Heather M Johnson

University of Wisconsin, Madison, Madison, MS, United States

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Publications (15)83.27 Total impact

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    ABSTRACT: Young adults with hypertension have the lowest prevalence of controlled blood pressure compared to middle-aged and older adults. Uncontrolled hypertension, even among young adults, increases future cardiovascular event risk. However, antihypertensive medication initiation is poorly understood among young adults and may be an important intervention point for this group. The purpose of this study was to compare rates and predictors of antihypertensive medication initiation between young adults and middle-aged and older adults with incident hypertension and regular primary care contact. A retrospective analysis PARTICIPANTS: Adults ≥ 18 years old (n = 10,022) with incident hypertension and no prior antihypertensive prescription, who received primary care at a large, Midwestern, academic practice from 2008-2011. The primary outcome was time from date of meeting hypertension criteria to antihypertensive medication initiation, or blood pressure normalization without medication. Kaplan-Meier analysis was used to estimate the probability of antihypertensive medication initiation over time. Cox proportional-hazard models (HR; 95 % CI) were fit to identify predictors of delays in medication initiation, with a subsequent subpopulation analysis for young adults (18-39 years old). After a mean follow-up of 20 (±13) months, 34 % of 18-39 year-olds with hypertension met the endpoint, compared to 44 % of 40-59 year-olds and 56 % of ≥ 60 year-olds. Adjusting for patient and provider factors, 18-39 year-olds had a 44 % slower rate of medication initiation (HR 0.56; 0.47-0.67) than ≥ 60 year-olds. Among young adults, males, patients with mild hypertension, and White patients had a slower rate of medication initiation. Young adults with Medicaid and more clinic visits had faster rates. Even with regular primary care contact and continued elevated blood pressure, young adults had slower rates of antihypertensive medication initiation than middle-aged and older adults. Interventions are needed to address multifactorial barriers contributing to poor hypertension control among young adults.
    Journal of General Internal Medicine 02/2014; · 3.28 Impact Factor
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    ABSTRACT: Young adults meeting hypertension diagnostic criteria have a lower prevalence of a hypertension diagnosis than middle-aged and older adults. The purpose of this study was to compare the rates of a new hypertension diagnosis for different age groups and identify predictors of delays in the initial diagnosis among young adults who regularly use primary care. A 4-year retrospective analysis included 14 970 patients, at least 18 years old, who met clinical criteria for an initial hypertension diagnosis in a large, Midwestern, academic practice from 2008 to 2011. Patients with a previous hypertension diagnosis or prior antihypertensive medication prescription were excluded. The probability of diagnosis at specific time points was estimated by Kaplan-Meier analysis. Cox proportional hazard models (hazard ratio; 95% confidence interval) were fit to identify predictors of delays to an initial diagnosis, with a subsequent subset analysis for young adults (18-39 years old). After 4 years, 56% of 18-24-year-olds received a diagnosis compared with 62% (25-31-year-olds), 68% (32-39-year-olds), and more than 70% (≥40-year-olds). After adjustment, 18-31-year-olds had a 33% slower rate of receiving a diagnosis (18-24 years hazard ratio 0.66, 0.53-0.83; 25-31 years hazard ratio 0.68, 0.58-0.79) compared with adults at least 60 years. Other predictors of a slower diagnosis rate among young adults were current tobacco use, white ethnicity, and non-English primary language. Young adults with diabetes, higher blood pressures, or a female provider had a faster diagnosis rate. Provider and patient factors are critical determinants of poor hypertension diagnosis rates among young adults with regular primary care use.
    Journal of Hypertension 10/2013; · 4.22 Impact Factor
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    ABSTRACT: The mechanisms by which smoking cessation reduces cardiovascular disease risk are unclear. We evaluated longitudinal changes in carotid intima-media thickness among current smokers enrolled in a prospective, randomized smoking cessation clinical trial. Subjects were enrolled in a randomized, double-blind, placebo-controlled trial of 5 smoking cessation pharmacotherapies and underwent carotid ultrasonography with carotid intima-media thickness measurement. Subjects were classified as continuously abstinent (biochemically confirmed abstinence at 6 months, 1 year, and 3 years post-quit attempt), intermittently abstinent (reported smoking at one of the three time points), or smoked continuously (reported smoking at all three time points). The primary endpoint was the absolute change (mm) in carotid intima-media thickness (ΔCIMT(max)) before randomization and 3 years after the target quit date. Pearson correlations were calculated and multivariable regression models (controlling for baseline CIMT(max) and research site) were analyzed. Among 795 subjects (45.2 ± 10.6 years old, 58.5% female), 189 (23.8%) were continuously abstinent, 373 (46.9%) smoked continuously, and 233 (29.3%) were abstinent intermittently. There was a greater increase in carotid intima-media thickness among subjects who were continuously abstinent than among those who smoked continuously (p = 0.020), but not intermittently (p = 0.310). Antihypertensive medication use (p = 0.001) and research site (p<0.001) independently predicted ΔCIMTmax--not smoking status. The greatest increase in carotid intima-media thickness among continuous abstainers was related to increases in body-mass index (p = 0.043). Smoking status did not independently predict ΔCIMT(max); increasing body-mass index and antihypertensive medication use were the most important independent predictors. The rapid reduction in cardiovascular disease events observed with smoking cessation is unlikely to be mediated by changes in subclinical atherosclerosis burden. ClinicalTrials.gov NCT00332644.
