Mikael Rostila, PhD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Rostila: 

-  Surviving women were 25 percent and men 15 percent more likely to die from heart attack after the death of a sibling, compared to people who had not lost a sibling.

-  Increased risk of death from heart attack was four to six and a half years after the death of a sibling among women and two to six and a half years after among men.

-  No notable increased risk of heart attack occurred immediately after their siblings died.

-  If their sibling died of heart attack, the risk of heart attack death in the following years rose 62 percent among women and 98 percent among men.

JAHA: What are the major implications of this work?

Dr. Rostila: Healthcare providers should follow bereaved siblings to help recognize signs of acute or chronic psycho-social stress mechanisms that could lead to heart attack. We might be able to prevent heart attacks and other heart-related conditions by treating these siblings early on and recommending stress management.

JAHA: How did you get the idea to do this study?

Dr. Rostila: During my career I have been interested in the links between social networks and health, for instance, I wrote my thesis about social capital and health. However, it is not only the presence of a social relationship that could have severe health effects. Also the loss of a relationship could influence health. A family may be considered the simpliest form of a social network and the loss of a family member could therefore be considered a traumatic and stressful event. While previous studies have examined whether the loss of other family members might trigger myocardial infarction, the impact of grief following the loss of an adult sibling has been largely overlooked. To the extent that siblings are also beloved, provide companionship and support, one would expect that death of an adult sibling -- as much as the death of other family members (e.g. spouse, parents, children) – could be considered a stressful life event

JAHA: What was your biggest obstacle in completing this study?

Dr. Rostila: Despite the obvious strengths of the use of total population register data such data does not include detailed individual information that is required to uncover the actual causal mechanisms that link sibling deaths and myocardial infarction. Ideally, one would like to have access to biological and genetic data, detailed information on diseases from medical records, more information on shared childhood social environment and family characteristics and detailed data on personal and relational characteristics which is unfortunately not included in the registers

JAHA: What was your most unexpected finding?

Dr. Rostila: That our results suggest that this association between the loss of a sibling and having a heart attack is more likely to occur some years after bereavement. Most previous studies suggest that bereavement could trigger myocardial infarction through acute psycho-physiological stress mechanisms ("the so called broken heart syndrome"). Deaths from broken-heart usually appear within the first few hours and days after a stressful event while our findings suggests effects in the longer-term.

JAHA: What do you plan to do next, based on these current findings?

Dr. Rostila: The loss of a parent at adult ages - as a trigger of myocardial infarction - is also rarely studied. In the future we therefore aim to study whether parental loss could increase the risk of myocardial infarction in the shorter and longer-term. We are however also interested in how sibling loss influence other diseases and causes of death such as suicide, stroke, and cancer.

JAHA: What do you like to do in your free time?

Dr. Rostila: I enjoy exercise like running and going to the gym. I also enjoy travelling and experiencing new countries and cultures. I have two small children so of course I want to spend as much time as possible with them during my free time.

JAHA: What is your favorite sports team or musical group?

Dr. Rostila: In particular i follow the Swedish national team in Ice hockey and soccer since I am Swedish. My local favorite team in soccer and Ice hockey is Djurgården from Stockholm, Sweden. I enjoy all kinds of contemporary music but U2, Coldplay and Bruce Springsteen have been my favorites for a long time.

To read Dr. Rostila's full article, click here

Profile originally published April 16, 2013

Yueh Z. Lee, MD, PhD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Lee: We found that that the spatial distributions of calcifications along the aorta from different strains of apoe mice using a novel carbon nanotube x-ray based micro-computed tomography CT system. 

JAHA: What are the major implications of this work?

Dr. Lee: Our carbon nanotube based x-ray source allows improved cardiac gating as compared to conventional x-ray sources; this device offers new ways to assist researchers in evaluating cardiac pathology in difficult to image mouse models.

JAHA: How did you get the idea to do this study?

