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Eat smarter- How to boost your cardiovascular health and lower your blood pressure with functional foods – Watermelon

It’s finally summer. Warmer temperatures and local Farmer’s markets motivate us to eat lots of fresh fruits and greens. A healthy summer diet maintains our health and can be even supportive in the management of various diseases. For example, some patients with treated blood pressure are able to taper off blood pressure medications by eating not only healthier but also smarter, losing weight and exercising more.

American Heart Association guidelines recommend eating 9 servings of fresh fruit and vegetables per day. Although reasonable, it is often difficult to implement these recommendations into one’s busy life. In addition to consuming more fruits and greens, is it possible to eat smarter and implement more so-called functional foods to positively affect blood pressure and ultimately cardiovascular health?

One of my friends brought my attention to the beneficial effects of watermelon. Since then I am hooked. For me, watermelon in the form of juice works best – either in the office or during work outs to help with next day muscle soreness.

Watermelons are sweet and popular fruits of summer, originating from sub-Saharan Africa, usually consumed fresh in slices, diced in fruit salads, or as juice. They contain more than 90% of water and are low in fat. Against popular belief watermelons are neither high caloric nor do they have high sugar levels. They contain approximately 6-7 g total sugars which is half of total sugars found in apples, bananas, mangos, sweet cherries, kiwis, pineapples etc., and comparable to blackberries, blueberries, grapefruits, and oranges, just to name a few.

Studies have shown that watermelon can lower blood pressure and improve arterial compliance. Watermelons seem to work like an anti-aging remedy on arteries. But how does watermelon reduce blood pressure and make arteries “younger”?

Watermelon contains three functional important bioactive components: lycopene, arginine and citrulline. These are potent antioxidants and converted into nitric oxide, the principal vasodilatory molecule produced by endothelial cells, the inner layer of your arteries. For decades, doctors have prescribed nitroglycerin which gets converted to nitric oxide in patients with chronic angina to dilate heart arteries and relieve chest pain.  

A variety of factors can reduce the production of nitric oxide and ultimately lead to increased arterial stiffness and higher blood pressure levels such as aging, unhealthy diets, and poor exercise habits. Many people reach for arginine supplements, but the body does not absorb it well. Citrulline on the other hand is easy absorbed and converted into arginine and ultimately nitric oxide.

Watermelon provides these artery-bioactive compounds and studies indicate beneficial influence on cardiovascular health. For example, one study showed that higher lycopene levels improve arterial compliance. Watermelon bioactive compounds also seem to be anti-inflammatory and to positively impact cholesterol levels including lowering of the so-called “bad” LDL cholesterol without impacting the “good” HDL cholesterol.

In addition, watermelon is also a good food source of glutamine and Vitamin C, both of which display antioxidant properties and have been shown to enhance arterial dilation. Studies that have examined the effects of watermelon on vascular function support the notion that this functional food may improve blood pressure and arterial stiffness. 

As recommended by the American Heart Association guidelines for the detection, prevention, management and treatment of high blood pressure, a healthy lifestyle is an integral part of health maintenance and high blood pressure should be treated with lifestyle changes and in some patients with medication.

So, as long as the watermelon season lasts, let’s be health smart and add it to our diet: fresh in slices, diced in fruit salads, or as juice and take advantage of this natural remedy.

References:

