hypertension – Page 2 – The Early Career Voice

Clinical Significance of Sigmoid Shaped Interventricular Septum

August 27, 2018March 28, 2019 Fawaz Alenezi, MD, MSc 

A sigmoid-shaped interventricular septum (SIS) is generally considered a normal part of the aging process and is of little clinical significance. However, certain patients with SIS may experience clinical symptoms, such as dyspnea upon effort and different types of cardiac arrhythmias. SIS is frequently observed on transthoracic echocardiography (TTE) and in cardiac magnetic resonance (MR) imaging modality in daily clinical practice. However, nothing usually occurs in subjects with SIS, and the clinical significance of the presence of SIS is unclear.

The precise mechanisms leading to isolated SIS have yet to be determined, but plausible reasons exist as to why the basal septum might be uniquely susceptible to hypertrophy. For example, Laplace’s law states that the larger a vessel’s radius, the larger the wall tension required to withstand internal fluid pressures. Because the longitudinal fibers of the basal septum have some of the largest radii in the human heart, they would be expected to experience the greatest inward component of wall stress. This is compounded by the fact that the basal septum is the last part of the ventricle to be electrically activated, so contractions from other myocardial segments further increase its wall stress (Fig. 1). Moreover, the additional load created by pressure from the right ventricle exerts additional stress on the septum. Therefore, it is conceivable that the basal septum hypertrophies earlier than other LV regions in response to increased afterload as it already operates under higher loading conditions.

Clinical Significance of Sigmoid Shaped Interventricular Septum

Prospective studies suggest that up to 20% of cardiovascular cohorts may have isolated SIS. Some researchers have reported that the cause of SIS may be aging or arteriosclerosis. This may involve a change in the spatial relationship between ascending aorta (AA) and left ventricle (LV) due to elongation or tortuosity of arteriosclerotic AA. An alternative hypothesis suggests that SIS may be a form of cardiomyopathy. However, there is no evidence to support such a hypothesis due to the limited capabilities of traditional TTE. Use of other diagnostic approaches like CMR may be needed where characteristics of LV myocardium and the spatial relationship between AA and LV and degree of arteriosclerosis of AA can be evaluated simultaneously.

It is known that LV hypertrophy with different remodeling patterns is one of the major cardiac manifestations of hypertensive heart disease, and echocardiographic LV hypertrophy could be detected in 20-40% of patients with arterial hypertension. However, there are often no specific echocardiographic features for hypertensive patients at the early stage of disease. Previous echocardiographic studies have described asymmetric septal hypertrophy with a localized septal thickening at the basal-mid portion in patients with hypertrophic cardiomyopathy or aortic valve stenosis.

Basal-septal hypertrophy may also occur in a subset of older normal subjects, with normal wall thickness (WT) elsewhere, and is considered to be an age-related anatomic variant. This morphologic echocardiographic sign is termed as septal bulge (SB), sigmoid septum, or discrete upper septal thickening or knuckle. A large community-based population study reported that SB was documented frequently in elderly individuals with higher systolic blood pressure (BP). It was shown that the overall prevalence of SB was 1.5% and was markedly higher (18%) in the eighth decades of life.

Although pathologic and echocardiographic observations have indicated that SB is a structural response in hypertensive patients, the nature and significance of the SB in subclinical arterial hypertension was never investigated. In addition, despite the fact that BP can be easily measured, AH sometimes cannot be diagnosed due to the underreported BP reading in the casual or self-measured BP measurement. BP measurement with appropriate tools is essential to diagnosing AH early as well as to guiding AH management. It has been shown that, besides resting BP measurement in the office, arterial hypertension could be clinically diagnosed by 24-hour ambulatory BP monitoring (ABPM) as well as exercise stress test in some resting normotensive individuals.

Focal hypertrophy of the basal inter-ventricular septum can be seen in up to 20% of cardiac patients without HCM, being more prevalent in the elderly and hypertensives. While it’s anatomical location plausibly renders it more susceptible to hypertrophy, evidence suggests that the basal septum enlarges mainly due to pressure overload from hypertension. This discrete upper septal hypertrophy is associated with exertional LVOT obstruction and SOB, and appears symptomatically amenable to β -blockade. While diastolic dysfunction likely also contributes to symptoms in this condition, the data to date are equivocal. Focused analyses conducted using a consensus definition of SB, in patients undergoing simultaneous assessment of myocardial systolic and diastolic performance during physiological exercise, are needed to further understand the clinical relevance of this entity.

