology (WIC) Member Section!
  4. Cardiology ESo. EAPCI Women Committee.
  5. Cardiology ESo. Women in Electrophysiology.
  6. Interventions SoCA. Women in Innovations.

“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.”

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Fast Forward to Spring, Slowly Fall Back to the Normal Heart

As the days become longer and the weather gets warmer, it’s that time of year again. Daylight saving time has been observed in most parts of the United States, and it’s time to manually set the clock one hour forward. When the clocks go forward, we ‘lose’ one hour of sleep. Even you try to compensate by forcing yourself to sleep more, your body might not follow your brain’s instructions due to the constant biological clock system, circadian rhythms. In a simple way, sudden disruption of sleep schedule could cause sleep deprivation and misalignment. The consequences of sleep disruption could have profound impacts, especially on cardiovascular health.

Why do we have daylight saving time?

In the United States, it’s scheduled to be the second weekend of March. In the European countries, the daylight saving normally is on the last weekend of March in spring. The idea is pretty much the same. The origin of daylight saving dated back to 1784, Benjamin Franklin proposed to adjust clocks for economic reasons. About 130 years later, Great Britain started to enact the daylight-saving rule to reduce energy costs during the war. Other countries then followed suit.

What are the health consequences?

One of the main consequences of forwarding one hour of clocks is sleep disruption. Despite the common opinion that shifting one hour of sleep ahead is inconsequential, increased sleep fragmentation and sleep latency present a cumulative effect of sleep loss at least across the following week, possibly longer (1). Circadian rhythms, commonly known as the internal clock, can directly or indirectly regulate many important biological functions such as sleep and locomotor activities, feeding and drinking behavior, core body temperature, endocrine activity, metabolism, autonomic and sympathetic activity, and many others (2).

What can we do to mediate the effects?

In 2020, the American Academy of Sleep Medicine published a statement calling for the abolition of daylight saving (3). It discussed acute and chronic harmful effects of sudden transition of sleep schedule attributed to daylight saving. The academy said, “the shift, by disrupting the body’s natural clock, could cause an increased risk of stroke and cardiovascular events, and could lead to more traffic accidents”. A call for permanent daylight saving time has been advocated and discussed both in European countries and in the United States. Just recently, United States senates approved a bill to make daylight saving permeant, the Sunshine Protection Act. Whether it will get approved by the House of Representatives and President Joe Biden, it’s still unknown.

At the moment, there are a few approaches to facilitate a smooth transition to the spring season. Common practices of good sleep hygiene such as avoiding caffeine and alcohol consumption late at night, following a consistent sleep schedule, using relaxation techniques to facilitate a stress-free sleep, avoiding screen exposure before bed, avoiding eating too close to bedtime would be some good starts. It’s also recommended to adjust clock time gradually to the daylight saving time a few days before and increase morning sun exposure to facilitate internal clock re-adjustment after daylight saving. Don’t expect your body can suddenly adjust to a new time schedule, treat it like jet lag. Allow some time for your body to recover and take it slowly to be your normal self.

REFERENCE

  1. Manfredini, R., Fabbian, F., Cappadona, R., & Modesti, P. A. (2018). Daylight saving time, circadian rhythms, and cardiovascular health. Internal and Emergency Medicine, 13(5), 641–646.
  2. Young, M. E., & Bray, M. S. (2007). Potential role for peripheral circadian clock dyssynchrony in the pathogenesis of cardiovascular dysfunction. Sleep Medicine, 8(6), 656–667.
  3. Rishi MA, Ahmed O, Barrantes Perez JH, et al. Daylight saving time: an American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2020;16(10):1781–1784.

 

“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.”

