A Cluster-Randomized Trial of Blood-Pressure Reduction in Black Barbershops.

BACKGROUND: Uncontrolled hypertension is a major problem among non-Hispanic black men, who are underrepresented in pharmacist intervention trials in traditional health care settings. METHODS: We enrolled a cohort of 319 black male patrons with systolic blood pressure of 140 mm Hg or more from 52 black-owned barbershops (nontraditional health care setting) in a cluster-randomized trial in which barbershops were assigned to a pharmacist-led intervention (in which barbers encouraged meetings in barbershops with specialty-trained pharmacists who prescribed drug therapy under a collaborative practice agreement with the participants' doctors) or to an active control approach (in which barbers encouraged lifestyle modification and doctor appointments). The primary outcome was reduction in systolic blood pressure at 6 months. RESULTS: At baseline, the mean systolic blood pressure was 152.8 mm Hg in the intervention group and 154.6 mm Hg in the control group. At 6 months, the mean systolic blood pressure fell by 27.0 mm Hg (to 125.8 mm Hg) in the intervention group and by 9.3 mm Hg (to 145.4 mm Hg) in the control group; the mean reduction was 21.6 mm Hg greater with the intervention (95% confidence interval, 14.7 to 28.4; P<0.001). A blood-pressure level of less than 130/80 mm Hg was achieved among 63.6% of the participants in the intervention group versus 11.7% of the participants in the control group (P<0.001). In the intervention group, the rate of cohort retention was 95%, and there were few adverse events (three cases of acute kidney injury). CONCLUSIONS: Among black male barbershop patrons with uncontrolled hypertension, health promotion by barbers resulted in larger blood-pressure reduction when coupled with medication management in barbershops by specialty-trained pharmacists. (Funded by the National Heart, Lung, and Blood Institute and others; ClinicalTrials.gov number, NCT02321618 .).

Sustainability of Blood Pressure Reduction in Black Barbershops.

BACKGROUND: We developed a new model of hypertension care for non-Hispanic black men that links health promotion by barbers to medication management by American Society of Hypertension-certified pharmacists and demonstrated efficacy in a 6-month cluster-randomized trial. The marked reduction in systolic blood pressure (BP) seen at 6 months warranted continuing the trial through 12 months to test sustainability, a necessary precondition for implementation research. METHODS: We enrolled a cohort of 319 black male patrons with systolic BP ≥140 mm Hg at baseline. Fifty-two Los Angeles County barbershops were assigned to either a pharmacist-led intervention or an active control group. In the intervention group, barbers promoted follow-up with pharmacists who prescribed BP medication under a collaborative practice agreement with patrons' primary care providers. In the control group, barbers promoted follow-up with primary care providers and lifestyle modification. After BP assessment at 6 months, the intervention continued with fewer in-person pharmacist visits to test whether the intervention effect could be sustained safely for 1 year while reducing pharmacist travel time. Final BP and safety outcomes were assessed in both groups at 12 months. RESULTS: At baseline, mean systolic BP was 152.4 mm Hg in the intervention group and 154.6 mm Hg in the control group. At 12 months, mean systolic BP fell by 28.6 mm Hg (to 123.8 mm Hg) in the intervention group and by 7.2 mm Hg (to 147.4 mm Hg) in the control group. The mean reduction was 20.8 mm Hg greater in the intervention (95% CI, 13.9-27.7; P<0.0001). A BP <130/80 mm Hg was achieved by 68.0% of the intervention group versus 11.0% of the control group ( P<0.02). These new 12-month efficacy data are statistically indistinguishable from our previously reported 6-month data. No treatment-related serious adverse events occurred in either group over 12 months. Cohort retention at 12 months was 90% in both groups. CONCLUSIONS: Among black male barbershop patrons with uncontrolled hypertension, health promotion by barbers resulted in large and sustained BP reduction over 12 months when coupled with medication management by American Society of Hypertension-certified pharmacists. Broad-scale implementation research is both justified and warranted. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifier: NCT 02321618.