    PLoS ONE 01/2012; 7(4):e35332. · 3.53 Impact Factor
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    ABSTRACT: Carotid ultrasound screening (CUS) has been recommended for cardiovascular disease risk prediction, but its effectiveness in clinical practice is unknown. The purpose of this study was to prospectively determine the effects of office-based CUS on physician decision making and patient health-related behaviors. Physicians from five nonacademic, community practices recruited patients aged ≥40 years with ≥1 cardiovascular disease risk factor. Abnormal results on CUS (AbnlCUS) were defined as carotid intima-media thickness >75th percentile or carotid plaque presence. Subjects completed questionnaires before and immediately after CUS and then 30 days later to determine self-reported behavioral changes. Odds ratios (ORs) for changes in physician management and patient health-related behaviors were determined from multivariate hierarchical logistic regression models. There were 355 subjects (mean age, 53.6 ± 7.9 years; mean number of risk factors, 2.3 ± 0.9; 58% women); 266 (74.9%) had AbnlCUS. The presence of AbnlCUS altered physicians' prescription of aspirin (P < .001) and cholesterol medications (P < .001). Immediately after CUS, subjects reported increased ability to change health-related behaviors (P = .002), regardless of their test results. Subjects with AbnlCUS reported increased cardiovascular disease risk perception (OR, 4.14; P < .001) and intentions to exercise (OR, 2.28; P = .008), make dietary changes (OR, 2.95; P < .001), and quit smoking (OR, 4.98; P = .022). After 30 days, 34% increased exercise frequency and 37% reported weight loss, but these changes were not predicted by the CUS results. AbnlCUS modestly predicted reduced dietary sodium (OR, 1.45; P = .002) and increased fiber (OR, 1.55; P = .022) intake. Finding abnormal results on CUS had major effects on physician but not patient behaviors.
    Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 07/2011; 24(7):738-47. · 2.98 Impact Factor
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    ABSTRACT: Ethnicity has been identified as a risk factor not only for having type 2 diabetes but for increased morbidity and mortality with the disease. Current American Diabetes Association (ADA) guidelines advocate screening high-risk minorities for diabetes. This study investigates the effect of minority status on diabetes screening practices in an ambulatory, insured population presenting for yearly health care. This is a retrospective population-based study of patients in a large, Midwestern, academic group practice. Included patients were insured, had ≥1 primary care visit yearly from 2003 to 2007, and did not have diabetes but met ADA criteria for screening. Odds ratios (ORs), 95% confidence intervals (CI), and predicted probabilities were calculated to determine the relationship between screening with fasting glucose, glucose tolerance test, or hemoglobin A(1c) and patient and visit characteristics. Of the 15,557 eligible patients, 607 (4%) were of high-risk ethnicity, 61% were female, and 86% were ≥45 years of age. Of the eight high-risk factors studied, after adjustment, ethnicity was the only factor not associated with higher diabetes screening (OR = 0.90 [95% CI 0.76-1.08]) despite more primary care visits in this group. In overweight patients <45 years, where screening eligibility is based on having an additional risk factor, high-risk ethnicity (OR 1.01 [0.70-1.44]) was not associated with increased screening frequency. In an insured population presenting for routine care, high-risk minority status did not independently lead to diabetes screening as recommended by ADA guidelines. Factors other than insurance or access to care appear to affect minority-preventive care.
