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The global epidemic of hypertension is largely uncontrolled and hypertension remains the leading cause of noncommunicable disease deaths worldwide. Suboptimal adherence, which includes failure to initiate pharmacotherapy, to take medications as often as prescribed, and to persist on therapy long-term, is a well-recognized factor contributing to the poor control of blood pressure in hypertension. Several categories of factors including demographic, socioeconomic, concomitant medical-behavioral conditions, therapy-related, healthcare team and system-related factors, and patient factors are associated with nonadherence. Understanding the categories of factors contributing to nonadherence is useful in managing nonadherence. In patients at high risk for major adverse cardiovascular outcomes, electronic and biochemical monitoring are useful for detecting nonadherence and for improving adherence. Increasing the availability and affordability of these more precise measures of adherence represent a future opportunity to realize more of the proven benefits of evidence-based medications. In the absence of new antihypertensive drugs, it is important that healthcare providers focus their attention on how to do better with the drugs they have. This is the reason why recent guidelines have emphasize the important need to address drug adherence as a major issue in hypertension management.

Objective: The Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) study is the first stroke prevention trial to include protocol-driven intensive management of multiple risk factors. In this prespecified analysis, we aimed to investigate the relationship between risk factor control during follow-up and outcome of patients in the medical arm of SAMMPRIS., Methods: Data from SAMMPRIS participants in the medical arm (n = 227) were analyzed. Risk factors were recorded at baseline, 30 days, 4 months, and then every 4 months for a mean follow-up of 32 months. For each patient, values for all risk factor measures were averaged and dichotomized as in or out of target., Results: Participants who were out of target for systolic blood pressure and physical activity, as well as those with higher mean low-density lipoprotein cholesterol and non-high-density lipoprotein, were more likely to have a recurrent vascular event (stroke, myocardial infarction, or vascular death) at 3 years compared to those who had good risk factor control. In the multivariable analysis, greater physical activity decreased the likelihood of a recurrent stroke, myocardial infarction, or vascular death (odds ratio 0.6, confidence interval 0.4-0.8)., Conclusions: Raised blood pressure, cholesterol, and physical inactivity should be aggressively treated in patients with intracranial atherosclerosis to prevent future vascular events. Physical activity, which has not received attention in stroke prevention trials, was the strongest predictor of a good outcome in the medical arm in SAMMPRIS., Clinicaltrialsgov Identifier: NCT00576693., (© 2016 American Academy of Neurology.)

Background: To reduce the cardiovascular disease burden, Healthy People 2020 established US hypertension goals for adults to (1) decrease the prevalence to 26.9% and (2) raise treatment to 69.5% and control to 61.2%, which requires controlling 88.1% on treatment., Methods and Results: To assess the current status and progress toward these Healthy People 2020 goals, time trends in National Health and Nutrition Examination Surveys 1999 to 2012 data in 2-year blocks were assessed in adults ≥18 years of age age-adjusted to US 2010. From 1999 to 2000 to 2011 to 2012, prevalent hypertension was unchanged (30.1% versus 30.8%, P=0.32). Hypertension treatment (59.8% versus 74.7%, P<0.001) and proportion of treated adults controlled (53.3%-68.9%, P=0.0015) increased. Hypertension control to <140/<90 mm Hg rose every 2 years from 1999 to 2000 to 2009 to 2010 (32.2% versus 53.8%, P<0.001) before declining to 51.2% in 2011 to 2012. Modifiable factor(s) significant in multivariable logistic regression modeling include: (1) increasing body mass index with prevalent hypertension (odds ratio [OR], 1.44); (2) lack of health insurance (OR, 1.68) and <2 healthcare visits per year (OR, 4.24) with untreated hypertension; (3) healthcare insurance (OR, 1.69), ≥2 healthcare visits per year (OR, 3.23), and cholesterol treatment (OR, 1.90) with controlled hypertension., Conclusions: The National Health and Nutrition Examination Survey 1999 to 2012 analysis suggests that Healthy People 2020 goals for hypertension ([1] prevalence shows no progress, [2] treatment was exceeded, and [3] control) have flattened below target. Findings are consistent with evidence that (1) obesity prevention and treatment could reduce prevalent hypertension, and (2) healthcare insurance, ≥2 healthcare visits per year, and guideline-based cholesterol treatment could improve hypertension control., (© 2014 American Heart Association, Inc.)

