Association of Coronary Plaque With Low-Density Lipoprotein Cholesterol Levels and Rates of Cardiovascular Disease Events Among Symptomatic Adults.

Importance: Atherosclerosis burden and coronary artery calcium (CAC) are associated with the risk for atherosclerotic cardiovascular disease (ASCVD) events, with absence of plaque and CAC indicating low risk. Whether this is true in patients with elevated levels of low-density lipoprotein cholesterol (LDL-C) is not known. Specifically, a high prevalence of noncalcified plaque might signal high risk. Objective: To determine the prevalence of noncalcified and calcified plaque in symptomatic adults and assess its association with cardiovascular events across the LDL-C spectrum. Design, Setting, and Participants: This cohort study included symptomatic patients undergoing coronary computed tomographic angiography from January 1, 2008, to December 31, 2017, from the seminational Western Denmark Heart Registry. Follow-up was completed on July 6, 2018. Data were analyzed from April 2 to December 2, 2021. Exposures: Prevalence of calcified and noncalcified plaque according to LDL-C strata of less than 77, 77 to 112, 113 to 154, 155 to 189, and at least 190 mg/dL. Severity of coronary artery disease was categorized using CAC scores of 0, 1 to 99, and ≥100, where higher numbers indicate greater CAC burden. Main Outcomes and Measures: Atherosclerotic cardiovascular disease events (myocardial infarction and stroke) and death. Results: A total of 23 143 patients with a median age of 58 (IQR, 50-65) years (12 857 [55.6%] women) were included in the analysis. During median follow-up of 4.2 (IQR, 2.3-6.1) years, 1029 ASCVD and death events occurred. Across all LDL-C strata, absence of CAC was a prevalent finding (ranging from 438 of 948 [46.2%] in patients with LDL-C levels of at least 190 mg/dL to 4370 of 7964 [54.9%] in patients with LDL-C levels of 77-112 mg/dL) and associated with no detectable plaque in most patients, ranging from 338 of 438 (77.2%) in those with LDL-C levels of at least 190 mg/dL to 1067 of 1204 (88.6%) in those with LDL-C levels of less than 77 mg/dL. In all LDL-C groups, absence of CAC was associated with low rates of ASCVD and death (6.3 [95% CI, 5.6-7.0] per 1000 person-years), with increasing rates in patients with CAC scores of 1 to 99 (11.1 [95% CI, 10.0-12.5] per 1000 person-years) and CAC scores of at least 100 (21.9 [95% CI, 19.9-24.4] per 1000 person-years). Among those with CAC scores of 0, the event rate per 1000 person-years was 6.3 (95% CI, 5.6-7.0) in the overall population compared with 6.9 (95% CI, 4.0-11.9) in those with LDL-C levels of at least 190 mg/dL. Across all LDL-C strata, rates were similar and low in those with CAC scores of 0, regardless of whether they had no plaque or purely noncalcified plaque. Conclusions and Relevance: The findings of this cohort study suggest that in symptomatic patients with severely elevated LDL-C levels of at least 190 mg/dL who are universally considered to be at high risk by guidelines, absence of calcified and noncalcified plaque on coronary computed tomographic angiography was associated with low risk for ASCVD events. These results further suggest that atherosclerosis burden, including CAC, can be used to individualize treatment intensity in patients with severely elevated LDL-C levels.

Association between low density lipoprotein cholesterol and all-cause mortality: results from the NHANES 1999-2014.

The association between low density lipoprotein cholesterol (LDL-C) and all-cause mortality has been examined in many studies. However, inconsistent results and limitations still exist. We used the 1999-2014 National Health and Nutrition Examination Survey (NHANES) data with 19,034 people to assess the association between LDL-C level and all-cause mortality. All participants were followed up until 2015 except those younger than 18 years old, after excluding those who died within three years of follow-up, a total of 1619 deaths among 19,034 people were included in the analysis. In the age-adjusted model (model 1), it was found that the lowest LDL-C group had a higher risk of all-cause mortality (HR 1.708 [1.432-2.037]) than LDL-C 100-129 mg/dL as a reference group. The crude-adjusted model (model 2) suggests that people with the lowest level of LDL-C had 1.600 (95% CI [1.325-1.932]) times the odds compared with the reference group, after adjusting for age, sex, race, marital status, education level, smoking status, body mass index (BMI). In the fully-adjusted model (model 3), people with the lowest level of LDL-C had 1.373 (95% CI [1.130-1.668]) times the odds compared with the reference group, after additionally adjusting for hypertension, diabetes, cardiovascular disease, cancer based on model 2. The results from restricted cubic spine (RCS) curve showed that when the LDL-C concentration (130 mg/dL) was used as the reference, there is a U-shaped relationship between LDL-C level and all-cause mortality. In conclusion, we found that low level of LDL-C is associated with higher risk of all-cause mortality. The observed association persisted after adjusting for potential confounders. Further studies are warranted to determine the causal relationship between LDL-C level and all-cause mortality.