Dr. Fawaz Abdulaziz M Alenezi is a Clinical Imaging Fellow at the Duke University Health Systems. He conducts medical research on the derivation and validation of novel echocardiographic approaches to myocardial deformation and a new echocardiographic technique which assists patients with heart ventricular function.

How the Immune System Favors Females in Pulmonary Artery Hypertension? Another Regulatory T Cell Story.

August 21, 2018 Dalia Gaddis, PhD

While it is commonly thought that cardiovascular disease is a man’s disease, CVD is the number one killer of women with the same number of deaths per year as cancer, diabetes and respiratory disease combined (according to 2015 statistical data from AHA). In addition, women exhibit different and more silent symptoms of heart attacks. There is a lot of interest in the difference between how males and females respond to CVD. A lot of emphasis is put on hormonal differences, but the immune system also seems to play an important role in this disparity. Females have a more robust immune system and therefore respond faster to infections providing more protection than in males. However, a more responsive immune system also means a more reactive immune system that can result in increased incidence of autoimmune diseases, such as rheumatoid arthritis and lupus.

Part of the difference in the immune system response in females can be attributed to the fact that multiple immune-related genes are expressed on the X chromosome. Since females have two alleles of the X chromosomes and males have only one, it is evident that females express more genes that regulate immune system functions. One of these genes is Foxp3, the key transcription factor for regulatory T cells, an adaptive immune cell which I have discussed before in a previous post. Regulatory T cells play an important protective role in CVD, especially in atherosclerosis and hypertension.

Pulmonary artery hypertension (PAH) is a fatal cardio-pulmonary disorder where the pulmonary arterioles narrow leading to a right ventricular fibrosis, heart failure and death. Regulatory T cells play an important role in this disease as animal models that lack regulatory T cells are more susceptible to PAH. Adding regulatory T cells back prevents the development of PAH showing the protective power of these cells. A recent study published in the journal Circulation Research, shows that in the absence of regulatory T cells, females rats are more prone to PAH than male animals due to a lower levels of PGI2, a pulmonary vasodilator, and the lack of the enzyme COX-2 that regulated PGI2. The researchers conducting the study show that by transferring regulatory T cells into these rats, these immune cells were sufficient to restore the levels of COX-2 and PGI2, as well as other immune inhibitory molecules PDL1 and IL-10. The authors suggest that regulatory T cells have both a direct and indirect effects on the arteries. The direct effects are exerted on the endothelial cells directly via COX-2 and PGI2, and the indirect effect is through the release of inhibitory molecules such as IL-10 and TGF, both of which would result in immune suppression and preventing inflammation. The results from this report suggested that females are more reliant on regulatory T cells for protection against PAH.

These new findings highlight the subtlety of immune regulation between females and males and further proves that in addition to hormonal differences, immune regulation disparities between genders that can alter the outcome of cardiovascular diseases. By understanding more about gender differences in CVD and the immune system, and figuring out ways to manipulate these subtle differences, scientists hope to achieve a more personalized and effective therapies to women versus men to combat CVD.

Dalia Gaddis Headshot

Dalia Gaddis is a postdoctoral fellow at the La Jolla Institute for Allergy and Immunology. She has a Ph.D. in microbiology and immunology. She is currently working on understanding the interactions between the immune system and atherosclerosis development

Post-Call Hypertension – Physician Health in High Stress Specialties

June 4, 2018 David Werho, MD

Should we be getting hazard pay for taking in-house call? As awareness of physician wellness topics (most buzzworthy: #burnout) is growing, it’s important to realize that we, as physicians, are human and have all the requisite needs for health, wellness, rest, and routine as our patients do.

A few weeks ago, I had a routine doctor’s appointment for myself, which I had scheduled on a post-call morning (when else do we have time to take care of ourselves?). As she took my blood pressure and repeated it twice, the MA seemed flustered. I’ve been quite healthy my whole life and had never had an issue with hypertension. Of course, the new AHA hypertension guidelines do put me closer to the at-risk group, but I’ve still been well below the cutoffs and I’m (relatively) young. My systolic during this visit was above 140. Admittedly, I had just had a Venti coffee and a Monster energy drink in the waning hours of the call night, but this was very unusual for me.