 

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Taking the Guesswork out of HFpEF

With an aging population and a higher burden of comorbidities, the proportion of heart failure patients with a preserved ejection fraction, i.e. ejection fraction ≥ 50% is increasing.1 Heart failure with preserved ejection fraction (HFpEF) now accounts for more than half of all heart failure hospitalizations. Despite the increasing prevalence, HFpEF remains a nebulous entity. HFpEF is often alluded to without a complete understanding of the underlying pathophysiology. Diagnosing HFpEF can be challenging as opposed to heart failure with reduced ejection fraction (HFrEF). With a normal ejection fraction, attributing dyspnea to cardiac congestion without performing invasive hemodynamic testing requires good clinical suspicion and judgment. Moreover, euvolemic patients with compensated HFpEF can have elevated filling pressures and dyspnea only with exertion. Non-invasive measurement of cardiac pressures can be inconclusive and invasive cardiopulmonary exercise testing (CPET) is considered the gold standard in this population.2 However its routine use is not feasible as it is an invasive and technically complex procedure with limited availability. An algorithm incorporating clinical and non-invasive parameters can help stratify patients’ probability of having HFpEF. The utility of risk scores, such as the CHA2DS2-VASc, TIMI, and Wells’ scores, is well established in the field of cardiovascular disease. There has been research into developing similar algorithms/ prediction scores for the diagnosis of HFpEF. Here, we discuss 2 proposed scoring systems for HFpEF- H2FPEF and HFA-PEFF.

H2FPEF Score

Reddy and colleagues at Mayo Clinic, Rochester developed the H2FPEF score to help physicians discriminate HFpEF from non-cardiac causes of dyspnea in symptomatic patients without obvious fluid overload.3 The score was developed from a cohort of 414 patients with an ejection fraction ≥ 50%, who underwent invasive hemodynamic exercise testing for definitive evaluation of unexplained dyspnea. Different clinical and echocardiographic markers were evaluated through logistic regression to identify variables associated with HFpEF. Ultimately 6 routinely available variables (BMI > 30 kg/m2, atrial fibrillation, hypertension treated with ≥ 2 medications, pulmonary artery systolic pressure > 35 mmHg, age > 60 years, and E/e’ > 9) were used for the model. Each variable was assigned a point based on the strength of association observed with HFpEF diagnosed via invasive testing (Figure 1). The final score had good discriminatory power (area under the curve = 0.84) for differentiating HFpEF from other causes of dyspnea. As the score increased from 0 to 9, so did the probability of HFpEF. The robustness of the model was validated through sensitivity analyses and a test cohort of 100 patients. The authors proposed a Bayesian approach- using a low score (0-1) to rule out HFpEF, a high score (6-9) to make a diagnosis of HFpEF, and an intermediate score (2-5) to consider additional testing.

The major limitation of this important model is the setting of the study. It was conducted at a single institute serving as a referral center, which may not truly represent the general population. It is reassuring that the score has been validated in small external cohorts.4,5 Moreover, an analysis from the TOPCAT trial population showed that patients with a higher H2FPEF score had an increased risk of adverse outcomes, suggesting a prognostic value of the score.6

Figure 1. H2FPEF Score proposed by Reddy et al. https://doi.org/10.1161/CIRCULATIONAHA.118.034646

HFA-PEFF Score

In 2020, the Heart Failure Association (HFA) and the European Society of Cardiology (ESC) released a consensus recommendation for diagnosing HFpEF, proposing the stepwise HFA-PEFF algorithm.7 This recommendation centers around the use of the HFA-PEFF score. The proposed scoring system uses echocardiographic parameters and natriuretic peptide (BNP and NT-proBNP) levels. The variables are divided into major and minor criteria across 3 domains- functional, morphological, and biomarker (Figure 2). Parameters within a domain are not additive, hence the score can be used even when certain values are not available. Each domain can contribute a maximum of 2 points and the total score ranges from 0 to 6. A total score of 5-6 is considered diagnostic of HFpEF while a score of 0-1 makes HFpEF unlikely. An intermediate score of 2-4 warrants further testing with non-invasive or invasive functional testing.