Dr. Lee: The idea was a natural synergy between two novel technologies from UNC Chapel Hill – the invention of the carbon nanotube x-ray source (Otto Zhou) and the apoe mouse (Nobuyo Maeda). As a translational imaging scientist, I sought to bring the two teams together for the project.

JAHA: What was your biggest obstacle in completing this study?

Dr. Lee: Comparing data from histological samples and 3-D CT data remains a challenge.

JAHA: What was your most unexpected finding?

Dr. Lee: The blur induced by motion was more significant than we anticipated in the mouse.

JAHA: What do you plan to do next, based on these current findings?

Dr. Lee: We are developing other clinical and pre-clinical applications of our carbon nanotube x-ray source in cardiac imaging.

JAHA: What do you like to do in your free time?

Dr. Lee: I enjoying spending my free time traveling with my family and dragon boat racing when the opportunity arises.

To read Dr. Lee's full article, click here

Profile originally published April 9, 2013

David McManus, MD, ScM

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. McManus: We examined rates of, and complications from, new-onset and prevalent atrial fibrillation (AF) in approximately 24,000 Cardiovascular Research Network participants with heart failure. We found that AF was quite common among participants with HF and that the odds of being hospitalized for HF, hospitalized for any reason, or dying were similar between those with HF and preserved systolic function vs. those with HF and reduced systolic function.

JAHA: What are the major implications of this work?

Dr. McManus: We explored the epidemiology and impact of AF in a population of patients with heart failure, further stratified by systolic function. We emphasize that AF is an important complication of HF, irrespective of HF subtype (HF with preserved vs. reduced systolic function).

JAHA: How did you get the idea to do this study?

Dr. McManus: I am a cardiac electrophysiologist interested in the epidemiology and treatment of AF, particularly in high-risk and understudied populations such as those with heart failure.

JAHA: What was your biggest obstacle in completing this study?

Dr. McManus: Familiarizing myself with the Cardiovascular Research Network, its methods and personnel seemed daunting at first. However, I had great mentorship and analytic support from coauthors and colleagues with CVRN expertise, such as Dr. Jerry Gurwitz, Robert Goldberg, and Alan Go.

JAHA: What was your most unexpected finding?

Dr. McManus: I was surprised at precisely how impactful AF was on rates of adverse events in patients with HF and preserved systolic function, even after adjusting for their age and other important comorbidities.

JAHA: What do you plan to do next, based on these current findings?

Dr. McManus: We plan to further explore the impact of AF and its treatments on the prognosis of patients with HF, and vice versa.

JAHA: What do you like to do in your free time?

Dr. McManus: I am the proud father of two energetic kids and future cardiovascular researchers, Elyse and Vivian. We like to ski and read together.

JAHA: What is your favorite sports team or musical group?

Dr. McManus: I am perhaps the most avid Patriots fan in the electrophysiology community. I was quite disappointed by the outcome of the AFC championship game.

To read Dr. McManus' full article, click here

Profile originally published April 2, 2013

David Hasan, MD

JAHA:  Tell us about the key findings from your recent article in JAHA.

Dr. Hasan:  Previously we did a retrospective analysis of a large clinical trial (ISUIA) and found that daily aspirin decreased the risk of aneurysm rupture by 60%. The current study provides evidence that aspirin attenuates inflammation of the wall of human cerebral aneurysms, which we suspect contributes to aneurysm progression to rupture. 

JAHA: What are the major implications of this work?

Dr. Hasan:  Inflammation is a strong potential cause of aneurysm rupture. Aspirin can attenuate this process leading to decreased risk of rupture.

JAHA:  How did you get the idea to do this study?

Dr. Hasan:  Growing evidence that inflammation contributes to aneurysm formation and rupture, and aspirin has anti-inflammatory effect.

JAHA:  What was your biggest obstacle in completing this study?