Global perspective of familial hypercholesterolaemia: a cross-sectional study from the EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC).

BACKGROUND: The European Atherosclerosis Society Familial Hypercholesterolaemia Studies Collaboration (FHSC) global registry provides a platform for the global surveillance of familial hypercholesterolaemia through harmonisation and pooling of multinational data. In this study, we aimed to characterise the adult population with heterozygous familial hypercholesterolaemia and described how it is detected and managed globally. METHODS: Using FHSC global registry data, we did a cross-sectional assessment of adults (aged 18 years or older) with a clinical or genetic diagnosis of probable or definite heterozygous familial hypercholesterolaemia at the time they were entered into the registries. Data were assessed overall and by WHO regions, sex, and index versus non-index cases. FINDINGS: Of the 61 612 individuals in the registry, 42 167 adults (21 999 [53·6%] women) from 56 countries were included in the study. Of these, 31 798 (75·4%) were diagnosed with the Dutch Lipid Clinic Network criteria, and 35 490 (84·2%) were from the WHO region of Europe. Median age of participants at entry in the registry was 46·2 years (IQR 34·3-58·0); median age at diagnosis of familial hypercholesterolaemia was 44·4 years (32·5-56·5), with 40·2% of participants younger than 40 years when diagnosed. Prevalence of cardiovascular risk factors increased progressively with age and varied by WHO region. Prevalence of coronary disease was 17·4% (2·1% for stroke and 5·2% for peripheral artery disease), increasing with concentrations of untreated LDL cholesterol, and was about two times lower in women than in men. Among patients receiving lipid-lowering medications, 16 803 (81·1%) were receiving statins and 3691 (21·2%) were on combination therapy, with greater use of more potent lipid-lowering medication in men than in women. Median LDL cholesterol was 5·43 mmol/L (IQR 4·32-6·72) among patients not taking lipid-lowering medications and 4·23 mmol/L (3·20-5·66) among those taking them. Among patients taking lipid-lowering medications, 2·7% had LDL cholesterol lower than 1·8 mmol/L; the use of combination therapy, particularly with three drugs and with proprotein convertase subtilisin-kexin type 9 inhibitors, was associated with a higher proportion and greater odds of having LDL cholesterol lower than 1·8 mmol/L. Compared with index cases, patients who were non-index cases were younger, with lower LDL cholesterol and lower prevalence of cardiovascular risk factors and cardiovascular diseases (all p<0·001). INTERPRETATION: Familial hypercholesterolaemia is diagnosed late. Guideline-recommended LDL cholesterol concentrations are infrequently achieved with single-drug therapy. Cardiovascular risk factors and presence of coronary disease were lower among non-index cases, who were diagnosed earlier. Earlier detection and greater use of combination therapies are required to reduce the global burden of familial hypercholesterolaemia. FUNDING: Pfizer, Amgen, Merck Sharp & Dohme, Sanofi-Aventis, Daiichi Sankyo, and Regeneron.

Phytosterol supplementation in the treatment of dyslipidemia in children and adolescents: a systematic review / Suplementação de fitoesteróis no tratamento da dislipidemia em crianças e adolescentes: uma revisão sistemática

ABSTRACT Objective: To carry out a systematic review on the effects of phytosterol supplementation on the treatment of dyslipidemia in children and adolescents. Data sources: Review in the SciELO, Lilacs, Bireme, PubMed and Web of Science databases, with no time limit. Descriptors: phytosterols or plant sterols and dyslipidemias, hypercholesterolemia, cholesterol, children, adolescent, in English and Portuguese. The articles included were published in Portuguese, English or Spanish and evaluated the effect of phytosterol supplementation in pediatric patients with dyslipidemia. Documents that involved adults or animals, review papers, case studies and abstracts were excluded. Two authors performed independent extraction of articles. Of 113 abstracts, 19 were read in full and 12 were used in this manuscript. Data synthesis: Phytosterol supplementation to reduce cholesterol levels has been shown to be effective in reducing LDL-cholesterol levels by approximately 10%, with reductions above 10% in LDL-cholesterol levels observed after 8 to 12 weeks of intervention. Studies have not shown significant changes in HDL-cholesterol and triglyceride levels. Based on the absence of adverse effects, its use seems to be safe and of good tolerance in children and adolescents. Conclusions: Phytosterol supplementation seems to be of great therapeutic aid for the treatment of hypercholesterolemia in children and adolescents. Further studies assessing the long-term effect of phytosterol supplementation are necessary.

