Skip main navigation

Circulation on the Run: January 9, 2024

  • Carolyn S.P. Lam, MBBS, PhD orcid
  • W. Gregory Hundley, MD orcid
  • Peder L. Myhre, MD, PhD orcid
Originally published 10.1161/podcast.20240108.684387

Dr. Greg Hundley:

Welcome listeners, to this January 9th issue of Circulation on the Run. I am one of your co-hosts, Dr. Greg Hundley, Associate Editor, Director of the Pauley Heart Center at VCU Health in Richmond, Virginia.

Dr. Peder Myhre:

And I'm the other co-host, Dr. Peder Myhre from Akershus University Hospital at the University of Oslo, Norway.

Dr. Greg Hundley:

Peder, this week's feature discussion is very germane to the world of athletics, and the feature discussion is going to be investigating sudden cardiac death in the United States NCAA or National Collegiate Athletic Association. We'll have a follow-up, a cohort over 20 years, so very interesting feature. But before we get to that, how about we grab a cup of coffee and jump into some of the other articles in the issue?

Dr. Peder Myhre:

Yes. Let's go, Greg. Do you want to go first today?

Dr. Greg Hundley:

Absolutely. Peder, our first paper today is a clinical focus and is going to address preeclampsia, which shares numerous risk factors with cardiovascular diseases. In here this team in association with corresponding author Lucas Bacmeister from the University Heart Center of Freiburg, aimed to assess the potential utility of high sensitivity cardiac troponin I values during pregnancy in predicting preeclampsia occurrence and to accomplish this, they measured high sensitivity troponin I levels in 3,721 blood samples from 2,245 pregnant women from four international prospective cohorts.

Three analytical approaches were employed. One, a cross-sectional analysis of all women using a single blood sample. Two, a longitudinal analysis of high sensitivity cardiac troponin I trajectories in women with multiple samples and then finally three, an analysis of prediction models incorporating high sensitivity cardiac troponin I, maternal factors, and the soluble FMS like tyrosine kinase-1 placental growth factor ratio.

Dr. Peder Myhre:

Oh, nice, so more data on this beautiful biomarker, high sensitivity troponin and now in patients who have experienced preeclampsia. So what did they find, Greg?

Dr. Greg Hundley:

Yes, Peder. So women with high sensitivity cardiac troponin I levels in the upper quarter had higher odds ratios for preeclampsia occurrence compared to women with levels in the lower quarter. Associations were driven by preterm preeclampsia and remain significant when using high sensitivity cardiac troponin I as a continuous variable adjusted for confounders.

Now also, a series of prediction models were constructed and as assessed by likelihood ratio tests the addition of high-sensitivity cardiac troponin I to each prediction model significantly improved the respective prediction model overall that did not incorporate high-sensitivity troponin I, particularly for those with preterm preeclampsia.

So Peder, these exploratory findings uncover a potential role for high-sensitivity cardiac troponin I as a complementary biomarker in the prediction of preeclampsia. Following validation in prospective studies, high-sensitivity cardiac troponin I alongside maternal factors may either be considered as a substitute for angiogenic biomarkers in healthcare systems where they are sparse or unavailable or as an enhancement to establish prediction models utilizing angiogenic markers.

Dr. Peder Myhre:

Nice. So, troponin again proves as a very strong risk predictor in now-imprint preeclampsia. Very nice summary, Greg thank you. And now we're going to talk about primary aldosteronism because Greg, Renin-independent aldosteronism refers to production of aldosterone from one or both adrenal glands, independent of regulation by renin and angiotensin II, which results in appropriate activation of the mineral corticoid receptor MR and its downstream consequences. And we typically think of this in patients with hypertension, but primary aldosteronism also leads to higher risk of adverse cardiovascular outcomes compared with essential hypertension, even independent of blood pressure. And growing evidence suggests that milder and subclinical forms of aldosteronism are highly prevalent, yet their contribution to cardiovascular disease is not well characterized until this large population-based study from the CARTA gene cohort in Quebec Canada, which comes to us from corresponding author Gregory Hundemer from University of Ottawa. And these investigators measured aldosterone, renin and the aldosterone to renin ratio in 1,284 participants aged 40 to 69 years and associated this with the following measurements of cardiovascular health. So first arterial stiffness and then adverse cardiac remodeling captured via cardiac magnetic resonance imaging and finally incident hypertension.

