hidden

Innovative Pathways To Antioxidant Therapy

disease potentially cause by oxidation

Cardiovascular disease (CVD) has been responsible for increased mortality and morbidity rates in our society for generation with no end in sight. There is a paradigmatic shift in medical practice as it pertains to treating CVD, rather than physicians and scientist looking at this as a single organ disease, we are now considering the pathophysiological condition to include genetic inheritance and lifestyle that imparts changes to the heterogeneity of molecular, cellular and organs systems.

It is well accepted that a number of risk factors contribute to the onset of CVD to include poor nutrition, lack of physical activity, hypertension, obesity, diabetes and certain forms of cancer. My research has focused on the role reactive oxygen species (ROS) have played on the onset on CVD due to increased vascular inflammation. ROS is a common term that is used to address the highly regulated enzymatic process that can be either antimicrobial or damaging to an organ system. Oxidative stress has been thought to be a balancing act between oxidants and antioxidants, but the mechanism of using high antioxidant foods have not rendered any changes in oxidative outcomes. There is new research that is being conducted by Cortese-Krott et al. (2017) that is identifying a new and integrative biology concept known as redox regulation. In their study, they have defined various chemical interactions of reactive sulfur species, reactive nitrogen species, and ROS along with downstream biological targets as reactive species interactome (RSI). This group suggest RSI serves to sense multiple stressors and adjust metabolic needs accordingly. This model identifies thiols as an important source of ROS in addition to the cysteine redox switches.

More research is necessary to determine whether efficiency of these new developments; however, we cannot evade the concept of ROS leading to an enhanced immune response that contributes to the disease process. It is my opinion, that this new development will open a new mechanistic pathway to understand the pathophysiology that leads to CVD and increase the intersystemic approaches that are used to treat the chronic inflammatory response that leads to CVD.

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.

hidden

E-Cigarettes, Cigars, And Commercial Cigarettes

JUUL Perspective

Adopted from www.juullabs.com/our-story
There was a recent article released on AHA Newsroom discussing a lawsuit to expedite the FDA review of electronic (e)-cigarettes and cigars. The article highlights the premises behind the suit filed by several groups to include medical, public health, and pediatricians due to a lengthy delay by the FDA in reviewing laws surrounding e-cigarettes and cigars. These products such as JUUL, are becoming more popular among younger generations due to the increased number of flavors available (mango, crème brulè, and fruit medley), which has been shown to cause cardiovascular (CV) effects.  These electronic products are being marketed as being a cleaner, more stylish product that makes cigarette cessation easier, but there is no evidence to that affect.

I was quite surprised to read this because during the AHA EPI | Lifestyle Specialty Conference there was a topic on the dangers of e-cigarettes and its metabolic toxicity as compared to commercial cigarettes. There is increasing research being conducted on the use of e-cigarettes and the impact they have on the population. The lawsuit filed in the federal court in Maryland, is important because the products will remain on the market indefinitely during the review process with no set deadline for completion. Additionally, advertisements are being targeted toward youth causing an uproar with parents and school officials due to overwhelming incidences of bathroom smoking.

During the Stamler session of the EPI | Lifestyle meeting, Lloyd-Jones discussed the risk of considering these products as safe under the premise of them emitting vapor, when they are producing aerosols (a mixture of particles and water) that can contribute to the onset of chronic diseases. These particulate matters produced are equivalent to the size and concentration of commercial cigarettes with similar incidences of toxin-induced CVD. E-cigarettes have been shown to decrease nitric oxide by 16% after 5 minutes but long term exposure slows the heart rate subsequently preventing vasodilation. Chronic inhalation of e-cigarette or cigar vapor was demonstrated to induce pro-inflammatory and pro-fibrotic proteins such as IL-8, angiopoietin-1 by 31 fold, and EGF by 25 fold. There was additional evidence that kidneys, heart, and liver rendered a significant increase in pro-fibrotic pathway activation and altered CV function and elevated blood pressure. Some of the more alarming data demonstrate, among the common side effects of chronic use of e-cigarettes/cigars are popcorn lung and inflammation that leads to organ damage that cause cardiorenal and hepatic disease.