Dr. Hasan:  Obtaining IRB approval because of concerns that aspirin would worsen SAH if patients ruptured. Previous studies showed that aspirin does not worsen outcome in patients with SAH secondary to ruptured aneurysms.

JAHA:  What was your most unexpected finding?

Dr. Hasan:  Finding a clear effect of aspirin in a small group of patients.

JAHA:  What do you plan to do next, based on these current findings?

Dr. Hasan:  Propose a larger study to determine the effects of aspirin on inflammation in the wall of human cerebral aneurysms, using a new promising imaging protocol (ferumoxytol-enhanced MRI).

JAHA:  What do you like to do in your free time?

Dr. Hasan:  Teach my English Bulldog (Duke) how to skate.

JAHA:  What is your favorite sports team or musical group?

Dr. Hasan:  The Dallas Cowboys

To read Dr. Hasan's full article, click here

Profile originally published March 28, 2013

Gordon Tomaselli, MD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Tomaselli: This is a prospective observational study of patients who were candidates for ICD implantation for primary prevention of sudden death. These are generally stable heart failure or post-MI patients. As this is a description of the cohort the major findings are to follow. Some of the key features of this cohort are a much larger representation of non-white mostly African-American patients, a rich biorepository with all patients having blood drawn and stored at baseline and follow-up visits in addition to digital ECGs.

JAHA: What are the major implications of this work?

Dr. Tomaselli: The major implications are the development of a well phenotyped cohort to explore the utility of non-traditional biomarkers of risk such as genotype, mRNA and microRNA expression, metabolites, dynamic ECG metrics and in a subset of patients cMRI and CT imaging.  We will also have a rather long followup for this group allowing us to determine the short and long-term benefits of the ICD in this cohort.

JAHA: How did you get the idea to do this study?

Dr. Tomaselli: A well know shortcoming of primary ICD deployment are the limitations in our ability to identify patients with primary prevention indications at risk mostly likely to benefit from this invasive and expensive treatment. 

JAHA: What was your biggest obstacle in completing this study?

Dr. Tomaselli: The recent rates of use of primary prevention ICDs has slowed some either by patient or physician preference. It raises the possibility that the group enrolled may have changed over the enrollment period.

JAHA: What was your most unexpected finding?

Dr. Tomaselli: Perhaps, not totally unexpected, the preliminary data demonstrate that the overall mortality rate is greater than the appropriate shock rate by the ICD. It reinforces the concept that there are competing risks for death in this group that are not prevented by the ICD.

JAHA: What do you plan to do next, based on these current findings?

Dr. Tomaselli: We will be doing a comprehensive analysis of mortality, ICD therapy and risk once enough events are accrued. We have genotype the entire cohort and done RNA, protein, metabolic and ECG studies on the group.

JAHA: What do you like to do in your free time?

Dr. Tomaselli: Free time is in short supply, when there is any spending time with family, helping coach recreation council basketball and baseball

JAHA: What is your favorite sports team or musical group?

Dr. Tomaselli: I know you do not want to hear this: New York Yankees

Eclectic musical taste Classical to Vintage rock e.g. Clapton

To read Dr. Tomaselli's full article, click here

Profile originally published March 19, 2013

Amanda Fretts, PhD, MPH

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Fretts:  Our analysis examined the association of plasma phospholipid and dietary ALA with the development of atrial fibrillation among older adults who participated in the Cardiovascular Health Study. Our results indicate no association of either plasma phospholipid or dietary ALA on risk of atrial fibrillation.

JAHA:  What are the major implications of this work?

Dr. Fretts: The burden of atrial fibrillation is increasing as the population ages. As such, it is important to better understand factors associated with risk of developing atrial fibrillation. Although our results showed no association of ALA with atrial fibrillation among older adults who consume an American diet, this is a very important finding.

JAHA:  How did you get the idea to do this study?

