Deficiency in 25-hydroxyvitamin D (25[OH]D) is a treatable condition that has been associated with coronary artery disease and many of its risk factors. A practical time to assess for 25(OH)D deficiency, and to initiate treatment, is at the time of an acute myocardial infarction. The prevalence of 25(OH)D deficiency and the characteristics associated with it in patients with acute myocardial infarction are unknown. In this study, 25(OH)D was assessed in 239 subjects enrolled in a 20-hospital prospective myocardial infarction registry. Patients enrolled from June 1 to December 31, 2008, had serum samples sent to a centralized laboratory for analysis using the DiaSorin 25(OH)D assay. Normal 25(OH)D levels are ≥30 ng/ml, and patients with levels <30 and >20 ng/ml were classified as insufficient and those with levels ≤20 ng/ml as deficient. Vitamin D levels and other baseline characteristics were analyzed with the linear or Mantel-Haenszel trend test. Of the 239 enrolled patients, 179 (75%) were 25(OH)D deficient and 50 (21%) were insufficient, for a total of 96% of patients with abnormally low 25(OH)D levels. No significant heterogeneity was observed among age or gender subgroups, but 25(OH)D deficiency was more commonly seen in non-Caucasian patients and those with lower social support, no insurance, diabetes, and lower activity levels. Higher parathyroid hormone levels (45.3 vs 32.7 pg/ml, p = 0.029) and body mass indexes (31.2 vs 29.0 kg/m 2 , p = 0.025) were also observed in 25(OH)D-deficient subjects. In conclusion, vitamin D deficiency is present in almost all patients with acute myocardial infarction in a multicenter United States cohort.
From the current body of evidence, it is clear that there is an association between cardiovascular (CV) disease and vitamin D deficiency. However, the prevalence of vitamin D deficiency as well the characteristics associated with it in patients presenting with acute myocardial infarction (AMI) is unknown. This is an important gap in knowledge, because vitamin D deficiency is readily treatable and, if common in patients with AMI, can identify an opportunity to recognize, initiate treatment, and potentially improve the outcomes of deficient patients. This was a substudy of the Translational Research Investigating Underlying Disparities in Acute Myocardial Infarction Patients’ Health Status (TRIUMPH) registry to describe the prevalence of vitamin D deficiency at the time of AMI care.
Methods
We studied subjects enrolled in TRIUMPH. This registry collected information on patients admitted for AMI through chart abstraction, detailed patient interviews, as well as serum samples at 24 United States hospitals from April 11, 2005, to December 31, 2008. Inclusion criteria were very similar to TRIUMPH’s predecessor, the Prospective Registry Evaluating Myocardial Infarction: Events and Recovery (PREMIER), and included patients aged ≥18 years with biomarker evidence of myocardial injury (elevated troponins or creatinine kinase-MB), supporting evidence of AMI (e.g., prolonged ischemic signs or symptoms, electrocardiographic ST-segment changes) who presented <24 hours after symptom onset.
In the last 239 patients consenting to baseline blood work in the enrollment period of June 1 to December 31, 2008, patients also had 25-hydroxyvitamin D (25[OH]D) levels quantified from the centralized laboratory that was performing all other analysis. Data in TRIUMPH were collected through chart abstraction, standardized in-depth interviews by trained hospital research staff members 24 to 72 hours after AMI admission, and serum sample collection during admission. Patient data included demographics including age, gender, and race as well as marital status, education, access to health insurance, and employment status, region of country, as well as season at time of admission. Collected clinical variables included hypercholesterolemia, hypertension, peripheral arterial disease, diabetes mellitus, previous AMI, previous angina, previous percutaneous coronary intervention or coronary artery bypass surgery, previous stroke, chronic lung disease, chronic renal failure, chronic heart failure, nonskin cancer, smoking, body mass index, family history of coronary artery disease, and history of depression. Other collected data included blood pressure, apolipoprotein A1, glycosylated hemoglobin, insulin, troponin, pro–brain natriuretic peptide, calcium, phosphate, a lipid panel, and 25(OH)D and parathyroid hormone.