Dr. Greg Hundley:

Very interesting. So evaluating Peder, the renin-angiotensin-aldosterone axis, and then looking at long-term outcomes pertaining to cardiovascular health of which some are going to be subclinical in nature. So what did they find?

Dr. Peder Myhre:

Yes, exactly. So at baseline, the mean blood pressure was a 123 over 72 millimeters mercury, and 57% of patients had established hypertension. And there was a higher aldosterone to renin ratio indicative of renin independent aldosteronism, so that is subclinical primary aldosteronism. And this was associated with increased arterial stiffness and with adverse cardiac remodeling including increased left atrial volume, left ventricular mass and higher aldosterone renin ratio was also associated with the higher odds of left ventricular hypertrophy and a higher odds of developing incident hypertension with an odds ratio of 1.3. And all the aforementioned associations were consistent when assessing participants with normal blood pressure in isolation and consistent when adjusting for baseline blood pressure.

So, to conclude independent of brachial measured blood pressure, a biochemical phenotype of subclinical primary aldosteronism is negatively associated with cardiovascular health, including greater arterial stiffness, adverse cardiac remodeling and incident hypertension.

Dr. Greg Hundley:

Very nice Peder. What a great study and beautiful description. And now Peder, we're going to switch and review a study that is going to evaluate hypertrophic cardiomyopathy. And Peder, as we know, hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy and is classically caused by pathogenic or likely pathogenic variants in genes encoding for sarcomere proteins. Now not all subclinical variant carriers will manifest clinically overt disease as penetrance. So the proportion of gene positive who developed disease is variable, it's age dependent and not reliably predicted. So this team in association with corresponding author Carolyn Ho from Brigham and Women's Hospital performed a systematic search of the literature employed random effects generalized linear mix model meta analyses to contrast the cross-sectional prevalence and penetrance of sarcomere genes in two different contexts.

First, clinically based studies on patients and families with hypertrophic cardiomyopathy versus population community-based studies. And then second, longitudinal family clinical studies were also analyzed to investigate the rate of phenotypic conversion from some clinical to overt hypertrophic cardiomyopathy during the follow-up period.

Dr. Peder Myhre:

Okay, so we are going to learn about the relationship between the phenotype and the genotype in hypertrophic cardiomyopathy. What did they find?

Dr. Greg Hundley:

Right, so Peder penetrance varied from 32% for myosin light chain to 55% for myosin binding protein C to 60% for troponin T and troponin I and 65% for myosin heavy chain or MYH7 as we often read about. Now, population-based genetic studies demonstrated that pathogenic or likely pathogenic sarcomere variants are present in the background population, but at a low prevalence of less than 1%. The penetrance of hypertrophic cardiomyopathy and incidentally identified pathogenic or likely pathogenic variant carriers was also substantially lower, approximately 11%, ranging from 0% in the Atherosclerosis Risk In Community study or ARIC to 18% in the UK Biobank. And then finally Peder in longitudinal family studies, the pooled phenotypic conversion across all genes was 15% over an average of eight years of follow-up starting and beginning at a mean age of 16 years.

So Peder, what can we conclude? Well from this research, the penetrance of pathogenic and likely pathogenic variants is highly variable and influenced by currently undefined and context-dependent genetic and environmental factors. And therefore additional longitudinal studies are needed to improve understanding of true lifetime penetrance in families and in the community, and to identify drivers of the transition from subclinical to overt clinically expressed hypertrophic cardiomyopathy.

