cardiovascular disease

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How to Protect Your Aging Heart

Huan Wang, PhD

“Man is as old as his arteries.” –Thomas Sydenham

Cardiovascular diseases are commonly associated with unhealthy lifestyles. Do you know that age is a strong predictor of cardiovascular diseases in both men and women? As you grow older, your risks of suffering a heart attack, to have a stroke, or to develop coronary heart disease and heart failure are getting much higher. Ageing research has been evolving rapidly in the recent decades. In the early days, ageing research was mostly focused on Alzheimer’s disease and related dementias. To improve quality of life in ageing population, other symptoms of ageing including physiological function decline start to capture scientific community’s attention. In AHA Scientific Sessions 2021, a panel of experts and professionals in the field talked about novel strategies to promote healthy vascular aging.

To prevent cardiovascular diseases in aging populations, there are many take-home messages from today’s live session. Dr. Blumenthal from Johns Hopkins University used a simple “ABCDEF” approach1 to highlight the most recent development in cardiovascular diseases management based on most recent scientific discoveries and epidemiological results. Two of the major factors: Diet and Exercise, which are closely associated with body weight management, are further elaborated by Drs. Willett and Donato, respectively.

Dr. Willett is a professor of Epidemiology and Nutrition from Harvard Medical School. He challenged the recommendation of Dietary Guidelines for Americans (DGA). Dr. Willett encouraged the public to focus on evidence-based dietary recommendation, and to evaluate epidemiological studies by using randomized control trials with risk factor, disease incidence and mortality outcomes and prospective epidemiological studies with equal intensity intervention of 12-month and longer. Aside from canonical discussion of dietary recommendation based on health benefits, Dr. Willett raised a pertinent point in environmental sustainability. “How to feed 2 billion people in 2050?” he asked. Climate change is a global crisis and agriculture plays a pivotal role in fighting it. In “the Omnivore’s Dilemma”, Michael Pollan talked about how livestock production is responsible for much of the carbon footprint of global agriculture. The best practice for specific diets to prolong healthy life needs to take into consideration of reducing carbon footprint.

Vascular ageing is comprised of multiple processes including cellular senescence, inflammation and oxidative stress2. Dr. Donato talked about how ageing affects endothelial cell function and habitual aerobic exercise improves endothelial function in men. He also raised an interesting point: this beneficial effect of exercise on endothelial function is sex dependent. More research on sex differences needs to help us understand how to promote healthy ageing. DNA damage is associated with vascular aging. Dr. Shanahan discussed the signaling pathways involving in DNA damage and cellular senescence-associated phenotypes on vascular calcification. Inhibition of DNA damage agents can mediate vascular calcification progression. Can we use DNA damage as a biomarker to detect vascular ageing?

The “One-size-fits-for-all” approach in disease prevention and treatment requires a new perspective. In 2015, Precision Medicine Initiative was launched to accelerate research in disease treatment and prevention by considering individual differences in people’s genes, environments and lifestyles. With the development of next-generation sequencing, risk factors for coronary artery diseases require a modification. Dr. Wolford discussed her research on incorporating genetic backgrounds for disease prediction using polygenic risk scores3. It’s only the beginning of an exciting era using precision medicine as a tool for disease prevention and intervention in cardiovascular diseases.

To protect an aging heart, many approaches need to be implemented. Healthy lifestyles, nice environment and consideration of individual differences are all part of a clue.

REFERENCE

  1. Feldman DI, Wu KC, Hays AG, Marvel FA, Martin SS, Blumenthal RS, Sharma G. The Johns Hopkins Ciccarone Center’s expanded ‘ABC’s approach to highlight 2020 updates in cardiovascular disease prevention. American Journal of Preventive Cardiology. 2021;6:100181.
  2. Donato AJ, Machin DR, Lesniewski LA. Mechanisms of Dysfunction in the Aging Vasculature and Role in Age-Related Disease. Circulation Research. 2018;123(7):825–848.
  3. Wolford BN, Surakka I, Graham SE, Nielsen JB, Zhou W, Gabrielsen ME, Skogholt AH, Brumpton BM, Douville N, Hornsby WE, Fritsche LG, Boehnke M, Lee S, Kang HM, Hveem K, et al. Utility of family history in disease prediction in the era of polygenic scores. medRxiv. 2021:2021.06.25.21259158.

“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.”
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Cancer Warriors losing battle to heart disease?