While hospitals have widely adopted quality improvement (QI) initiatives, primary care practices continue to face unique challenges to QI implementation. The purpose of this article is to outline a strategy for promoting QI in primary care practices by introducing specially trained nurses. Two case examples are described, one with a QI nurse external to the practice and one with a nurse internal to the practice. Lessons learned and barriers and facilitators to QI in primary care are presented. Barriers and facilitators are identified in the following categories: practice infrastructure, practice leadership, and practice organizational culture. Implications for primary care practitioners and avenues for future work are discussed.

Background: Joint National Committee goal blood pressure for all adults was <140/<90 mm Hg or lower from 1984 to 2013. Adults aged ≥60 years (older) have mainly isolated systolic hypertension, with major trials attaining systolic blood pressure <150 but not <140 mm Hg. The main objective was to assess changes in hypertension control to <140/<90 mm Hg in younger (aged <60 years) and older adults and <150/<90 mm Hg in the latter., Methods and Results: National Health and Nutrition Examination Surveys (NHANES) 1988 to 1994, 1999 to 2004, and 2005 to 2010 were analyzed in adults aged ≥18 years. From 1988 to 1994 to 2005 to 2010, hypertension control to <140/<90 mm Hg improved in older (31.6% to 53.1%; P<0.001) and younger (45.7% to 55.9%; P<0.001) patients. The age gap in control declined from 14.1% (P<0.01) in 1988 to 1994 to 2.8% (P=0.13) in 2005 to 2010. Better hypertension control reflected increased percentages of older (55.6% to 77.5%) and younger (34.6% to 54.7%) patients on treatment and treated older (45.7% to 64.9%) and younger (56.8% to 73.4%) patients controlled (all P<0.001). Control to <150/<90 mm Hg rose from 48.8% to 69.9% in older adults. Antihypertensive medication number and percentages on ≥3 medications increased in both age groups but increased more in older patients (P<0.01). Blood pressure control was higher in both age groups with ≥2 healthcare visits per year and on statin therapy., Conclusions: The age gap in hypertension control to <140/<90 mm Hg was virtually eliminated in 2005 to 2010 as clinicians intensified therapy, especially in older patients in whom isolated systolic hypertension predominates, controlling 70% to <150/<90 mm Hg. More frequent healthcare visits and the use of statin therapy may improve hypertension control in all adults., (© 2014 American Heart Association, Inc.)

Background: Hypertension doubles coronary heart disease (CHD) risk. Treating hypertension only reduces CHD risk ≈25%. Treating hypercholesterolemia in hypertensive patients reduces residual CHD risk >35%., Methods and Results: To assess progress in concurrent hypertension and hypercholesterolemia control, National Health and Nutrition Examination Surveys 1988 to 1994, 1999 to 2004, and 2005 to 2010 were analyzed. Hypertension was defined by blood pressure ≥140/≥90 mm Hg, current medication treatment, and 2-told hypertension status; blood pressure <140/<90 defined control. Hypercholesterolemia was defined by ATP III criteria based on 10-year CHD risk, low-density lipoprotein cholesterol (LDL-C), and non-high-density lipoprotein cholesterol; values below diagnostic thresholds defined control. Across surveys, 60.7% to 64.3% of hypertensives were hypercholesterolemic. From 1988 to 1994 to 2005 to 2010, control of LDL-C rose (9.2% [95% confidence interval (CI), 6.6%-11.9%] to 45.4% [95% CI, 42.6%-48.3%]), concomitant hypertension and LDL-C (5.0% [95% CI, 3.3%-6.7%] to 30.7% [95% CI, 27.9%-33.4%]), and combined hypertension, LDL-C, and non-high-density lipoprotein cholesterol (1.8% [95% CI, 0.4%-3.2%] to 26.9% [95% CI, 24.4%-29.5%]). By multivariable logistic regression, factors associated with concomitant hypertension, LDL-C, and non-high-density lipoprotein cholesterol control (odds ratio [95% CI]) were statin (10.7 [8.1-14.3]) and antihypertensive (3.32 [2.45-4.50]) medications, age (0.77 [0.69-0.88]/10-year increase), ≥2 healthcare visits/yr (1.90 [1.26-2.87]), black race (0.59 [0.44-0.80]), Hispanic ethnicity (0.62 [0.43-0.90]), cardiovascular disease (0.44 [0.34-0.56]), and diabetes mellitus (0.54 [0.42-0.70])., Conclusions: Despite progress, opportunities for improving concomitant hypertension and hypercholesterolemia control persist. Prescribing antihypertensive and antihyperlipidemic medications to achieve treatment goals, especially for older, minority, diabetic, and cardiovascular disease patients, and accessing healthcare at least biannually could improve concurrent risk factor control and CHD prevention.