Of course, I had it rechecked when I wasn’t full of caffeine and low on sleep and the values were back in the normal range. However, when I mentioned this encounter to some of my more experienced colleagues, they were not surprised. Apparently, there is a silent epidemic of hypertension and diabetes plaguing otherwise healthy cardiac intensivists that begins in the early-mid-career range. Colleagues and colleagues of colleagues have all been touched by this phenomenon, but I can’t find much of anything about how to address this in the literature.

There are several recent studies linking shift work with hypertension. And it makes sense that the chronic stress of frequently being in a hospital for 12-24 hours continuously with a phone/pager that could go off with a disaster or emergency at any second may begin to take its toll on your arteries in mid-life. But there are not really any great solutions at this point. We need to be around to take care of our patients. In the era of increasing in-house attending physician coverage in cardiac ICU’s, this is only likely to get worse.

The common sense bullet points seem to be the focus of many of the anti-burnout physician wellness programs: good nutrition, adequate/regular exercise, sleep/rest, resilience, and self-care behaviors. However, I think another important aspect is prevention. Any of us beginning our careers in these high-stress shift-work specialties should be proactive in reducing our cardiovascular risk as much as possible and as early as possible. And we should be active participants in seeing our own physicians so they can screen for these issues; better patients are better doctors.

David K. Werho, MD is an Assistant Clinical Professor at the University of California San Diego and a Pediatric Cardiac Intensivist at Rady Children’s Hospital – San Diego. His research focuses on pediatric cardiac ICU outcomes as well as interventions and curriculum development in medical education. He tweets @DWerho and contributes to the Pediatric Cardiac Intensive Care Society Newsletter as editor and contributor.

Un-complementing The Immune System Improves Hypertension

May 17, 2018 Dalia Gaddis, PhD

Even though I have been studying immunology for 15 years, I am constantly fascinated by how elaborately involved the immune system is in different diseases and conditions. I have written previously about the intricate relationship between the immune system and heart disease. In this blog, I will be highlighting the role of the immune system in hypertension, focusing on a new study that examined the role of complements and regulatory T cells in hypertension.

According to the CDC, there are 75 million people – a third of the population – in the USA with hypertension. Another third of the population is at risk, being at a pre-hypertensive state. With the change in blood pressure guidelines that was announced at the end of 2017, it is expected that the number of people affected with hypertension will increase substantially. While half of the patients with hypertension have their high blood pressure under control, hypertension still contributes to more than 1,000 deaths per day in the US.

It is evident that the immune system is involved during hypertension. Activated immune cells can infiltrate target organs such as the perivascular tissue and the kidneys. Macrophages, an innate immune and phagocytic cell, contribute to hypertension by increasing inflammation and oxidative burst. T cells, a key adaptive immune cell, can also be found infiltrating aortas, perivascular tissue, vascular vessels as well as the kidneys, where they can produce inflammatory mediators. The lack of the above two cell types has been shown to reduce blood pressure in angiotensin II infusion mouse models.

A recent study in Circulation Research examined how the complement system affected regulatory T cells during hypertension. The authors show that two complement receptors, C3aR and C5aR, are increased on regulatory T cells, an anti-inflammatory T cells that protects against heart disease. The increase in complement receptors led to a reduction of the protective regulatory T cells in hypertensive mice. By deleting the two complement receptors, the authors show that there is a decrease in systolic and diastolic blood pressure and regulatory T cells were preserved in the angiotensin II treated mice. The authors also show that similar increase in C5aR is found in patients with hypertension.

Complements are a part of the immune system that enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells, having beneficial effects in immune defense. It is already known that ischemia is a potent activator of the complement system and the activated complement system play a role in tissue damage during myocardial infarction and contribute to atherosclerosis progression. There are studies to show that inhibition of the complement system can reduce myocardial infarction. Can the inhibition of the complement system assist in hypertension reduction in patients? Would scientists be able to design therapies that limit the activation of the complement system to benefit hypertensive patients without complete abrogation of the complements anti-microbial properties? There are still many uncertainties about how the scientific community can manipulate the complement system to benefit patients with hypertension, but I think the more advances we make in understanding how the different players in the immune system affect hypertension and other heart related conditions, the better we fair in getting closer to new therapies against heart disease.