With e-cigarettes and cigars gaining in popularity, I think there should be more research geared toward understanding the impact they have on the general population. There are ongoing studies exploring second-hand and third-hand smoke on vascular and pulmonary health. FDA has made efforts to reduce the level of nicotine in commercial cigarettes to minimally- or non-addictive levels, but for e-cigarettes and cigars are exempt from those requirements making it potentially unlawful and harmful to public health. Furthermore, they have delayed the deadline for filing applications until August 2021 for commercial cigarettes/cigars and other combustible produces until August 2022. I would venture to say, these studies have indicated adverse inflammatory events that will be multiplied by the time the applications are filed, let alone reviewed. Although companies producing e-cigarettes/cigars are not soliciting to children, the flavors they are manufacturing are enticing to the younger generations. In addition, arguments have been made to the affect that there is no diacetyl contained in these pods. Because they have substituted diacetyl with benzoic acid,, the potential of oxidation of the scavenging agent enhance the opportunity for oxyradicals to be produced within the vascular system subsequently increasing inflammatory responses that lead to vascular injury.

Food for thought, there were issues of these pods exploding due to leaks but the overall health outcome may be worse than the threat of combustion. So, if the cost of e-cigarettes/cigars were to be calculated, does it make sense to spend $10 per pack to increase the potential for a chronic disease by subjecting our youth (and the public) to the aerosols from combustible products? Is it in the best interest of the public for nicotine containing products to be regulated?

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.

hidden

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

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:

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. Session 11 – The William B. Kannel MD Memorial Lectureship in Preventative Cardiology
  6. 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.
  7. 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.

hidden

Surviving A Deadly Heart Attack

With cardiovascular disease (CVD) being the leading cause of mortality and morbidity among the western population, it is not a long shot for one to think almost everyone knows someone that has encountered heart disease or the symptoms thereof. Not surprising that I had the opportunity to meet these people whom I am now writing.

 

Heart month heart image

There was a cardiologist at a well-known and respected institution that suggested, her patient, a 60 year old man with two occluded arteries and only a functioning aorta (widow maker) had on average 10 years to live. The patient had one silent heart attack and one where he sought medical treatment. During that time the cardiologist attempted to place a stent to reopen the artery, but had no success due to the “amount of scarring.” Which is why the patient was left with two arteries occluded. I am left to wonder, with all the research that is being conducted to extend life and improve cardiac health including but not limited to pharmaceuticals and the surgical techniques, why is there nothing that can be done other than sending this patient home with a bleak outlook on the next several years of his life. That patient is still alive and doing well, thanks for asking. That is not an isolated case of patients being sent home hopeless. I came across a story on Facebook (2014) about a 58 year old lady that was on hospice for the last four years. She presented to the hospital in full cardiac arrest. The emergency medical team was performing compressions until she arrived at the hospital; thankfully they were able to revive her. She previously suffered 3 heart attacks resulting in 2 triple bypass surgeries, but after that 4rd heart attack in August 2010 the doctors said there was nothing they could do to improve her [cardiac] health. Before you are alarmed, she had multiple chronic illnesses by this time: 3 myocardial infarction (MI), congestive heart failure, diabetes, breast cancer (resulting in double mastectomy), hypertension, and renal failure. Since she was not a good candidate for dialysis, she had a poor prognosis. She was taken off all her medications (from a cocktail of 19 pills to 4, which were for CVD symptoms and a morphine tablet for pain) and the end of life care team made worked diligently to make her comfortable until she passed.  The medical providers alerted the family that she could pass on at any time. That was in 2010, it is now 2018 and she is STILL alive and well! Both patients are.  So, what allowed this Facebooker to live so long with no major arteries? How is this even possible? Is it a case of faith/a miracle alone (which is what the Facebook post suggest) or something that can be medically/scientifically explained? What about the man from the former story? Is 10 years the best he could hope for or is the case with the latter possible in his case? Is there anything we can do pharmaceutically to drive the system toward the former?

