Causes of Troponin Elevation and Associated Mortality in Young Patients.

BACKGROUND: While increased serum troponin levels are often due to myocardial infarction, increased levels may also be found in a variety of other clinical scenarios. Although these causes of troponin elevation have been characterized in several studies in older adults, they have not been well characterized in younger individuals. METHODS: We conducted a retrospective review of patients 50 years of age or younger who presented with elevated serum troponin levels to 2 large tertiary care centers between January 2000 and April 2016. Patients with prior known coronary artery disease were excluded. The cause of troponin elevation was adjudicated via review of electronic medical records. All-cause death was determined using the Social Security Administration's death master file. RESULTS: Of the 6081 cases meeting inclusion criteria, 3574 (58.8%) patients had a myocardial infarction, while 2507 (41.2%) had another cause of troponin elevation. Over a median follow-up of 8.7 years, all-cause mortality was higher in patients with nonmyocardial infarction causes of troponin elevation compared with those with myocardial infarction (adjusted hazard ratio [HR] 1.30; 95% confidence interval [CI], 1.15-1.46; P < .001). Specifically, mortality was higher in those with central nervous system pathologies (adjusted HR 2.21; 95% CI, 1.85-2.63; P < .001), nonischemic cardiomyopathies (adjusted HR 1.66; 95% CI, 1.37-2.02; P < .001), and end-stage renal disease (adjusted HR 1.36; 95% CI, 1.07-1.73; P = .013). However, mortality was lower in patients with myocarditis compared with those with an acute myocardial infarction (adjusted HR 0.43; 95% CI:, 0.31-0.59; P < .001). CONCLUSION: There is a broad differential for troponin elevation in young patients, which differs based on demographic features. Most nonmyocardial infarction causes of troponin elevation are associated with higher all-cause mortality compared with acute myocardial infarction.

Sorafenib-Associated Heart Failure Complicated by Cardiogenic Shock after Treatment of Advanced Stage Hepatocellular Carcinoma: A Clinical Case Discussion.

Background. Sorafenib, an oral tyrosine kinase inhibitor (TKI), targets multiple tyrosine kinase receptors (TKRs) involved in angiogenesis and tumor growth. Studies suggest that inhibition of TKR impacts cardiomyocyte survival. Inhibition of VEGF signaling interrupts angiogenesis and is associated with the development of hypertension and compensatory hypertrophy. Compensated hypertrophy ultimately leads to heart failure. Case Description. A 76-year-old man with a past medical history of systolic heart failure due to ischemic cardiomyopathy and stage IIIC hepatocellular carcinoma (HCC) presented with symptoms of decompensated heart failure. Four months prior to admission, he was started on sorafenib. Results. Our patient was treated with intravenous furosemide and guideline directed therapy. Clinical status was complicated by the development of low cardiac output and shock requiring inotropic support. Careful titration of heart failure medication led to hemodynamic improvement and discontinuation of dobutamine. Conclusion. Greater awareness of sorafenib cardiotoxicity is essential. As TKI usage grows for treatment of cancers, heart failure-related complications will increase. In our patient, routine heart failure management and cessation of sorafenib led to clinical improvement. Future studies on the treatment of sorafenib cardiotoxicity should be explored further in this unique patient population.

Environmental lead and childhood blood lead levels in US children: NHANES, 1999-2006.

Although blood lead levels in the United States have fallen dramatically since 1980, there remain subgroups of children with high blood lead levels. We assessed the relationship between environmental lead sources and blood lead levels in children ages 1 to 5 years from the National Health and Nutrition Examination Survey (NHANES), 1999-2006. Modeled ambient air lead levels and industrial lead releases at the census-tract level were assigned to each child's residence with adjustment for confounding factors. Of 3,223 children, 272 (8.4%) had blood lead levels ≥ 5 ug/dL. Industrial releases (2,252 vs 1,696 lbs/mi2) and ambient air lead levels (2.28 vs 1.75 ng/m3) were greater in exposed versus unexposed children. For every 10,000 lb/mi2 increase in inverse distance squared weighted exposure, there was a 1.13% increase (95% CI: 0.45%, 1.81%) in blood lead (p = .001).

A case-crossover analysis of the impact of PM(2.5) on cardiovascular disease hospitalizations for selected CDC tracking states.

BACKGROUND: Information is currently being collected by the CDC Environmental Public Health Tracking (EPHT) network on hospitalizations due to Acute Myocardial Infarction (AMI) and there is interest by CDC in exploring the relationship between fine particulate matter (PM2.5) and other cardiovascular (CVD) outcomes in the context of the EPHT program. The goal of this study was to assess the short term effects of daily PM(2.5) air pollution levels on hospitalizations for CVD for seven states within the CDC EPHT network (Florida, Massachusetts, New Hampshire, New Jersey, New Mexico, New York, and Washington). METHODS: Hospitalization data was obtained for 2001-2008 admissions for circulatory disease (primary discharge diagnosis of ICD-9 codes 390-459) from data stewards in those states and included admission date, age, gender, and zip code of residence. We used CMAQ-derived predicted daily PM2.5 data as estimated by EPA at the centroid of each Census Bureau Zip Code Tabulation Area (ZCTA) and linked to zip code of patient residence. A time-stratified case-crossover study design with conditional logistic regression was used to evaluate the short-term association of PM2.5 on risk of non-elective hospitalizations for CVD. Specifically, we considered all circulatory disease, ischemic heart disease, acute myocardial infarction, heart failure, cardiac arrhythmia, cerebrovascular disease and peripheral vascular disease endpoints. RESULTS: Data were obtained on over 7,500,000 hospitalizations for this time period. Mean annual PM2.5 exposure levels were lowest for New Mexico and Washington (6.5 µg/m3 PM2.5 and 8.4 µg/m3 PM2.5). New Jersey, New York and Massachusetts exhibited the highest annual averages for PM2.5, (12.8 µg/m3, 11.1 µg/m3 and 10.8 µg/m3), respectively. The Northeast states (Massachusetts, New Jersey, New Hampshire and New York) exhibited significant effects of PM2.5 during the cooler months across most disease categories after adjustment for ozone and maximum apparent temperature. Ischemic heart disease risk per 10 µg/m3 increase in PM2.5 varied from 1.02 to 1.05 for the cooler months. The largest lag effect was noted on lag days 0 and 1. New Mexico and Washington exhibited no cool or warm month significant effects. Although Florida showed no cooler month effects, significant increases were noted in odds ratios for the warm weather months for all outcomes except peripheral vascular disease. This study is one of the first large scale applications of linkage of hospitalization data by state with national US EPA statistically modeled air pollution data. The results demonstrate that state-wide, there are multiple cardiovascular outcomes in addition to AMI which may be impacted by particulate air pollution.