RESUMO Objetivo: Realizar uma revisão sistemática sobre os efeitos da suplementação de fitoesteróis no tratamento da dislipidemia em crianças e adolescentes. Fontes de dados: Revisão nos bancos SciELO, Lilacs, Bireme, Pubmed e Web of Science, sem limite de tempo. Descritores: phytosterols or plant sterols, dyslipidemias, hypercholesterolemia, cholesterol, children, adolescent, nas línguas inglesa e portuguesa. Os artigos incluídos foram publicados nos idiomas português, inglês ou espanhol e avaliaram o efeito da suplementação de fitoesteróis em pacientes pediátricos com dislipidemia. Estudos que envolviam adultos ou animais, trabalhos de revisão, estudos de caso e resumos foram excluídos. A extração independente de artigos foi realizada por dois autores. Do total de 113 resumos, 19 foram lidos na íntegra, e 12 utilizados neste manuscrito. Síntese de dados: A suplementação de fitoesteróis para a redução dos níveis de colesterol mostrou-se eficiente, de forma a promover a redução de aproximadamente 10% dos níveis de LDL-colesterol, sendo observadas reduções acima de 10% em 8 a 12 semanas de intervenção. Os estudos não mostraram alterações significantes nos níveis de HDL-colesterol e triglicérides. Com base na ausência de efeitos adversos, seu uso parece ser seguro e de boa tolerância em crianças e adolescentes. Conclusões: A suplementação com fitoesteróis parece ser de grande auxílio terapêutico para o tratamento da hipercolesterolemia em crianças e adolescentes. São necessários mais estudos que avaliem o efeito em longo prazo da suplementação de fitoesteróis.

Cardiovascular event rates and trajectories of LDL-cholesterol levels and lipid-lowering therapy in patients with atherosclerotic cardiovascular disease: A population-based cohort study.

BACKGROUND: An understanding of cardiovascular event rates and low-density lipoprotein cholesterol (LDL-C) levels and trajectories in patients with atherosclerotic cardiovascular disease is needed to evaluate treatment goals and adherence to guidelines. METHODS: We conducted a population-based cohort study in the North and Central Denmark Regions. Patients with prevalent atherosclerotic cardiovascular disease (myocardial infarction, non-hemorrhagic stroke, or peripheral artery disease) during 2006-2009 were identified. All patients received lipid-lowering therapy (statins or ezetimibe) and had LDL-C levels ≥1.8 mmol/L at baseline (January 1, 2010). We followed patients for 6 years until a primary composite outcome of cardiovascular death, myocardial infarction, non-hemorrhagic stroke, hospitalization for unstable angina, or coronary revascularization. Additionally, we characterized changes in LDL-C levels and use of statins during follow-up. RESULTS: The study included 10,772 patients (median age 69.2 years, 60.4% male). The overall event rate for the primary outcome was 62.7 (95% confidence interval: 59.2-66.2) per 1000 person-years. This event rate was higher among men than among women and increased with age and baseline LDL-C levels. Approximately 25% of patients with LDL-C measurements during follow-up achieved LDL-C levels below 1.8 mmol/L. Of the approximately two-thirds of patients using statins at the end of follow-up, nearly all patients (97%) received high-intensity therapy. CONCLUSIONS: In this population of patients with atherosclerotic cardiovascular disease, we found high cardiovascular event rates, which increased with baseline LDL-C levels. Although most patients were on high-intensity statin therapy at end of follow-up, only one-quarter reached the guideline-recommended target LDL-C level ≤ 1.8 mmol/L.

Association Between Low-Density Lipoprotein Cholesterol (LDL-C) Level and Unfavorable Outcomes in Participants of Ischemic Stroke without Diabetes: A Multi-Center Retrospective Study.