the vascular endothelial growth factor graphic

In a 2018 study by Manavski et al, it was suggested that angiogenesis after ischemia is due to clonal expansion of endothelial cells. Indicating there is, indeed, a scientific rationale for the revascularization of the aforementioned hearts. After an MI there is significant scar tissue leading to the inability for the heart to provide the necessary oxygen and nutrients to other organ systems, known as ischemia. The newly ischemic environment potentiates the growth of new vessels to compensate for the loss of cardiac output due to the MI. These vessels are said to be generated through a mechanism known as angiogenic sprouting; in excess this pathological growth that can promote tumor formation. The signaling molecule vascular endothelial growth factor (VEGF) is hallmark in the formation of new vessels, but it is also highly expressed in cancers. Before we get off track, let’s think about the mechanisms in play in an MI. monocytes are attracted to an insult in the vessel, they differentiate into macrophages, those macrophages take up oxidized low density lipoproteins, and since they cannot process them, they die (undergo apoptosis). In ischemia macrophages promote the development of collateral vessels, but in tumors macrophages (M2) produce proangiogenic factors while educating the macrophage as what phenotype to take on – Tumor or cardiac. There are signals in the body that include VEGF and Ang1 that keep endothelial cells inactive to promote vessel stabilization. Furthermore, an oxygen sensor helps the endothelial cells to normalize and readapt to oxygen supply to the organ tissues. There are a battery of enzymes that play a role in vessel maturation which is too exhaustive for this blog, but mainly sprouting is impaired by inhibition of VEGF and S1P receptor signaling is the stabilizer for the vasculature.

In conclusion, having a heart attack is not necessarily a death sentence. Even when all the arteries to the heart of occluded. It is not the norm, but the human body is an overwhelmingly amazing in compensating for the loss of some pathways. Our bodies have system in place with mechanism to support life even when the answers evade medicine and science. With the passion to conduct research, we are finding ways to make our heart health better daily. As we explore mechanistic pathways to reduce oxidative stress, inflammation, and other underlying pathways, it is up to each individual to maintain a healthy heart by following the guidelines set in place by the American Heart Association. As for the patients above, they are working with their medical teams to maintain a healthy life. May I suggest you all continue to seek your physicians’ advice on how to improve/maintain your heart health?


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.

hidden

Killing Cardiac Cells

chambers of the heart imageI was in the mall one day and the saleswoman started talking about her health issues. For starters, I am not sure why she entrusted me with this information, but okay. So why is that conversation interesting enough to write about? Well, the lady was 20 years of age and she had undergone several cardiovascular challenges, including a cardiac ablation. I had heard of other people having this procedure done but I had not thought much about it (I looked it up but not in much detail), until I met this young lady. So, I started wondering:

  1. What is the underlying pathology that causes one to need to have the procedure?
  2. What is the average age of patients undergoing the procedure?
  3. What is cardiac ablation?
  4. How commonly is this procedure done?

Cardiac ablation is the use of catheters to target and kill off specific cells within the heart, generally in the atrium. The adult mammalian myocardium has a negligible ability to regenerate once damage has occurred. Thus, rather than undergoing cardiomyogenesis (the formation of myocardium/heart muscles), fibrous tissue is instead formed. This phenomenon raised more questions for me, so I did literature searches…then more literature searches…then read more literature. The more I read, the more I felt I needed to read to understand why cardiologist would choose this procedure. Following a myocardial infarction (heart attack) a significant number of cardiomyocytes die leading to an enhanced inflammatory reaction. This cardiac event results in dead myocardial tissue being replaced with interstitial and perivascular collagen deposition. The presence of fibrosis can lead to pressure overload, increased blood pressure or potentially aortic stenosis. However, a patient that has suffered from myocardial infarction would not be a good candidate for cardiac ablation. So, who would be a good fit to undergo such a procedure? Usually it is a patient exhibiting cardiac arrhythmias, including atrial fibrillation (AF or AFib), supraventricular tachycardia (SVT), and Wolff-Parkinson-White Syndrome (WPW). Because this subject is enormous, I will only focus on AF due to the fact that it is the most common cause of arrhythmias treated with catheter ablation.

Pathophysiology of Atrial Fibrillation
AF is characterized by an abnormal heartbeat (quivering or irregular heartbeat) that causes the heart to ineffectively move blood into the ventricles. The onset of AF could be due to family history (genetics), but controllable risk factors are hypertension and valvular heart disease. The cardiovascular consequence of AF includes: 

  1. Coronary artery disease
  2. Mitral stenosis
  3. Mitral regurgitation
  4. Left atrial enlargement
  5. Hypertrophic cardiomyopathy
  6. Congenital Heart Disease
  7. Cerebrovascular Accident

AF is considered the most common arrhythmic disease and it affects about 4% of the population. The prevalence of AF increase with age (<0.2% under 50 year of age (yoa), 4% are 60-70 yoa, and ~15% >80 yoa), with patients suffering from it has an average age between 75-85 yoa. In the U.S., there was a significant number of deaths (>200,000) resulting from AF in 2015, which is reason enough to pursue aggressive therapies to control this heart rhythm disorder.

