Live Streaming Into Scientific Sessions 2018

AHA Scientific Sessions 2018 was a unique experience for me – unable to attend the meeting, I live-streamed the sessions (first time ever for a conference!). Two of my most favorite sessions this year were the panel discussion for advanced heart failure (HF) patients, “The Metabolic Face of Heart Failure,” and the mini-symposium on “Cutting Edge in Cardiovascular Science.”

One of the main highlights in the session Metabolic Face of HF, moderated by Dr Lynne Stevenson, was the talk by cardiovascular stalwart Dr. E. Braunwald, Brigham and Women’s Hospital. Dr. Braunwald spoke of the significance and latest practices in the use of Sodium-Glucose Cotransporter-2 (SGLT2) inhibitors, a class of FDA-approved drugs for type-2 diabetes. He indicated how SGLT2 inhibitors should be explored beyond diabetes treatment and these class of drugs can benefit HF patients as well. “I had to learn about blood clotting 30 years ago, which was difficult,” he modestly admitted as he clarified the renal effects of SGLT2 inhibition. His views also seemed to resonate with Dr. Subodh Verma, St. Michael’s Hospital, Toronto and Dr. John McMurray, Glasglow University, as they covered SGLT2 inhibitors in HF, as well.

Other speakers at this session, Dr. Neha Pagidipati, Duke University and Dr. Lewandowski, Ohio State University, touched upon aspects of stroke and metabolism regulating HF, respectively. While Dr. Pagidipati compared the risk of cardiovascular diseases and stroke with the risks of diabetes, Dr. Lewandowski explained how metabolic regulator PPAR-a (transcriber of genes in fat metabolism) could be a player explored in targeted therapy.

The session ‘Cutting Edge in Cardiovascular Science’ had presenters covering diverse strategies in dealing with cardiovascular therapy, ranging from computational screening to identifying small molecule compounds, to decoding neurovascular networks and the gut microbiome. Dr. Stanley Hazen from Cleveland Clinic presented his work on understanding the microbes in the gut and their role in driving cardiovascular diseases. Dr. Hazen explained how food like red meat, which are rich in components like phosphatidyl serine, activates the gut microbiome. He described the significance of trimethylamine N-oxide (TMAO) pathway in liver and its association with HF, stroke and cardiovascular diseases. He also strategized the use of enzyme in TMAO pathway as targets of small molecule inhibitors.

Dr. Joseph Loscalzo, Brigham and Women’s Hospital, explained how repurposing drugs and finding drug targets computationally could help precision medicine vastly. He also offered his expertise and tools as open access to AHA members. Finally, Dr. Costantino Iadecola, Cornell, elaborated on the heart-brain connectome. He brought attention to the fact that dementia, known to cause hardening of arteries, led to Alzheimer’s, but we all forgot about the vascular complications of this. He bridged this connection between neurovascular dysfunction and cognitive impairment and went on to explain his research on the intake of high salt in diet caused dementia in mice models. To learn of such versatile range of topics in a session was illuminating, to say the least!

Researchers must spend time thinking about applications of their current projects beyond their own niche – this is the only way we can widen our horizons with existing tools.



High Sodium Consumption: The Next Public Health Endeavor?

We hear it everywhere. “Don’t put too much salt on your food, it’s not good for you.” It is a statement that is so frequently said by doctors to their patients, by concerned family members to their loved ones, that it has almost become part of our culture. Off the top of my head, I can think of a dozen movies where the main protagonist gets the table salt taken away from them because they have high blood pressure.

With that said, as noted by the AHA’s “Common High Blood Pressure Myths” article1, adding table salt to your food is not the main culprit causing medical problems. It is the hidden sodium in our processed foods.

Recently, I took it upon myself to pay a closer look at my diet. Like many American, I eat out a lot. Given that most fast food restaurants are starting to note the calories within their food, I started to realize it was easy to keep up with the CDC-recommended calorie count of roughly 2,300 calories per day2. However, the one variable that always kept coming up high in my diet was sodium.

It’s not like I was eating hamburgers everyday either. I started to realize simple condiments pushed the sodium in my food to astronomical numbers. A serving of hot sauce, broth in my ramen noodles, even pickles, would cause my sodium intake to leap despite a low-calorie count. On restaurant menus, I always saw in small letters the warning that “guidelines recommend a 2,000 mg daily sodium consumption”, and next to it, I would find a food entrée that had twice that amount in a single serving. As a physician, I was recommending sodium restriction to all my patients as an easy treatment for their many comorbidities, and yet, I had a difficulty following my own recommendations. Sodium is everywhere and trying to keep its consumption in check is a challenge.

So why is high sodium bad?

Initially, clinicians attributed sodium’s harmful effects to its association with high blood pressure3. Multiple meta-analysis and randomized control trials have shown a strong positive correlation between high sodium intake and elevated systolic blood pressure. As we know, high blood pressure is associated with a myriad of health complications affecting the heart, kidneys, and the brain. Thus, given sodium’s relationship with the number one cause of cardiovascular related death worldwide, it would make sense that sodium restriction has become the first-line treatment for hypertension.

Yet, new research presented at this year’s AHA Scientific Sessions is suggesting that there may be more adverse effects associated with high sodium consumption than just its effect on blood pressure. During the “Cutting Edge in Cardiovascular Science” presentation at Sessions, Dr. Constantino Ladecalo of Weill Cornell Medicine presented evidence in mice studies correlating high sodium consumption to neurovascular and cognitive impairment in the absence of hypertension. Outlined in a paper published recently in Nature Neuroscience4, Dr Ladecola presented a molecular pathway that may connect the effect of sodium in the small intestine with reduced resting blood flow to the brain, leading to cognitive impairment. The “gut-brain connection” as so called by Dr. Ladecola, may be a new frontier in medicine.

While Dr. Ladecola and his team suggested that this molecular pathway may be a new target for prevention of cognitive impairment, to me, their findings reinforced the fact that we need to return to the basics in our treatment of cardiovascular disease: lifestyle changes and nutrition. Previous endeavors in public health have helped eliminate several illnesses that were common such as thiamine deficiency, so why not attempt the same with sodium? As the evidence builds against high sodium consumption, it may be time for us to take a more active look at how we can address it. Can we work together with major food distributors to reduce sodium in their food? Should chain restaurants inform consumers of the sodium value in their foods as they do with calories currently? I am not sure of the answer to these questions as they can be very difficult endeavors to focus on.

What are your thoughts on sodium?

  1. American Heart Association. “Common High Blood Pressure Myths” October 31, 2016 “http://www.heart.org/en/health-topics/high-blood-pressure/the-facts-about-high-blood-pressure/common-high-blood-pressure-myths”
  2. Kotchen TA, Cowley AW, Frohlich ED. Salt in health and disease–a delicate balance. N Engl J Med. 2013;368(26):2531-2.
  3. Center for Disease Control. “Most Americans Should Consume Less Salt” June 11, 2018 National Center for Chronic Disease Prevention and Health Promotion , Division for Heart Disease and Stroke Prevention “https://www.cdc.gov/salt/index.htm”
  4. Faraco G, Brea D, Garcia-bonilla L, et al. Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response. Nat Neurosci. 2018;21(2):