Dr. Peder Myhre:

Nice, that was really interesting to learn about. And thank you for summarizing that, Greg. And now we're going to move into preclinical science and talk about endothelial cells because Greg, as you know, endothelial cell damage and loss leads to cardiovascular diseases such as atherosclerosis, hypertension, and limb ischemia. And generation of new endothelial cells, either through proliferation or differentiation from endothelial progenitor cells provides the building blocks to promote vascular repair and tissue regeneration. And in large vessels such as arteries, endothelial cell proliferation has been hard to study due to their infrequent proliferation. And these investigators led by co-corresponding authors, Dr. Zhou and He from Shanghai in China, developed a novel genetic system for temporally seamless recording of endothelial cell proliferation in vivo in order to enhance our understanding of these endothelial cells in greater arteries.

Dr. Greg Hundley:

Oh Peder, really great description. So what did they find?

Dr. Peder Myhre:

So they made three main findings. So first their tracing reveals that 3% approximately of aortic endothelial cells undergo proliferation per month in adult mice during homeostasis. Second, they also demonstrate that the orientation of aortic endothelial cell division is generally parallel to the direction of blood flow. And finally they show that endothelial cell proliferation is significantly increased in diseases such as hypertension or Type II diabetes. And this may be a new therapeutic target for treating endothelial damage in these diseases.

Dr. Greg Hundley:

Oh, great description, Peder. Well, we've got some other articles in the mailbag and first Peder, there's an exchange of letters between Professors Čulić and Liu regarding the article, “Extreme Temperature Events, Fine Particular Matter, and Myocardial Infarction Mortality.” Also, there's an ECG Challenge from Professor Raposo Salas: “Is It a Twofer?” And then next Molly Robbins, just fantastic. And she's got Highlights from our Circulation Family of Journals in November and it highlights the following: First among young patients with hypertrophic cardiomyopathy and association of storage disease and pre-excitation, and that is reported in Circulation Arrhythmia and Electrophysiology; next, the associations of coronary and cerebrovascular, microvascular dysfunction, heart failure and cognitive dysfunction are reported in Circulation Heart Failure. Next, the incorporation of cost-effectiveness evaluations in clinical cardiology guidelines is reported in Circulation Cardiovascular Quality and Outcomes.

Following this, investigators report an association of pericardial enhancement on cardiac MRI after cardiac surgery with low-grade inflammation. And that is reported in Circulation Cardiovascular Imaging. And then finally, there's an analysis of cardiac CT characteristics prior to redo TAVR for the risk of coronary occlusion and that is reported in Circulation Cardiovascular Interventions.

Dr. Peder Myhre:

Thank you, Greg. Then there is a Research Letter from Dr. Dickfeld entitled “Baseline-Twelve-Lead ECG Characteristics in Genetically Modified Porcine Cardiac Xenotransplants.” And finally, we have this very nice collection of papers, a new series entitled Centennial Collection, and that is really celebrating that the American Heart Association is 100-years-old this year in 2024. So to start this off, no other than Eugene Braunwald is summarizing the advances in cardiology during the past century. So this is a must read. But now Greg, do you want to move on to the feature discussion?

Dr. Greg Hundley:

You bet.

Dr. Spencer Carter:

Welcome listeners to this week's feature discussion for Circulation on the Run. I'm your host Dr. Spencer Carter, and I'm a Cardiology Fellow at UT Southwestern in Dallas. I am joined by the corresponding author for our paper today, Dr. Kimberly Harmon. She is a Professor of Family Medicine and Sports Medicine and also Head Football Physician at the University of Washington. We have the pleasure of having her joining us today. We are also joined by our Handling Editor, Dr. Mark Link, also from the University of Texas Southwestern, welcome to you both.

Dr. Kimberly Harmon:

Thank you.

Dr. Mark Link:

Thank you.

Dr. Spencer Carter:

So today we will discuss the key findings of a paper in the sports medicine realm, talking specifically about cardiac arrest in NCAA athletes. It is a 20-year study looking at sudden cardiac death in this population and it was published in this week's issue of Circulation. The study sought to answer questions involving the etiology of these cardiac arrests. And Kim, would you mind walking us through some background on your paper?