Enrolled patients’ serum samples were sent to a centralized laboratory (CRL, Lenexa, Kansas) for analysis using the DiaSorin (Saluggia, Italy) 25(OH)D assay. Normal 25(OH)D levels are ≥30 ng/ml, and we classified patients with levels <30 and >20 ng/ml as insufficient and those with levels ≤20 ng/ml as deficient ( Table 1 ).
| Serum 25(OH)D (ng/mL) | Vitamin D Status |
|---|---|
| ≤20 | Deficient |
| 21–29 | Insufficient |
| ≥30 | Sufficient |
The DiaSorin 25(OH)D assay uses an in vitro radioimmunoassay for quantitative determination of 25(OH)D and other hydroxylated vitamin D metabolites in human serum or plasma. This assay consists of a 2-step procedure in which (1) a rapid extraction of 25(OH)D and other hydroxylated metabolites from serum or plasma with acetonitrile is performed, at which time (2) the sample is assayed using an equilibrium radioimmunoassay procedure based on an antibody with specificity to 25(OH)D. The sample, antibody, and tracer are incubated for 90 minutes at 20°C to 25°C. Phase separation is accomplished after a 20-minute incubation at 20°C to 25°C with a second antibody precipitating complex. A nonspecific binding/addition buffer is added after this incubation before centrifugation to aid in reducing nonspecific binding. Assay precision was evaluated at DiaSorin by testing 4 control levels spanning the curve over 23 operating days in 40 assays. Each assay included the 4 controls × 2 extractions (4 replications). Levels of 25(OH)D and other baseline characteristics were analyzed using linear or Mantel-Haenszel trend tests.
Results
During the enrollment period of June 1 to December 31, 2008, 239 patients from 20 of the 24 TRIUMPH sites consented to baseline blood work and had 25(OH)D levels assessed via the DiaSorin radioimmunoassay method. The total population mean age was 57.6 ± 11.4 years, and 73.2% of the enrolled subjects were men ( Table 2 ).
| Variable | 25(OH)D (ng/ml) | p Value | |
|---|---|---|---|
| ≤20 | >20 | ||
| (n = 179) | (n = 60) | ||
| Age (yrs) | 57.0 ± 11.5 | 59.4 ± 10.9 | 0.151 |
| Men | 129 (72%) | 46 (77%) | 0.487 |
| Women | 50 (28%) | 14 (23%) | |
| Caucasian | 127 (71%) | 51 (85%) | 0.031 |
| BMI (kg/m 2 ) | 31.2 ± 6.6 | 29.0 ± 5.5 | 0.025 |
| Obese (BMI ≥30 kg/m 2 ) | 83 (49%) | 27 (47%) | 0.791 |
| Marital status | |||
| Married | 98 (55%) | 41 (68%) | 0.073 |
| Divorced/separated | 46 (26%) | 12 (20%) | |
| Widowed | 11 (6%) | 3 (5%) | |
| Single | 23 (12%) | 4 (7%) | |
| Avoid service | 61 (34%) | 13 (22%) | 0.092 |
| Education | |||
| Did not finish high school | 33 (19%) | 5 (8%) | 0.129 |
| Completed high school | 42 (24%) | 15 (25%) | |
| Some college/vocational school | 60 (34%) | 22 (37%) | |
| Graduated from college | 28 (16%) | 12 (20%) | |
| Postgraduate degree | 15 (8%) | 6 (10%) | |
| High school | 145 (82%) | 55 (92%) | 0.063 |
| Low social support | 31 (18%) | 3 (5%) | 0.015 |
| No health insurance | 42 (24%) | 6 (10%) | 0.026 |
| Medical costs burden | 0.307 | ||
| Severe burden | 23 (13%) | 4 (7%) | |
| Moderate burden | 12 (7%) | 5 (9%) | |
| Somewhat of a burden | 25 (14%) | 7 (11%) | |
| A little burden | 12 (7%) | 6 (10%) | |
| No burden at all | 103 (59%) | 37 (63%) | |
| Live alone | 42 (24%) | 9 (15%) | 0.161 |
| Region | 0.093 | ||
| Midwest | 72 (48%) | 20 (39%) | |
| Northeast | 19 (13%) | 5 (10%) | |
| Southeast | 28 (19%) | 10 (19%) | |
| Southwest | 25 (17%) | 14 (27%) | |
| West | 6 (4%) | 3 (6%) | |
| Season | 0.124 | ||
| April to June | 2 (1%) | 0 (0%) | |
| July to September | 67 (38%) | 31 (52%) | |
| October to December | 109 (61%) | 29 (48%) | |
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