  1. Vlachopoulos C, Xaplanteris P, Aboyans V, Brodmann M, Cífková R, Cosentino F, et al. The role of vascular biomarkers for primary and secondary prevention. A position paper from the European Society of Cardiology Working Group on peripheral circulation: Endorsed by the Association for Research into Arterial Structure and Physiology (ARTERY) Society. Atherosclerosis. 2015; 241(2): 507–532.
  2. Seals DR, Kaplon RE, Gioscia-Ryan RA, LaRocca TJ. You’re only as old as your arteries: translational strategies for preserving vascular endothelial function with aging. Physiology (Bethesda). 2014; 29(4):250–264.
  3. Ellis AC, Dudenbostel T, Locher JL, Crowe-White K. Modulating Oxidative Stress and Inflammation in Elders: The MOXIE Study. J Nutr Gerontol Geriatr. 2016 Oct-Dec;35(4):219-242.
  4. Figueroa A, Sanchez-Gonzalez MA, Perkins-Veazie PM, Arjmandi BH. Effects of watermelon supplementation on aortic blood pressure and wave reflection in individuals with prehypertension: a pilot study. Am J Hypertens. 2011; 24(1):40–44.
  5. Figueroa A, Sanchez-Gonzalez M, Wong A, Arjmandi B. Arterial stiffness and blood pressure are reduced after watermelon supplementation in obese with prehypertension and hypertension. The FASEB Journal. 2012; 26:385.
  6. Figueroa A, Wong A, Hooshmand S, Sanchez-Gonzalez MA. Effects of watermelon supplementation on arterial stiffness and wave reflection amplitude in postmenopausal women. Menopause. 2013; 20(5):573–577.

Tanja Dudenbostel Headshot

Tanja Dudenbostel is an Internist, Hypertension Specialist within Cardiology at the University of Alabama at Birmingham where I divide my time as an Assistant Professor between clinical research and seeing patients in cardiology.

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Women’s Health: Premature Coronary Heart Disease In Young Women And Health Disparities – Will Cinderella Make It To The Ball?

Every 80 seconds a woman dies from a heart attack or stroke. Once thought to be predominantly a problem of men, coronary heart disease remains the leading cause of morbidity and mortality for women in the US and worldwide. Gender differences have been recognized, but knowledge gaps in gender differences regarding pathophysiology, clinical presentation, diagnosis, and optimal acute and chronic treatment strategies for heart attacks and co-existing or resulting complications such as heart failure are still existing.

Despite stunning improvements in cardiovascular mortality in women in the last two decades, the annual coronary heart disease mortality rate has remained greater for women than for men. The observed narrowing of outcomes between women and men has been attributed to improved therapy for established cardiovascular disease and to primary and secondary preventive interventions. However, women are less likely to receive evidence-based care and have worse outcomes than men and the observed decline in heart attack event rates or heart attack associated deaths in the US in women remains significant higher than in men.

In addition to this unresolved gender gap, we are now facing a new phenotype of premature coronary heart disease. Recent evidence has shown the emergence of unfavorable trends in coronary heart disease and related mortality in younger individuals 35-55 years of age worldwide over the last decade.

While a substantial decline in AMI event rates or MI deaths in the US in the past decade is absent in young women.

Over the last decade, hospitalizations for acute coronary syndrome in women 40-49 years of age have increased all over the world.
Similar, as observed in the general population, young women are more affected than their male counterparts with more hospitalization for heart attacks, 2-fold higher crude 30-day hospital readmissions rate, and higher mortality rates. These unfavorable age and sex-specific trends in coronary heart disease may be attributable to distinct risk factors and an emerging cardiovascular phenotype of increasing obesity, diabetes mellitus, and high fat-salt-sugar consumption rates among young individuals.

Regardless of age, more women than men will die within the first year after they had their first heart attack. Young women who have their first heart attack in their 40s do worse than their male counterparts.

The mechanisms, likely multi-factorial, contributing to excess risk and inferior health among young women remain unclear. Young women are thought to have a different underlying gender-specific biology and disease manifestation and distinctive psychosocial stressors that interfere with health behaviors and interact with biology.

Racially/ethnically diverse young women are more affected by coronary heart disease and have their first heart attack at an even younger age than white women.

Further, ethnically diverse women are less likely to be referred to coronary arteriogram present with their incident AMI at an even younger age than white women, have a higher mortality.

Short-comings in evidence-based care, referral for coronary angiogram, reperfusion strategies, admission to intensive care units are more pronounced in diverse than white non-Hispanic women.

Trends of worse risk profile and higher mortality among younger women persist with continuing reports of excess in-hospital and early and late mortality compared with men.

Clinical and autopsy data point to a different pathophysiology in young women.

From a pathophysiological perspective, there are predominantly 3 major vascular events underlying thrombotic coronary occlusions responsible for myocardial infarction: plaque rupture, plaque erosion, and calcific nodule. Plaque rupture is by far the most common cause, responsible in three quarter of men and in half of women with fatal myocardial infarction.  