High Carbon Monoxide Levels from Charcoal Combustion Mask Acute Endothelial Dysfunction Induced by Hookah (Waterpipe) Smoking in Young Adults.

BACKGROUND: Hookah smoking is marketed to youth as a harmless alternative to cigarettes. Although cigarette smoking acutely impairs endothelial function, the effect of smoking fruit-flavored hookah tobacco is unknown. Because charcoal traditionally is used to heat the hookah tobacco in the waterpipe, hookah smoke delivers tobacco toxicants and nicotine plus charcoal combustion products: not only carbon-rich nanoparticles, oxidants that may destroy nitric oxide and impair endothelial function, but also large amounts of carbon monoxide (CO), a putative vasodilator molecule. METHODS: To test the acute effect of hookah smoking on endothelial function, in young adult hookah smokers (n=30, age 26±1 years, mean±SE), we measured plasma nicotine, exhaled CO, and brachial artery flow-mediated dilation (FMD) before and after charcoal-heated hookah smoking. To remove the effect of charcoal combustion, the same measurements were performed when the same flavored hookah tobacco product was heated electrically (n=20). As a positive internal control, we studied age-matched cigarette smokers (n=15) who smoked 1 cigarette. To isolate the effect of the CO boost on FMD, hookah smokers (n=8) inhaled a 0.1% CO gas mixture to approximate their CO boost achieved with charcoal-heated hookah smoking. RESULTS: Nicotine levels increased similarly with all types of smoking, whereas exhaled CO increased 9- to 10-fold more after charcoal-heated hookah than after either electrically heated hookah or cigarette smoking. FMD did not decrease after smoking charcoal-heated hookah but instead increased by +43±7% ( P<0.001). In contrast, FMD decreased by -27±4% ( P<0.001) after smoking electrically heated hookah, comparable to the decrease after cigarette smoking. FMD increased markedly by 138±71% ( P<0.001) after breathing CO gas, 2.8 times more than the increase induced in the same subjects after smoking charcoal-heated hookah ( P<0.001), despite comparable increases in exhaled CO (24±1 versus 28±3 ppm, hookah versus CO). CONCLUSIONS: Smoking hookah tobacco, similar to cigarette tobacco, acutely impairs endothelial function. With traditional charcoal-heated hookah smoking, the acute endothelial dysfunction is masked by high levels of carbon monoxide, a potent vasodilator molecule generated by charcoal combustion. With respect to large-artery endothelial function, smoking hookah is not harmless. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifiers: NCT03616002 and NCT03067701.

Impact of a Patient-Centered Behavioral Economics Intervention on Hypertension Control in a Highly Disadvantaged Population: a Randomized Trial.

BACKGROUND: Uncontrolled hypertension contributes to disparities in cardiovascular outcomes. Patient intervention strategies informed by behavioral economics and social psychology could improve blood pressure (BP) control in disadvantaged minority populations. OBJECTIVE: To assess the impact on BP control of an intervention combining short-term financial incentives with promotion of intrinsic motivation among highly disadvantaged patients. DESIGN: Randomized controlled trial. PARTICIPANTS: Two hundred seven adults (98% African American or Latino) aged 18 or older with uncontrolled hypertension attending Federally Qualified Health Centers. INTERVENTION: Six-month intervention, combining financial incentives for measuring home BP, recording medication use, BP improvement, and achieving target BP values with counseling linking hypertension control efforts to participants' personal reasons to stay healthy. MAIN MEASURES: Primary outcomes: percentage achieving systolic BP (SBP) < 140 mmHg, percentage achieving diastolic BP (DBP) < 90 mmHg, and changes in SBP and DBP, all after 6 months. Priority secondary outcomes were SBP < 140 mmHg, DBP < 90 mmHg, and BP change at 12 months, 6 months after the intervention ended. KEY RESULTS: After 6 months, rates of achieving target BP values for intervention and control subjects respectively was 57.1% vs. 40.2% for SBP < 140 mmHg (adjusted odds ratio (AOR) 2.53 (1.13-5.70)), 79.8% vs 70.1% for DBP < 90 mmHg (AOR 2.50 (0.84-7.44)), and 53.6% vs 40.2% for achieving both targets (AOR 2.04 (0.92-4.52)). However, at 12 months, the groups did not differ significantly in these 3 measures: 39.5% vs 35.0% for SBP (AOR 1.20 (0.51-2.83)), 68.4% vs 75.0% for DBP (AOR 0.70 (0.24-2.09)), and 35.5% vs 33.8% for both (AOR 1.03 (0.44-2.42)). Change in absolute SBP and DBP did not differ significantly between the groups at 6 or 12 months. Exploratory post hoc analysis revealed intervention benefit only occurred among individuals whose providers intensified their regimens, but not among those with intensification but no intervention. CONCLUSIONS: The intervention achieved short-term improvement in SBP control in a highly disadvantaged population. Despite attempts to enhance intrinsic motivation, the effect was not sustained after incentives were withdrawn. Future research should evaluate combined patient/provider strategies to enhance such interventions and sustain their benefit. TRIAL REGISTRATION: NCT01402453; http://clinicaltrials.gov/show/NCT01402453.