Dr. Fretts: Many studies have shown that long-chain n-3 fatty acids derived from seafood, particularly eicosapantaenoic acid (EPA) and docosahexaenoic acid (DHA), are associated with a lower risk of AF. However, the relationship of ALA, a medium-chain n-3 fatty acid derived from plants and found in foods like canola oil and walnuts, is unclear. As plant-derived fatty acids are cheaper and have a greater worldwide availability than seafood, a better understanding of the relationship of ALA with atrial fibrillation is of public health importance. 

JAHA: What was your biggest obstacle in completing this study?

Dr. Fretts:  I have worked with many complex data sets in the past. However, the Cardiovascular Health Study is unique in that there were two recruitment periods (1989-1990 and 1992-1993) and many measures were collected annually. As this was my first analysis using data from the Cardiovascular Health Study, it took me quite a long time to become familiar with the data.

JAHA:  What was your most unexpected finding?

Dr. Fretts: In the Cardiovascular Health Study, fatty acids derived from fish (EPA and DHA) were associated with a lower risk of AF. As such, we expected ALA (a fatty acid derived from plants) to be associated with a lower risk of AF. Although we did not find an association of ALA and AF in this cohort, we need to examine the relationship in non-fish eating populations with other types of diets.

JAHA:  What do you plan to do next, based on these current findings?

Dr. Fretts: We’d like to examine the relationship of ALA with other cardiovascular outcomes in the Cardiovascular Health Study. Additionally, exploring the relationship of ALA and atrial fibrillation in populations with other types of diets is of interest.

JAHA: What do you like to do in your free time?

Dr. Fretts: I live in the Pacific Northwest, so when it’s not raining, I like to take advantage of living close to the mountains and spend time hiking, camping, or snowshoeing. I also enjoy gardening in the summer months. 

To read Dr. Fretts' full article, click here

Profile originally published March 12, 2013

Yoshihiko Kakinuma, MD, PhD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Kakinuma: The non-neuronal cardiac cholinergic system producing extremely more ACh by ventricular cardiomyocytes plays a beneficial role in protecting cardiomyocytes against myocardial infarction. The key mechanism is expected to render cardiomyocytes utilize more glucose and less oxygen. 

JAHA: What are the major implications of this work?

Dr. Kakinuma: Non-neuronal cardiac cholinergic system plays a role in decreasing oxygen demand by cardiomyocytes and in accelerating angiogenesis.

JAHA: How did you get the idea to do this study?

Dr. Kakinuma: From our previous study showing that cardiomyocytes synthesize ACh of their own.

JAHA: What was your biggest obstacle in completing this study?

Dr. Kakinuma: The concept that cardiomyocytes synthesize ACh is not yet well known and accepted by

others.

JAHA: What was your most unexpected finding?

Dr. Kakinuma: This engineered heart, i.e., a ChAT overexpressing heart, is resistant to no flow conditions in Langendorff apparatus and fairly easy to restart the ventricular beating after reperfusion.

JAHA: What do you plan to do next, based on these current findings?

Dr. Kakinuma: The cellular mechanisms of this non-neuronal cardiac cholinergic system should be profoundly clarified. 

To read Dr. Kakinuma's full article, click here

Profile originally published March 5, 2013

Alka Kanaya, MD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Kanaya: We found that brachial artery flow mediated dilation (FMD) results differed from endothelial function biomarkers for those with pre-diabetes.  While biomarkers of endothelial function (PAI-1, E-selectin, sICAM-1, and vWF) were more uniform in association with glucose levels with higher levels of biomarkers associated with higher glucose levels.  However, the pattern of association with FMD was different—with the pre-diabetes IFG group having higher FMD levels than those with normal or diabetic glucose levels. This was most notable in whites with normal BMI.

JAHA: What are the major implications of this work?

Dr. Kanaya: This discordance between FMD and biomarker results raises the possibility of differential effects of insulin signaling in the endothelium vs. the skeletal muscles or other organs. It may also give us some clues about why some studies have found harmful associations between IFG and future events while others have not. 

