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Racial/Ethnic Disparities in Cardiovascular Outcomes

On-Demand Webinar

Health & Wellness

Although the health and life expectancy has increased for Americans over the last century, a mortality gap between black and white individuals has persisted since the 1960s. The higher rate of mortality in black individuals is driven by an increased risk of hypertension, obesity, cardiovascular disease, and other chronic diseases in black individuals. In this webinar, Dr Keith Ferdinand will review how to address ethnic disparities in cardiovascular disease.



Learning objectives:
–    Describe CVD disparities in risk factor prevalence and outcomes in the United States
–    Highlight genomic variation and social determinants in CVD
–    Discuss strategies to eliminate disparities among racial/ethnic minorities


Keith C. Ferdinand, MD, FACC, FAHA, FNLA, FASPC
Gerald S. Berenson Endowed Chair in Preventive Cardiology, Professor of Medicine, Tulane University School of Medicine, New Orleans, LA


Time of talk: 30 minutes

Jun 30, 2020

Good day. I'm Dr. Keith C. Ferdinand, the Gerald Berenson Endowed Chair in preventive cardiology and professor of medicine at the Tulane University School of Medicine in New Orleans. I will be pleased to discuss with you racial ethnic disparities in cardiovascular outcomes. Here are my disclosures. The learning objectives first is to describe cardiovascular disease disparities in risk factor, prevalence and outcomes in the United States. I’ll then highlight genomic variation and social determinants of health as they relate to cardiovascular disease. And finally, we'll discuss strategies to eliminate disparities among racial ethnic minorities. Past is Prologue. This is unequal treatment that was written in 2002 from the National Academy of Science and unfortunately what they said then stands today. First bullet Health, life expectancy, and overall care has improved drastically for all Americans over the last century. Secondly, the distribution of benefits, however, has not occurred equitably. There's a current mortality gap between blacks and whites, which has persisted since the 1960s. Finally, this mortality gap is driven by a combination of higher risk for hypertension, diabetes, obesity, myocardial infarction, stroke, chronic kidney disease, end stage renal disease, and cardiovascular mortality, especially premature cardiac death. This is an interesting study from Dr. Sidney, who looks at mortality rates. On the left, you see non-Hispanic whites. On the right, non-Hispanic blacks. And note that although the Y axis is similar for both of the groups, there clearly is a higher risk of all cardiovascular disease in the blacks compared to the whites. Furthermore, an interesting finding that Dr. Sidney has described is that the decline that we've previously seen in mortality rates of all forms of cardiovascular disease now appears to be plateauing, and some data suggest they may even be an increase. Nevertheless, for all forms of cardiovascular disease, including heart disease and stroke, the rates for death, heart end points are higher in blacks versus whites. Here's another way of looking at similar data. Note that Hispanics tend to actually have lower death rates than either whites or blacks, but the leading death rate is in non-Hispanic blacks compared to non-Hispanic whites. This then leads to a decrease in life expectancy with the shortest life expectancy of all the major racial ethnic groups being non-Hispanic black males. And note that non-Hispanic black females have a life expectancy which is equally similar to non-Hispanic white males as compared to non-Hispanic white females. Almost suggesting that being a black female removes the protective effect of being female. Now, why do Hispanics have what appears to be a favorable mortality rate? We really don't know. But here are three possibilities. First of all, there's a healthy migrant effect where Hispanic immigrants may have been selected, self selected, that is for good health and robustness. Secondly, there may be a salmon bias. This describes that Hispanic residents may actually return to their country of origin when they become very ill to die. And finally, there may be a cultural effect, and that is despite poverty and social disadvantage, status, intact family structure, lifestyle behaviors and social networks may confer somewhat of a protective barrier against these negative effects of lower SES and minority status. Perhaps the main driver of these poor outcomes in cardiovascular disease in African-Americans or US blacks, is hypertension. And here you can see compared to Hispanics and non-Hispanic whites, a significant higher age adjusted hypertension related death rates in blacks. Furthermore, when you look at the prevalence of hypertension itself in the dark gray, the rates in non Spanish blacks are clearly higher than other racial ethnic groups. And although for all groups the control rates are poor when compared to whites. Specifically for blacks. Poorly controlled hypertension is the primary driver of an increase in cardiovascular mortality. What can we do therefore to improve hypertension control across all populations? This is directly from the latest 2017 ACC/AHA High Blood Pressure guideline. Pay attention first to adherence. Using once daily dosing is possible in combination pills and promote active lifestyle modification. I put a box around what I think is very important. That is team based care using a wide range of health professionals, not only physicians but also nurse practitioners, clinical nurses and pharmacists, and note part of their team is the patient, him or herself, the staff and their relatives and friends. Electronic health records, telehealth strategies which have now become very important. Performance measures and financial incentives all may play a part, and at the top I put a box around what I think is really important that is shared decision making where the patient becomes a large component of his or her care. As I've mentioned, African-Americans are clearly a high risk population when using the ASCVD risk estimator from the pooled cohorts as promulgated by the American Heart Association, American College of Cardiology therefore, along with the variable measurements in terms of gender, cholesterol, HDL, systolic blood pressure, the presence or absence of diabetes, extra points are given for race. This is not necessarily driven by any genetics at all, but these are observational data that suggests that