Gaganpreet Kaur

Your cancer treatment may be over, but does it continue to cause side effects to your body? Chemotherapy and radiation have revolutionized the survival rates among cancer patients, but so is the development of cardiovascular diseases (CVD) in cancer survivors. The scientific session 2021 program committee organized an educational session on cardio-oncology, which included talks by experts on heart health after cancer treatment, feedback link between heart and cancer, racial disparities, and new clinical imaging technology. The session was moderated by Dr. Susan Gilchrist from Houston, TX, Dr. Daniel Addison from Columbus, OH, and Dr. Mary Branch from Oak Ridge, NC. However, my favorite part was a short talk by Ms. Kikkan Randall, the first American cross-country skier to win Olympic gold along with her teammate. The session walked through the science journey and a patient journey and provided us perspective on a healthy heart from both expert’s and patient’s point of view.

Cardiovascular diseases are the leading non-cancerous cause of death among cancer survivors. Cardiac dysfunction, atherosclerosis, arrhythmia, and valvular diseases are major complications observed among cancer survivors. The first speaker in the cardio-oncology session was Dr. Saro Armenian from the City of Hope Comprehensive Cancer Center. He started by discussing the nature of the problem using the “Multiple-Hit” hypothesis, where he discussed how the margin of safety declines following cancer diagnosis and treatment. He further addressed the effect of tumor and cancer therapies on cardiac output, pulmonary function, muscle integrity, and oxygen-carrying capacity, all events ultimately causing cardiovascular aging among patients. He further walks us through how clonal hematopoiesis (a condition where we accumulate somatic mutation in the blood) can be the underlying cause of cardiovascular aging and drive CVD development among cancer patients. You can further read about clonal hematopoiesis and premature aging in one of his publications:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7192097/

After a fantastic talk on premature cardiovascular aging in cancer patients, Dr. Clyde Yancy provided an exciting perspective on racial disparities. Adverse differences in numerous cancer burdens exist among specific population groups in the United States. For example, African American men are 111% more like to develop prostate cancer, whereas American Indian/Alaska Natives are twice as likely to develop liver and bile duct cancer. Similarly, racial, and ethnic health care disparities are present in cardio-oncology due to structural racism, higher prevalence of CVD risk factors, and reduced access to specialty care. A multidisciplinary approach involving stakeholders, health care policymakers, clinicians, scientists, and patients is required to resolve these disparities. Lastly, Dr. Clyde Yancy highlighted the importance of diverse population-based study and, in addition to genetic factors, phenotyping the social determinants of CV health. Read one of his recent publications about how poverty can increase the risk of heart problems:

https://pubmed.ncbi.nlm.nih.gov/34240286/

The third talk was from Dr. Rudolf A. de Boer from University Medical Center Groningen about reverse cardio-oncology. When I think about cardio-oncology, I always think about how cancer patients end up developing heart problems. However, he explained how the reverse could be true. He shared preclinical findings on how heart failure promotes tumor growth. Both CVD and cancer share several risk factors. Further, angiogenesis and inflammation under CVD conditions can increase the risk of tumor development. To learn more about cardio-oncology, refer to his recent review: https://www.ahajournals.org/doi/pdf/10.1161/JAHA.119.013754

There were additional highlights on crosstalk on clinical imaging by Dr. Ana Barac from MedStar Heart. She listed the importance of cardiac imaging, echocardiography, and cardiac MRI.

Lastly, Olypoam Kikkan Randall, a cancer survivor, shared how she stayed committed to the 10-minute rule to keep her active despite adversity. Exercise training has been shown to confer beneficial effects in cancer patients at CVD risk. Here is an interesting article documenting a scientific statement from AHA for cancer survivors to manage cardiovascular outcomes. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000679

“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.”
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Can your leg and arm tell a failing heart?

Huan Wang, PhD

For the heart’s health condition, everything is interconnected. Other parts of the body might be reflective or instigators of a failing heart. Among all of the important issues related to cardiovascular disease, skeletal muscle is on top of that list. Conventionally, the main function of skeletal muscle is tightly related to physical capabilities. It’s only the partial facts. Skeletal muscle plays a pivotal role in supporting our physical well-being in many ways that are more than organizational. The relationship between skeletal muscle mass and cardiometabolic health starts to attract the researcher’s attention.

