air pollution and heart disease

Yet another study found an increase in heart disease in people exposed to air pollution/fine-particulate matter exposure (see cad air pollution lancet2016 in dropbox, or doi.org/10.1016/ S0140-6736(16)00378-0). details:

--6795 participants. aged 45-84, enrolled in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) from 6 different US cities (Baltimore, Chicago, LA County, New York City, St Paul, Winston-Salem)
--median age 62, 53% women, 39% white, 12% Chinese, 27% black, 22% Hispanic), 50-80% with at least some post-high school education, 15% smokers, BMI 28, 45% with hypertension and SBP 128 mmHg, 12% diabetic, 15% on statins and cholesterol/HDL/LDL=190/50/115
--followed 10 years with repeated measurements of coronary artery calcium by CT (CAC score) as well as carotid artery intima-media thickness (CIMT); concentrations of fine particulate matter (PM2.5, which reflects particulate matter <2.5 mm in diameter) and nitrogen oxides (NOx) were estimated based on residence-specific spatio-temporal pollution concentration models, which include community-specific measurements, monitoring data and geographical predictors.
--baseline CAC was 145 Agatston units, which is already pretty elevated, but not so surprising for the demographics of the study (see https://www.mesa-nhlbi.org/Calcium/input.aspx for the MESA CAC score: input age, sex, race/ethnicity and CAC score to get a sense of the meaning of the score)

--results:
    --overall, CAC increased on average by 24 Agatston units/yr and CIMT 12mm/yr.
    --participant-specific air pollutant concentrations averaged over the years 2000-2010 ranged: for PM2.5 from 9.2-22.6 mg PM2.5/m3 and for NOx​ from 7.2-139.2 parts/billion (ppb) [PM2.5 highest in LA County, NOx highest in New York City]
    --for each 5 mg PM2.5/m3 increase, CAC progressed by 4.1 Agatston units/yr (CI 1.4-6.8), controlling for the usual suspects (age, sex, ethnicity, BMI, physical activity, smoking/second-hand smoke, employment, total and HDL cholesterol, triglycerides, statin use, neighborhood socioeconomic index, level of education, income)
    ​--for each 40 ppb increase in NOx, CAC progressed by 4.8 Agatston units/yr (0.9-8.7). this relationship was stronger in hypertensive, non-obese individuals and in those >65 yo.
    --no clear association with CIMT

commentary:
--there have been many studies over the past 1-2 decades finding a relationship between particulate exposure or air pollution with atherosclerotic disease (MI, strokes). the current study was a prospective long-term one which looked at the process of atherosclerosis itself. My reading of the literature is that CIMT is a much less accurate predictor of atherosclerotic events than the CAC (CIMT really measures arterial injury more than atherosclerosis itself). and CAC has really good sensitivity and specificity for clinical atherosclerotic events over an array of clinical settings (it' s the best of the nontraditional cardiac risk factors).
--this study provides strong evidence that the relationship between particulate exposure/air pollution and heart disease is mediated through atherosclerosis (vs simply being from endothelial dysfunction, arrhythmias, etc), that the process is dose-related and progressive, and that there would be a reasonable expectation that improving air quality would lead to improvements in atherosclerosis-related outcomes. Though I should add that there are also data from the MESA study that endothelial dysfunction may also play a role: see Krishnam RM. J Am Coll Cardiol 2012; 60:2158; and there was a small study at our health center in Boston finding an association between particulate exposure and cardiac autonomic function within hours of the exposure: see Lee M. Am J Cardiol 2016; 117:151)
--though I think this study is quite impressive regarding the relationship between air pollution and atherosclerosis, it would be interesting to see more granular data: was this as true for those with no underlying atherosclerosis by CAC at baseline? also, was there a difference in actual clinical events (vs just changes in the surrogate marker of CAC; though as a perspective, there are a slew of other studies finding increased strokes/MIs)?  
--so, again, on an individual level, it is useful to incorporate air quality as one of our many risk factors for clinical atherosclerotic disease both in terms of nonpharmacologic therapies (weight, diet, exercise, stress reduction, etc), perhaps with further education around minimizing exposure to air pollution on particularly bad days, and for use of meds (statins, etc). and, on a society level, and especially with increasing pollution in many countries associated with "modernization" and perhaps exacerbated further by climate change, this study reinforces the importance of public health initiatives to decrease air pollution/particulate exposures.



Comments

Post a Comment

if you would like to receive the near-daily emails regularly, please email me at gmodest@uphams.org

Popular posts from this blog

cystatin c: better predictor of bad outcomes than creatinine

  another article found significant discordance between creatinine and cystatin C in assessing renal function,  finding that the latter correlated most strongly with both renal and non-renal adverse clinical outcomes (see   ckd cystatin c better than creat AJKD2023  in  dropbox or doi: 10.1053/ j.ajkd.2023.04.002)   Details: -- 158,601 adults who were in the Stockholm Creatinine Measurements (SCREAM) project and had testing of creatinine and cystatin C on the same day during a healthcare encounter, from 2010-2018     -- >400,000 outpatient tests were done for both creatinine and cystatin C levels -- mean age 62, 48% female -- mean eGFR by creatinine (   eGFR cr ) 80; mean eGFR by cystatin C ( eGFR cys  ) 73 -- mean stage of renal insufficiency: 39%  eGFR cr   90+; 38%  eGFR cr  60-89; 12%  eGFR cr  45-59; 7.1%  eGFR cr  30-44; 3.2%  eGFR cr  15-29, 0.7%  eGFR cr ...
Read more

diabetes DPP-4 inhibitors and the risk of heart failure

the FDA just came out with a safety alert about 2 DPP-4 inhibitors and the increased risk of heart failure (released 04/05/2016)(see  http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm494252.htm?source=govdelivery&utm_medium=email&utm_source=govdelivery ​ ). details: --saxagliptin and alogliptin were singled out because of 2 clinical trials in diabetic patients with heart disease. in each trial more patients taking these meds were hospitalized for heart failure vs those on placebo     --in the saxagliptin trial: 3.5% were hospitalized for heart failure (vs 2.8% on placebo). risk factors included prior heart failure or kidney disease     --in the alogliptin trial: 3.9% were hospitalized for heart failure (vs 3.3% on placebo) --recommendation by the FDA:     -- we should consider stopping these drugs if the patient develops heart failure ...
Read more

UPDATE: ASCVD risk factor critique

I decided to do an extensive update of my prior ASCVD (atherosclerotic cardiovascular disease) risk analysis and critique of risk calculators, with much more information about the “non-traditional” risk factors. I felt that there should be more data/clarification, since I think we are really undertreating/not preventing the most common cause of death by relying on the current ASCVD risk calculators   -- Cardiovascular risk models:      -- many of us rely on the various cardiovascular risk models to determine the appropriate approach to patients, and these are often integrated into the electronic medical records      -- these risk models have several very important limitations:          -- they are typically based on community data, eg from the Framingham study etc. But, in clinical practice, we are dealing with the individual and not the community:          ...
Read more