Disparities in cardiovascular disease risk and treatment: demographic comparison.

BACKGROUND: Cardiovascular morbidity and mortality can be prevented by identification and modification of specific risk factors. Ethnic minorities have a higher incidence of cardiovascular risk factors. Additionally, ethnic minorities often reside in medically underserved areas and are subject to health care disparities. We hypothesized that ethnic minorities residing in medically underserved areas would experience greater health care disparities related to cardiovascular disease (CVD) prevention and treatment compared with those residing near an urban academic medical center. METHODS: We performed a retrospective chart review (N = 200) comparing an urban academic medical center with a rural community center. We evaluated the effects of ethnicity, demographics, and the absence or presence of CVD on cardiovascular risk factor prevalence, risk factor reduction, and CVD prevention and treatment. RESULTS: We found that Hispanics had more cardiovascular risk factors, including diabetes mellitus and low high-density lipoprotein cholesterol, compared with non-Hispanic whites. However, there were no ethnically based differences in risk factor prevalence by location. Additionally, ethnicity had no impact on the management of cardiovascular risk factors. However, patients with CVD residing in the rural location, regardless of ethnicity, received significantly fewer secondary prevention treatments compared with patients residing near the urban academic medical center, including aspirin or antiplatelets (p < .0001); beta-blockers or calcium channel blockers (p < or = .0001); diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers (p = .014); and statins (p < or = .0001). CONCLUSIONS: Hispanics have more CVD risk factors than non-Hispanic whites but receive equivalent prevention initiatives. Residing in a rural, medically underserved area, regardless of ethnicity, was associated with the largest CVD treatment and health care disparity.

Methimazole-induced hypothyroidism paradoxically decreases homocysteine.

Clinical hypothyroidism is associated with hyperhomocysteinemia, whereas the opposite is seen in hyperthyroidism. The effects of mild thyroid dysfunction on homocysteine concentrations are not known. We performed the following study to investigate this. Total homocysteine, vitamins B6 and B12, folate, fibrinogen, plasminogen activator inhibitor type 1, and lipids were measured in 11 subjects at baseline and after methionine loading. Subjects began methimazole (MMI), 40 mg daily, and were restudied during 2 stages of hypothyroidism. Liothyronine was added and subjects were restudied once thyrotropin normalized. Methimazole was stopped and studies were repeated during 2 stages of hyperthyroidism. Data were analyzed using repeated-measures analysis of variance. Post-methionine homocysteine decreased in each hypothyroid study compared with baseline (28.8+/-10.7, 27.5+/-9.9 vs 34.4+/-9.2 micromol/L, respectively). In addition, both fasting and post-methionine homocysteine decreased in the euthyroid/MMI study arm compared with baseline despite equivalent thyrotropin values (fasting, 7.5+/-3.0 vs 8.8+/-3.5 micromol/L, P<.05; and post-methionine, 27.2+/-10.6 vs 34.4+/-9.2 micromol/L, P<.05, respectively). Fasting homocysteine decreased in the first hyperthyroidism study arm compared with baseline (6.6+/-2.3 vs 8.8+/-3.5 micromol/L, P<.05) and post-methionine homocysteine decreased in both hyperthyroid arms compared with baseline (25.2+/-8.1, 24.2+/-10 vs 34.4+/-9.2 micromol/L, P<.05 respectively). In conclusion, mild thyroid dysfunction changes homocysteine metabolism. Unexpectedly, our results suggest a homocysteine-lowering effect of MMI.

Patient knowledge improves glycemic control: is it time to go back to the classroom?

BACKGROUND: Over the last two decades, pharmaceutical intervention for the treatment of type 2 diabetes has expanded. Studies over this same time demonstrated the benefits of tight glycemic control. Unfortunately, despite the availability of novel therapies, glycemic control remains problematic. Nonpharmacologic interventions need to be explored, including patient empowerment. Improving patient knowledge of diabetes may ultimately improve glycemic control. To test this hypothesis, we compared patients' diabetes knowledge with their glycemic control. METHODS: The Michigan Diabetes Knowledge Test, designed by the University of Michigan, was administered to patients with type 2 diabetes at three University of New Mexico primary care clinics. Patient records were reviewed. The most recent hemoglobin A1c (HbA1c) value was recorded. The data were analyzed using linear regression analysis. RESULTS: Seventy-seven patients completed surveys and had HbA1c values available. Only questions 1 to 14 of the 23-question survey were used because they pertained specifically to type 2 diabetes. HbA1c was inversely correlated with the number of questions answered correctly on the test (r = -.337, p < .003). Using "all subsets" regression, a correct response to questions 1, 3, and 9 specifically correlated with a lower HbA1c (p < .0001). CONCLUSIONS: These results demonstrate that an inverse linear relationship exists between performance on this diabetes test and HbA1c values. Improvement in patient knowledge of diabetes and the importance of treatment may indeed improve glycemic control and ultimately decrease complications. Studies aimed at empowering patients with disease knowledge may help control the ramifications of the growing diabetes epidemic.

Potential association of thyrotoxicosis with vitamin B and folate deficiencies, resulting in risk for hyperhomocysteinemia and subsequent thromboembolic events.

OBJECTIVE: To describe a patient with severe thyrotoxicosis attributable to Graves' disease who had a thrombotic cerebrovascular accident and hyperhomocysteinuria, which resolved on correction of the thyrotoxicosis, and to present findings in a pilot study undertaken to investigate the relationship among thyrotoxicosis, homocysteine, folate, and vitamin B(12). METHODS: We present a case report of the index case, with clinical and laboratory details. For the investigative analysis, 21 patients who were 18 to 50 years old and had newly diagnosed, untreated Graves' disease and 10 age-and sex-matched euthyroid control subjects were studied. Of the patients with Graves' disease, 11 underwent studies both at diagnosis and after treatment. Fasting blood tests were performed for thyrotropin, free thyroxine, homocys-teine, vitamin B(12), folate, and methylmalonic acid, a marker of vitamin B(12) deficiency. RESULTS: Vitamin B(12), folate, homocysteine, and methylmalonic acid levels were not significantly different between the thyrotoxic and control or posttreatment groups. In patients with thyrotoxicosis, however, free thyroxine was positively correlated with both homocysteine (r = 0.67; P = 0.03) and methylmalonic acid (r = 0.89; P = 0.003). CONCLUSION: The positive correlation between free thyroxine levels and both homocysteine and methylmalonic acid suggests that thyrotoxicosis may be associated with functional vitamin B(12) deficiency. Such a deficiency may result in clinically important hyperhomocysteine-mia.