As we know, skeletal muscle mass decreases during the aging process, while cardiometabolic health often declines. A recently published epidemiology study investigated the relationship between skeletal muscle mass and cardiovascular disease in a group of adults (3042 people) without pre-existing cardiovascular risk in a 10-year follow-up study, ATTICA1. After adjusting for various confounders, this study showed a significant inverse association between skeletal muscle mass and cardiovascular incidence (HR 0.06, 95% CI 0.005 to 0.78). Moreover, it showed that people in the highest skeletal muscle mass group had 81% lower risk for a cardiovascular event. The results are quite intriguing. Does decreased skeletal muscle mass contribute to poor heart health or does a failing heart cause muscle mass decrease? It’s hard to figure out the cause and effect without understanding the relationship between skeletal muscle and the heart.

Chronic heart diseases and heart failure impair muscle function2. In particular, many heart diseases affect exercise performance. For certain cardiac conditions such as atherosclerotic heart disease, exercise stress test is widely used to measure heart functional capacity, and also used as a diagnostic tool to evaluate the efficacy of treatment and predict prognosis. Cardiac function affects exercise performance in many ways and reduced cardiac output response to exercise leading to skeletal muscle hypoperfusion and lactic acidosis3. The pathophysiological mechanisms impairing skeletal muscle function in heart failure are discussed in a review, shown in Fig12. In heart failure, many stimuli contribute to skeletal muscle contractility apparatus dysfunction such as systemic inflammation, TGF family members, adrenergic signaling, decreased anabolic stimuli and increased calcium shuttling/overload (Fig. 1). Skeletal muscle atrophy can be caused by biological processes such as protein degradation, impaired growth factor signaling and skeletal muscle inflammation.

Heart failure with increased systemic inflammation can trigger skeletal muscle inflammation. it’s also true the other way around: skeletal muscle injury can cause local activation of innate immune system4. Danger-associated molecular patterns (DAMPs) can be released from dying myocytes. DAMPs encompass diverse mediators including alarmins (HMGB1, S100A8/9/12, S100B, IL1a, HSPs), bioactive lipids, extracellular matrix fragments and nucleotides (ATP, CpG, dsRNA)5. The impact of local skeletal muscle immune responses has been proved both harmful and beneficial. Traditionally, a stimulated immune response (M1-like macrophages) is a sign of disease. However, distinct macrophage subsets (M2-like macrophages) help tissue regeneration in chronic skeletal muscle pathologies6. The relationship between skeletal muscle damage and inflammation is complicated. And how they play a role in heart diseases require more research in the future.

To go back to the original question in this blog, the answer is a yes. Yes, skeletal muscle (leg and arm muscle) can tell the basic condition of the heart. And is it good for your heart if there is more muscle mass? Maybe. The absolute muscle mass does not tell us the function of the muscle, other aspects of muscle, for example, different types of fiber may hold the key.

References

  1. Tyrovolas S, Panagiotakos D, Georgousopoulou E, Chrysohoou C, Tousoulis D, Haro JM, Pitsavos C. Skeletal muscle mass in relation to 10 year cardiovascular disease incidence among middle aged and older adults: the ATTICA study. Journal of Epidemiology and Community Health. 2020;74(1):26 LP – 31.
  2. Kennel PJ, Mancini DM, Schulze PC. Skeletal Muscle Changes in Chronic Cardiac Disease and Failure. Comprehensive Physiology. 2015;5(4):1947–1969.
  3. Lunde PK, Sjaastad I, Schiøtz Thorud H-M, Sejersted OM. Skeletal muscle disorders in heart failure. Acta Physiologica Scandinavica. 2001;171(3):277–294.
  4. Lavine KJ, Sierra OL. Skeletal muscle inflammation and atrophy in heart failure. Heart failure reviews. 2017;22(2):179–189.
  5. Chan JK, Roth J, Oppenheim JJ, Tracey KJ, Vogl T, Feldmann M, Horwood N, Nanchahal J. Alarmins: awaiting a clinical response. The Journal of Clinical Investigation. 2012;122(8):2711–2719.
  6. Villalta SA, Deng B, Rinaldi C, Wehling-Henricks M, Tidball JG. IFN-γ Promotes Muscle Damage in the <em>mdx</em> Mouse Model of Duchenne Muscular Dystrophy by Suppressing M2 Macrophage Activation and Inhibiting Muscle Cell Proliferation. The Journal of Immunology. 2011;187(10):5419 LP – 5428.