Notably, the HFA-PEFF score did not utilize demographic and clinical parameters and the power of the score was not assessed. However, an independent study later demonstrated its validity in two separate cohorts.8

Figure 2. HFA-PEFF Score proposed by HFA and ESC. https://doi.org/10.1002/ejhf.1741

Both of the above scoring systems have been received with enthusiasm, given the lack of a clear definition and diagnostic framework for HFpEF. Studies evaluating the 2 scores have also been published. Parcha and colleagues studied the generalizability of the H2FPEF and HFA-PEFF scores in an analysis of participants with unexplained dyspnea from prior HFpEF trials and the Atherosclerosis Risk in Communities (ARIC) study.9 They found that both the scores could rule out HFpEF with a greater than 99% success rate but the H2FPEF score had a higher specificity than the HFA-PEFF score. Amanai and colleagues calculated H2FPEF and HFA-PEFF scores in patients with HFpEF referred for stress echocardiography.10 They found that both scores had similarly high positive and negative predictive values and a correlation with abnormal hemodynamics during exercise. Another study in the ARIC population also found that both high H2PEFF and HFA-PEFF scores were associated with increased risk of heart failure hospitalizations or death, suggesting the prognostic value of both.11

Both H2FPEF and HFA-PEFF are validated and easy-to-use scores using readily available clinical, laboratory, and echocardiographic parameters. The use of these scores in the appropriate patient and context can aid in the timely and accurate diagnosis of HFpEF. Growing recognition and emergence of effective therapies such as SGLT2 inhibitors are important strides for improving outcomes for patients with HFpEF.

References:

  1. Borlaug BA. Evaluation and management of heart failure with preserved ejection fraction. Nat Rev Cardiol. 2020;17(9):559-573. doi:10.1038/s41569-020-0363-2
  2. Sorajja P, Borlaug BA, Dimas VV, et al. SCAI/HFSA clinical expert consensus document on the use of invasive hemodynamics for the diagnosis and management of cardiovascular disease. Catheter Cardiovasc Interv. 2017;89(7):E233-E247. doi:10.1002/ccd.26888
  3. Reddy YNV, Carter RE, Obokata M, Redfield MM, Borlaug BA. A Simple, Evidence-Based Approach to Help Guide Diagnosis of Heart Failure With Preserved Ejection Fraction. Circulation. 2018;138(9):861-870. doi:10.1161/CIRCULATIONAHA.118.034646
  4. Sepehrvand N, Alemayehu W, Dyck GJB, et al. External Validation of the H2F-PEF Model in Diagnosing Patients With Heart Failure and Preserved Ejection Fraction. Circulation. 2019;139(20):2377-2379. doi:10.1161/CIRCULATIONAHA.118.038594
  5. Segar MW, Patel KV, Berry JD, Grodin JL, Pandey A. Generalizability and Implications of the H2FPEF Score in a Cohort of Patients With Heart Failure With Preserved Ejection Fraction. Circulation. 2019;139(15):1851-1853. doi:10.1161/CIRCULATIONAHA.118.039051
  6. Myhre PL, Vaduganathan M, Claggett BL, et al. Application of the H2 FPEF score to a global clinical trial of patients with heart failure with preserved ejection fraction: the TOPCAT trial. Eur J Heart Fail. 2019;21(10):1288-1291. doi:10.1002/ejhf.1542
  7. Pieske B, Tschöpe C, de Boer RA, et al. How to diagnose heart failure with preserved ejection fraction: the HFA-PEFF diagnostic algorithm: a consensus recommendation from the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur J Heart Fail. 2020;22(3):391-412. doi:10.1002/ejhf.1741
  8. Barandiarán Aizpurua A, Sanders-van Wijk S, Brunner-La Rocca HP, et al. Validation of the HFA-PEFF score for the diagnosis of heart failure with preserved ejection fraction. Eur J Heart Fail. 2020;22(3):413-421. doi:10.1002/ejhf.1614
  9. Parcha V, Malla G, Kalra R, et al. Diagnostic and prognostic implications of heart failure with preserved ejection fraction scoring systems. ESC Heart Fail. 2021;8(3):2089-2102. doi:10.1002/ehf2.13288
  10. Amanai S, Harada T, Kagami K, et al. The H2FPEF and HFA-PEFF algorithms for predicting exercise intolerance and abnormal hemodynamics in heart failure with preserved ejection fraction. Sci Rep. 2022;12(1):13. doi:10.1038/s41598-021-03974-6
  11. Selvaraj S, Myhre PL, Vaduganathan M, et al. Application of Diagnostic Algorithms for Heart Failure With Preserved Ejection Fraction to the Community. JACC Heart Fail. 2020;8(8):640-653. doi:10.1016/j.jchf.2020.03.013

“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.”