Sodium nitrate alleviates functional muscle ischaemia in patients with Becker muscular dystrophy.

Becker muscular dystrophy (BMD) is a progressive X-linked muscle wasting disease for which there is no treatment. BMD is caused by in-frame mutations in the gene encoding dystrophin, a structural cytoskeletal protein that also targets other proteins to the sarcolemma. Among these is neuronal nitric oxide synthase mu (nNOSµ), which requires specific spectrin-like repeats (SR16/17) in dystrophin's rod domain and the adaptor protein α-syntrophin for sarcolemmal targeting. When healthy skeletal muscle is exercised, sarcolemmal nNOSµ-derived nitric oxide (NO) attenuates α-adrenergic vasoconstriction, thus optimizing perfusion. In the mdx mouse model of dystrophinopathy, this protective mechanism (functional sympatholysis) is defective, resulting in functional muscle ischaemia. Treatment with a NO-donating non-steroidal anti-inflammatory drug (NSAID) alleviates this ischaemia and improves the murine dystrophic phenotype. In the present study, we report that, in 13 men with BMD, sympatholysis is defective mainly in patients whose mutations disrupt sarcolemmal targeting of nNOSµ, with the vasoconstrictor response measured as a decrease in muscle oxygenation (near infrared spectroscopy) to reflex sympathetic activation. Then, in a single-arm, open-label trial in 11 BMD patients and a double-blind, placebo-controlled cross-over trial in six patients, we show that acute treatment with oral sodium nitrate, an inorganic NO donor without a NSIAD moiety, restores sympatholysis and improves post-exercise hyperaemia (Doppler ultrasound). By contrast, sodium nitrate improves neither sympatholysis, nor hyperaemia in healthy controls. Thus, a simple NO donor recapitulates the vasoregulatory actions of sarcolemmal nNOS in BMD patients, and constitutes a putative novel therapy for this disease.

Simulating Strategies for Improving Control of Hypertension Among Patients with Usual Source of Care in the United States: The Blood Pressure Control Model.

BACKGROUND: Only half of hypertensive adults achieve blood pressure (BP) control in the United States, and it is unclear how BP control rates may be improved most effectively and efficiently at the population level. OBJECTIVE: We sought to compare the potential effects of system-wide isolated improvements in medication adherence, visit frequency, and higher physician prescription rate on achieving BP control at 52 weeks. DESIGN: We developed a Markov microsimulation model of patient-level, physician-level, and system-level processes involved in controlling hypertension with medications. The model is informed by data from national surveys, cohort studies and trials, and was validated against two multicenter clinical trials (ALLHAT and VALUE). SUBJECTS: We studied a simulated, nationally representative cohort of patients with diagnosed but uncontrolled hypertension with a usual source of care. INTERVENTIONS: We simulated a base case and improvements of 10 and 50%, and an ideal scenario for three modifiable parameters: visit frequency, treatment intensification, and medication adherence. Ideal scenarios were defined as 100% for treatment intensification and adherence, and return visits occurring within 4 weeks of an elevated office systolic BP. MAIN OUTCOME: BP control at 52 weeks of follow-up was examined. RESULTS: Among 25,000 hypothetical adult patients with uncontrolled hypertension (systolic BP ≥ 140 mmHg), only 18% achieved BP control after 52 weeks using base-case assumptions. With 10/50%/idealized enhancements in each isolated parameter, enhanced treatment intensification achieved the greatest BP control (19/23/71%), compared with enhanced visit frequency (19/21/35%) and medication adherence (19/23/26%). When all three processes were idealized, the model predicted a BP control rate of 95% at 52 weeks. CONCLUSION: Substantial improvements in BP control can only be achieved through major improvements in processes of care. Healthcare systems may achieve greater success by increasing the frequency of clinical encounters and improving physicians' prescribing behavior than by attempting to improve patient adherence to medications.

