Neighborhood deprivation increases risk for HF

Clyde W. Yancy, MD, MSc, MACC, FAHA, MACP, FHFSA

These findings are important because we are accustomed to thinking about the risk for heart disease — in this case, HF — at the patient level: high BP, coronary disease, diabetes, familial tendencies towards cardiomyopathy, etc. In fact, these data allow us to expand our prism and to think more globally about the risk for HF as a function of the neighborhood dynamics. This is important because the paper demonstrates an evident truth that after adjustment for the usual risk attributed to the development of heart failure, there remain independent contributions from the neighborhood dynamic that cannot be dismissed.

The investigators used a neighborhood deprivation index, which is based largely on markers of socioeconomics. With this new tool, these investigators were able to very capably demonstrate that depending on the extent to which there is more stress on the neighborhood dynamic, there is a subsequent and not insignificant increase in the risk for HF. That’s the news embedded in this research. There are important non-patient-related factors that account for at least some of the burden of heart failure. As we continue to engage in conversations about preventing HF and focus on the overt, ie, targeting obesity and especially hypertension, maybe diabetes, we now much consider the neighborhoods.

We cannot dismiss the importance of what has heretofore been described as the built environment; we now understand that a major component of the built environment is in fact the neighborhood and the community. All of these things come together and create an intersection of risk that really does predispose to HF.

If we take this just one step further, for many years, we’ve been accustomed to assigning disease risk as a function of race, African Americans in this case. We have taken this even further and used race as a means to describe more malignant disease and a more aggressive natural history. However, given that many who are self-described by race live in similar circumstances and similar neighborhoods, a new dynamic emerges. What happens when those are the same individuals that are more likely to be hypertensive, more likely to be obese, more likely to live in neighborhoods with more neighborhood stress? Is that not part of the dynamic that is the reason for the excess number of cases of HF observed, and might we not be able to intervene, specifically and very clearly, might not we be able to narrow the evidence of disparities by targeting not the individual, but targeting the neighborhoods along with the known risk factors? That in my mind is very exciting and brings to our attention new approaches to reduce the burden of disease in at-risk populations.

We can never re-engineer a person, nor can we rework the genetic underpinnings of diseases, but we can certainly re-engineer communities. We can certainly target risk, and maybe that is an alternative way to achieve a meaningful reduction in the disease burden that we’ve currently ascribed to race.

The important takeaway from this paper is the necessity to involve others in the conversation. We have not previously interfaced with city planners, social engineers or those who build/maintain/fund our social safety net, but we should, as meaningful contributions to health are possible with a more global focus. As cardiologists, especially those with a focus in heart failure and prevention, we’re very facile, very adept at talking about controlling BP, talking about focusing on those things that we know describe health: a healthy diet, being physically active, an appropriate weight and managing all the other metabolic parameters like lipid levels and blood glucose, but persons with a different set of skills, expertise other than that which we have really ought be the ones we would turn to, to say, “How can we re-engineer a community?” For example, how can we increase the space available for exercise? How can we make certain that there’s a safe area for exercise? How can we ensure that there’s access to fresh fruits and vegetables? What about air quality? What about water quality? What can we do to be certain that the components of the environment that are absolutely beyond the control of the individual short of moving to a new neighborhood are at least positioned in a way that they advantage health and not disadvantage health.

hat might happen now is to go beyond the first step. The first step here was geocoding. We’ve known for quite some time that we can look at the ZIP code and, for the most part, predict the burden of CVD by ZIP code across the country. In fact, we know that there are a number of ZIP codes where a fair proportion of the HF we’ve seen in this country are well localized. I applaud these investigators for going beyond the ZIP code and developing a neighborhood deprivation index.

The next step would be akin to an intervention that relocates an at-risk individual from a neighborhood with a deprivation index that is adverse to one that has a neutral deprivation index. What then happens to the subsequent development of HF? It takes some time for that kind of work to evolve, but the answer would be invaluable.
An alternative approach might be to modify the neighborhood, ie, address those characteristics of neighborhood deprivation which are modifiable. Again, I speak to parks, areas to exercise, safe spaces, availability of fresh fruits and vegetables, transportation to medical facilities and access to primary care. What happens if you step in and re-engineer those communities real-time, do you change the burden of disease? That would be very provocative, but again would likely require a generation of change to see the effects. Again, it may be beyond the usual realm of the clinical trial, but nonetheless, it would be important work to pursue.

We are transitioning to a very different conversation in the HF space. For decades, we’ve talked about treating symptomatic HF, chronic HF, acute decompensated HF and advanced HF. We’ve always suggested that prevention was a good thing, but over the last 2 to 3 years, we have particularly embraced the importance of having conversations about preventing HF. It appears in the updated HF guidelines. It appears in the hypertension guidelines. It is an evident truth now that we can screen for, anticipate and, if you will, prevent the development of HF by targeting the things that we know to be amiss. This takes us another step further and adds more to the conversation about prevention and reminds us that we have to go beyond patient-level factors to successfully accomplish prevention.

If there is no other takeaway from this paper, that one important takeaway should be the following: HF can be prevented. It’s no longer a theoretical consideration. There are steps that can be taken to prevent HF, and we should be very forthright in trying to make that happen.