Multi-Disciplinary Approach And Decision Sharing In Geri-Cardio-Oncology

April 23, 2018March 28, 2019 Fawaz Alenezi, MD, MSc 

Incorporating a geriatric assessment tool into the care of the geriatric cardio-oncology patient is crucial. The use of comprehensive geriatric assessments has been shown to improve overall survival, quality of life, and physical function, while decreasing hospitalizations and nursing home placement in the geriatric population. While cancer is the number one cause of mortality in patients between 60 and 79 years, heart disease is most common in people aged 80 and older. More than 40% of these cancer survivors above the age of 50 will develop cardiovascular (CV) disease. In general, older patients are affected by a number of factors, including concomitant comorbidities as well as other physiologic and functional changes that can affect prognosis, treatment, and outcomes of cancer.

Cancer therapeutics including traditional chemotherapy, targeted therapy, radiotherapy, and hormonal therapy all have short- and long-term systemic effects, often involving multiple organs. However, CV toxicities have been most concerning and can result in irreversible CV damage or reversible cardiac dysfunction. These cardiotoxic manifestations can include left-ventricular (LV) dysfunction and heart failure, myocardial ischemia and infarction, hypertension (HTN), and arrhythmias such as QT prolongation. Less frequently, these complications consist of myocarditis or pericarditis.

Anthracycline-induced cardiotoxic effects are dose dependent, and those who develop late cardiotoxicity have a high mortality. Risk factors include cumulative dose, bolus administration, high single dose, prior radiotherapy, simultaneous use of other cardiotoxic agents, female gender, bimodal age distribution, existing CV disease, elevation of cardiac biomarker during and after cancer treatment, as well as time since completion of cancer therapy. A second class of frequently used cardiotoxic agents are targeted therapies including monoclonal antibody-based tyrosine kinases (bevacizumab, trastuzumab) and small molecule tyrosine kinase inhibitors (sorafenib, sunitinib, lapatinib). HTN is a common adverse event whose mechanism is not well understood but has been attributed to the inhibition of vascular endothelial growth factor. Progression of or acceleration of ischemic disease is more common with radiation therapy Agents such as bleomycin, etoposide, cisplatin, 5-fluorouracil have been implicated in the development of myocardial ischemia including myocardial infarction.

Risk factors for chemotherapy-related cardiac complications should be assessed in all patients diagnosed with cancer who are being considered for cancer therapy, whether it be the administration of biologics, chemotherapy, or radiation therapy. Given that advancing age has been associated with cardiac complications from chemotherapy using anthracyclines or trastuzumab-based treatments, it is recommended that all elderly patients prescribed these medications should be educated about risk stratification and risk modification. Risk stratification remains difficult in elderly patients at risk for cardiotoxicity. A comprehensive evaluation of CV comorbidities such as HTN, diabetes, dyslipidemia, and smoking needs to be evaluated prior to start of therapy.

Those patients receiving high-dose anthracyclines, high-dose radiation, and history of prior cardiac disease are at greatest risk for cardiac dysfunction are at highest risk for cardiotoxicity. Cancer-specific mortality is often higher in older patients, likely due to the impact of age-related factors. Pre-treatment evaluation of LV systolic function is a standard part of many treatment protocols. However, the utility of this approach has been debated due to a low prevalence of asymptomatic LV systolic dysfunction, with this strategy missing most patients that will ultimately have cardiotoxicity. Serum biomarkers may be useful in predicting cardiotoxicity and the role of baseline assessment of serum biomarkers prior to cancer treatment in predicting cardiotoxicity is being evaluated. An echocardiogram is the most important tool for serial evaluation of the heart during cancer therapy. Ejection fraction should be determined using biplane method of discs, according to the American Society of Echocardiography guideline. Current recommendations for imaging surveillance include monitoring of LV systolic function during treatment with both anthracyclines and trastuzumab. Current National Comprehensive Cancer Network guidelines suggest cardiac monitoring at baseline, 3, 6, and 9 months after initiating therapy for trastuzumab therapy, upon completion of treatment, and every six months for 2 years following completion of treatment.