“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.”
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Housing and Health Equity in Cardiovascular Disease

William Aitken, MD

So far, 2020 has been a year of public health crises. By early spring, it was apparent that people living in socio-economically disadvantaged areas were being hit hardest by Covid-19 [1]. In these same areas, people across the United States took to the streets protesting the murder of George Floyd, an unarmed Black man – in police custody [2]. In the words of James Baldwin, “It demands great spiritual resilience not to hate the hater whose foot is on your neck, and an even greater miracle of perception and charity not to teach your child to hate.”, and we as a country are still looking for this resilience [3]. Among the many consequences of this year’s events, these tragedies have really prompted a long, hard look at our healthcare system. One recently published article that was particularly heartening to read was the American Heart Association’s Council on Epidemiology and Prevention and Council on Quality of Care and Outcomes Research Scientific Statement on “Importance of Housing and Cardiovascular Health and Well-Being”. It outlines how housing stability, quality, affordability, and neighborhood environment are linked to cardiovascular disease. The statement doesn’t shy away from evidence of how increased psychosocial stress in the Black community and other social determinants of health are associated with cardiovascular health disparities.

The world has changed profoundly over the past year and while we continue to strive to show charity to others in our everyday encounters, I look forward to reading more research that will help inform how we as a community can better address health inequity.

References:

“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.”
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Keep Out The Rain

Anberitha Matthews, PhD

cvd umbrella

It has been well established that cardiovascular disease (CVD) is a condition that leads to chronic symptoms that are generally thought of as a primary disease. However, vascular injury leads to subsequent disease such as metabolic disease, obesity, high blood pressure and kidney disease. There are several contributing factors starting a person on the path of having cardiovascular disease. Some of these include:

  1. Oxidative (ox)stress—potentially results in DNA damage
  2. Increased low density lipid (LDL) that can become oxidized into oxLDLs
  3. Overeating/over-nutrition leads to hormonal imbalances and subsequently obesity and/or metabolic disease
  4. Distress/Eustress is controversial, but the body does not know the difference and they can both lead to shear stress due to increased blood flow through laminar areas of the vascular system.
  5. Toxins that come produced within the body (endobiotics) or enter the body from outside source (xenobiotics). Environmental effects have strong impacts on how the body responds. It is important to manage the things that are within one’s control such as smoking, exercise, and consuming a well-balanced diet.

With people livings becoming busier, it is easy to miss the warning signs. A slight weight gain here or a headache there. What then can be done about the progression of CVD and other disease states such as hypertension? I am glad you asked. Controlling hypertension for example can be maintained by making lifestyle changes consisting of exercising at least 150 minutes per week, modifying one’s diet to potentially include the dash diet, and reducing stress levels. This sounds like a lot but planning ahead is key. Often times I find myself going to a fast food restaurant because I have gotten too hungry to cook, or because I have not had time to go shopping. When I plan ahead and purchase my food for a week and pack healthy snacks, I evade the urge to go for those french fries (my go-to weapon against hunger). Additionally, I find I am less stressed if I spend some time performing rigorous exercises or get moving throughout the day. I attempt at least 250 steps every hour and 10,000 steps over the course of the day.

However, the symptoms are not the same for everyone, thus one should know what to look for to identify vascular disease early as well as forming a trusting relationship with a primary care provider because, “You’re the Cure”!! Let’s keep this conversation going. Follow me on Twitter (@AnberithaT) or on my site. I will take a deeper look at each of these topics and discuss what, if anything, can be done to combat or control these symptoms.

 
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Paradigms and Progress in HIV and Cardiovascular Health

Allison Webel, PhD

 “Led by a new paradigm, scientists adopt new instruments and look in new places” – Thomas S. Kuhn

For a lot of rational (and some irrational) reasons, hearing the word HIV evokes fear, anger, and sadness. When I first heard about HIV, I was an elementary school student in late 1980’s and at that time, HIV was almost always a death sentence.  But today that is not the case.  Today, due to the hard work of scientists, patients, volunteers, advocates, and countless others, HIV is a chronic, manageable disease. An accomplishment epitomized by the oldest known person living with HIV recently turning 100 years old.

living with HIV graph

While this progress and longevity should be celebrated, the flip-side of age is that it is the primary driver of cardiovascular disease (CVD). In fact, this longevity has ushered in a new era where adults living with HIV are at exceptionally high risk of cardiovascular diseases including heart attacks, heart failure, and stroke. A recent meta-analysis by Anoop Shah, MD, from the University of Edinburgh, found that the global burden of HIV-associated cardiovascular disease has tripled in the past 20 years, especially in low and middle-income countries. Now, after more than two decades of accumulating evidence in this field, the American Heart Association released earlier this month a Scientific Statement on the characteristics, prevention and management of cardiovascular disease in people living with HIV.