Dr. Kimberly Harmon:

Yeah, I first became interested in this topic actually in 2001 after one of my women's basketball players had a sudden cardiac arrest. And the first question I asked myself was like, oh my gosh, what did I miss? And the second one was, how often does this happen? And at the time there wasn't a lot out there, or at least it was suggested that it was very infrequent. And so that sort of began sort of this odyssey that really has resulted in this paper and two previous papers that we published in Circulation, the 5-year results in the 10-year results as well. And what we found is that sudden cardiac arrest is really more common than certainly was thought 20 years ago, occurs about 1 in 50,000 overall. But if you look into subgroups, in particular men or males and black athletes and in certain sports and particular basketball and football seems to occur more frequently in those. And so that was sort of findings that have been consistent through the years.

What was interesting and unique about this particular paper is that we've seen over the last 10 years that the rate of sudden cardiac death in athletes has gone down. So that was an interesting finding.

Dr. Spencer Carter:

And that's definitely good news. And this is a topic that hits home close to my heart, no pun intended as a former college athlete. So I'm going to involve Dr. Link in this part as well. But I'd like to move on to the study design and methods. Can you tell us a little bit about how you arranged the study and how you looked at the data?

Dr. Kimberly Harmon:

Yeah, so the first four years of data are actually in retrospective looking at media reports and then looking at a database that the NCAA creates called the Resolutions Database and once an NCAA athlete dies of any cause, their school reports it to the NCAA and at the convention they have a moment of silence for them. And so we look at this list and try and find what everybody died from. If we don't know or if it appears to be cardiac, we requested autopsies. We also did systematic media reports, and in this particular paper collaborated with the National Center for Catastrophic Sports Injury Research, which also keeps the database of sudden cardiac death and arrest. And we get claims data, insurance claims data from the NCAA on if an athlete dies, they're entitled to death benefit. And so those that have died from sudden cardiac arrest, they report those numbers to us.

And so we have different sources of case identification to try and make sure that we get them all. As I said, the first four years was retrospective in nature, but since then it's been prospective in nature and so we look at these cases as they come along.

Dr. Spencer Carter:

That's super interesting. Now, did you guys find that you were able to get all of the information that you were looking for or do you think that there was something that you would've liked to have that for some reason wasn't available?

Dr. Kimberly Harmon:

Well, you need two things to get a good incidence rate, you need a numerator and you need a denominator. When the NCAA, one of the real advantages of using that population for this type of research is that we have a great denominator. So we know how many people there are, we know if they're male or female, we know what sport they are and we actually know what race they are and that ethnicity. And so it's a very rich database in terms of denominator. The numerator is a harder thing to get at and so, or case identification. And so there's no mandatory reporting in the United States of sudden cardiac arrest or death. There has been in the NCAA for the last five years or so, and that data goes to the NCCSIR. And so, we use multiple sources in to try and get the numerator, but I'm sure that there's cases that we missed even though we got as many as we could and we had multiple sources. And so if anything, these numbers are an underestimate.

Dr. Spencer Carter:

Yeah, certainly. And so the other thing I wanted to know, it's obviously a very tragic event when a collegiate athlete or any athlete experiences a cardiac arrest. And I'm going to involve Dr. Link here. And just to ask, because he's also an expert in this field, when you hear that an athlete has had sudden cardiac arrest, whether it be on the field at practice, what are some things that go through your head in terms of potential etiologies for that?

Dr. Mark Link:

Well, this paper's a very nice paper on that. I mean, traditionally it was thought that hypertrophic cardiomyopathy was the most common, but I think more and more data is showing us that that's actually not the most common anymore. And it's a mix and you always worry or wonder about what the underlying heart disease is, and there has to be a complete evaluation of the survivor. And if they die, they should have an autopsy also in order to try to figure out what they had and screen their family members for it.

Dr. Kimberly Harmon:

Mark, you make a really good point and that they need an autopsy to try and figure out the cause. And our system of autopsies and coroners in the United States is a patchwork and it's less than ideal. And so there's limitations in terms of what you can do with some autopsy data because they may not have the expertise to really get down to the exact cause. But this is the best that we could tell from what was reported. We have autopsy data.

Dr. Mark Link:

Yeah, no, and I think genetic testing is very useful also. And the problem with genetic testing is insurances won't pay for genetic testing for a dead person. So if they make it to the hospital, you should send off genetic testing as quickly as possible.