Collaborative assessment by oncologists, cardiologists and geriatricians before the start of chemotherapy can lead to early identification of patients at risk as well as discussions about the utility and benefits of cardiotoxic medications as opposed to potential alternative therapies. In some situations, alternative noncardiotoxic chemotherapy regimens may be considered. A lower-intensity chemotherapy regimen, however, should not be prescribed based simply on a patient’s risk factors or concern for potential cardiac complications, as this has been shown to potentially worsen clinical cancer outcomes. Cardiologists and oncologists may be less familiar with and often have limited to no training in routinely performing geriatric assessments and systematically evaluating for frailty. Within the gericardio-onc collaborative framework, the geriatrician is well positioned to take an active leadership role in advocating for the patient, assisting with decision-making, and facilitating screening and long-term monitoring of CV complications.

Cardiac dysfunction developing during or after the completion of cancer therapy is a growing heath concern that should be addressed in a multidisciplinary setting. There is a need for research on early biomarkers of toxicity as well as monitoring, surveillance, and treatment of older patients with cancer receiving potentially cardiotoxic therapy. The results of several studies are imperative in determining how best to risk-stratify and treat elderly patients with cancer while preserving their quality of life and functional outcomes.

Dr. Fawaz Abdulaziz M Alenezi is a post-doctorate associate at the Duke University Health Systems. He conducts medical research on the derivation and validation of novel echocardiographic approaches to myocardial deformation and a new echocardiographic technique which assists patients with heart ventricular function.

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

April 17, 2018 Tanja Dudenbostel, MD

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 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.

On My Way To NoLa – AHA EPI | Lifestyle Specialty Conference

March 19, 2018March 23, 2023 Anberitha Matthews, PhD

The AHA EPI | Lifestyle Specialty Conference will be smaller and more specific than any conference that I have attended. My conference experience has consisted of, for the most part, international meetings that are held in large venues such as Experimental Biology (EB) in the San Diego Conference Center. This center boast 525,701 gross ft2 on the ground level and 90,000 ft2 of column-free space in the Sails Pavilion on Upper Level. EB uses this vast conference space to house over 14,000 researchers, 400 oral sessions that are hosted by 6 societies and 35 guest societies. To attend an event of this size can prove to be too exhaustive to experience everything that is being offered. I have opted to attend the AHA EPI | Lifestyles specialty conference because it is smaller and focused on Health Promotion: Risk Prediction to Risk Prevention.

Since Bailey DeBarmore went into great detail outlining the schedule for the meeting, I will not expound on that any further. Although I have more of a molecular biology/biomedical background that focus on oxidative stress in the microvasculature, I was surprised to see this meeting offered topics that would enhance not only my knowledge of health promotion, but also contribute to my scientific research. The section Hypertension: Guidelines and Prevention, Rapid Fire Oral Presentations consist of several researchers/clinicians that will present their work in 10 minute burst, giving the vibe of “speed dating”. This is an interesting way to present topics, but it is also challenging! From my experience, there is so much to say and so little time to say it. Which, is true. The topics are so specific, one is required to have background knowledge of the topic to understand the speakers’ findings. It is also a good way for the listener to gain a vast amount of information in a short time.

Additionally, I am excited about several of the sessions that will be held at AHA EPI |Lifestyle Specialty Conference. My career trajectory has taken me through proteomics, genomics, and metabolomics as mechanistic tools to elucidate the onset of inflammation, and subsequently, cardiovascular disease. The intersection between theoretical prediction of a disease to the onset of the disease, and ultimately the prevention of the disease by reducing the risk is the obvious pathway of ameliorating chronic diseases. The topic of interest to me, due to the time constraints, are as follows:

Session 2 – Hypertension Guidelines and Prevention. Now that the new guidelines are beginning to be accepted among the clinical/scientific communities, it will be interesting to learn more about the methods being initiated to accomplish these new levels.
Session 5 – Cardiovascular Biomarkers I expect will introduce more detail about the markers clinicians use for early identification of cardiovascular disease and what can be done to truncate its occurrence.
Session 6 – Hot off the Press – there are several new articles that have been released this year. Among them, Schoenthaler et al addressed social needs of hypertensive patients.
         a. For decades there has been arguments as to whether one should have a low fat or low carbohydrate diet to lose a weight. This study by Gardner et al, will add to what we know about the impact diet have on weight loss in overweight adults using genotype patterns and/or insulin secretions as the associated factors.
         b. The study by Powell-Wiley et al, suggest there is a correlation between crime and physical activity and obesity among African American women. Since we know there are many variables that plays a role in obesity and physical activity, I am interested to learn more about their study and what variables were tested to come to the conclusions that they have drawn.
         c. Fuchs et al explored the use of low-dose diuretics to optimize prehypertensive values as a means of lowering blood pressure.
         d. Banck et al discussed racial disparities among young adulthood modifiable risk factors in the incidence of type 2 diabetes during middle adulthood as a modifiable risk factor.
Session 10 – I have learned about 3 of the omics and the more I learn the more that seem to be identified. The Omics section, I will imagine, will cover the well-known, proteomics, genomics and metabolomics; however, some that are exciting, due to them being novel to me, are the Trans-Omics and Phenomics.
Session 11 – The William B. Kannel MD Memorial Lectureship in Preventative Cardiology
Session 12 – The debate will cover some of the Pros and Cons of medical cost. The main argument when it comes to cardiovascular care is the rising cost of medical treatment. This session will cover some of the cost associated with cardiovascular disease treatment, and I hope, some ways that they can be overcome by prevention.
It is my desire, during this AHA EPI | Lifestyles conference to disseminate information that will assist in empowering clinicians, researchers, and the general population of methods that can be taken to promote health and a healthy lifestyle. Hope to see you there in person or online to share thoughts on the lessons learned during this conference.

Anberitha Matthews, PhD is a Postdoctoral Fellow at the University of Tennessee Health Science Center in Memphis TN. She is living a dream by researching vascular injury as it pertains to oxidative stress, volunteers with the Mississippi State University Alumni Association, serves as Chapter President and does consulting work with regard to scientific editing.

Empowering Patients To Treat Hypertension – Self-monitoring

March 12, 2018 Neal Parikh, MD

Precision medicine, when applied to prevention, can identify opportunities for an individual to reduce their cardiovascular risk. Resulting interventions are personalized and may take advantage of the latest science, including genetics. Such interventions may presuppose that basic risk factors – such as hypertension and diabetes – have been identified and maximally controlled. Intervening upon more recently identified risk factors may have less or no impact if dominant risk factors such as hypertension are not adequately controlled.

In contrast, population health interventions could indiscriminately improve health for individuals by targeting well-accepted, high-stakes risk factors. For example, although hypertension is accepted as the leading risk factor for cardiovascular disease, we see patients every day with poorly controlled blood pressure in the clinic and hospital. Controlling such risk factors could raise the bar more uniformly so that more people may benefit from the additional gains of precision prevention.

Engaging patients in their own health care may be an effective strategy. For example, in the recently published TASMINH4 trial from the United Kingdom, patients empowered to monitor their blood pressure at home and present the data to their doctors had improved blood pressure control, as compared to individuals receiving routine care.¹

While such research can be frustratingly complex to perform and interpret, the benefits of standardizing and incorporating sound methods for improving blood pressure control cannot be understated. Translating this into clinical practice may require a new information infrastructure and possibly changes to reimbursement schemes, due to the possible added burden of reviewing additional data.

In this era of enthusiasm for precision medicine, we should continue to pursue population health and implementation science with equal gusto, especially in countries with high health care disparities such as the United States.

References:

McManus RJ, Mant J, Franssen M, Nickless A, Schwartz C, Hodgkinson J, et al. Efficacy of self-monitored blood pressure, with or without telemonitoring, for titration of antihypertensive medication (TASMINH4): an unmasked randomized controlled trial. Lancet. 2018. https://doi.org/10.1016/S0140-6736(18)30309-X

Neal S. Parikh, MD, earned his MD from Weill Cornell Medical College and completed residency training in neurology at the same institution. He is now an NIH T32 neuro-epidemiology and vascular neurology fellow at New York-Presbyterian Hospital/Columbia University Medical Center. He tweets @NealSParikhMD and contributes to Blogging Stroke as a blogger.

Hypertension In 2017— Individual VS Public Health Goals

January 26, 2018March 28, 2019 Fawaz Alenezi, MD, MSc 

Hypertension has obviously been one of the main stays of cardiovascular (CV) medicine for a long time and it is the single most modifiable CV risk factor in the world today. Hypertension had a great deal of evolution since publication of the landmark 1977 Joint National Committee report there has been progressive improvement in awareness, treatment, and control of high blood pressure (BP). Although several BP guidelines have been published since 2003, the 2017 guideline is the most comprehensive that has a new classification, definition and different goals for BP reductions.