Autopsy studies have shown that particularly in young women, plaque erosions rather than ruptures are more common. This is of particular interest given that myocardial infarction without obstructive coronary heart disease is more common at younger ages and among women. Further, nonatherosclerotic etiologies of acute coronary syndrome, such as spontaneous coronary artery dissection frequently affects younger women and a recent statement by the American Heart Association provides an overview of the Current State of the Science of Spontaneous Coronary Artery Dissection

As a physician-scientist who encounters frequently young adults with cardiovascular disease, I am curious what future studies will reveal about this new phenotype of premature coronary artery disease regarding pathophysiology, optimal primary prevention, diagnosis and treatment strategies.

I am also wondering, despite stunning improvements in cardiovascular mortality in women in the last two decades, if we will be able to close the disparity gap in young women with cardiovascular disease and if Cinderella will make it to the ball.

References:

1) Acute Myocardial Infarction in Women. A Scientific Statement From the American Heart Association. Laxmi S. Mehta, Theresa M. Beckie, Holli A. DeVon, Cindy L. Grines, Harlan M. Krumholz, Michelle N. Johnson, Kathryn J. Lindley, Viola Vaccarino, Tracy Y. Wang, Karol E. Watson, Nanette K. Wenger and on behalf of the American Heart Association Cardiovascular Disease in Women and Special Populations Committee of the Council on Clinical Cardiology, Council on Epidemiology and Prevention, Council on Cardiovascular and Stroke Nursing, and Council on Quality of Care and Outcomes Research. Circulation. 2016;133:916-947
2) Ghazi L, Oparil S, Calhoun DA, Lin CP, Dudenbostel T. Distinctive Risk Factors and Phenotype of Younger Patients With Resistant Hypertension: Age Is Relevant. Hypertension. 2017 May;69(5):827-835. PMID: 28348010 PMCID: PMC5402755
3) Hayes SN, Kim ESH, Saw J, Adlam D, Arslanian-Engoren C, Economy KE, Ganesh SK, Gulati R, Lindsay ME, Mieres JH, Naderi S, Shah S, Thaler DE, Tweet MS, Wood MJ; American Heart Association Council on Peripheral Vascular Disease; Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Genomic and Precision Medicine; and Stroke Council. Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association. Circulation. 2018 Feb 22.

 

Tanja Dudenbostel Headshot
Tanja Dudenbostel is an Internist, Hypertension Specialist within Cardiology at the University of Alabama at Birmingham where I divide my time as an Assistant Professor between clinical research and seeing patients in cardiology.

 

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Women’s Heart Disease – The Interdisciplinary Road Ahead

Every 80 seconds a woman dies from a heart attack or stroke. Once thought to be predominantly found in men, coronary heart disease remains the leading cause of morbidity and mortality for women in the US and worldwide. There have been significant improvements in cardiovascular mortality in women in the last two decades with narrowing of outcomes between women and men which have been attributed to improved therapy for established cardiovascular disease and to primary and secondary preventive interventions. However, women are less likely to receive evidence-based care and have worse outcomes than men. Gender differences have been recognized, but vast knowledge gaps in gender differences regarding pathophysiology, clinical presentation, diagnosis, and optimal acute and chronic treatment strategies for heart attacks and co-existing or resulting complications such as heart failure remain. The AHA Scientific Statement “Acute Myocardial Infarction in Women” provides a comprehensive review of the current evidence.
 
At the opening plenary session of the American College of Cardiology ACC.18 meeting in Orlando, Florida, the pioneer of women’s cardiology Dr. Nanette Kass Wenger gave her inspiring Simon Dack keynote lecture on Heart Disease & Women titled “Understanding the Journey-The Past, Present and Future of CVD in Women.”
 
In “Steps on the journey” Dr. Wenger gave a comprehensive review of the early beginnings and showed how far we have come. Some interesting anecdotes were also shared such as that the first women’s heart disease meeting in Iowa in the 1950s was to help women prevent heart attacks in husbands.
 