Directed at all who support adults living with HIV, this statement is a general roadmap for raising awareness about the increasing burden of CVD in this population. However, it offers few new tools for providers to use, due primarily to the lack of high-quality “clinical trial data on how to prevent and treat cardiovascular diseases in people living [and aging] with HIV investigating cardiovascular endpoints” said Matthew J. Feinstein, M.D., M.Sc., chair of the writing group for the statement and assistant professor of medicine at the Feinberg School of Medicine, Northwestern University.

Still, what the existing (mostly observational) evidence allowed the writing group to do was to develop a pragmatic approach to assessing and preventing cardiovascular disease in treated HIV (Figure above). This approach includes the following:

  • Ensure all patients living with HIV are on effective HIV treatment
  • Determine risk of cardiovascular disease using tools such as ACC/AHA 10-year ASCVD risk estimator and a family history
  • Optimize lifestyle approach to prevention (e.g., smoking cessation, physical activity, healthy diet intake)
  • If at high risk and between the ages of 40-75 years, talk with the patient about the risks and benefits of lipid-lowering therapy while exercising caution for drug-drug interactions

Yet, while the new AHA Scientific Statement will be an important catalyst for the field, in many ways it creates more questions than answers. For example, are we shifting to a new paradigm in HIV care? Do we need new tools to help reduce CVD in this population or are the general recommendations for risk stratification and lifestyle optimization sufficient?  What is the most effective way to get either existing or new clinical tools to the high-risk patients living with HIV?

Fortunately, some of these questions are starting to be answered. The REPRIEVE study is the first large scale (>8,000 people) clinical trial to test if a daily statin reduces cardiovascular disease in adults living with HIV. Results are expected in the next 3-4 years. Additionally, the PRECluDe grants at the National Heart, Lung, and Blood Institute have stimulated new implementation science research focused on understanding how to best adapt effective CVD prevention studies to the real-world settings where people living with HIV receive their health care. These initiatives, coupled with ongoing research on the discovery of mechanisms of CVD and the testing of CVD prevention interventions in people living with HIV, will eventually allow for the development of guidelines on the prevention and management of CVD in HIV—the true instrument needed to help improve cardiovascular health for all adults living with HIV.

 
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Five Lessons From My Heart Attack Patients

Akl Fahed, MD, MPH

In only few months, I leave my clinic where I have been seeing patients with heart disease for the past three years. It was not until I started discussing with them the transition to a new cardiologist that I appreciated the unique relationship we have built.  It has only been few years since we first met in in the Emergency Department in the middle of the night as they were having a heart attack, but somehow this journey feels longer.  I witnessed their heart attacks change their lives in many different ways, as they learned to cope, recover and carry on in life with a story to tell. Being one of the characters in their stories, I learned five lessons about life that will stay with me.

 

1- You can make any terrible event a wake up call or the beginning of the end.

A big heart attack or sudden cardiac arrest is arguably the most terrible event one could experience. As my patients recovered from such an event and came to see me in clinic, I could tell that the event changed them, either to the better or to the worse. While some lost weight, started training regularly, left their high stress jobs, or decided to travel the world, others became even more sedentary, gained weight, and started lamenting their bad luck and “missed opportunity” for good health.  It was striking to observe those two trajectories of opposite directions. Like my heart attack patients, when you are faced with a terrible event in life, you can either use it as a wake up call to do better afterwards or fall off a ledge and spiral down. You decide your own fate.

 

2- A supporting family is worth all the medicine of the world.

One patient after another, it became clear to me that the presence of a supporting family member that cares for you during difficult times is worth the most state-of-the-art medicine. It is that person that ensures that your food is low in salt and has no butter, that you do your daily exercise and not miss your medication, that you come to your appointments and ask all the right questions, or that simply hold your hand and tell you it’s going to be okay when things turn sour.

 

3- You’re as old as you think you are.

I met a 90 year-old woman who had a big heart attack and went for the most aggressive therapies. A year later she still shows to my clinic fully groomed and cheerful telling me she picked up dancing and life could not be any better.  I also met a 50 year-old man who after a small heart attack gave up on enjoying life or hoping for better future and couldn’t be convinced otherwise.

 

4- Faith, hope, and courage are your best friends when you’re not in control.

When patients are waiting for a high risk surgery or intervention, they simply are not in control of their fate. I found that those that fared well had three unique characteristics. First, they had faith in themselves, their doctors, or God. Second, they always hoped for the best. Third, they had the courage to face a difficult reality when things don’t go as well.  Whenever you’re not in control, let faith, hope, and courage always be your best friends.

 

5- Write your best story today because you never know when it ends.