Background: Despite progress, many hypertensive patients remain uncontrolled. Defining characteristics of uncontrolled hypertensives may facilitate efforts to improve blood pressure control., Methods and Results: Subjects included 13,375 hypertensive adults from National Health and Nutrition Examination Surveys (NHANESs) subdivided into 1988 to 1994, 1999 to 2004, and 2005 to 2008. Uncontrolled hypertension was defined as blood pressure ≥140/≥90 mm Hg and apparent treatment-resistant hypertension (aTRH) when subjects reported taking ≥3 antihypertensive medications. Framingham 10-year coronary risk was calculated. Multivariable logistic regression was used to identify clinical characteristics associated with untreated, treated uncontrolled on 1 to 2 blood pressure medications, and aTRH across all 3 survey periods. More than half of uncontrolled hypertensives were untreated across surveys, including 52.2% in 2005 to 2008. Clinical factors linked with untreated hypertension included male sex, infrequent healthcare visits (0 to 1 per year), body mass index <25 kg/m2, absence of chronic kidney disease, and Framingham 10-year coronary risk <10% (P<0.01). Most treated uncontrolled patients reported taking 1 to 2 blood pressure medications, a proxy for therapeutic inertia. This group was older, had higher Framingham 10-year coronary risk than patients controlled on 1 to 2 medications (P<0.01), and comprised 34.4% of all uncontrolled and 72.0% of treated uncontrolled patients in 2005 to 2008. We found that aTRH increased from 15.9% (1998-2004) to 28.0% (2005-2008) of treated patients (P<0.001). Clinical characteristics associated with aTRH included ≥4 visits per year, obesity, chronic kidney disease, and Framingham 10-year coronary risk >20% (P<0.01)., Conclusion: Untreated, undertreated, and aTRH patients have consistent characteristics that could inform strategies to improve blood pressure control by decreasing untreated hypertension, reducing therapeutic inertia in undertreated patients, and enhancing therapeutic efficiency in aTRH.

Unlabelled: Numerous studies have demonstrated the value of team-based care to improve blood pressure (BP) control, but there is limited information on whether these models would be adopted in diverse populations. The purpose of this study was to evaluate whether a collaborative model between physicians and pharmacists can improve BP control in multiple primary care medical offices with diverse geographic and patient characteristics and whether long-term BP control can be sustained. This study is a randomized prospective trial in 27 primary care offices first stratified by the percentage of underrepresented minorities and the level of clinical pharmacy services within the office. Each office is then randomized to either a 9- or 24-month intervention or a control group. Patients will be enrolled in this study until 2012. The results of this study should provide information on whether this model can be implemented in large numbers of diverse offices, if it is effective in diverse populations, and whether BP control can be sustained long term., Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00935077.

The purpose of this study was to determine if prereatment with taurolidine, a known anti-endotoxin agent, would attenuate the hemodynamic and respiratory responses associated with endotoxin induced lung injury in a large animal model in a randomized controlled study under license from the Department of Health. All animals underwent a general anesthetic. Vascular catheters were placed in the femoral artery and in the femoral vein. A Swan-Ganz Catheter was inserted for measurement of pulmonary artery pressure. Animals were randomized into three groups: Control, with measurements taken at baseline and half hourly up to 90 min; Endotoxin, receiving 5microg/Kg E. coli endotoxin intravenously after baseline measurements; and Endotoxin + Taurolidine, receiving 5g of taurolidine via intraperitoneal infusion 1 h before endotoxin administration. Main outcome measures were mean systemic arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), arterial oxygen tension (pO2), serum endotoxin concentration, and pulmonary myeloperoxidase. Endotoxin induced a significant lung injury characterized by an increase in pulmonary artery pressure, hypoxia, and systemic hypotension. Pretreatment with intraperitoneal taurolidine significantly attenuated these hemodynamic and respiratory changes. Serum endotoxin concentration was also significantly reduced as was lung myeloperoxidase. The data suggest that taurolidine may have a therapeutic role in preventing the lung injury seen in endotoxemia.