Can I ask a question of Kim, because I'm intrigued by this. First of all, great study, I loved it, but the way I see there's actually three explanations for this decrease in sudden cardiac death, and I'm curious to hear your opinion about this. I mean, one is that it's actually decreased, it's possible. The second is that screening has decreased it, which I kind of doubt, but what I think is that we're so much better at resuscitation and that more people are resuscitated and then they won't make it into the database because as I understand from you, because we've talked about this, it doesn't include the resuscitated athletes, it only includes the dead athletes. So what do you think is accounting for this?

Dr. Kimberly Harmon:

I think that you're exactly right. That the primary reason we've seen a decrease is probably improved resuscitation. Not only improved resuscitation, but improved recognition of sudden cardiac arrest because used to be an athlete went down and you're like, oh, it's like a seizure, they passed out. And now sort of the first thing you should think of when an athlete is unconscious rapidly is that it's sudden cardiac arrest until proven otherwise. So I think there's better recognition. Certainly the emergency action plan is now required by the NCAA. We practice it every year, and so there's more access to defibrillators. So survival is more likely with quick access to defibrillation. And so I think that probably the most likely reason is because of improved resuscitation.

As you know, I'm an advocate of screening and I would like to think that it's improved screening, but we don't know that yet. And so our next project is going to be to try and look at the sudden cardiac arrest aspect of this in addition to the sudden cardiac death.

Dr. Spencer Carter:

All of this is super interesting. And so I know we have touched on the results a little bit, but Kim, just for our listeners, would you mind outlining for us some of your key findings in this study?

Dr. Kimberly Harmon:

So the key findings are that the overall incidence of sudden cardiac arrest in an NCAA athlete is 1 in 63,000. That is different and less than we saw in our previous studies, and that there are still high risk groups that persist. And those high risk groups are males, black athletes, and athletes in certain sports. And those sports are basketball and football and particularly male basketball players seem to be at a high risk. And the next question should likely be why is that? And I have no idea. And if anybody can figure that out, that would be great, but that's another thing that we need to look at in the future. And I think when we look at incidents, sometimes people want to say the incidence is this, but we really have to understand that there's certain high risk groups, and so it's inaccurate.

So if I was to say the risk of breast cancer for people is 1 in 16, that underestimates the risk of breast cancer in women and overestimates the risk of breast cancer in men. And the same thing can happen with sudden cardiac arrest if we don't get down to those subgroups where there's vastly different rates between women and men. And so I think that we need to have that granular information.

Dr. Spencer Carter:

Yeah, certainly. So very interesting that that specific demographic, black male basketball player seems to be the most likely to have cardiac arrest. And correct me if I'm wrong, but it sounds like that has been shown in prior studies as well that that specific demographic is at higher risk. And I'm sure we could speculate on many potential reasons for that. But I wanted to ask you, other than that demographic, are there any other racial or sports demographics in particular that you noticed any significantly increased risk in?

Dr. Kimberly Harmon:

So football's higher as well. Then after that we start to get into track and field sort of athletes. The highest female sport is female cross country. And I guess when you start thinking about when you screen how aggressively you should screen, part of the question becomes do you screen everybody and sort of no persons left behind or do you screen your high-risk groups? And there's all sorts of different ethical questions about that and things, but people have different risk thresholds as well. One in 10,000 is a lot, but you take that risk if you ride motorcycles. And so people's risk thresholds are different. And so I think that all goes into the mix when sort of figuring out whether something is high or low. And then you also need resources if you're going to screen, you need somebody that can do it correctly. And so there's a lot of factors to consider.

Dr. Spencer Carter:

Certainly. And I'm sure particularly the screening, seems like it would be more extensive for collegiate athletes, especially in the NCAA than say high school athletes. And so to Mark's point earlier, have we gotten better with that screening? Have we gotten better with resuscitation? Do you think that that accounts for the decrease that we've seen in sudden cardiac death over time?