The new guideline defines normal BP as below 120/80 mmHg and elevated blood pressure as 120 to 129 mm Hg systolic with a diastolic pressure below 80 mm Hg. Stage 1 hypertension is defined as 130 to 139 mmHg systolic or 80 to 89 mmHg diastolic, and stage 2 hypertension as 140/90 mm Hg or higher (the old definition of hypertension). What is now called stage 1 hypertension was previously labeled “prehypertension” a term meant to alert patients and to prompt physicians to provide lifestyle education to help delay development of hypertension.

Adults with an average systolic BP of 130 to 139mmHg or diastolic BP of 80 to 89mmHg have about a 2-fold increase in CV disease risk compared with a normal BP (SBP < 120 mmHg and DBP < 80 mmHg). Unlike previous guidelines, the 2017 guideline emphasizes individualized CV risk assessment and aggressive management of BP at levels of 140/90 mm Hg or higher in patients with a 10-year risk of CV events of more than 10%. Although the 10% 10-year-risk designation is not based on randomized, controlled trials, patients with BP of 130 to 139/80 to 89 mmHg would still receive non-pharmacologic treatment, unless they had a 10-year risk above 10%; in that case, a single antihypertensive agent is recommended, in concert with lifestyle changes.

Accurate and proper measurement of BP is the first most important and critical step to the diagnosis hypertension. In addition to careful BP measurement, the new guideline highlights the increasingly important role of out-of-office BP readings for confirming hypertension and recognizing white-coat and masked hypertension. It also emphasizes contemporary strategies to improve BP control, including ways to successfully implement and sustain non-pharmacological interventions, improve medication adherence, use a structured team-based approach to care, and take advantage of health information technology.

According to the new BP definitions, prevalence of hypertension increased and there is concern that a new disease designation can become a mandate for pharmacologic treatment without consideration of the patient’s risk level. However, this was an area of discussion and was explained very well in this version of guidelines. Although there are positive aspects of targeting higher-risk people with lower blood pressure for risk-factor modification, an individualized approach to hypertension can help determine the best choice for first-line therapy.

In the public health level there is a morbidity and mortality benefit, but in the individual patient level this may be hard to achieve specifically in asymptomatic patients. We are still not doing well in lowering BP and almost half of the patients are not achieving the individualized goals. However, this is the biggest place where we can have an effect and obviously why there is a national concern! It’s reasonable to consider more aggressive treatment goals in the highest-risk patients, but understanding the guideline and considering each patient according to their risk factors and complex medicine problems become more critical.

New Hypertension Guidelines: Why Neurologists Should Pay Attention

December 11, 2017 Neal Parikh, MD

Scientific Sessions generated a great deal of buzz in the traditional and social media spheres, particularly with regards to the new ACC/AHA High Blood Pressure Guidelines. The lay media was quick to note that nearly half of the US population will now be considered hypertensive, and some doctors expressed concern that some patients may incur undue harm from over-zealous anti-hypertensive therapy.

It is important first to note that the guidelines do not require or recommend that individuals with blood pressure values falling in the “Elevated Blood Pressure” or “Stage I Hypertension” categories be reflexively treated with anti-hypertensive medication. There is room for consideration of overall-risk and prior cardiovascular events. There is an explicit role for non-pharmacological therapy. Some have noted that that while the number of individuals now considered “hypertensive” will increase, the number requiring pharmacological treatment will not increase as dramatically.

That said, why should neurologists pay attention? First, the previously-used term “pre-hypertensive” is decidedly not alarming. The updated guidelines’ use of “elevated blood pressure” is clear and unambiguous; patients and their physicians will be prompted to action earlier. Given that hypertension is a leading risk factor for stroke, we will hopefully see stroke rates decrease with time. Second, neurologists should pay attention because some patients may see us more frequently than their primary care physicians. We should be aware of these guidelines so that we are prepared to appropriately counsel and/or refer patients with elevated blood pressure. A check-in for a migraine or epilepsy medication refill may yield an opportunity to reduce long-term cardiovascular risk!

I look forward to seeing the public health gains materialize from dissemination and implementation of these guidelines.

Neal S. Parikh, MD, earned his MD from Weill Cornell Medical College and completed residency training in neurology at the same institution. He is now an NIH T32 neuro-epidemiology and vascular neurology fellow at New York-Presbyterian Hospital/Columbia University Medical Center. He tweets @ NealSParikhMD and contributes to Blogging Stroke as a blogger.