As an initial step in testing the hypothesis that high oleic acid concentrations contribute to vascular remodeling in obese hypertensive patients by activating protein kinase C (PKC), the effects of oleic acid on primary cultures of rat aortic smooth muscle cells (RASMCs) were studied. Oleic acid, an 18-carbon cis-monounsaturated fatty acid (18:1 [cis]), from 25 to 200 mumol/L significantly increased [3H]thymidine uptake in RASMCs with an EC50 of 41.0 mumol/L and a maximal response of 196 +/- 15% of control (P < .01). Oleic acid from 25 to 200 mumol/L caused a concentration-dependent increase in the number of RASMCs in culture at 6 days, reaching a maximum of 210 +/- 13% of control at 100 mumol/L (P < .001). PKC inhibition with 4 mumol/L bisindolyImaleimide I and PKC depletion (alpha, mu, iota, and zeta) with 24-hour exposure to 200 nmol/L phorbol 12-myristate 13-acetate in RASMCs eliminated the mitogenic effects of oleic acid but did not reduce responses to 10% FBS. Stimulation of intact cells with oleic acid induced a peak increase of cytosolic PKC activity, reaching 328 +/- 8% of control (P < .001), but did not enhance PKC activity in the membrane fraction (105 +/- 4%, P = NS). The oleic acid-induced increase of PKC activity in cell lysates was similar in the presence and absence of Ca2+, phosphatidylserine, and diolein (maximum response, 360 +/- 4% versus 342 +/- 9% of control, P = NS). Unlike phorbol 12-myristate 13-acetate, oleic acid over 24 hours did not downregulate any of the four PKC isoforms detected in RASMCs. Oleic acid treatment activated mitogen-activated protein (MAP) kinase. PKC depletion in RASMCs eliminated the rise in thymidine uptake, activation of PKC, and activation of MAP kinase in response to oleic acid. In contrast to oleic acid, 50 to 200 mumol/L stearic (18:0) and elaidic (18:1 [trans]) acids, which are less effective activators of PKC than oleic acid, did not enhance thymidine uptake. These data suggest that oleic acid induces proliferation of RASMCs by activating PKC, particularly one or more of the Ca(2+)-independent isoforms, and raise the possibility that the higher oleic acid concentrations observed in obese hypertensive patients may contribute to vascular remodeling.

Psychologic studies of hypertension have usually focused on the relationship of anger and anxiety to clinic or laboratory blood pressure (BP). Yet, average blood pressure outside of the clinic has proven to be a more important predictor of hypertensive complications. In this study, we have isolated two groups of borderline hypertensives--one group that maintained high blood pressure outside of the clinic and another whose average BP returned to normal at home. All 33 subjects were given psychometric instruments for measuring various components of anger and anxiety: Spielberger's State-Trait Personality Inventory, the Anger Expression Scale, and the State Anger Reaction Scale. The high home BP group reported greater intensity of anger, although they suppressed their expression of anger to a greater extent. The groups did not differ in anxiety. Also, blood pressure variability was not different between the two groups. It is suggested that the psychologic differences found in the group of higher-risk borderline hypertensives may, through autonomic arousal, contribute to the later development of established hypertension.

Arterial compliance, assessed by the stroke volume-pulse pressure relationship, was measured in 32 patients with a high cardiac output together with borderline hypertension and 26 control subjects with normokinetic borderline hypertension. Measurements were obtained in the supine position both before and after 0.2 mg/kg intravenous propranolol. Baseline arterial compliance was significantly greater in the hyperkinetic group (P less than 0.01). The inter-group difference was no longer significant after the administration of propranolol, since compliance tended to increase in the normokinetic group and decrease in the hyperkinetic group. Therefore, disparities in vascular beta-adrenergic tone between hyperkinetic and normokinetic borderline hypertensive patients probably contribute to group differences in arterial compliance.