Dr. Kimberly Harmon:

I think the resuscitation for sure, the screening question is out there because we've been screening. NCAA athletes, they're required to be screened. We've been screening with history and physical, most Power Five or highly resourced schools will add ECG to that, but not all. And so there's a real question whether we do a better job one way or another and the jury's out in that and this study doesn't answer that.

Dr. Spencer Carter:

Yeah, certainly. And then one additional question I had, and Mark, feel free to respond to this as well. Do you think that the exercise or the nature of exercise that these athletes are doing in any way contributes to their likelihood of having a cardiac arrest?

Dr. Kimberly Harmon:

When we think about etiology, one of the things, the most frequent cause was autopsy negative, sudden unexplained death. So a pathologically normal heart, which we think is likely electrical disease. But the second most common thing is idiopathic left ventricular hypertrophy with fibrosis. And so that doesn't meet the definition of hypertrophic cardiomyopathy. But these may have been things that were, we don't know what this represents. Is this physiologic? Is it from the type of exercise that people do? Is it undeclared cardiomyopathy? We don't have genetic testing as Mark mentioned on most of these things. So we don't know whether it's congenital or acquired or what this represents and that's another area that we need to sort of delve into further. But Mark, getting back to the type of exercise contributes to the higher risk. I'm interested in your thoughts.

Dr. Mark Link:

We have a lot of studies that show exercise is beneficial for you. I mean, if you look at quartiles, the most active quartile always has the lowest mortality, but there is a signal that over exercising, and that's unusual I think, can actually be harmful to the heart and certainly increase the risk of a-fib. So I'd hate people to go away from this thinking exercise is harmful to you because that's not what we've seen in all of our studies. That exercise is beneficial. And I'd want people to go away from this thinking that.

Dr. Kimberly Harmon:

100% agree, exercise is medicine, it's great for you. And the question still is sort of why we see this signal in both white and black basketball players.

Dr. Spencer Carter:

So it sounds like in summary, the incidence of sudden cardiac death has decreased over time, and we talked about potential reasons for that. It also sounds like male sex, black race and basketball in particular are associated with a higher incidence of sudden cardiac death related to the sport. Are there any other key takeaways that you think that we should come away from this paper knowing, and are there any implications that you want to emphasize for how we take care of these athletes testing that should be done prior to competition or evaluation when these events happen?

Dr. Kimberly Harmon:

So let me take the first part of that question first in terms of if there's any other points. I think one of the interesting things that we found in the study is that we didn't see a big increase in cardiac deaths in athletes due to myocarditis. And so there's been a lot of concern with that, particularly at the beginning of the pandemic, whether this was going to cause a lot of problems. And after 2020, there's one death due to myocarditis, and that was giant cell myocarditis, so not related to COVID. And so I think another important takeaway, at least the data went to June of 2022. So at least from January or February 2020 when the COVID pandemic started to the time we stopped collecting data, we didn't see an increase in deaths due to myocarditis in athletes. And so I think that that was another interesting point.

Your second question was whether this had implications on the way we take care of athletes. I think that the importance of emergency action plans and recognizing sudden cardiac arrest is highlighted in this for sure, and that's going to get the people that have witnessed arrest, right? But half of these athletes still died not when they were exercising or within an hour of exercise, they died at rest or in their sleep. So those are the ones that are least likely to be resuscitated, we think, because it's not witnessed. And so that's where I think screening might potentially come in. So I think that studies have shown that ECG is much more likely to detect abnormalities if they're present. And so if the resources are available to add ECG screening, it is my opinion that it should be added. That is Kim's opinion. Other people have other opinions.

Dr. Mark Link:

I want to thank Kim for sending this. This is a fantastic paper for Circulation. And if you look at figures 1 and 3, they'll be included in every presentation on athletes for the next five years.

Dr. Kimberly Harmon:

Like the ones from the 2011 article, which is a 5-year article, is my most cited article ever because people included that figure for a lot and this is a better figure.

Dr. Mark Link:

Yeah, we'll all be seeing this figure hundreds of times.

Dr. Kimberly Harmon:

Well, I really appreciate you guys taking this article.