    Diabetes care 06/2011; 34(6):1289-94. · 7.74 Impact Factor
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    Archives of internal medicine 03/2011; 171(6):589-91. · 11.46 Impact Factor
  • Heather M Johnson, James H Stein
    Journal of Nuclear Cardiology 02/2011; 18(1):153-62. · 2.85 Impact Factor
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    ABSTRACT: the effects of smoking and smoking cessation on lipoproteins have not been studied in a large contemporary group of smokers. This study was designed to determine the effects of smoking cessation on lipoproteins. this was a 1-year, prospective, double-blind, randomized, placebo-controlled clinical trial of the effects of 5 smoking cessation pharmacotherapies. Fasting nuclear magnetic resonance spectroscopy lipoprotein profiles were obtained before and 1 year after the target smoking cessation date. The effects of smoking cessation and predictors of changes in lipoproteins after 1 year were identified by multivariable regression. the 1,504 current smokers were (mean [SD]) 45.4 (11.3) years old and smoked 21.4 (8.9) cigarettes per day at baseline. Of the 923 adult smokers who returned at 1 year, 334 (36.2%) had quit smoking. Despite gaining more weight (4.6 kg [5.7] vs 0.7 kg [5.1], P < .001], abstainers had increases in high-density lipoprotein cholesterol (HDL-C) (2.4 [8.3] vs 0.1 [8.8] mg/dL, P < .001), total HDL (1.0 [4.6] vs -0.3 micromol/L [5.0], P < .001), and large HDL (0.6 [2.2] vs 0.1 [2.1] micromol/L, P = .003) particles compared with continuing smokers. Significant changes in low-density lipoprotein (LDL) cholesterol and particles were not observed. After adjustment, abstinence from smoking (P < .001) was independently associated with increases in HDL-C and total HDL particles. These effects were stronger in women. despite weight gain, smoking cessation improved HDL-C, total HDL, and large HDL particles, especially in women. Smoking cessation did not affect LDL or LDL size. Increases in HDL may mediate part of the reduced cardiovascular disease risk observed after smoking cessation.
    American heart journal 01/2011; 161(1):145-51. · 4.65 Impact Factor
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    ABSTRACT: Cigarette smoking has been associated with increases in C-reactive protein (CRP) and leukocyte counts (white blood cell [WBC]); however, the effects of smoking intensity and smoking cessation on inflammatory markers have not been evaluated prospectively in a large, modern cohort of current smokers. White blood cell count and high-sensitivity CRP were measured in current smokers enrolled in a randomized, prospective clinical trial of 5 smoking cessation pharmacotherapies. Smoking intensity parameters included cigarettes per day, pack-years, Fagerström Test of Nicotine Dependence score, and carbon monoxide levels. C-reactive protein also was measured after 1 year with assessment of abstinence status. The 1,504 current smokers (58% female) were (mean [SD]) 44.7 (11.1) years old, smoked 21.4 (8.9) cigarettes per day, and had a smoking burden of 29.4 (20.4) pack-years. Log(CRP) was not associated with any marker of smoking intensity, except for a weak correlation with pack-years (r = 0.05, P = .047). In contrast, statistically significant correlations were observed between all 4 markers of smoking intensity and WBC count (all P ≤ .011). In multivariable models, waist circumference (P < .001) and triglycerides (P < .05), but no markers of smoking intensity, were associated with log(CRP). However, pack-years (P = .002), cigarettes per day (P = .013), carbon monoxide (P < .001), and Fagerström Test of Nicotine Dependence (P < .001) were independently associated with WBC count. After 1 year, log(CRP) (P = .296) and changes in log(CRP) (P = .455) did not differ between abstainers and continuing smokers. Smoking intensity is associated with increased WBC count, but not CRP levels. Smoking cessation does not reduce CRP. The relationship between CRP and smoking intensity may be masked by CRP's stronger relationship with adiposity.
    American heart journal 09/2010; 160(3):458-63. · 4.65 Impact Factor
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    James H Stein, Heather M Johnson
    Journal of the American College of Cardiology 04/2010; 55(15):1608-10. · 14.09 Impact Factor
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    ABSTRACT: The purpose of this study was to determine whether smoking cessation improves flow-mediated dilation (FMD) of the brachial artery. The long-term effects of continued smoking and smoking cessation on endothelial function have not been described previously. This was a 1-year, prospective, double-blind, randomized, placebo-controlled clinical trial of the effects of 5 smoking cessation pharmacotherapies. FMD was measured by B-mode ultrasonography before and 1 year after the target smoking cessation date. Cessation was verified by exhaled carbon monoxide levels. DeltaFMD was compared among study arms and between subjects who successfully quit smoking and those who continued to smoke. Predictors of baseline FMD and DeltaFMD were identified by multivariable regression. The 1,504 current smokers (58% female, 84% white) were 44.7 +/- 11.1 years of age and smoked 21.4 +/- 8.9 cigarettes/day. Baseline FMD was similar in each treatment arm (p = 0.499) and was predicted by BA diameter (p < 0.001), reactive hyperemia blood flow (p < 0.001), high-density lipoprotein cholesterol (p = 0.001), and carbon monoxide (p = 0.012) levels. After 1 year, 36.2% quit smoking. FMD increased by 1% (6.2 +/- 4.4% to 7.2 +/- 4.2%) after 1 year (p = 0.005) in those who quit, but did not change (p = 0.643) in those who continued to smoke. Improved FMD among quitters remained significant (p = 0.010) after controlling for changes in brachial artery diameter, reactive hyperemia, low-density lipoprotein cholesterol, and the presence of a home smoking ban. Despite weight gain, smoking cessation leads to prolonged improvements in endothelial function, which may mediate part of the reduced cardiovascular disease risk observed after smoking cessation. (Smoking Cessation Medications: Efficacy, Mechanisms and Algorithms; NCT00332644).