JAHA: How did you get the idea to do this study?

Dr. Kanaya: I am interested in studying what factors explain higher prevalence of diabetes in ethnic minority groups vs. European white populations. We are studying South Asians in a prospective cohort study to determine etiologic and prognostic factors associated with diabetes and CVD. Endothelial function was a novel aspect worth studying in South Asians and comparing them to other US ethnic groups.

JAHA: What was your biggest obstacle in completing this study?

Dr. Kanaya: The most difficult part of this study was to understand and explain the novel findings with the differential effects observed by the FMD and the endothelial biomarkers for the IFG group.

JAHA: What was your most unexpected finding?

Dr. Kanaya: See above.

JAHA: What do you plan to do next, based on these current findings?

Dr. Kanaya: We are conducting a larger prospective cohort of 900 South Asians currently (called the Mediators of Atherosclerosis in South Asians Living in America study) which has been created to be parallel in methods and measures to the MESA study. We plan to remeasure endothelial function in this larger study to confirm our original findings.  We will also be examining prospective associations of endothelial function with diabetes incidence in both MESA and MASALA. 

JAHA: What do you like to do in your free time?  

Dr. Kanaya: I like to travel internationally with my family, cook and practice yoga.

JAHA: What is your favorite sports team or musical group? 

Dr. Kanaya: The San Francisco 49ers, Favorite band is U2.

To read Dr. Kanaya's full article, click here

Profile originally published February 26, 2013

Tatsuya Iso, MD, PhD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Iso: PPARg induces expression of FABP4 and FAT/CD36 in capillary endothelial cells to promote FA transport into heart. This system is activated in the postprandial state after prolonged fasting.

JAHA: What are the major implications of this work?

Dr. Iso: Our findings identify capillary endothelium as promising target cells for controlling metabolism of energy substrates in the heart. That is, our demonstration in vivo opens a new research area on the role of trans-endothelial material transport system for the treatment and prevention of cardio-metabolic disease, such as heart failure and metabolic syndrome.

JAHA: How did you get the idea to do this study?

Dr. Iso: We found that FABP4 is strongly expressed in capillary endothelial cells, by immunohistochemistry. FABP4 is cytosolic fatty acid chaperon and one of the most famous PPARg target genes. These findings led me to come up with the idea.

JAHA: What was your biggest obstacle in completing this study?

Dr. Iso: While we were working on this project, a similar study was published in Journal of Clinical Investigation 2009 by Kanda et al.  Adding new data and new story was tough.

JAHA: What was your most unexpected finding?

Dr. Iso: Uptake of ¹²⁵I-BMIPP in hearts was comparable between wild-type and endothelial PPARg KO mice during fasting. We expected remarkable difference. We finally found difference of fatty acid uptake after olive oil gavage.

JAHA: What do you plan to do next, based on these current findings?

Dr. Iso: We will estimate function of endothelial FABP4 and FAT/CD36 by generating endothelial-specific KO mice.

JAHA: What do you like to do in your free time?

Dr. Iso: I play with my kids. Ski,skate, watching movies, etc.

JAHA: What is your favorite sports team or musical group?

Dr. Iso: Lakers when I used to live in Los Angeles. Now, Japan national football team.

To read Dr. Iso's full article, click here

Profile originally published February 19, 2013

Steven P. Dunn, PharmD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Dunn: Our major findings are twofold: One, that the analysis of proton pump inhibitor (PPI) use in the CREDO population whereby the antiplatelet efficacy of clopidogrel may be interfered with, is by and large consistent with previously published randomized, controlled trials such as TRITON and PLATO. Second, that in a randomized, controlled trial of single antiplatelet therapy with aspirin-only versus clopidogrel-only (CAPRIE), PPI use significantly impacted the efficacy of clopidogrel, but not aspirin (p-value for interaction 0.047).

JAHA: What are the major implications of this work?