Cocaine-induced vasoconstriction in the human coronary microcirculation: new evidence from myocardial contrast echocardiography.

BACKGROUND: Cocaine is a major cause of acute coronary syndrome, especially in young adults; however, the mechanistic underpinning of cocaine-induced acute coronary syndrome remains limited. Previous studies in animals and in patients undergoing cardiac catheterization suggest that cocaine constricts coronary microvessels, yet direct evidence is lacking. METHODS AND RESULTS: We used myocardial contrast echocardiography to test the hypothesis that cocaine causes vasoconstriction in the human coronary microcirculation. Measurements were performed at baseline and after a low, nonintoxicating dose of intranasal cocaine (2 mg/kg) in 10 healthy cocaine-naïve young men (median age, 32 years). Postdestruction time-intensity myocardial contrast echocardiography kinetic data were fit to the equation y=A(1-e(-ßt)) to quantify functional capillary blood volume (A), microvascular flow velocity (ß), and myocardial perfusion (A×ß). Heart rate, mean arterial pressure, and left ventricular work (2-dimensional echocardiography) were measured before and 45 minutes after cocaine. Cocaine increased mean arterial pressure (by 14±2 mm Hg [mean±SE]), heart rate (by 8±3 bpm), and left ventricular work (by 50±18 mm Hg·mL(-1)·bpm(-1)). Despite the increases in these determinants of myocardial oxygen demand, myocardial perfusion decreased by 30% (103.7±9.8 to 75.9±10.8 arbitrary units [AU]/s; P<0.01) mainly as a result of decreased capillary blood volume (133.9±5.1 to 111.7±7.7 AU; P<0.05) with no significant change in microvascular flow velocity (0.8±0.1 to 0.7±0.1 AU). CONCLUSIONS: In healthy cocaine-naïve young adults, a low-dose cocaine challenge evokes a sizeable decrease in myocardial perfusion. Moreover, the predominant effect is to decrease myocardial capillary blood volume rather than microvascular flow velocity, suggesting a specific action of cocaine to constrict terminal feed arteries.

Using insights from behavioral economics and social psychology to help patients manage chronic diseases.

Despite a revolution in therapeutics, the ability to control chronic diseases remains elusive. We present here a conceptual model of the potential role of behavioral tools in chronic disease control. Clinicians implicitly accept the assumption that patients will act rationally to maximize their self-interest. However, patients may not always be the rational actors that we imagine. Major behavioral barriers to optimal health behavior include patients' fear of threats to health, unwillingness to think about problems when risks are known or data are ambiguous, the discounting of risks that are far in the future, failure to act due to lack of motivation, insufficient confidence in the ability to overcome a health problem, and inattention due to pressures of everyday life. Financial incentives can stimulate initiation of health-promoting behaviors by reducing or eliminating financial barriers, but may not produce long-term behavior change without additional interventions. Strategies have been developed by behavioral economists and social psychologists to address each of these barriers to better decision-making. These include: labeling positive behaviors in ways consistent with patient life goals and priorities; greater focus on more immediate risks of chronic diseases; intermediate subgoals as steps to a large health goal; and implementation of specific plans as to when, where, and how an action will be taken. Such strategies hold promise for improving health behaviors and disease control, but most have not been studied in medical settings. The effectiveness of these approaches should be evaluated for their potential as tools for the clinician.