Her impactful vision on how to expand the landscape of women’s cardiovascular health research in the next decade struck a nerve with me and made me re-think some of the concepts we are applying in academic cardiology. Dr. Wenger called for an expansion of women’s cardiovascular health research to include social determinants of health as nearly 80% of heart outcomes depend on social factors. Women’s Heart Health is not solely a medical problem and clinical research cannot happen in a vacuum in the hospital. A variety of factors contribute to women’s cardiovascular health and need to be considered for maintenance of health and cure of disease. Women’s Heart Heath needs to be extended. Factors like beliefs and behaviors, the local community, economic, environmental, ethical, legislative/political, public policy – all these social determinants need to be included in heart disease research in women.
 
My take away for the future was that we cannot longer compartmentalize and that programs focusing on Women’s Heart Heath need to involve all programs available- not only cardiology. It needs to be an interdisciplinary approach to learn more about physiology, psychology and ecology of health for best outcomes and to tackle Women’s Heart Health.
 
Dr. Wenger quoted the French Victor Hugo in her inspiring lecture.
 
“There is nothing as powerful as an idea whose time has come.”
Victor Hugo
Histoire d’un crime, 1977
 

Tanja Dudenbostel Headshot

Tanja Dudenbostel is an Internist, Hypertension Specialist within Cardiology at the University of Alabama at Birmingham where I divide my time as an Assistant Professor between clinical research and seeing patients in cardiology.

 

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Lipid-lowering Therapy In Young Adults: Do We Need To Re-invent The Wheel Or Just Align It?

Elevated cholesterol levels or hypercholesterolemia can be found for years or even decades, before individuals present with cardiovascular disease and complications such as myocardial infarction, stroke, or sudden cardiac death. The diagnosis of hypercholesterolemia and its treatment along with healthy lifestyle changes including a healthy diet and exercise as well as blood pressure control, are cornerstones of long-term cardiovascular health.1

There has been a substantial decline in cardiovascular disease mortality in the last decade due to improved awareness, therapy for established cardiovascular disease and primary and secondary preventive interventions.1 However, this observation is absent in young adults.2 Over the last decade, unfavorable trends in coronary heart disease and related mortality in younger individuals, i.e. 35-55 year-old, have emerged.2

We have previously shown that there is a phenotype of young adults with premature hypertension and development of resistant hypertension in their 30s.3 This phenotype has been characterized in a cross-sectional study of 2068 patients seen in a university referral clinic for resistant hypertension. In this study 45% of consecutively seen patients were younger than 55 years of age. Amongst them, 23% had high lipids, 25% were obese, 19% had diabetes, and 13% had obstructive sleep apnea. Cardiovascular events such a s history of myocardial infarction, stroke, or heart failure were prevalent were found in >20%. The majority of these predominately obese, resistant hypertensive individuals have excessive aldosterone, cortisol and sodium levels, conditions that are associated with increased cardiovascular morbidity and mortality, independent of blood pressure levels.

Lipid-lowering drugs, so-called statins, have been shown to reduce cardiovascular disease and mortality. Lipid lowering with statins in patients with hypercholesterolemia has a proven survival benefit for both primary prevention (ie, in patients without clinical evidence of coronary disease) and secondary prevention (ie, in patients with established coronary disease), even when serum cholesterol concentrations are “normal” for the population or borderline high. The mechanisms by which lipid-lowering therapy is beneficial are incompletely understood since absolute levels of cholesterol before or during treatment only explain parts while cholesterol-independent effects have been also described.1 Among the non-lipid mechanisms that may be involved are plaque stabilization, reduced inflammation, improvement of endothelial and arterial function, and decreased blood clotting.
 
