American Heart Association Tobacco Regulation and Addiction Center, which is funded by the U.S. Food and Drug Administration and National Heart, Lung, and Blood Institute.

Cardiovascular disease is a leading cause of morbidity and mortality worldwide, and a key barrier to improved outcomes is medication non-adherence. The aim of this study is to review the role of mobile health (mHealth) tools for improving medication adherence in patients with cardiovascular disease. We performed a systematic search for randomized controlled trials that primarily investigated mHealth tools for improving adherence to cardiovascular disease medications in patients with hypertension, coronary artery disease, heart failure, peripheral arterial disease, and stroke. We extracted and reviewed data on the types of mHealth tools used, preferences of patients and healthcare providers, the effect of the mHealth interventions on medication adherence, and the limitations of trials. We identified 10 completed trials matching our selection criteria, mostly with <100 participants, and ranging in duration from 1 to 18 months. mHealth tools included text messages, Bluetooth-enabled electronic pill boxes, online messaging platforms, and interactive voice calls. Patients and healthcare providers generally preferred mHealth to other interventions. All 10 studies reported that mHealth interventions improved medication adherence, though the magnitude of benefit was not consistently large and in one study was not greater than a telehealth comparator. Limitations of trials included small sample sizes, short duration of follow-up, self-reported outcomes, and insufficient assessment of unintended harms and financial implications. Current evidence suggests that mHealth tools can improve medication adherence in patients with cardiovascular diseases. However, high-quality clinical trials of sufficient size and duration are needed to move the field forward and justify use in routine care.

Quantification of coronary artery calcium (CAC) has been shown to be reliable, reproducible, and predictive of cardiovascular risk. Formal CAC scoring was introduced in 1990, with early scoring algorithms notable for their simplicity and elegance. Yet, with little evidence available on how to best build a score, and without a conceptual model guiding score development, these scores were, to a large degree, arbitrary. In this review, we describe the traditional approaches for clinical CAC scoring, noting their strengths, weaknesses, and limitations. We then discuss a conceptual model for developing an improved CAC score, reviewing the evidence supporting approaches most likely to lead to meaningful score improvement (for example, accounting for CAC density and regional distribution). After discussing the potential implementation of an improved score in clinical practice, we follow with a discussion of the future of CAC scoring, asking the central question: do we really need a new CAC score?

To inform the study and regulation of emerging tobacco products, we sought to identify sensitive biomarkers of tobacco-induced subclinical cardiovascular damage by testing the cross-sectional associations of smoking with 17 biomarkers of inflammation in 2,702 GENOA study participants belonging to sibships ascertained on the basis of hypertension. Cigarette smoking was assessed by status, intensity (number of cigarettes per day), burden (pack-years of smoking), and time since quitting. We modeled biomarkers as geometric mean (GM) ratios using generalized estimating equations (GEE). The mean age of participants was 61 ±10 years; 64.5% were women and 54.4% African American. The prevalence of smoking was 12.2%. After adjusting for potential confounders, 6 of 17 biomarkers were significantly higher among current smokers at a Bonferroni adjusted p-value threshold (p<0.003). High sensitivity C-reactive protein was the most elevated biomarker among current smokers when compared to never smokers [GM ratio = 1.39 (95% CI: 1.23, 1.57); p <0.001]. Among former smokers, each pack-year of cigarettes smoked was associated with a 0.4% higher serum level of hsCRP [GM ratio = 1.004 (95% CI: 1.001, 1.006); p = 0.002] and each 5-year lapsed since quitting was associated with a 4% lower serum level of hsCRP [GM ratio = 0.96 (95% CI: 0.93, 0.99); p = 0.006]. However, we found no significant association of smoking intensity or burden with biomarkers of inflammation among current smokers. HsCRP appears to be the most sensitive biomarker of inflammation associated with cigarette smoking of those investigated, and could be a useful biomarker of smoking-related injury for the study and regulation of emerging tobacco products.