  
Dr. Dunn: The CREDO data is largely reassuring in the interventional cardiology arena in combination with previously published data. In fact, I think this data set nicely illustrates what we’ve largely seen as concerning signals in observational studies may just reflect confounded data as PPI use “worsened” adverse cardiovascular event rates in both the clopidogrel and placebo 1-year primary endpoint. The CAPRIE data suggests that the PPI drug interaction may be more significant in patients receiving single antiplatelet therapy with clopidogrel.

JAHA: How did you get the idea to do this study?

  
Dr. Dunn:  I was fortunate to have access to some of the individuals who had worked on the CREDO and CAPRIE clinical trial programs and spoke early-on to people within Sanofi and BMS. When the mechanistic potential for this interaction was first described, it seemed logical to me that the randomized data sets would be valuable information to examine, especially when the observational and registry data begin to emerge that this was potentially a serious issue. Fortunately, these two trials had the foresight to capture all concomitant medication use.

JAHA: What was your biggest obstacle in completing this study?

  
Dr. Dunn: It was very difficult to merge and combine the findings from two disparate clinical trials which essentially concluded opposite findings. While this makes for good contrast, it was difficult to rationalize how this could be possible and make a cohesive manuscript.

JAHA: What was your most unexpected finding?

  
Dr. Dunn: The data from CAPRIE were very unexpected to us. To our knowledge, this is the only data from a randomized, controlled trial which demonstrates harm in patients receiving both PPI therapy and clopidogrel versus a comparator.

JAHA: What do you plan to do next, based on these current findings?

  
Dr. Dunn:  I think it would be very valuable to obtain more information about patients taking single antiplatelet therapy with clopidogrel only and whether the interaction is more significant in this particular population of patients. This occurs often, for example, in ischemic stroke prevention.

JAHA: What do you like to do in your free time?

  
Dr. Dunn:  I enjoy spending time with my family and am very busy keeping up with my two-and-a-half year old daughter. Outside of that, I “dabble” in technology and more outdoorsy stuff like hiking, mountain biking, golfing, and “technical” outdoors activities like photography.

JAHA: What is your favorite sports team or musical group?

  
Dr. Dunn:  I am a Western Pennsylvania native so of course I am a Pittsburgh Steelers fan!

To read Dr. Dunn's full article, click here

Profile originally published February 12, 2013

Kathryn A. Britton, MD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Britton: Thoracic periaortic adipose tissue (TAT) is a type of ectopic fat that surrounds the aorta, and has been postulated to have a local toxic effect on the vasculature.  We examined categories of individuals discordant for periaortic and visceral fat in order to better understand the potential specificity of the association of different fat depots with cardiometabolic risk factors.  We found that high TAT was uniquely associated with a higher prevalence of cardiovascular disease, smoking, and low-HDL.

JAHA: What are the major implications of this work?

Dr. Britton: Our findings suggest that individuals with high TAT, even in the absence of high VAT, are characterized by a uniquely adverse cardiometabolic profile.

JAHA: How did you get the idea to do this study?

Dr. Britton: We were interested in establishing the unique risk factor correlates of high thoracic periaortic fat. 

JAHA: What was your biggest obstacle in completing this study?

Dr. Britton: Thoracic periaortic and visceral fat are highly correlated which makes it more challenging to disentangle the specific associations of TAT versus visceral fat with cardiometabolic risk factors.  Thus, we specifically looked at discordant categories to better capture the unique associations of high TAT versus high visceral fat. 

JAHA: What was your most unexpected finding?

Dr. Britton: We were surprised and intrigued to find that men with high thoracic periaortic fat in the absence of high VAT had a higher prevalence of current smoking.  This finding, taken in conjunction with previous findings that thoracic periaortic fat is associated with peripheral artery disease (for which smoking is a major risk factor) and that smoking appears to influence the biology of adipose tissue, will be interesting to pursue in further experimental and observational studies. 