In 2013 the American College of Cardiology and American Heart Association developed a new guideline for the management of hyperlipidemia. While previous guidelines recommended to initiate or adjust predominantly in response to lipid values these 2013 ACC/AHA guidelines target patients to fixed dose of statin therapy corresponding to atherosclerotic cardiovascular disease (ASCVD) or other risk factors. The four at-risk populations of individuals that are thought to benefit from statin therapy based on this guideline include:

  1. Adult patients with clinical ASCV
  2. Adult patients with primary elevations of LDL–C ≥190 mg/dL
  3. Patients 40-75 years of age with diabetes and LDL–C 70 to 189 mg/dL without clinical ASCVD
  4. Patients 40-75 years of age without clinical ASCVD or diabetes with LDL–C 70 to 189 mg/dL and have an estimated 10-year ASCVD risk of 7.5% or higher

In our cohort half of obese young patients under the age of 40 would per se not qualify to be treated with a statin. Patients between the ages of 40-55 are in the majority of cases not considered “eligible” since age is one of the most powerful nominators in the risk calculator and, anecdotally, when we evaluate these patients for statin eligibility for primary prevention, we usually calculate an estimated 10-year CVD risk score of <5%.

At their first visits we always discuss life style changes, since younger patients may be more motivated to eat healthier, exercise, and lose weight, but consistent, successful lifestyle changes are often difficult to accomplish.

When we consider statin treatment for primary prevention even if the ASCVD risk score is <7.5%, there are a lot of unknowns. Aside from statins being contraindicated in young women who are or want to become pregnant or are breastfeeding, it is not known if there are short-term benefits of therapy. There are few data on the safety of statins over decades of therapy and possible side effects of statin therapy could outweigh potential benefits.

Furthermore, we don’t know whether long-term treatment leads to better outcomes and who are the individuals who are going to benefit. With evolving advances in precision medicine, we may be able to “customize” primary prevention especially for this group and identify young individuals in whom premature cardiovascular events can be prevented.

However, the question remains: how can we prevent cardiovascular events in young adults?

Data of young adults who suffered a cardiovascular event will help to elucidate underlying mechanisms and optimal therapy regimens. 
 

Premature CHD in young adults versus CHD 02012018

This problem has been recognized and resulted in the YOUNG-MI Registry, a retrospective study examining a cohort of young adults age ≤50 years with a first-time MI.  The study uses electronic health records of 2 large academic centers, as well as detailed chart review of all patients, to generate high-quality longitudinal data regarding the clinical characteristics, management, and outcomes of patients who experience a myocardial infarction at a young age. Findings are thought to provide important insights regarding prevention, risk stratification, treatment, and outcomes of cardiovascular disease in this understudied population, as well as identify disparities which, if addressed, can lead to further improvement in patient outcomes.  

In a recent study from this registry, Singh et al. analyzed retrospectively the statin eligibility of young adults after a myocardial infarction. In this study the statin eligibility, based on the 2013 ACC/AHA guidelines and 2016 USPSTF recommendations, for primary prevention in adults <50 years who experienced a first-time type 1 myocardial infarction were evaluated. The median age of analyzed patients was 45 years, 20% were women, the majority had at least 1 traditional cardiovascular risk factor and 57% had experienced a ST-segment elevation myocardial infarction. Surprisingly, the median estimated 10-year atherosclerotic cardiovascular disease risk score was only 4.8% (interquartile range 2.8-8.0%). Only 49% and 29% would have met criteria for statin eligibility as per the 2013 ACC/AHA guidelines and 2016 USPSTF recommendations, respectively. These findings were even more noticeable in women where 63% were not eligible for statins according to either one of the guidelines as opposed to 46% of men only. To summarize these findings, the majority of young adults who present with a heart attack would not have met current guideline-based treatment thresholds for statin therapy prior to their myocardial infarction.

It highlights the need for better risk assessment tools for young adults.  Further, much more needs to be known about risk profiles, optimal prevention, and treatment to improve outcomes in these young understudied adults.

References

  1. Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH, Goldberg AC, Gordon D, Levy D, Lloyd-Jones DM, McBride P, Schwartz JS, Shero ST, Smith SC, Jr., Watson K, Wilson PW, Eddleman KM, Jarrett NM, LaBresh K, Nevo L, Wnek J, Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke FW, Shen WK, Smith SC, Jr., Tomaselli GF and American College of Cardiology/American Heart Association Task Force on Practice G. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129:S1-45.
  2. Ghazi L, Oparil S, Calhoun DA, Lin CP and Dudenbostel T. Distinctive Risk Factors and Phenotype of Younger Patients With Resistant Hypertension: Age Is Relevant. Hypertension. 2017;69:827-835.
  3. Ghazi L, Dudenbostel T, Xing D, Ejem D, Turner-Henson A, Joiner CI, Affuso O, Azuero A, Oparil S, Calhoun DA, Rice M and Hage FG. Assessment of vascular function in low socioeconomic status preschool children: a pilot study. J Am Soc Hypertens. 2016.
     