BACKGROUND The impact of low-density lipoprotein cholesterol (LDL-C) levels on outcomes in patients with non-diabetic acute ischemic stroke remains uncertain. The objective of this study was to explore whether LDL-C could refine outcomes after acute ischemic stroke in patients with non-diabetic acute ischemic stroke. MATERIAL AND METHODS A multi-center, retrospective, clinical-based study was conducted within eight hospitals between January 2015 and August 2016. Adjusted odds ratio (aOR) was used for measurement of unfavorable outcome which was evaluated by the modified Rankin Scale (mRS) score at 6 months after acute ischemic stroke, estimated categorically according to multivariate logistic regression. RESULTS A total of 1614 participants with non-diabetic acute ischemic stroke were enrolled, of which 376 patients (23.3%) had unfavorable neurologic outcomes at 6 months. After multivariate analysis comparing 4 LDL-C levels by quartiles (Q), we found that compared to Q1 (LDL-C level ≤2.41 mmol/L), there was a significant association between the frequency of unfavorable outcomes and levels of LDL-C (Q3: 2.95-3.54 mmol/L) for all participants (adjusted odds ratio [aOR]=0.63; 95% CI: 0.44-0.92, P=0.016) and patients with first ever strokes (aOR=0.52; 95% CI: 0.31-0.87, P=0.013). CONCLUSIONS Compared to lower LDL-C levels, non-diabetic patients with LDL-C levels in Q3 (2.95-3.54 mmol/L), were less likely to have unfavorable functional outcomes at 6 months after acute ischemic stroke. Managing HDL-C is one of the most important steps for the recovery of acute ischemic stroke.

Cholesterol: Can't Live With It, Can't Live Without It.

Given its role in many biochemical processes essential to life, cholesterol remains a topic of intense research. Of all the plasma lipids, cholesterol is distinctive because it is a precursor to steroidogenic molecules, some of which regulate metabolism, and its blood concentration in the form of low- and high-density lipoprotein cholesterol (HDL-C) are positive and negative risk factors for atherosclerotic cardiovascular disease (ASCVD). New research, however, has challenged the widely held belief that high HDL-C levels are atheroprotective and is showing that both low and high plasma HDL-C levels confer an increased risk of ASCVD. Furthermore, it is disputing the widely cited mechanism involved in reverse cholesterol transport. This review explores the evolution of cholesterol research starting with the Gofman and Framingham studies, the development of traditional and emerging lipid-lowering therapies, and the role of reverse cholesterol transport in HDL cardioprotection.

Familial hypercholesterolaemia.

Familial hypercholesterolaemia is a common inherited disorder characterized by abnormally elevated serum levels of low-density lipoprotein (LDL) cholesterol from birth, which in time can lead to cardiovascular disease (CVD). Most cases are caused by autosomal dominant mutations in LDLR, which encodes the LDL receptor, although mutations in other genes coding for proteins involved in cholesterol metabolism or LDLR function and processing, such as APOB and PCSK9, can also be causative, although less frequently. Several sets of diagnostic criteria for familial hypercholesterolaemia are available; common diagnostic features are an elevated LDL cholesterol level and a family history of hypercholesterolaemia or (premature) CVD. DNA-based methods to identify the underlying genetic defect are desirable but not essential for diagnosis. Cascade screening can contribute to early diagnosis of the disease in family members of an affected individual, which is crucial because familial hypercholesterolaemia can be asymptomatic for decades. Clinical severity depends on the nature of the gene that harbours the causative mutation, among other factors, and is further modulated by the type of mutation. Lifelong LDL cholesterol-lowering treatment substantially improves CVD-free survival and longevity. Statins are the first-line therapy, but additional drugs, such as ezetimibe, bile acid sequestrants, PCSK9 inhibitors and other emerging therapies, are often required.

Hematoma Expansion: Clinical and Molecular Predictors and Corresponding Pharmacological Treatment.