Functional sympatholysis is impaired in hypertensive humans.

In healthy individuals, sympathetic vasoconstriction is markedly blunted in exercising muscles to optimize blood flow to the metabolically active muscle fibres. This protective mechanism, termed functional sympatholysis, is impaired in rat models of angiotensin-dependent hypertension. However, the relevance of these findings to human hypertension is unknown. Therefore, in 13 hypertensive and 17 normotensive subjects we measured muscle oxygenation and forearm blood flow (FBF) responses to reflex increases in sympathetic nerve activity (SNA) evoked by lower body negative pressure (LBNP) at rest and during moderate-intensity rhythmic handgrip exercise. In the normotensives, LBNP caused decreases in oxygenation and FBF (−16 ± 2% and −23 ± 4%, respectively) in resting forearm but not in exercising forearm (−1 ± 2% and −1 ± 3%, respectively; P < 0.05 vs. rest). In the hypertensives, LBNP evoked decreases in oxygenation and FBF that were similar in the resting and exercising forearm (−14 ± 2% vs. −12 ± 2% and −20 ± 3% vs. −13 ± 2%, respectively; P > 0.05), indicating impaired functional sympatholysis. In the hypertensives, SNA was unexpectedly increased by 54 ± 11% during handgrip alone. However, when SNA was experimentally increased during exercise in the normotensives, sympatholysis was unaffected. Treatment for 4 weeks with the angiotensin receptor blocker irbesartan, but not with the thiazide-type diuretic chlorthalidone, restored sympatholysis in the hypertensives. These data provide the first evidence that functional sympatholysis is impaired in hypertensive humans by a mechanism that appears to involve an angiotensin-dependent increase in sympathetic vasoconstriction in the exercising muscles.

Premise, promise, and potential limitations of invasive devices to treat hypertension.

Invasive device-based therapies for drug-resistant hypertension are undergoing active clinical investigation. The two approaches are 1) permanent implantation of a carotid baroreceptor pacemaker and 2) radiofrequency catheter ablation of the renal nerves. Both are designed to reduce the sympathetic nervous system component of drug-resistant hypertension. Several excellent comprehensive articles have reviewed each of these devices separately. In contrast, this brief article aims to provide a conceptual framework for evaluating the premise, promise, and potential limitations of both invasive antihypertensive therapies.

Sympathetic nerves and the progression of chronic kidney disease during 5/6 nephrectomy: studies in sympathectomized rats.

1. Chronically increased sympathetic nerve activity is present during chronic kidney disease (CKD); however, its role in contributing to hypertension or the progression of CKD remains poorly understood. The aim of the present study was to determine whether neonatal sympathectomy attenuates hypertension in 5/6 nephrectomized rats and affects renal structure and function in a blood pressure-independent manner. 2. We performed 5/6 nephrectomy (referred to as CKD) in both sympathetically intact and sympathectomized (injected neonatally with guanethidine; referred to as CKD + Sympath) male Sprague-Dawley rats. Sham-operated sympathetically intact and sympathectomized rats (Sham and Sham + Sympath, respectively) were used as controls. Radiotelemetry was used to monitor blood pressure throughout the 6 week duration of the study, after which renal function and histology were assessed. 3. Overall average systolic arterial pressure and final urinary protein excretion were significantly lower in CKD + Sympath compared with CKD rats (168 +/- 7 mmHg and 33 +/- 5 mg/24 h vs. 184 +/- 6 mmHg and 66 +/- 7 mg/24 h, respectively). However, the level of proteinuria in the CKD + Sympath group was reduced to a greater extent than what would be expected solely on the basis of lower blood pressure. All other indices of renal function and histology were comparable between both CKD groups. All measurements were comparable between Sham and Sham + Sympath groups. 4. In conclusion, sympathectomy attenuated hypertension by approximately one-third in 5/6 nephrectomized rats. Furthermore, sympathetic nerves to the kidney during 5/6 nephrectomy may contribute to proteinuria in a blood pressure-independent manner.