Tanja Dudenbostel Headshot

Tanja Dudenbostel is an Internist, Hypertension Specialist within Cardiology at the University of Alabama at Birmingham where I divide my time as an Assistant Professor between clinical research and seeing patients in cardiology.

 

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Manual Versus Automated Office Blood Pressure Measurements

Although the awareness and treatment of hypertension has increased steadily over the past decade, it is estimated that approximately 50% of patients are still not adequately controlled. However, blood pressure measurement techniques vary widely and results from studies are difficult to compare. Further, office BP measurements depend on time, resources, and equipment.

In our referral Cardiology-Hypertension Clinic blood pressure is measured in different ways by different providers:BP measurement tools

  1. Manual
  2. attended automated office BP (AOBP) with 3 consecutive readings (Omron) or
  3. unattended attended automated office BP (AOBP) with 3 consecutive readings (Omron) or 6 consecutive readings (BPTrue).

“Attended” means that trained personnel stays in the room, while in unattended measurements trained personnel leaves the room and monitors are either programmed to take 3 or 6 consecutive readings.

These different approaches make it difficult to compare BP levels and to adjust medication to achieve target BP.

So what is the best way to measure blood pressure and which is the one we should stick to?

It is known that BPs taken manually can differ from those taken using an automated device in the clinic or office. Several studies have shown that manually taken BPs can be higher than AOBP.  Further, many clinicians prefer AOBP over manual BPs since it is an easy way to check BP several times.

With advances in technology, unattended AOPB measurements are possible. Research suggests that unattended blood pressure measurements are significantly lower than attended blood pressure measurements.

Clinical trials using AOBP usually pre-specify how to measure BP i.e. either attended while trained personnel stays in the room or unattended i.e. medical staff comes back after a few minutes and retrieves BP readings.

The importance of a consistent way to measure BP has come under scrutiny in the SPRINT study.

Although blood pressure measurements in this study were obtained using an automated measurement device, there were substantial differences in the methods used by the different SPRINT centers. In particular, medical staff were inconsistently present or absent when blood pressure readings were taken, between centers and perhaps within centers.

Blood pressure in SPRINT was defined as the average of three measurements taken with an automated measurement device. But until now it has not been entirely clear whether these measurements were obtained in the presence or absence of medical staff.

Results of a survey for the SPRINT trial showed that patients were completely alone during the measurement period at 43% of the sites and were alone (unattended) for part of the time at 29% of the sites. However, within sites significant internal variation in their BP measurement techniques (unattended and attended AOBP) may have occurred.
What is clear is that there are a variety of methods currently employed to measure BP in clinical trials and in the office, and that technique, environment, and equipment can influence BP levels obtained.

To put that in perspective for clinical practice we should take this into consideration and report how BP was measured when we communicate with our patients or colleagues.

Bp levels

Tanja Dudenbostel Headshot

Tanja Dudenbostel is an Internist, Hypertension Specialist within Cardiology at the University of Alabama at Birmingham where I divide my time as an Assistant Professor between clinical research and seeing patients in cardiology.

 

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Precision Medicine Through Big Data – A Game Changer

From clinical science supported by data to data science supported by clinicians

AHA Badge
We live in an era of a tremendous amount of information. Scientific research is particularly well suited by the possibilities offered by analyzing large sets of data. In the past, data has been locked up in individual data bases and were not openly shared or available. Over the last two decades access to data has been improved and more open sources for analyses are now available. With advancements in technology, including cloud computing, big data is now available to all researchers. Information gained from big data needs to be translated into knowledge.  Acute and chronic disease is a complex process and often displays itself in a variety of phenotypes with different outcomes. Consequently, data has to be complex in order to identify subgroups, to define disease phenotypes, and precise treatment strategies.

