Notes From Rounds: AHA Day Two

Adam Sturts, MSIV

Amyloid Heart Disease

In an effort to diversify on-site coverage at the American Heart Association (AHA) 2019 Scientific Sessions in Philadelphia this week, MD Magazine® enlisted the aid of an aspiring medical student to provide observations and key takeaways from the sessions he attended throughout the meeting.Adam Sturts, MSIV, a fourth-year medical student with a cardiology focus at Rowan University School of Osteopathic Medicine, is also a type 1 diabetic. His unique perspectives in both training rotations and direct patient care management drew him to learn more how the relay of conference information and data applies to patient benefits.Below is Sturts' journal of notes on the sessions he attended at AHA on Sunday, November 17. Medical students, care providers, and experts interested in contributing to MD Mag coverage can contact us here.I arrived on Sunday morning excited to attend the “Amyloid Heart Disease: Emerging from the Shadows into YOUR Practice” session. Before the session began, I decided to review cardiac amyloidosis pathophysiology.

The transthyretin gene codes for the TTR protein. The liver produces TTR, which is most stable as a tetramer. It circulates in the blood, functioning in thyroxine and retinol transportation. Isolated monomers can dissociate and infiltrate the myocardium, misfolding and forming amyloid plaques. This toxic infiltrative cardiomyopathy leads to myocardial stiffness, necrosis, diastolic dysfunction, and heart failure.

The first speaker, Omar Abou Ezzedine, MD, proposed that the ATTR cardiac amyloidosis prevalence rate among HFpEF patients is 6.5% to 7%. The prevalence is suspected to be even higher among African Americans because of the higher frequency of ATTR genetic variants (V122I) among this population. Interestingly, this gene variant is detectable through 23andMe genetic testing.

Frederick Ruberg, MD, discussed symptomatology and diagnostic considerations in his presentation “Making the Diagnosis in Your Practice: From History to Diagnostic Testing”. Interestingly, many non-cardiac symptoms may predate heart failure, such as carpal tunnel, spinal stenosis and peripheral neuropathy. Low voltage ECG in the presence of increased ventricular mass and/or persistently elevated cardiac biomarkers might also raise suspicion. Unfortunately, diagnosis of ATTR is often delayed as etiology may be confused with other causes of HFpEF.

The 2019 Heart Failure Association of the European Society of Cardiology expert consensus recommendations for diagnosis of HFpEF provide a new, stepwise approach to diagnosis. Included in these recommendations are details regarding scintigraphy to identify cardiac amyloidosis. In addition, the American Society of Nuclear Cardiology recently announced a multi-societal expert consensus recommendation for “Multimodality Imaging in Cardiac Amyloidosis.”

Lastly, Daniel Judge, MD, discussed “Medications for ATTR Amyloid Cardiomyopathy: Ready for Prime Time!” Judge emphasized 2 particular classes of drugs that appear to be beneficial.

Between Sessions

Recently approved by the FDA for the treatment of cardiomyopathy caused by ATTR, tafamidis stabilizes the TTR tetramer slowing the formation of amyloid. Patisiran is currently FDA approved for the treatment of polyneuropathy of hereditary transthyretin-mediated amyloidosis and is a double-stranded siRNA that causes degradation of TTR mRNA. The APOLLO-B clinical trial is currently underway to evaluate Patisiran’s efficacy in ATTR with cardiomyopathy. Unfortunately, these medications are expensive resulting in “financial toxicity.” -ASAfter this session, I walked over to the puppy exhibit where I found a variety of 12-week-old puppies frolicking. Two, in particular, caught my eye. I named one AFFIRM and the other RACE2.

I walked through an afternoon poster presentation with a coffee in my hand. Robust academic debate and discussion filled the atmosphere. One poster entitled “The Relationship Between Atrial Fibrillation and Coffee” caught my attention. Here, I met Nandini Mehra, MD, a third-year internal medicine resident from Mayo Clinic who hopes to pursue a career as a cardiac electrophysiologist.