While I learned so much from the stories of those patients who made it to my clinic, many did not, and their stories ended in the hospital. As you go through life, live every day to the fullest and write your best story page by page, because you really never know when it ends.
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What Are the 7 Steps to A Heart Healthy Lifestyle

Renee Bullock-Palmer, MD

The key ‘take home’ points for patients based on the latest 2019 American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines on Primary Prevention of Cardiovascular disease.

Introduction

Following the theme of Preventive Lifestyle from the 2018 American Heart Association meeting, EPI | Lifestyle 19,  the Cardiology community eagerly awaited the release of the highly anticipated 2019 American College of Cardiology (ACC)/American Heart Association (AHA) Guidelines on Primary Prevention of Cardiovascular disease1. These guidelines were released at the recent ACC annual scientific meeting in New Orleans, Louisiana March 16-18, 2019. There is an increased focus on the importance of lifelong adherence to a heart healthy lifestyle of eating heart healthily and maintaining a physically active lifestyle. There were also new recommendations with regards to use of aspirin for primary prevention. These recommendations have caused some anxiety with regards to use of aspirin, a common drug used by many persons over the last several decades hoping to prevent heart disease. Cardiologists have already received questions from their patients regarding aspirin use and the recently release prevention guidelines. In this blog I will focus on the key take home messages for patients from these prevention guidelines and the seven steps to heart healthy living outlined in the guidelines.

 

Where should I begin?

A heart healthy lifestyle is one that is important to start at any age, and the earlier this is started in life, the better the degree of prevention. Living a heart healthy lifestyle should first begin with an assessment of your cardiovascular (CV) risk which is defined as the probability/chance of an individual having a cardiovascular event, such as a heart attack or stroke, over the next 10 years. CV risk is based on family history of premature heart disease, age, gender, ethnicity, history of tobacco smoking, level of physical activity, diet, the presence of diabetes, hypertension and/or hyperlipidemia.

Your CV risk should be assessed by your physician. Based on your history, physical exam and blood testing, a CV risk profile can be assessed and calculated based on the ACC AHA CV risk calculator. After your risk is calculated, your physician can customize their recommendations based on your CV risk profile. Most times further testing may not be necessary. However, for individuals with an elevated CV risk score further testing may be recommended. These tests may include a Cardiac CT scan without contrast to assess for the presence and degree of calcification of the blood vessels of the heart, which suggests the presence of hardening of the blood vessels known as atherosclerosis. This atherosclerosis indicates a high CV risk as it is a usual precursor for heart attacks and strokes and for patients with this finding further treatment and/or testing may be recommended by your physician.

 

Next steps

There are 7 main take home messages for healthy individuals preventing heart disease, the first three steps are focused on living a healthy lifestyle. The last 4 steps focuses on recommendations related to medical therapy and should be actively discussed with your provider to customize recommendations based on your CV risk profile.

 

Step 1 – Heart Healthy Diet 

A diet that is focused on eating fresh fruits, vegetables, legumes, nuts and whole grains is recommended. Sweetened drinks, processed foods, foods with a high content of sodium, and foods containing trans fats and saturated fats should be avoided.

 

Step 2 – Physically Active Lifestyle 

Maintaining a physically active lifestyle is also recommended with at least 150 minutes a week of moderate intensity exercise such as a brisk walk or 75 minutes a week of high intensity exercise such as playing basketball, rowing, et cetera. Generally, maintaining physical activity should be a daily regimen rather than focused on 1 or 2 days a week which was emphasized in the 2018 updated second edition of the Physical Activity guidelines that were released by the Department of Health and Human services2.

 

Step 3 – Cessation of Tobacco Smoking 

Tobacco smoking is the single most potent reversible risk factor for cardiovascular disease. It is recommended that tobacco smoking is avoided to prevent the development of cardiovascular disease. This recommendation is relevant for all age groups.

 

Step 4 – Maintaining Healthy Cholesterol Levels 

Your cholesterol levels should be checked by your physician on a regular basis as determined by your provider and latest guidelines. Based on your individual CV risk, your physician may opt to start medical therapy to manage your cholesterol or may opt to perform further testing such as a non-contrast Cardiac CT to determine calcifications in the blood vessels of the heart reported as a “CAC score.” This CAC score will assist your physician to determine the need for medical therapy and/or further testing.

 

Step 5 – Maintaining a Healthy Blood Pressure 

Achieving and maintaining a healthy blood pressure of <130/80 is recommended. This may or may not require medical therapy as determined by your physician. A physically active lifestyle, low sodium diet and a diet rich in fruits and vegetables are helpful in maintaining a healthy blood pressure.