I recently attended the AHA Scientific Sessions meeting the “Early Career Day” to learn more about the AHA – Precision Medicine Platform (AHA-PMP) to access and also upload my own data and use the provided workspace, which is especially great for teams. Additionally, to AHA-PMP other data portals were presented and explored in small groups. These open portals included cardiovascular, cerebrovascular, and diabetes research such as the Cardiovascular Disease Knowledge Portal (CVDKP; broadcvdi.org), cerebrovascularportal.org (CDKP) and the type2diabetesgenetics.org (T2DKP) portal.

The goal of these platforms is to accelerate analyses of the genetics of cardiovascular and cerebrovascular disease as well as diabetes. For example, the CVDKP is an open-access resource that facilitates the translation of genomic data into actionable knowledge for better understanding and treatment of cardiovascular disease. For example data in the CVDKP are from 4 large Consortia namely the Atrial Fibrillation Consortium (AFGen), the Global Lipids Genetics Consortium (GLGC), the Myocardial Infarction Genetics Consortium (MIGen), and the CARDIoGRAMPlusC4D Consortium. The CVDKP was built on the Knowledge Portal platform originally designed for the Type 2 Diabetes Knowledge Portal (type2diabetesgenetics.org), which was produced by the Accelerating Medicines Partnership In Type 2 Diabetes.  It is part of the Knowledge Portal Network, which also includes the Cerebrovascular Disease Knowledge Portal (CDKP: cerebrovascularportal.org). Data in the CVDKP include GWAS data for CVD and other traits (anthropometric, glycemic, renal, and psychiatric traits), exome chip data, whole exome sequence data, disease-agnostic genomic resources and epigenomic data. Further, with evolving results from big data a paradigm shift in science has been recognized. While over the last few decades medicine has been mostly clinical science supported by data; now medicine is about to become data science supported by clinicians and artificial intelligence and machine learning (deep learning)  plays an important role. This new frontier of data science, provides a greater opportunity especially for younger investigators to develop and drive their own projects.

However, despite the widely endorsement of sharing data and the availability of open sources and platforms, the rate that these data are accessed and utilized are still low. This is one reason AHA wants to promote these valuable resources further to advance our understanding in medicine and facilitate new therapies.

The perception that open source data are underutilized is supported by recent studies.  A just published analysis showed that for example cardiometabolic study data from patient-level clinical trial data are less accessed than previously assumed. In this study by Vaduganathan et al. data were extracted from ClinicalStudyDataRequest.com, a large, multi-sponsor data-sharing platform hosting individual patient-level data from completed studies sponsored by 13 pharmaceutical companies. Over the last 4 years, the platform had data from 3374 clinical trials, of which 537 evaluated cardiometabolic therapeutics covering 74 therapies and 398 925 patients. Diabetes mellitus and hypertension were the most common study topics with a median follow up time of 79 months. As of May 2017, despite availability of data from more than 500 cardiometabolic trials in a multi-sponsor data-sharing platform, ClinicalStudyDataRequest.com, only 15% of these trials and 29% of phase 3 or 4 clinical trials have been accessed by investigators and almost all researchers were from academic centers in North America and Europe. Of note, only half of the proposals were funded, and most proposals were for secondary hypothesis-generating questions. To date, after a median of 19 months (9-32 months) only 3 peer-reviewed articles have been published.

Further, when analyzed if male and female researchers were requesting data access equally, the investigators found that only 15 % of female researchers accessed data while the majority, with 85%, were men.

In conclusion, during “Early Career Day” I learnt that available open sources for big data analysis are underutilized and researchers who access scientific data are predominately men.  Data platforms provide a huge opportunity for researchers, and especially women, to generate hypotheses which may then lead to (further) funding.

 Tanja Dudenbostel Headshot
Tanja Dudenbostel is an Internist, Hypertension Specialist within Cardiology at the University of Alabama at Birmingham where I divide my time as an Assistant Professor between clinical research and seeing patients in cardiology.