Peripheral Blood Flow Changes to Cutaneous and Muscular Beds in Response to Acute Hookah Smoking.

Hookah (waterpipe) smoking is a growing tobacco epidemic. Though perceived as a safer tobacco alternative, hookah smoke contains, in addition to tobacco combustion products, large amounts of charcoal combustion products-implicated in cardiovascular disease-from the burning charcoal used to heat the flavored tobacco. To date, little is known on the vascular effects of hookah smoking. The aim of this study was to characterize the peripheral circulatory response to acute hookah smoking in cutaneous and muscular beds. In 21 healthy young adult habitual hookah smokers who did not smoke cigarettes (age 24 ± 1 years, mean ± SE), we measured plasma nicotine, exhaled carbon monoxide, skin blood flow (laser Doppler velocimetry) and calf muscle blood flow (strain-gauge plethysmography) before and for up to 60 minutes after ad lib hookah smoking. In nine subjects, nonsmoking time-control studies were performed. Hookah smoking, which increased plasma nicotine by 5.8 ng/ml (from 0.6 ± 0.1 to 6.4 ± 1.3, p <0.001) and exhaled carbon monoxide by 27 ppm (from 2.7 ± 0.2 to 29.5 ± 2.2, p <0.001), decreased skin blood flow by 23% (20.1 ± 2.8 to 14.8 ± 1.9 units, p <0.001) and increased skeletal muscle blood flow by 34% (2.3 ± 0.1 to 2.9 ± 0.2 units, p = 0.010). These responses required more than one hour to recover after smoking cessation. All cardiovascular parameters were unchanged in the nonsmoking time-control studies. Although perceived to be innocuous, hookah smoking produces acute cutaneous vasoconstriction with skeletal muscle vasodilation, a dissociated pattern of peripheral blood flow responses that is characteristic of nicotine and carbon monoxide. In conclusion, these findings provide objective evidence to challenge the perception that hookah smoking is a safer tobacco alternative.

Simultaneous noninvasive recording of electrocardiogram and skin sympathetic nerve activity (neuECG).

neuECG, the simultaneous noninvasive recording of ECG and skin sympathetic nerve activity (SKNA), directly records sympathetic nerve activity over a long period of time. It can be used to measure sympathetic tone in healthy subjects and in subjects with non-cardiovascular diseases. The electrical activity that can be measured on the surface of the skin originates from the heart, the muscle or nerve structures. Because the frequency content of nerve activity falls in a higher frequency range than that of the ECG and myopotential, it is possible to use high-pass or band-pass filtering to specifically isolate the SKNA. neuECG is voltage calibrated and does not require invasive procedures to impale electrodes in nerves and thus has advantages over microneurography. Here, we present a protocol that takes <10 min to set up. The neuECG can be continuously recorded over a 24-h period or longer. We also describe methods to efficiently analyze neuECG from humans using commercially available hardware and software to facilitate adoption of this technology in clinical research.

Inhibition of nitric oxide synthase evokes central sympatho-excitation in healthy humans.

Animal studies have indicated that nitric oxide is a key signalling molecule involved in the tonic restraint of central sympathetic outflow from the brainstem. Extension of these findings to humans has been difficult because systemic infusion of nitric oxide synthase (NOS) inhibitors increases blood pressure due to inhibition of endothelial NOS, resulting in activation of the arterial baroreflex and subsequent inhibition of central sympathetic outflow. To overcome this confounding inhibitory influence of the baroreflex, in the current study we directly measured skin sympathetic nerve activity (SNA), which is not under baroreceptor control. Healthy, normotensive humans were studied before, during a 60 min intravenous infusion of the NOS inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME; 4 mg kg(1)), and for 120 min following the infusion (i.e. 180 min total). Skin SNA and arterial blood pressure (BP) were continuously measured. BP was increased from baseline at the end of the l-NAME infusion (14 +/- 2 mmHg; P < 0.05) and remained significantly elevated for the remainder of the experiment (18 +/- 3 mmHg; P < 0.05). Similarly, systemic NOS inhibition produced time-dependent increases in skin SNA, such that skin SNA was elevated at the end of the l-NAME infusion (total activity, 200 +/- 22% baseline; P = 0.08) and was further increased at the end of the study protocol (total activity, 350 +/- 41% baseline; P < 0.05). Importantly, skin SNA remained unchanged during time and hypertensive (phenylephrine) control experiments. These findings indicate that pharmacological inhibition of NOS causes sympathetic activation and support a role of nitric oxide in central sympathetic control in humans.