Treatment
The European Society of Cardiology (ESC) released guidelines that summarized the current evidence that is available to physicians in selecting the best strategy for managing diseases, taking into consideration the risk-benefit ratio of diagnosis and therapeutic means. The recommended guidelines has shifted to focus on the identification of ‘truly low-risk’ patients (<65 with AF alone that does not need antithrombotic therapy) rather than ‘high-risk’ patients. Based on the earlier guidelines for treating AF, a patient of age >20 would not be considered for ablation therapy, so I wondered…what are the alternative treatments? I found they can either be drugs, such as: 1) Novel oral anticoagulants (blood thinners) fall into two categories (Oral direct factor Xa inhibitors or Oral direct thrombin) and 2) Left atrial ablation—introduced by American College of Cardiology Foundation, American Heart Association, and the Heart Rhythm Society.

To read more about these treatment, please be directed to European Heart Journal for the ESC Guidelines. Here I will focus on cardiac ablation.

Cardiac Ablation
Cardiac ablationThe normal mammalian heart is composed of tight layers of myocytes that are separated by small clefts creating a matrix network. The cardiac matrix network is divided into three constituents. The matrix network is collagen-based and serves as a scaffold for various components of the cell as well as transmission of contractive forces that keep the cells in correct timing with neighboring cells. When the heart undergoes damage, the resulting fibrosis disrupts the coordination of this myocardial excitation-contraction leading to hypertension. Subsequently, loss of collagen impair transduction, which causes the uncoordinated contraction of the cardiac muscle bundles (the quivering or fluttering that is felt with AF) or generation of re-entry circuits (irregular heartbeat).

The ablation process will depend on the patient medical condition, past cardiac history, and the ablation technique chosen. There are several types of catheter ablation

a) Radiofrequency ablation-use radiofrequency generators to deliver a current, in a point by point fashion around the pulmonary vein, creating a circular scar around each vein.

b) Cryoablation—uses a single catheter that travels through the femoral vein in the groin to the left atrium. The balloon end (halo) of the catheter has a refrigerant that freezes the tissue it comes in contact with creating a scar.

c) Surgical ablation—generally used when open heart surgery is being conducted.
          i. Mini Maze-use 3-5 incisions on the front and side of the chest to insert the catheter to freeze/heat cardiomyocytes
          ii. Convergent—uses both surgical and catheter based techniques.

Catheter ablation is generally an outpatient procedure, but it should not be taken lightly. As with most consumers, cost comes to mind. How can cardiologist/electrophysiologist conduct such a procedure in so short of a time and charge so much? The answer is simple. The technology used in ablation is extensive; mapping equipment, cardioverter/defibrillator and catheter, recording apparatus, stimulators, and junction boxes. I am overwhelmed just thinking about it all!

Wrap it up…
Cardiovascular disease is a consequence of a lot of factors. Understanding the various procedures that the cardiologists are explaining can be daunting. Even with the expansive literature that is available it is difficult to determine how a procedure will work for each patient, especially with regard to the side effects. For example, in a 2010 study for rhythmic control (294 patients), there was no significant difference between patients that received the catheter ablation compared to those taking antiarrhythmic drugs as a first line of intervention. Catheter ablation is said to be more effective than antiarrhythmic drugs, but the recurrence of AF is significant during long term follow up. Early recurrence of AF is the best predictor of whether one will have a recurrence later. In an observational study conducted at high volume clinics, there was a 39% hospitalization rate post catheter ablation. However, catheter ablation has been deemed reasonable for first line of therapy for AF when patients have paroxysmal AF and low risk for procedures with complications; which is interesting since the majority of studies are inherently biased toward the experienced centers. It is reasonable to speculate that people, such as the saleswoman in the mall, who visit small low volume clinics, contribute to increased rates of hospitalization rates.