JAHA: What do you plan to do next, based on these current findings?

Dr. Britton: We are interested in looking at changes in TAT over time since many of the individuals in this study are undergoing follow-up CT scans six years later.  In addition, we are interested in examining the association of TAT with other manifestations of cardiovascular disease.  We are also interesting in performing prospective studies examining the association of TAT with different health outcomes over time. 

JAHA: What do you like to do in your free time?

Dr. Britton: I enjoy spending time with my family and friends, and especially enjoy outdoor activities, such as running, walking, and cross-country skiing.  I also enjoy traveling and most recently spent two weeks in Turkey. 

JAHA: What is your favorite sports team or musical group?

Dr. Britton: Although I have lived in Boston for the past 10 years, I was born and raised in New York, and am a longstanding NY Yankee fan. 

To read Dr. Britton's full article, click here

Profile originally published February 5, 2013

Karen Siu Ling Lam, MD

JAHA: Tell us about the key findings from your recent article in JAHA.

Dr. Lam: In 1847 Chinese healthy subjects with no known cardiovascular diseases (heart disease or stroke) we found that a high level of adipocyte fatty acid binding protein (A-FABP) in their blood could predict whether they would develop cardiovascular diseases in 12 years. Their risk was increased by 50% for every unit increase in log-transformed A-FABP level, even after taking into consideration the effect of known cardiovascular risk factors like high blood pressure or cholesterol, diabetes and obesity. It should be noted that A-FABP is a hormone released from the fat cells and inflammatory cells with its blood level being elevated in overweight or obese subjects.

JAHA: What are the major implications of this work?

Dr. Lam: The implications are that A-FABP, which has been shown to be associated with increased cardiovascular diseases in animals, probably also contributes to the development of these diseases in humans. Furthermore, we have shown that measuring its level in our blood can potentially help to identify who are at increased risk of cardiovascular diseases and therefore should receive more intensive preventive measures, including healthy life-style and medications to control the known cardiovascular risk factors. Its use as a “risk marker” in this regard is additive to that of “C-reactive protein”, a marker already used in clinical practice to predict the risk of heart disease and stroke.

JAHA: How did you get the idea to do this study?

Dr. Lam: This is the continuation of our research on A-FABP since 2006 when we first demonstrated its presence in the human circulation and its association with obesity and other atherosclerotic risk factors in humans (Clin Chem 2006). We subsequently demonstrated that a high blood level of A-FABP was associated with atherosclerotic changes in the carotid arteries which supply the brain (ATVB 2007), and could predict the development of the metabolic syndrome (Circulation 2007) and type 2 diabetes (Diabetes Care 2007), two conditions which predispose to cardiovascular diseases. A high level of A-FABP also predicted early death after stroke (Neurology 2011). We therefore investigated whether it could predict the development of cardiovascular disease in the subjects in the Hong Kong Cardiovascular Risk Factors Prevalence Study (CRISP) that we have been following up for 12 years.

JAHA: What was your biggest obstacle in completing this study?

Dr. Lam: The greatest difficulty was in getting the study subjects to return for follow-up assessment repeatedly during the 12 years. This was achieved through the patience and dedication of our research nurses and doctors.

JAHA: What was your most unexpected finding?

Dr. Lam: Our most unexpected finding was that the blood level of adiponectin, another hormone from the fat cells which showed some protection against cardiovascular diseases in animal studies, did not show any suggestion of a protective effect in our study.

JAHA: What do you plan to do next, based on these current findings?

Dr. Lam: We plan to collaborate with other centers to establish A-FABP as a predictive marker of cardiovascular disease for clinical use.

JAHA: What do you like to do in your free time?

Dr. Lam: I enjoy jogging, hiking and reading.

JAHA: What is your favorite sports team or musical group?

Dr. Lam: Not applicable.


To read Dr. Lam's full article, click here
Profile originally published January 29, 2013