    Journal of the American College of Cardiology 03/2010; 55(18):1988-95. · 14.09 Impact Factor
  • Journal of The American College of Cardiology - J AMER COLL CARDIOL. 01/2010; 55(10).
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    ABSTRACT: This study characterized the determinants of carotid atherosclerosis in a large contemporary sample of current smokers. Associations between risk factors, carotid intima-media thickness (CIMT), and carotid plaque presence were determined by multivariable regression. Participants included 1504 current smokers (58% female) who were a median (interquartile range) of 44.7 (38-53) years old and smoked 25 (15-40) pack-years; 55% had plaque. Pack-years, age, male sex, nonwhite race, body mass index, systolic blood pressure, small low-density lipoproteins (LDLs), and total high-density lipoproteins were independently associated with CIMT (model R(2) =0.434, P<.001). Pack-years (odds ratio [OR], 1.14 per 10 pack-years; P=.001), age (OR, 1.75 per 10 years; P<.001), body mass index (OR, 0.91 per 5 kg/m(2) ; P=.035), and small LDLs (OR, 1.11 per 100 nmol/L; P<.001) were independently associated with carotid plaque presence (model χ(2) =210.7, P<.001). The association between pack-years and carotid plaque was stronger in women (OR, 1.09 per 10 pack-years, P(interaction) =.018).
    Preventive Cardiology 01/2010; 13(4):166-71.
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    ABSTRACT: Smoking is associated with decreased high-density lipoprotein cholesterol (HDL-C) and elevated triglycerides. To evaluate the effects of five markers of smoking intensity on lipoprotein concentrations and particle sizes in a large, modern cohort of current smokers. Fasting nuclear magnetic resonance spectroscopy lipoprotein profiles were obtained in a large cohort of current smokers enrolled in a smoking cessation trial. Multivariate linear regression models were constructed to determine predictors of lipoprotein fractions. Models included age, sex, race, waist circumference, level of physical activity and alcohol consumption. Smoking intensity parameters included: current cigarettes smoked/day, pack-years, the Fagerström Test of Nicotine Dependence (FTND) score, and carbon monoxide (CO) levels. The 1,504 subjects (58% women, 84% white) had a mean (standard deviation) age of 45 (11.0) years. They smoked 21.4 (8.9) cigarettes/day (29.4 [20.4] pack-years). HDL-C (42.0 [13.5] mg/dL) and total HDL particles (30.3 [5.9] μmol/L) were low. Cigarettes smoked/day independently predicted higher total cholesterol (p=0.009), low-density lipoprotein cholesterol (p=0.023), and triglycerides (p=0.002). CO levels predicted lower HDL-C (p=0.027) and total HDL particles (p=0.009). However, the incremental R(2) for each marker of smoking intensity on each lipoprotein was small. Relationships between the FTND score and lipoproteins were weak and inconsistent. Participants in the lowest quintiles of current smoking, pack-years, and CO had more favorable lipoproteins (all p<0.04). Among current smokers, increased smoking burden is associated with small increases in total cholesterol, LDL-C, and triglycerides. Increased recent smoke exposure is associated with small decreases in HDL-C and HDL particles.
    Journal of Clinical Lipidology 12/2009; 3(6):372-8. · 3.59 Impact Factor
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    ABSTRACT: We sought to evaluate the predictors of carotid intima-media thickness (CIMT) progression in young adults and to determine whether they differed between the sexes. Although risk factors for the progression of atherosclerosis in middle-aged and elderly adults are well known, they are less well understood in young adults. CIMT is a validated measure of subclinical atherosclerosis. B-mode ultrasound images of the far walls of both carotid arteries were obtained in 336 young adults in the Bogalusa Heart Study, whose mean+/-SD age was 32.3+/-3.0 years. CIMT and risk factors were measured at baseline (1995-1996) and after 5.8+/-0.6 years. Multivariable regression was used to determine the predictors of CIMT progression. CIMT progression rates in women (0.015+/-0.024 mm/y) and men (0.020+/-0.027 mm/y) were not statistically different after controlling for body mass index (P=0.155). Smoking was a statistically significant predictor of common and composite CIMT progression in both sexes. In men, systolic blood pressure was an independent predictor of internal carotid and composite CIMT progression, fasting glucose predicted common CIMT progression, and family history predicted composite CIMT progression. In young adults, smoking was a consistent predictor of short-term CIMT progression in men and women. Traditional risk factors also predicted CIMT progression in men.
    Stroke 04/2007; 38(3):900-5. · 6.16 Impact Factor