I am, furthermore interested in knowing whether there is a decrease in cardiac output post catheter ablation. If this procedure is killing off specific cells in the heart and leaving scar tissue, what are the downstream effects of this cardiac cell death? Especially in patients that have repeated catheter ablations. If there is a decrease in cardiac output, and the kidney filters 20% of the cardiac output daily, then what effect does cardiac ablation have on the renal system? Could this procedure enhance renal failure? I have had conversations with other people who have had cardiac ablations that later suffered from renal failure necessitating dialysis. Since all conditions are patient specific, there is no evidence that catheter ablation is connected to renal failure to my knowledge, but I wonder if anyone else had that observation.

To sum up the conversation I had with the young lady in the mall. She started her cardiac journey at an early age. She has gone through oral anticoagulant drugs, catheter ablation, and open-heart surgery. By the age of 20, that is a lot for one to have gone through. She was in such distress about having to undergo yet another catheter ablation that she was seeking answers to help her understand what she was going through and how to make informed decisions about her care. How can patients be better educated on what is going on with their bodies when visiting medical professionals? People are told to take responsibility for their care, but what if they do not understand enough to know what to ask?

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.

hidden

Tardiness Of Science Leads To Public Skepticism

Man with heart surgery scar

AHA17 introduced the new and controversial blood pressure measurement guidelines during its annual conference in Anaheim, CA, raising skepticism among the masses. However, before I get into what the new recommendations are, let’s review how blood pressure measurements were initially established. Historically, over the last century blood pressure was unstudied by the scientific and clinical communities. The realization of the importance of blood pressure to health was first observed over 4,000 years ago by Huang-Ti, the yellow Emperor of China, with the discovery that people who ate too much salt had “harder” pulses and subsequently suffered from more strokes. Precise blood pressure measurements did not come about until Samuel Siegfried Ritter von Basch developed the sphygmomanometer for clinical use in 1880. The concept of hypertension, previously termed hyperpiesia, did not make an appearance until 1896 with the introduction of auscultating Korotkoff sounds (the sounds heard through the stethoscope when the artery is occluded by the sphygmomanometer and pressure released slowly). Having this new technology revolutionized the means of measuring blood pressure.

As the technique for blood pressure measurement developed over the years, so did the basis for the clinical diagnosis of hypertension. However, there was still debate as to how to treat it. In 1949, Charles Friedberg suggested in the textbook “Diseases of the Heart” that mild ‘benign’ hypertension (210/100 mmHg) should not be treated. During this era, blood pressure treatment was so controversial that the common thought was, ‘the greatest danger to a person with high blood pressure was knowing, because some fool will try to reduce it’. To put that statement into perspective, this was still a time when people were bled by leeches to reduce blood pressure leading to increased incidences of death due to the treatment regimen. The next era of treatment was to do nothing. Researchers started to explore the idea that high blood pressure was a compensatory mechanism, which should not be tampered even if clinicians were certain it could be controlled. This line of thinking lead to a significant increase in morbidity and mortality due to the prevalence of cardiovascular disease caused in part by the untreated blood pressure. With this revelation, high blood pressure treatment and diagnosis was forever changed, starting with the level that is considered to be high (140/80 mmHg).

The first clinical breakthrough in hypertension treatment was the discovery of diuretics. The addition of this drug class reduced strokes and ischemic heart disease by ~50% between 1972 and 1994. Once beta blockers came on the scene for the use of angina, researchers found, by accident none the less, that they additionally lowered blood pressure. How about that?! With research advancing in the area of hypertension, there have been several drugs to come on the market to lower blood pressure including calcium channel blockers and sartan drugs. These medications have had enormous benefit in reducing cardiovascular disease.

This leads us to the new classifications of normal and high blood pressure. At AHA17, the new range for defining systolic/diastolic blood pressure in patients is as follows: normal (90-119 mmHg/60-79 mmHg), prehypertension stages I (120-139 mmHg /81-89 mmHg), and stage II (≥160 mmHg/ ≥100 mmHg), as well as isolated systolic hypertension (≥140 mmHg /<90 mmHg). These measurements are based on the average seated, relaxed blood pressure reading obtained over two or more office visits. Although these are the new recommendations, these numbers are interpreted in conjunction with the clinician’s understanding of the patient’s history. For example, if a patient has a blood pressure of 130/80 mmHg coupled with other chronic diseases, such as diabetes mellitus type 1 or 2 or kidney disease, then this might require more aggressive treatment than a patient with no underlying disease. Physicians will furthermore take into account a patient’s age and overall health when making the decision of how or when to medicate. For example, a patient with resistant hypertension (blood pressure that fails to be reduced with appropriate antihypertensive medicine) may require additional drugs. Because we know that hypertension can be a consequence of both environmental and behavioral factors, AHA still suggests that we adopt a healthy lifestyle that includes a diet focused on heart health, as well as incorporating exercise into our activities of daily living.