BACKGROUND: Hematoma expansion is a detrimental event of intracerebral hemorrhage (ICH) which results in progressive neurologic deteriorations and poor outcomes. OBJECTIVE: To summariz the current understanding of the mechanisms underlying hematoma expansion and discuss the potential approaches of treatment and prevention. RESULTS: Although the exact mechanism of hematoma expansion is unclear, accumulating evidences suggest that multiple clinical markers such as coagulation/hemostasis dysfunction, higher blood pressure and BRAIN scores, higher serum glucose and/or glycosylated hemoglobin A1c, serum creatinine, Factor XIII and international normalized ratio (INR), lower serum cholesterol or LDL cholesterol, and fibrinogen, may be correlated with incidents of hematoma expansion. Furthermore, activation of several molecular pathways (i.e. plasma kallikrein, von Willebrand factor, N-methyl-Daspartate and its receptor, cytokines/ adipokines, cellular fibronectin and apolipoprotein Eε2 allele) may lead to hematoma expansion. CONCLUSION: Prospective study for hematoma expansion How to predict the patients Who are at highest risk of hematoma expansion is more challengeable than restricting hematoma expansion itself following acute ICH. Seeking and detecting risk markers in plasma that can be intervened appropriately is meaningful for patients with potential hematoma expansion, which may contribute to improve clinical outcomes in patients suffering from ICH.

Declines in coronary heart disease incidence and mortality among middle-aged adults with and without diabetes.

PURPOSE: The purpose of the study was to investigate secular changes in coronary heart disease (CHD) incidence and mortality among adults with and without diabetes and to determine the effect of increased lipid-lowering medication use and reductions in low-density lipoprotein cholesterol (LDL-C) levels on these changes. METHODS: We analyzed data on participants aged 45 to 64 years from the Atherosclerosis Risk in Communities Study in 1987-1996 (early period) and the Reasons for Geographic and Racial Differences in Stroke Study in 2003-2009 (late period). Hazard ratios (HRs) for the association of diabetes and period with incident CHD and CHD mortality were obtained after adjustment for sociodemographics cardiovascular risk factors, lipid-lowering medication use, and LDL-C. RESULTS: After multivariable adjustment, diabetes was associated with an increased CHD risk during the early (HR = 1.99, 95% confidence interval = 1.59-2.49) and late (HR = 2.39, 95% confidence interval = 1.69-3.35) periods. CHD incidence and mortality declined between the early and late periods for individuals with and without diabetes. Increased use of lipid-lowering medication and lower LDL-C explained 33.6% and 27.2% of the decline in CHD incidence and CHD mortality, respectively, for those with diabetes. CONCLUSIONS: Although rates have declined, diabetes remains associated with an increased risk of CHD incidence and mortality, highlighting the need for continuing diabetes prevention and cardiovascular risk factor management.

Predictive factors of mortality in patients with acute mesenteric ischemia. A retrospective study.

AIM: The aim of this retrospective study was to evaluate the impact of some risk factors on mortality in patients with Acute mesenteric ischemia (AMI). MATERIALS AND METHODS: From September 2003 to August 2011, 200 patients were operated on for bowel infarction at our unit: 149 were included in the study. For each patient, socio-demographic (gender and age) and clinical data (extent of necrosis, predisposing factors, WBC, LDH, comorbidities) were collected from patients' clinical records. RESULTS: Of the 149 patients who underwent surgery, 57 (38.3%) died. A significantly higher mortality was associated with older age (79.9 versus 74.2 years, p < 0.01), higher LDH serum levels (695 versus 636 UI/L, p < 0.01), higher WBC (25.1 versus 22.5 X 103/mm3; p < 0.01), and extent of necrosis (p< 0.01). Otherwise, there was no correlation between comorbidities and mortality. Finally, multivariate analysis confirmed the significantly higher risk of death in patients with right colon and massive small bowel infarction (adjOR= 3.58; 95% CI=1.36-9.42) and intestinal perforation (adjOR=31.1; 95% CI=2.45-395.7). DISCUSSION: The results of our study suggest that the contribution of laboratory tests is limited, even if increased indexes of necrosis (such as LDH) associated with neutrophilic leukocytosis and metabolic acidosis, may help in defining diagnosis/ prognosis, though with low accuracy. CONCLUSIONS: The extent of necrosis and diagnostic delay seem to be the most important prognostic factors even after adjusting for confounding due to age, presence of comorbidities, and laboratory tests (LDH and WBC). KEY WORDS: Acute mesenteric ischemia, Mortality, Predictive factors.

Association of prestroke statin use and lipid levels with outcome of intracerebral hemorrhage.