Mehra chose to study this topic because her newly diagnosed atrial fibrillation (AF) patients often ask her if they should stop drinking coffee. She explained that there are “lots of studies in the past going both ways.”

Utilizing data from the Multi-Ethnic Study of Atherosclerosis (MERA), a publicly available database, she found that drinking coffee correlates with an increased incidence of atrial fibrillation. The strongest association was among those who drink 1 or more cups of coffee per week. In her subgroup analysis, she found the strongest increase in hazard ratio among those who drink 6 or more cups of coffee per day.

When asked if she had any recommendations for coffee drinkers like myself, she said, “Everything in moderation. This is not necessarily a causative relationship but it should make us think a little more about what we are putting into our bodies.”

Atrial Fibrillation

We also discussed the potential role of confounding factors like stress. Mehra admitted “I love coffee. I did start decreasing the amount of coffee I was drinking while working on this project. I was in the 6+ category per day but now down to a cup per day.” I found this study to be both interesting and thought-provoking but the data is not yet convincing enough for me to give up coffee. -ASNext, I attended “The Future of AF is Now — How Do I Answer My Patient’s New Questions?” headed by Paul Wang, MD. Wang discussed his approach to arrythmia detected on a wearable device. A variety of devices with the capability to detect arrhythmias are now available. The Apple Heart Study, which examined 400,000 patients with Apple Watches, showed that wearable devices have the ability to safely detect heart rate irregularities confirmed to be AF. Most work with an optical sensor that detects pulse waveform—newer watches have the ability to provide electrocardiograms.

Subclinical AF detection has increased with the use of wearable and implantable detection devices. The ASSERT and Ancillary MOST trials demonstrate that subclinical AF is associated with future clinical AF.

Studies have also demonstrated that subclinical AF is associated with future stroke. However, it is still unclear at what point these patients should be anticoagulated. Duration, frequency of episodes and concomitant risk factors should be considered. Wang voiced his own opinion during the presentation, which is that anticoagulation should be considered in these patients.

The AHA recently released a Scientific Statement, “Subclinical and Device-Detected Atrial Fibrillation: Pondering the Knowledge Gap,” which provides insight regarding prevalence, clinical significance and management of subclinical atrial fibrillation.

Next, Christine Albert discussed the role of lifestyle and risk factor modification in AF. Hypertension, body mass index, exercise, alcohol, and smoking are modifiable risk factors. Optimization of these risk factors can actually decrease the incidence and burden of atrial fibrillation, even among patients at higher risk of developing atrial fibrillation due to non-modifiable risk factors like age, genetics and Caucasian ethnicity.

Hypertension and body mass index are the biggest contributors. Even mild elevations in systolic blood pressure are associated with an increased risk of AF. For example, a patient with a systolic BP of 130 has a 37% higher risk of AF. Several large prospective cohort studies demonstrated that every kilogram increase in body weight increases the risk of AF by 5%. In 2017, Genetic Obesity and the Risk of Atrial Fibrillation — Causal Estimates from Mendelian Randomization, published in Circulation analyzed 7 prospective cohorts and determined that a causal relationship exists between BMI and AF incidence. In addition, it has been found that women who were overweight were more likely to present with persistent AF, which has worse health outcomes than paroxysmal AF.

Alcohol use is protective against cardiovascular disease but has been associated with an increased risk of AF. Albert recommended that we decrease alcohol intake to less than 2 drinks per day to reduce AF risk. Moderate exercise also decreases AF risk independent of its effects on blood pressure and weight. However, vigorous exercise has been associated with an increased risk of AF.

I believe that we should have a discussion with every AF patient regarding healthy lifestyle modifications. I hope that by doing this we can improve AF incidence, burden, symptoms, response to ablation and perhaps even drive more positive morbidity outcomes for these patients.

Although it had been a long weekend, I walked out of the AHA Scientific Sessions conference feeling excited about everything I have learned and the current state of cardiology research. Experiencing the 2019 AHA Scientific Sessions provided me with a new appreciation for research and its life-altering implications. I would also like to thank MD Mag for providing me with the opportunity to experience this conference and share my knowledge. -AS