A barber-based intervention for hypertension in African American men: design of a group randomized trial.

BACKGROUND: Barbershops constitute potential sites for community health promotion programs targeting hypertension (HTN) in African American men but such programs previously have not been formally evaluated. METHODS: A randomized trial (ClinicalTrials.gov no. NCT00325533) will test whether a continuous HTN detection and medical referral program conducted by influential peers (barbers) in a receptive community setting (barbershops) can promote treatment-seeking behavior and thus lower blood pressure (BP) among the regular customers with HTN. Barbers will offer a BP check with each haircut and encourage appropriate medical referral using real stories of other customers modeling the desired behaviors. A cohort of 16 barbershops will go through a pretest/posttest group-randomization protocol. Serial cross-sectional data collection periods (10 weeks each) will be conducted by interviewers to obtain accurate snapshots of HTN control in each barbershop before and after 10 months of either barber-based intervention or no active intervention. The primary outcome is BP control: BP <135/85 mm Hg (nondiabetic subjects) and <130/80 mm Hg (diabetic subjects) measured in the barbershop during the 2 data collection periods. The multilevel analysis plan uses hierarchical models to assess the effect of covariates on HTN control and secondary outcomes while accounting for clustering of observations within barbershops. CONCLUSIONS: By linking community health promotion to the health care system, this program could serve as a new model for HTN control and cardiovascular risk reduction in African American men on a nationwide scale.

Forgotten but not gone: the rediscovery of fatty heart, the most common unrecognized disease in America.

Until 60 years ago, fatty heart was an accepted clinical entity. Since then, its very existence has been questioned, despite the fact that 2 of 3 Americans are now obese or overweight and obesity has been shown to be correlated with cardiac functional abnormalities. In 2000, a syndrome of "lipotoxic cardiomyopathy" resembling earlier pathologic descriptions of fatty human hearts was described in rodents, and fatty infiltration of cardiomyocytes was subsequently reported in patients with congestive failure. Now, magnetic resonance spectroscopy has been adapted to permit routine noninvasive screening for fatty heart. The use of this technique in human volunteers indicates that cardiomyocyte fat correlates well with body mass index and is elevated in uncomplicated obesity. It is more severe when glucose tolerance becomes abnormal or diabetes is present. It is associated with impaired diastolic filling, even in seemingly asymptomatic obese volunteers. Because fatty heart can be readily prevented by lifestyle modification and pharmacologic interventions that reduce caloric intake and increase fatty acid oxidation, it seems important to recognize its existence so as to intervene as early as possible.

Superiority of Out-of-Office Blood Pressure for Predicting Hypertensive Heart Disease in Non-Hispanic Black Adults.

Black Americans suffer disproportionately from hypertension and hypertensive heart disease. Out-of-office blood pressure (BP) is more predictive for cardiovascular complications than clinic BP; however, the relative abilities of clinic and out-of-office BP to predict left ventricular hypertrophy in black and white adults have not been established. Thus, we aimed to compare associations of out-of-office and clinic BP measurement with left ventricular hypertrophy by cardiac magnetic resonance imaging among non-Hispanic black and white adults. In this cross-sectional study, 1262 black and 927 white participants of the Dallas Heart Study ages 30 to 64 years underwent assessment of standardized clinic and out-of-office (research staff-obtained) BP and left ventricular mass index. In multivariable-adjusted analyses of treated and untreated participants, out-of-office BP was a stronger determinant of left ventricular hypertrophy than clinic BP (odds ratio per 10 mm Hg, 1.48; 95% CI, 1.34-1.64 for out-of-office systolic BP and 1.15 [1.04-1.28] for clinic systolic BP; 1.71 [1.43-2.05] for out-of-office diastolic BP, and 1.03 [0.86-1.24] for clinic diastolic BP). Non-Hispanic black race/ethnicity, treatment status, and lower left ventricular ejection fraction were also independent determinants of hypertrophy. Among treated Blacks, the differential association between out-of-office and clinic BP with hypertrophy was more pronounced than in treated white or untreated participants. In conclusion, protocol-driven supervised out-of-office BP monitoring provides important information that cannot be gleaned from clinic BP assessment alone. Our results underscore the importance of hypertension management programs outside the medical office to prevent hypertensive heart disease, especially in high-risk black adults. Clinical Trial Registration- URL: https://www.clinicaltrials.gov. Unique identifier: NCT00344903.