BACKGROUND AND PURPOSE: It is unclear whether blood lipid profiles and statin use before intracerebral hemorrhage (ICH) are associated with its outcome. METHODS: The Helsinki ICH Study, a single-center observational registry of consecutive ICH patients, was used to study the associations between premorbid statin use, baseline lipid levels, and clinical outcome. RESULTS: The registry includes 964 ICH patients. Statin users (n=187; 19%) were significantly older, had more frequent comorbidities and medication, lower lipid levels, and higher admission Glasgow Coma Scale compared with nonusers. Modified Rankin Scale at discharge or mortality did not differ between statin users and nonusers. Compared with survivors, significantly lower total cholesterol and low-density lipoprotein cholesterol levels were observed in patients who died in hospital (median, 4.1 mmol/L [interquartile range, 3.6-4.4] versus 4.5 [3.8-5.1]; P<0.01; 1.9 mmol/L [1.4-2.5] versus 2.4 [1.8-3.0]; P<0.001, respectively), at 3 or 12 months. After adjusting for known ICH prognostic factors based on univariate analysis that is, age, National Institutes of Health Stroke Scale, Glasgow Coma Scale, ICH volume, and intraventricular location, lower low-density lipoprotein levels were independently associated with in-hospital mortality (odds ratio, 0.54 [95% confidence interval, 0.31-0.93]; P=0.028). CONCLUSIONS: Premorbid statin use did not affect the outcome of ICH, but lower low-density lipoprotein levels were associated with higher in-hospital mortality.

Meta-analysis methods and models with applications in evaluation of cholesterol-lowering drugs.

In this paper, we propose a class of multivariate random effects models allowing for the inclusion of study-level covariates to carry out meta-analyses. As existing algorithms for computing maximum likelihood estimates often converge poorly or may not converge at all when the random effects are multi-dimensional, we develop an efficient expectation-maximization algorithm for fitting multi-dimensional random effects regression models. In addition, we also develop a new methodology for carrying out variable selection with study-level covariates. We examine the performance of the proposed methodology via a simulation study. We apply the proposed methodology to analyze metadata from 26 studies involving statins as a monotherapy and in combination with ezetimibe. In particular, we compare the low-density lipoprotein cholesterol-lowering efficacy of monotherapy and combination therapy on two patient populations (naïve and non-naïve patients to statin monotherapy at baseline), controlling for aggregate covariates. The proposed methodology is quite general and can be applied in any meta-analysis setting for a wide range of scientific applications and therefore offers new analytic methods of clinical importance.

Pharmacist-led group medical appointments for the management of type 2 diabetes with comorbid depression in older adults.

BACKGROUND: Depression is associated with poor glycemic control, increased number of microvascular and macrovascular complications, functional impairment, mortality, and 4.5 times higher total health care costs in patients with diabetes. Shared medical appointments (SMAs) may be an effective method to attain national guideline recommendations for glycemic control in diabetes for patients with depression through peer support, counseling, problem solving, and improved access to care. OBJECTIVE: To test the efficacy as assessed by attainment of a hemoglobin A(1c) (A1C) <7% of pharmacist-led group SMA visits, Veterans Affairs Multidisciplinary Education in Diabetes and Intervention for Cardiac Risk Reduction in Depression (VA-MEDIC-D), in patients with type 2 diabetes mellitus. METHODS: This was a randomized controlled trial of VA-MEDIC-D added to standard care versus standard care alone in depressed patients with diabetes with A1C >6.5%. VA-MEDIC-D consisted of 4 once-weekly, 2-hour sessions followed by 5 monthly 90-minute group sessions. Each SMA session consisted of multidisciplinary education and pharmacist-led behavioral and pharmacologic interventions for diabetes, lipids, smoking, and blood pressure. No pharmacologic interventions for depression were provided. The change in the proportion of participants who achieved an A1C <7% at 6 months was compared. RESULTS: Compared to standard care (n = 44), a lower proportion of patients in VA-MEDIC-D (n = 44) had systolic blood pressure (SBP) <130 mm Hg at baseline, but were similar in other cardiovascular risk factors and psychiatric comorbidity. The change in the proportion of participants achieving an A1C <7% was greater in the VA-MEDIC-D arm than in the standard care arm (29.6% vs 11.9%), with odds ratio 3.6 (95% CI 1.1 to 12.3). VA-MEDIC-D participants also achieved significant reductions in SBP, low-density lipoprotein cholesterol, and non-high-density lipoprotein (HDL) cholesterol from baseline, whereas significant reductions were attained only in non-HDL cholesterol with standard care. There was no significant change in depressive symptoms for either arm. CONCLUSIONS: Pharmacist-led group SMA visits are efficacious in attainment of glycemic control in patients with diabetes and depression without change in depression symptoms.