African-Americans have higher risk for overall ASCVD and therefore African-American status as calculated gives a higher calculated risk. One of the other main causes of an increase in mortality is related to heart failure. This is a recent study looking at black men in the blue and black women in the orange. Note especially for younger adults, 35 to 64 years of age, a higher age adjusted death rates related to heart failure and CVD mortality in the blacks, both men and women. In older adults, there is somewhat less of a difference, but the rates compared to the match six for both men and women or higher in blacks than in whites. One of the problems with heart failure is that as the population ages and as we have difficulty controlling risk factors, especially hypertension, it is projected that the rates of heart failure will increase. Here, black is in the green, showing higher rates of projected heart failure extending out to 2030. Therefore, due to death, disability and extra costs, we as a society must do more to control these projected increases in heart failure. Why do you see differences in outcomes related to cardiovascular disease and a wide range of disease across populations? Is it nature which is genotype with the surrogate of race, ethnicity, or is it nurture our social environment? Here is a Venn diagram which describes when I think all of the various factors that may come into play. Starting at the top, we see environment, unhealthy diet, increase in sodium, decrease in potassium, physical inactivity, overweight and obesity status. That may indeed interact with certain genetics, tendencies for families to have higher levels of glucose, cholesterol or a greater tendency towards hypertension. But importantly, at the bottom, all of these intersect due to the social determinants of health, wealth and income, education, occupation, the lack of employment and health care access all play a major part and interact to cause an increase in disparities in cardiovascular disease. Diet plays a large component of the increase in cardiovascular mortality and diseases. This is from the REGARDS study that noted high southern diet intake was perhaps the largest mediator of a hypertension difference in blacks versus whites for both men and women. The second bullet described the southern diet high in fried foods, organ meats, processed meats, eggs, added fats, high fat dairy, sugar sweetened beverages and bread. The third bullet shows that the Southern diet may actually be associated with increased risk of a wide range of conditions beyond hypertension, including stroke, CHD, end stage renal disease, CKD, sepsis, cancer and even cognitive decline. There is an approach now to look at risk factors using what's called Mendelian randomization, and that is a person has inherited with a certain factor and is then observed over a lifetime. The factors in the red box of those which have been now found to be true positive risk factors including LDL cholesterol, triglycerides, lipoprotein little a and glucose. When studying lipids, we now can break the lipids not only into LDL versus HDL, but also into particle size, particle number, and the presence or absence of an LDL like particle called Lp(a), or lipoprotein a. Selecting therapy for the LDL cholesterol, the primary way of addressing this is with high intensity statins in high risk patients. The two high intensity statins are listed here Atorvastatin 40, 80 or Rosuvastatin 20, 40. Moderate and low intensity statins are also listed. But for all high risk patients, high intensity statins and in some cases moderate intensity statins are needed. What about cholesterol itself across populations? The latest ACC/AHA 2018 cholesterol guideline actually recommends that clinicians may want to consider in their decision making different race and ethnic factors. Indeed, for blacks, especially those who have premature cardiovascular disease, dyslipidemia itself is not the primary driver of the increase in cardiovascular outcomes when compared to whites. The second bullet describes other factors which may play a large part of this increase in risk, including hypertension, as we previously described. Obesity, type two diabetes, smoking and low physical activity. Nevertheless, when risk factors are identified, management may be suboptimal in African-Americans compared to whites. In the final bullet, there are issues related to socioeconomic status and a decreased access to health care, along with the lack of compliance with medications and partly due to the cost. Let's look at the guidelines, and I've highlighted in bold some salient factors across Asian Americans, Hispanic or Latino populations, and blacks. Going left to right, first of all, for lipids, Asian-Americans may actually have lower HDL compared to whites, and there may be an increase in triglycerides across all subgroups. In terms of blacks, they may have higher HDL levels, but lower triglyceride levels, which is clearly not protective in this population. At the bottom, in terms of risk decisions, coronary artery calcium score is beneficial as an additional marker for all populations. However, in blacks, they may have significantly lower prevalence of severe coronary artery calcium score despite their increase in cardiovascular mortality. This is also directly from the 2018 cholesterol management guideline in terms of intensity of statin therapy in response to LDL-C lowering, Japanese may be especially sensitive to statin, and the labeling for ROSUVASTATIN suggests recommending starting at a lower dose in Asians 5 mg versus the usual 10 to 20 milligrams. Note For blacks, in terms of safety, there may be higher baseline serum creatinine kinase. Creatinine kinase should not be used using normal values in this population since they may vary. What about patients who have severe hypercholesterolemia with LDLs of 190 and above? In this particular case, it may be a surrogate for familial hypercholesterolemia. In those particular patients maximally tolerated statin therapy is recommended as a Class 1 recommendation, regardless of whether or not there's obvious cardiovascular disease present. In the future, it's going to be suggested that we pay more attention to Lp(a). This is a National heart, Lung and Blood Institute working group. I was proud to be a member and what we described was that Lp(a) synthesized in the liver deposits in the coronary arteries goes to the carotids, the aortic valves in the periphery and may be an additional risk factor. It's also suggested that Lp(a) has different degrees of