Dr. Spencer Carter:

Well, Kim's opinion is what we're here for. So thank you so much for offering that. This has been an amazing discussion on a very thought-provoking paper. So thanks to you both, Dr., Kimberly Harmon, Dr. Mark Link. We appreciate you joining us today. And for our listeners, thank you so much for tuning in to this week's episode of Circulation on the Run. On behalf of Carolyn Lam, Greg Hundley and Peder Myhre, I'm Dr. Spencer Carter, your host, and we can't wait to have you join us for next week's episode. You can read more about this paper and this week's publication of Circulation.

Dr. Peder Myhre:

This program is copyright of the American Heart Association 2024. The opinions expressed by speakers in these podcasts are their own, and not necessarily those of the editors or of the American Heart Association. For more, please visit ahajournals.org.

{ "id": "main-menu", "list": [ { "text": "AHA Journals", "list": [ { "text": "AHA Journals Home", "link": "/" }, { "text": "Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB)", "list": [ { "text": "Journal Home", "link": "/journal/atvb" }, { "text": "Current Issue", "link": "/toc/atvb/current" }, { "text": "See All Issues", "link": "/loi/atvb" } ] }, { "text": "Circulation", "list": [ { "text": "Journal Home", "link": "/journal/circ" }, { "text": "Current Issue", "link": "/toc/circ/current" }, { "text": "See All Issues", "link": "/loi/circ" } ] }, { "text": "Circ: Arrhythmia and Electrophysiology", "list": [ { "text": "Journal Home", "link": "/journal/circep" }, { "text": "Current Issue", "link": "/toc/circep/current" }, { "text": "See All Issues", "link": "/loi/circep" } ] }, { "text": "Circ: Genomic and Precision Medicine", "list": [ { "text": "Journal Home", "link": "/journal/circgen" }, { "text": "Current Issue", "link": "/toc/circgen/current" }, { "text": "See All Issues", "link": "/loi/circgen" } ] }, { "text": "Circ: Cardiovascular Imaging", "list": [ { "text": "Journal Home", "link": "/journal/circimaging" }, { "text": "Current Issue", "link": "/toc/circimaging/current" }, { "text": "See All Issues", "link": "/loi/circimaging" } ] }, { "text": "Circ: Cardiovascular Interventions", "list": [ { "text": "Journal Home", "link": "/journal/circinterventions" }, { "text": "Current Issue", "link": "/toc/circinterventions/current" }, { "text": "See All Issues", "link": "/loi/circinterventions" } ] }, { "text": "Circ: Cardiovascular Quality & Outcomes", "list": [ { "text": "Journal Home", "link": "/journal/circoutcomes" }, { "text": "Current Issue", "link": "/toc/circoutcomes/current" }, { "text": "See All Issues", "link": "/loi/circoutcomes" } ] }, { "text": "Circ: Heart Failure", "list": [ { "text": "Journal Home", "link": "/journal/circheartfailure" }, { "text": "Current Issue", "link": "/toc/circheartfailure/current" }, { "text": "See All Issues", "link": "/loi/circheartfailure" } ] }, { "text": "Circulation Research", "list": [ { "text": "Journal Home", "link": "/journal/res" }, { "text": "Current Issue", "link": "/toc/res/current" }, { "text": "See All Issues", "link": "/loi/res" } ] }, { "text": "Hypertension", "list": [ { "text": "Journal Home", "link": "/journal/hyp" }, { "text": "Current Issue", "link": "/toc/hyp/current" }, { "text": "See All Issues", "link": "/loi/hyp" } ] }, { "text": "Journal of the American Heart Association (JAHA)", "list": [ { "text": "Journal Home", "link": "/journal/jaha" }, { "text": "Current Issue", "link": "/toc/jaha/current" }, { "text": "See All Issues", "link": "/loi/jaha" } ] }, { "text": "Stroke", "list": [ { "text": "Journal Home", "link": "/journal/str" }, { "text": "Current Issue", "link": "/toc/str/current" }, { "text": "See All Issues", "link": "/loi/str" } ] }, { "text": "Stroke: Vascular and Interventional Neurology", "list": [ { "text": "Journal Home", "link": "/journal/svin" }, { "text": "Current Issue", "link": "/toc/svin/current" }, { "text": "See All Issues", "link": "/loi/svin" } ] }, { "text": "AIM: Clinical Cases", "link": "/aimcc" } ] }, { "text": "Journal Information", "list": [ { "text": "About ", "link": "/podcasts/about" }, { "text": "Editorial Board", "link": "/podcasts/editorial-board" }, { "text": "Reprints", "link": "/commercial-reprints" }, { "text": "Customer Service and Ordering Information", "link": "/custserv" }, { "text": "AHA Journals RSS Feeds", "link": "/feeds.jsp" }, { "text": "For International Users", "link": "/international-users" }, { "text": "Institutions/Librarians FAQ", "link": "/custserv/institutionalFAQ" }, { "text": "Subscriber Help", "link": "/custserv/help" } ] }, { "text": "All Issues", "link": "/loi/podcasts", "className": "wide_dropdown_list", "list": [ { "content" : true } ] }, { "text": "Subjects", "list": [ { "text": "Arrhythmia and Electrophysiology ", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=arel" }, { "text": "Basic, Translational, and Clinical Research", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=btcr" }, { "text": "Critical Care and Resuscitation", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=ccr" }, { "text": "Epidemiology, Lifestyle, and Prevention", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=elp" }, { "text": "Genetics", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=gen" }, { "text": "Heart Failure and Cardiac Disease", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=hfcd" }, { "text": "Hypertension", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=hyp" }, { "text": "Imaging and Diagnostic Testing", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=idt" }, { "text": "Intervention, Surgery, Transplantation", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=ist" }, { "text": "Quality and Outcomes", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=qo" }, { "text": "Stroke", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=str" }, { "text": "Vascular Disease", "link": "/browse/podcasts?taxonomyUri=hwp-journal-coll&tagUri=vasc" } ] }, { "text": "Features", "list": [ { "text": "Bridging Disciplines", "link": "/browse/circ?taxonomyUri=featured&tagUri=bridging-disciplines" }, { "text": "Circulation at Major Meetings", "link": "/circ/circ-major-meetings" }, { "text": "Special Themed Issues", "link": "/circ/special-themed-issues" }, { "text": "Guidelines Put Into Perspective", "link": "https://www.ahajournals.org/circ/guidelines-perspective" }, { "text": "Circulation Supplements", "link": "/circ/supplements" }, { "text": "Cardiovascular Case Series", "link": "/browse/podcasts?taxonomyUri=features-menus&tagUri=circ-cv-case-series" }, { "text": "ECG Challenge", "link": "/browse/podcasts?taxonomyUri=features-menus&tagUri=circ-ecg-challenge" }, { "text": "Hospitals of History", "link": "/circ/hospitals-history" }, { "text": "On My Mind", "link": "/browse/podcasts?taxonomyUri=features-menus&tagUri=circ-on-my-mind" }, { "text": "Podcast Archive", "list": [ { "text": "Circulation on the Run", "link": "/circ/podcasts" }, { "text": "Subscribe to Circulation on the Run", "link": "/circ/subscribe-circulation-run" }, { "text": "#FITFAVES", "link": "/circ/fitfaves" } ] }, { "text": "Circulation Doodle", "link": "/circ/circulation-doodle" } ] }, { "text": "Resources & Education", "list": [ { "text": "AHA Guidelines and Statements", "link": "https://professional.heart.org/en/guidelines-and-statements", "target": "_blank" }, { "text": "Circulation CME", "link": "/circ/cme" }, { "text": "Information for Advertisers", "link": "https://www.wolterskluwer.com/en/solutions/lippincott-hcp-access/media-kits/circulation", "target": "_blank" } ] }, { "text": "For Authors & Reviewers", "list": [ { "text": "Instructions for Authors", "link": "/circ/author-instructions" }, { "text": "Submission Site", "link": "https://circ-submit.aha-journals.org/cgi-bin/main.plex", "target": "_blank" }, { "text": "AHA Journals EDI Editorial Board", "link": "/edi-editorial-board" }, { "text": "Author Reprints", "link": "/author-reprints" } ] } ] }