 

Step 6 – Maintaining a Healthy Glucose level and Adequate Control of Type 2 Diabetes Mellitus (DM)  

Adequate control of type 2 DM is important to prevent cardiovascular disease. A heart healthy diet as outlined previously in this blog along with one that is low in sugar and processed foods, as well as maintaining a physically active lifestyle, are vital in controlling DM. Additionally for diabetic patients on medications, Metformin is a primary line of treatment while newer drugs such as SGLT-2 inhibitor and GLP-1 receptor agonist are secondary line of treatment options for these patients to prevent the development of CV disease.

 

Step 7 – Aspirin Use

For decades aspirin has been useful in individuals with established CV disease to decrease risk of future cardiac events such as a heart attack. However, there is an increased risk of bleeding associated with aspirin use. For healthy individuals without established CV disease who have a low CV risk profile the increased risk of bleeding with aspirin use outweighs the benefit of cardiovascular disease prevention. For this reason it is recommended that use of aspirin for primary prevention of CV disease should be reserved only for selected patients with a high CV risk profile. Use of aspirin should therefore be discussed with your physician prior to considering starting or stopping an aspirin regimen.

 

Conclusion – Putting it all together!

The 2019 ACC AHA Primary Prevention guideline1 focuses on a heart healthy lifestyle and focuses on a patient centered approach that emphasizes active engagement and discussion between patient and physician to determine the best customized approach and recommendations based on an individual’s CV risk profile.

There are several patient related resources such as:

References:

  1. WRITING COMMITTEE MEMBERS, Arnett DK, Blumenthal RS, Albert MA, Michos ED, Buroker AB, Miedema MD, Goldberger ZD, Muñoz D, Hahn EJ, Smith Jr SC, Himmelfarb CD, Virani SS, Khera A, Williams Sr KA, Lloyd-Jones D, Yeboah J, McEvoy JW, Ziaeian B, ACC/ AHA TASK FORCE MEMBERS, O’Gara PT, Beckman JA, Levine GN, Chair IP, Al-Khatib SM, Hlatky MA, Birtcher KK, Ikonomidis J, Cigarroa JE, Joglar JA, Deswal A, Mauri L, Fleisher LA, Piano MR, Gentile F, Riegel B, Goldberger ZD, Wijeysundera DN, 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease, Journal of the American College of Cardiology (2019), doi: https://doi.org/10.1016/j.jacc.2019.03.010.
  2. The Physical Activity Guidelines for Americans: THe HHS Roadmap for an Active Healthy Nation. Second Edition. ADM Brett P. Giroir, MD

 

 
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Polygenic Scores in Cardiovascular Disease 

Akl Fahed, MD, MPH

For many decades, we knew that cardiovascular disease and several of its risk factors are heritable. This justifies why we often ask our patients about their family history, but is that truly the best measure for someone’s genetic liability to develop a disease?

Diseases such as myocardial infarction, type 2 diabetes, and atrial fibrillation are called complex traits. This is because their genetic liability comes from the summation of weak effects of many single nucleotide variations across the 3 billion nucleotides in our genome. This is different from monogenic diseases such as hypertrophic cardiomyopathy, which is due to a single but highly potent nucleotide variation in the cardiac sarcomere gene.

Owing to multiple large genome-wide association studies, a better understanding of the human genome and advances in statistical genomics methods, this polygenic liability of disease could now be measured in a single individual to predict where he or she falls on the genetic risk spectrum of disease. Over the past year, two high profile papers in Nature Genetics and JACC showed that polygenic scores can accurately predict coronary artery disease, as well as other diseases such as Type 2 Diabetes and Atrial Fibrillation.

A polygenic score is a number that is normally distributed in the population. Where your score is located on that bell-shaped curve determines your risk or protection from disease. While most of us will be in the middle, the unlucky person who happens to be in the upper tail of the distribution will carry several fold increased risk of CAD compared to the rest of us. This could be your 45 year-old patient, non-smoker with an LDL of 120mg/dL and no clinical risk factors who presents with a STEMI. On the other hand, I always wonder whether my 95 year-old grandpa who died of lung cancer with the cigarette in his mouth but a healthy heart actually was on the bottom tail of the CAD polygenic score distribution?

