Cost-effectiveness of lower targets for blood pressure and low-density lipoprotein cholesterol in diabetes: the Stop Atherosclerosis in Native Diabetics Study (SANDS) .

BACKGROUND: The Stop Atherosclerosis in Native Diabetics Study (SANDS) reported cardiovascular benefit of aggressive versus standard treatment targets for both low-density lipoprotein cholesterol (LDL-C) and blood pressure (BP) in diabetic individuals. OBJECTIVE: In this analysis, we examined within trial cost-effectiveness of aggressive targets of LDL-C ≤70 mg/dL and systolic BP ≤115 mmHg versus standard targets of LDL-C ≤100 mg/dL and systolic BP ≤130 mmHg. DESIGN: Randomized, open label blinded-to-endpoint 3-year trial. DATA SOURCES: SANDS clinical trial database, Quality of Wellbeing survey, Centers for Medicare and Medicaid Services, Wholesale Drug Prices. TARGET POPULATION: American Indians ≥ age 40 years with type 2 diabetes and no previous cardiovascular events. TIME HORIZON: April 2003 to July 2007. PERSPECTIVE: Health payer. INTERVENTIONS: Participants were randomized to aggressive versus standard groups with treatment algorithms defined for both. OUTCOME MEASURES: Incremental cost-effectiveness. RESULTS OF BASE-CASE ANALYSIS: Compared with the standard group, the aggressive group had slightly lower costs of medical services (-$116) but a 54% greater cost for BP medication ($1,242) and a 116% greater cost for lipid-lowering medication ($2,863), resulting in an increased cost of $3,988 over 3 years. Those in the aggressively treated group gained 0.0480 quality-adjusted life-years (QALY) over the standard group. When a 3% discount rate for costs and outcomes was used, the resulting cost per QALY was $82,589. RESULTS OF SENSITIVITY ANALYSIS: The use of a 25%, 50%, and 75% reduction in drug costs resulted in a cost per QALY of $61,329, $40,070, and $18,810, respectively. LIMITATIONS: This study was limited by use of a single ethnic group and by its 3-year duration. CONCLUSIONS: Within this 3-year study, treatment to lower BP and LDL-C below standard targets was not cost-effective because of the cost of the additional medications required to meet the lower targets. With the anticipated availability of generic versions of the BP and lipid-lowering drugs used in SANDS, the cost-effectiveness of this intervention should improve. Published by Elsevier Inc on behalf of the National Lipid Association.

Usefulness of quantitative assessment of electrocardiographic ST depression for predicting new-onset heart failure in American Indians (from the Strong Heart Study).

The qualitative electrocardiographic strain pattern of ST depression (STD) and T-wave inversion is strongly associated with coronary heart disease and left ventricular hypertrophy and is an independent predictor of new-onset heart failure in hypertensive participants. However, whether quantitative measures of STD in the lateral precordial leads predict new heart failure is unclear. Digital electrocardiograms were examined in 2,059 American-Indian participants in the second Strong Heart Study examination with no history of heart failure. The absolute magnitude of ST segment deviation was measured using computer to the nearest 5 microV in leads V(5) and V(6). During 5.7 +/-1.4 years of follow-up, heart failure developed in 77 participants (3.7%). Participants who developed heart failure had greater STD in leads V(5) or V(6) (-11 +/- 35 vs 12 +/- 27 microV; p <0.001) than those who did not. In univariate Cox analyses, STD was a significant predictor of new heart failure, with each 10-microV greater STD associated with a 31% greater risk of heart failure (hazard ratio [HR] 1.31, 95% confidence interval [CI] 1.24 to 1.39). Increasing STD grouped according to quartiles was strongly associated with the development of heart failure, with stepwise increasing risk of heart failure compared with the lowest quartile of STD for the second (HR 2.39, 95% CI 0.77 to 7.40), third (HR 3.01, 95% CI 1.00 to 9.08), and fourth quartiles of STD (HR 9.06, 95% CI 3.26 to 25.16). In Cox multivariate analyses controlling for age, gender, diabetes, coronary heart disease, albuminuria, and other baseline risk factors, STD remained a significant predictor of incident heart failure (HR 1.22, 95% CI 1.13 to 1.32 per 10-muV increment in STD; p <0.001). In conclusion, increasing STD in lateral precordial leads is strongly associated with increased risk of developing heart failure independent of other risk factors for new heart failure.

Quantitative assessment of electrocardiographic strain predicts increased left ventricular mass: the Strong Heart Study.

OBJECTIVES: This study was designed to examine the relation of computer-measured ST depression (STdep) in the lateral precordial leads to the presence of left ventricular hypertrophy (LVH). BACKGROUND: Qualitative abnormalities of repolarization in the lateral precordial leads of the electrocardiogram, as manifested by the strain pattern of T-wave inversion and STdep, are markers for LVH and adverse prognosis. However, the independent relationship of increased left ventricular (LV) mass to quantitative measures of STdep in these leads remains unclear. METHODS: Electrocardiograms and echocardiograms were examined in the second Strong Heart Study examination in 1,595 American Indian participants without evident coronary disease. The absolute magnitude of ST segment deviation above or below isoelectric baseline was measured by computer in leads V(5) and V(6), and participants were grouped according to gender-specific quartiles of maximal STdep. Left ventricular hypertrophy was defined by indexed LV mass >49.2 g/m(2.7) in men and >46.7 g/m(2.7) in women. RESULTS: Increasing STdep was associated with older age, greater pulse pressure, serum fibrinogen levels and urinary albumin/creatinine ratios, and with stepwise increases in LV mass (145 +/- 28 vs. 150 +/- 33 vs. 156 +/- 36 vs. 164 +/- 43 g, p < 0.001), indexed LV mass (38.2 +/- 7.7 vs. 39.3 +/- 8.7 vs. 40.5 +/- 9.4 vs. 44.0 +/- 11.0 g/m(2.7), p < 0.001), and prevalence of LVH (11.6 vs. 19.1 vs. 21.5 vs. 31.2%, p < 0.001). After controlling for clinical differences, increasing STdep remained strongly associated with increased prevalence of LVH (p = 0.0001). CONCLUSIONS: In the absence of evidence of coronary disease, increasing STdep in the lateral precordial leads is associated with increasing LV mass and increased prevalence of anatomic LVH.