There has been some controversy in the news and on social media about these changes. Whether these changes are in the best interest of the general population or in the interest of those who stand to gain from more people having hypertension. This could indeed lead to more patients taking medicine, and consequently more people having higher insurance premiums. It could also lead to more income for primary physicians and pharmaceutical companies. With these things being considered, none of them are more important than one’s health! There are things that cannot be controlled, such as age, sex and genetics, but that does not change the fact that it is the individual’s responsibility to live a healthy lifestyle and take control of their health care. This starts by knowing your risk, eating healthy, and regular exercise.

I know this is a lot of information to take in, but the real message here is: (1) do not allow social media to dictate your health. There are going to be a lot of things said by all types of people, but the best resource is your clinical staff. (2) Yes, regular medical appointments are still necessary to determine whether blood pressure should be treated or how it should be treated. (3) Although the blood pressure scale has changed slightly to incorporate more hypertensive stages, the definition of a healthy blood pressure has not really been modified. Experts (clinicians and scientist) are at odds as to whether patients over 70 years of age should be treated with additional medicines in order to reduce blood pressure. To add more antihypertensive drugs to a patient in such a vulnerable age group could lead to increased side effects such as hypotension, dizziness, increased prevalence of renal failure, enhanced fall risk, and alterations to activities of daily living. There are guidelines published in the JAMA for more information on the recommendations for the geriatric population. Science takes time. It takes a lot of studying to get the results that change the way experts view our clinical practice. It may seem to the general public that these data are tardy, but they are, in my opinion, timely.

I am interested in knowing more about the benefits of the new blood pressure scale and how this will tangibly change the occurrence of cardiovascular disease, cardiorenal disease, and chronic renal disease. I also wonder what questions will now arise in the general population regarding these new developments.
 

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.

hidden

Onsite Or Online…

keyboard and pen

Going to a conference is an exciting time. Walking into the conference hall with all the anticipation of meeting new people. Some that one only have the opportunity to see at one meeting or another, and learn more things that will reignite the passion that drove researchers to science in the first place. Conferences are also the time to recharge from the burnout that comes from writer’s block, the inability to come up with ideas to push your research forward, and alternative ways to look at things that have been being pondered with no solution or since of direction.

This year, the #AHA17 was out of my reach for various reasons. I could, however, attend via multimedia. This experience was different compared to being onsite, yet equally exhilarating in that it came with its own challenges and excitements. Attending to the technology limitations, such as converting from Windows to Mac, gaining access to meetings that were off limits, as well as managing time away from the laboratory duties while still be present in the lab. Once the sessions began, this means of attendance was more like attending a webinar; supersized. There were various aspects of the online tools that allowed me to be more interactive than with a live meeting, such as the ability to rewind and replay sections that were not clear; not possible with a webinar. I had the capability of looking up information that I did not understand in real time as well as ask questions. During live meetings, there are so many people vying for the speaker’s attention that it is impossible to ask during a live session and in webinars the question screen does not come up until after the webinar is over so remembering the question could be challenging.

Some of the sessions that I attended included Treating gum disease as a means of lowering blood pressure, the role of sleep deprivation in women’s propensity of cardiovascular disease, and how stress impacts obesity. All of which sparked a new way of thinking on the direction in which cardiovascular research is being driven. I was so enthralled with the topics, I could not pry myself away from my computer. I could only image the intense learning environment that was there in Anaheim during this conference and all that educational and mentoring opportunities that came with being onsite. Even though, I enjoyed my experience online, I feel being onsite is my favorite way of attendance. What is your favorite attendance method for conference?

Anberitha Matthews 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, serving as Chapter President and does consulting work with regard to scientific editing.