Just like the systolic blood pressure and the LDL cholesterol, polygenic scores are continuous measures of risk that require drawing cut-offs in order to practically classify patients and treat accordingly.  Defining those thresholds and determining how we act on them will be key for the successful implementation of those scores in clinical care. Anytime we draw thresholds to use in screening or treatment, there will be issues of sensitivity, specificity, outcomes, and value. After all, even cutoffs for risk factors that we’ve understood for decades, such as blood pressure and LDL cholesterol, continue to be debated from one guideline update to the other. The power of the polygenic scores is their wide availability and low cost (around $50 once for all diseases) as well as their ability to classify risk at an early stage in life (practically from birth) before clinical risk factors start appearing, which creates an opportunity to target disease early on before it develops.

The journey to clinical implementation of polygenic scores in cardiovascular disease still requires several steps. First, the current predictive ability of those scores declines in populations of non-European ancestry.  Development of scores that carry similar predictive ability across different ethnicities will be crucial to avoid widening healthcare disparities.  Second, prospective trials testing specific thresholds and interventions will be necessary to prove that implementation of those scores can lead to positive outcomes. For example, would targeting lower LDL thresholds in people with high polygenic scores reduce their risk of CAD?  Third, behavioral psychology studies could inform how young and healthy people react to information regarding their score. Ideally, you would want someone with higher score to engage in good lifestyle activities to mitigate his/her risk but also someone with a low score to not get falsely reassured and pick up poor lifestyle choices.  Fourth, clinical trials of existing and new therapies could be better informed with polygenic score stratification to pick up missed opportunities of benefit. One example would be that people at the upper tail of risk could benefit from treatment that when applied to the average population does not show a benefit.

Precision medicine in cardiovascular disease is happening and polygenic scores are one opportunity to prevent disease early on by targeting specific people at risk. Unlike the heritability informed by a positive family history which rarely changes management, the quantitative aspects of polygenic scores and our ability to validate their impact on outcomes prospectively and in different settings will change how we care for patients in the near future.

 
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It’s All In The Family

Nosheen Reza, MD

Our understanding of the genetic basis of adult-onset cardiomyopathy is rapidly evolving. Most of us learned to practice medicine in a paradigm that relied on detailed disease phenotyping, but now we have the ability to incorporate genetic and genomic information into routine clinical care. Even if you cannot remember the last time you thought about genes or pedigrees, here are a few modifications you can make to your practice today that will help you keep up with this exploding field of cardiovascular medicine.

 

1) Take a minimum three-generation family history in all patients with a primary cardiomyopathy.

  • The goals of taking a family history are to learn (1) whether the cardiomyopathy is familial, (2) about disease characteristics among family members, (3) if it is inherited in a specific pattern, and (4) to identify at-risk relatives.
  • Most adult-onset cardiomyopathies are inherited in an autosomal dominant pattern, but other inheritance patterns (e.g. dignetic, multigenic) are possible and need further study.
  • Importantly, an individual can have a genetic form of cardiovascular disease without having affected relatives. Most often, this is due to recessive inheritance, de novo mutations/variants, or reduced penetrance.

 

2) Use focused questions to obtain the family history.

  • The use of vague terms like “heart attack” can lead clinicians away from pursuing an inherited etiology of disease and prevent them detecting other important cardiovascular diagnoses like sudden cardiac death in family members.
  • Ask specific questions regarding heart failure symptoms (e.g. presence or absence of dyspnea at rest or on exertion, paroxysmal nocturnal dyspnea), arrhythmia symptoms (e.g. palpitations, presyncope, syncope with or without exertion), and sudden death (e.g. drowning, single-vehicle accidents) in family members.
  • Knowing about relatives’ cardiovascular procedures like arrhythmia ablation, cardiac surgery, device implantations, or heart transplantation can also be helpful.
  • If a multisystem syndrome like a laminopathy or Fabry disease is suspected, familiarize yourself with the extracardiac manifestations and include pertinent questions in your history.

 

3) Remember that diagnosing an individual with an inherited cardiovascular disease is just the first step in the process.

  • In cardiovascular genetics, a key concept is the transition of practice from individual patient-based care to family-based care. By incorporating the information you generate from your comprehensive multi-generational family history, you also gain insight into disease penetrance, expression, age of onset, and pleiotropy.
  • Generally, cardiomyopathies are considered “medically actionable” because evidence-based treatments to reduce morbidity and mortality exist.
  • Beyond just having effects on medical and device therapies, following this paradigm of family-based care also has implications for reproductive and family planning and lifestyle practices.

 

If you are interested in learning more about this topic, check out the 2018 update to the Heart Failure Society of America Practice Guideline on the Genetic Evaluation of Cardiomyopathy (PMID: 29567486).