BackgroundThere is a need to identify sensitive biomarkers of early tobacco‐related cardiovascular disease. We examined the association of smoking status, burden, time since quitting, and intensity, with markers of inflammation and subclinical atherosclerosis.Methods and ResultsWe studied 14 103 participants without clinical cardiovascular disease in ELSA‐Brasil (Brazilian Longitudinal Study of Adult Health). We evaluated baseline cross‐sectional associations between smoking parameters and inflammation (high‐sensitivity C‐reactive protein [hsCRP]) and measures of subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, and coronary artery calcium [CAC]). The cohort included 1844 current smokers, 4121 former smokers, and 8138 never smokers. Mean age was 51.7±8.9 years; 44.8% were male. After multivariable adjustment, compared with never smokers, current smokers had significantly higher levels of hsCRP (β=0.24, 0.19–0.29 mg/L; P<0.001) and carotid intima–media thickness (β=0.03, 0.02–0.04 mm; P<0.001) and odds of ankle‐brachial index ≤1.0 (odds ratio: 2.52; 95% confidence interval, 2.06–3.08; P<0.001) and CAC >0 (odds ratio: 1.83; 95% confidence interval, 1.46–2.30; P<0.001). Among former and current smokers, pack‐years of smoking (burden) were significantly associated with hsCRP (P<0.001 and P=0.006, respectively) and CAC (P<0.001 and P=0.002, respectively). Among former smokers, hsCRP and carotid intima–media thickness levels and odds of ankle‐brachial index ≤1.0 and CAC >0 were lower with increasing time since quitting (P<0.01). Among current smokers, number of cigarettes per day (intensity) was positively associated with hsCRP (P<0.001) and CAC >0 (P=0.03) after adjusting for duration of smoking.ConclusionsStrong associations were observed between smoking status, burden, and intensity with inflammation (hsCRP) and subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, CAC). These markers of early cardiovascular disease injury may be used for the further study and regulation of traditional and novel tobacco products.

Previous studies on animals have revealed that garlic (Allium sativum) is effective in reducing blood and tissue lead concentrations. The aim of this study was to investigate therapeutic effects of garlic and compare it with D-penicillamine in patients with chronic lead poisoning. After coordination and obtaining informed consent, clinical examinations and blood lead concentration (BLC) of 117 workers at a car battery industry were investigated. BLC was determined by heated graphite atomization technique of an atomic absorption spectrometer. The workers were randomly assigned into two groups of garlic (1200 lg allicin, three times daily) and D-penicillamine (250 mg, three times daily) and treated for 4 weeks. BLC was determined again 10 days post-treatment. Clinical signs and symptoms of lead poisoning were also investigated and compared with the initial findings. Clinical improvement was significant in a number of clinical manifestations including irritability (p = 0.031), headache (p = 0.028), decreased deep tendon reflex (p = 0.019) and mean systolic blood pressure (0.021) after treatment with garlic, but not D-penicillamine. BLCs were reduced significantly (p = 0.002 and p = 0.025) from 426.32 € 185.128 to 347.34 € 121.056 lg ⁄ L and from 417. 47 € 192.54 to 315.76 € 140.00 lg ⁄ L in the garlic and D-penicillamine groups, respectively, with no significant difference (p = 0.892) between the two groups. The frequency of side effects was significantly (p = 0.023) higher in D-penicillamine than in the garlic group. Thus, garlic seems safer clinically and as effective as D-penicillamine. Therefore, garlic can be recommended for the treatment of mild-to-moderate lead poisoning.

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We examined the utility of coronary artery calcium (CAC) for cardiovascular risk stratification among hypertensive adults, including those fitting eligibility for SPRINT (Systolic Blood Pressure Intervention Trial). Additionally, we used CAC to identify hypertensive adults with cardiovascular disease (CVD) mortality rates equivalent to those observed in SPRINT who may, therefore, benefit from the most intensive blood pressure therapy. Our study population included 16 167 hypertensive patients from the CAC Consortium, among whom 6375 constituted a "SPRINT-like" population. We compared multivariable-adjusted hazard ratios of coronary heart disease and CVD deaths by CAC category (0, 1-99, 100-399, ≥400). Additionally, we generated a CAC-CVD mortality curve for patients aged >50 years to determine what CAC scores were associated with CVD death rates observed in SPRINT. Mean age was 58.1±10.6 years. During a mean follow-up of 11.6±3.6 years, there were 409 CVD deaths and 207 coronary heart disease deaths. Increasing CAC scores were associated with increased coronary heart disease and CVD mortality (coronary heart disease-CAC 100-399: hazard ratio [95% CI] 1.88 [1.04-3.40], CAC ≥400: 4.16 [2.34-7.39]; CVD-CAC 100-399: 1.93 [1.31-2.83], CAC ≥400: 3.51 [2.40-5.13]). A similar increased risk was observed across 10-year atherosclerotic CVD risk categories and in the SPRINT-like population. A CAC score of 220 (confidence range, 165-270) was associated with the CVD mortality rate observed in SPRINT. CAC risk stratifies adults with hypertension, including those who are SPRINT eligible. A CAC score of 220 can identify hypertensive adults with SPRINT-level CVD mortality risk and, therefore, may be reasonable for identifying candidates for aggressive blood pressure therapy. (Hypertension. XXX;73:00-00.