elevated Lp(a) across populations. At the bottom in the middle, in the orange and dark red you see the degrees of elevated Lp(a) in persons of African descent and South Asians who have levels which appear to be higher than other continental ancestry groups. In terms of Lp(a) in African-Americans, therefore it appears to be higher than whites. And in the recent Jackson Heart study, there were informative markers that compared Lp(a) to African ancestry and suggested that there was a clear association. Therefore, Lp(a) in African-Americans and other groups is possibly associated with an increase in cardiovascular events. We should consider measuring Lp(a), especially in people who have premature cardiovascular disease, a family history of premature cardiovascular disease or family history of elevated Lp(a) familial hypercholesterolemia and patients who have recurrent cardiovascular disease despite statin therapy. And current recommendations is that Lp(a) since it is genetically based, should be measured or considered to be measured at least once in the dog's lifetime to better identify very high inherited risk. In terms of overcoming these cardiovascular disparities, the question always arises what can we as providers do? How can we address these considerations? First of all, adherence is a main problem in the control of hypertension, heart failure and cardiovascular disease. This is a working group state of the report in which we describe means of improving medication adherence and cardiometabolic disease. There were certain factors which could easily be identified as related to the effect adherence. This long list includes limited access to health care facilities, having an identifiable source for primary care is one of the best things a person can do to limit their cardiovascular risk. Low health literacy, meaning that the person may have difficulty understanding why he or she needs to do a certain test or take a certain medication. Culturally appropriate language, appropriate literature will help patients understand and become partners in their treatment. Lack of health care insurance persons who are uninsured often use emergency departments as their primary source of care, presenting too late in the cardiovascular sequelae when they have chest pain, shortness of breath, leg swelling or signs of a stroke. Cultural lay beliefs about illness and treatment. Patients need to have a better understanding of how we assess risk and why we treat patients who may appear to be asymptomatic. It may take extra time, but this will help overcome barriers which can affect adherence. Because we now are all in the COVID 19 pandemic, I would like to take some time to talk about the interactions of COVID 19 and the renin-angiotensin aldosterone system. We all know now the figure of the spiked SARS-CoV-2 virus. Note that the arrow points to the ACE2 receptor complex. That is where the spikes of the SARS virus actually enters into the cell. There has been some consideration that Angiotensin converting enzyme inhibitors and angiotensin receptor blockers may actually stimulate and upregulate ACE2 thereby increasing the entrance of the coronavirus into cells. Nevertheless, on the other hand, angiotensin 2 which is blocked by the angiotensin receptor blocker and decreased by the angiotensin converting enzyme inhibitors, has an adverse effect on the lung and other tissues. It has been suggested in angiotensin 2 increases acute lung injury, adverse myocardial remodeling, vasoconstriction and vascular permeability. Therefore, while increasing ACE2 may be one consideration, blocking the effects of angiotensin 2 with either ACE inhibitors or ARBs may actually be beneficial. The question then for the clinician is the following: What should we do with using RAAS antagonism in patients with COVID 19? This is a working group report from the combination of the American College of Cardiology, American Heart Association, and the Heart Failure Society of America. They suggest the following: the highest standard of care for our cardiovascular patients is our top priority. And while there are theoretical concerns with ACE and ARBs with COVID 19, there are no experimental or clinical data that clearly demonstrate either benefit or adverse outcomes among COVID 19 patients using ACE and ARBs. Therefore, their final conclusion at this time is that clinicians should be advised to not either add or remove RAAS blocking treatments beyond the actions that are based on standard clinical practice. We know controlling blood pressure, treating heart failure and chronic kidney disease with RAAS blocking agents is an important component of clinical care, and this particular statement suggests no action be taken based on theoretical concerns alone. I mentioned before adherence as being an important component of cardiovascular care, and one of the questions that arise is what can we do to increase health literacy? Particularly challenging in racial ethnic minorities, it is necessary to understand the significance of abnormal lab values and understand the conditions for which they are being treated. Almost half of patients with hypertension or diabetes have inadequate health literacy, less knowledge about their disease, less knowledge about important lifestyle modifications and essential self-management skills. As previously mentioned, therefore, multicultural, multilingual patient tools can be valuable in this area, and I show a depiction of some of the tools that are available on the web from the National Heart, Lung and Blood Institute. In terms of eliminating disparities, therefore, what action can we take? It's important to treat our patients with respect and spend the extra time for education and outreach. Here's a cartoon that's directly from the CDC showing a box lifting this person up with programs designed to reduce health disparities and reducing health disparities will bring us all closer to reaching health equity. In summary, therefore, I think we've shown that cardiometabolic and cardiovascular disparities by race and ethnicity, geography and socioeconomic status truly exists. They are sizable, they are multifactorial, but rarely due to genetics. Unfortunately, these disparities are persistent and unacceptable. Thank you for taking time to listen to this particular presentation.

This is a previously accredited webinar through the American Academy of Family Physicians created in 2020. The material was current as of the recording date. The views and opinions are those of the presenter. 
Page Published: October 17, 2023