Nocturia as an Unrecognized Symptom of Uncontrolled Hypertension in Black Men Aged 35 to 49 Years.

Background Hypertension is assumed to be asymptomatic. Yet, clinically significant nocturia (≥2 nightly voids) constitutes a putative symptom of uncontrolled hypertension. Black men with hypertension may be prone to nocturia because of blunted nocturnal blood pressure ( BP ) dipping, diuretic drug use for hypertension, and comorbidity that predisposes to nocturia. Here, we test the hypothesis that nocturia is a common and potentially reversible symptom of uncontrolled hypertension in black men. Methods and Results We determined the strength of association between nocturia (≥2 nightly voids) and high BP (≥135/85 mm Hg) by conducting in-person health interviews and measuring BP with an automated monitor in a large community-based sample of black men in their barbershops. Because nocturia is prevalent and steeply age-dependent after age 50 years, we studied men aged 35 to 49 years. Among 1673 black men (mean age, 43±4 years [ SD ]), those with hypertension were 56% more likely than men with normotension to have nocturia after adjustment for diabetes mellitus and sleep apnea (adjusted odds ratio, 1.56; 95% CI , 1.25-1.94 [ P<0.0001]). Nocturia prevalence varied by hypertension status, ranging from 24% in men with normotension to 49% in men whose hypertension was medically treated but uncontrolled. Men with untreated hypertension were 39% more likely than men with normotension to report nocturia ( P=0.02), whereas men whose hypertension was treated and controlled were no more likely than men with normotension to report nocturia ( P=0.69). Conclusions Uncontrolled hypertension was an independent determinant of clinically important nocturia in a large cross-sectional community-based study of non-Hispanic black men aged 35 to 49 years. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unqiue identifier: NCT 02321618.

Cardiac and skeletal muscle effects in the randomized HOPE-Duchenne trial.

OBJECTIVE: To assess the feasibility, safety, and efficacy of intracoronary allogeneic cardiosphere-derived cells (CAP-1002) in patients with Duchenne muscular dystrophy (DMD). METHODS: The Halt Cardiomyopathy Progression (HOPE)-Duchenne trial is a phase I/II, randomized, controlled, open-label trial (NCT02485938). Patients with DMD >12 years old, with substantial myocardial fibrosis, were randomized (1:1) to usual care (control) or global intracoronary infusion of CAP-1002 (75 million cells). Participants were enrolled at 3 US medical centers between January and August 2016 and followed for 12 months. An independent Data and Safety Monitoring Board provided safety oversight. Cardiac function and structure were assessed by MRI, and analyzed by a blinded core laboratory. Skeletal muscle function was assessed by performance of the upper limb (PUL). RESULTS: Twenty-five eligible patients (mean age 17.8 years; 68% wheelchair-dependent) were randomized to CAP-1002 (n = 13) or control (n = 12). Incidence of treatment-emergent adverse events was similar between groups. Compared to baseline, MRI at 12 months revealed significant scar size reduction and improvement in inferior wall systolic thickening in CAP-1002 but not control patients. Mid-distal PUL improved at 12 months in 8 of 9 lower functioning CAP-1002 patients, and no controls (p = 0.007). CONCLUSIONS: Intracoronary CAP-1002 in DMD appears safe and demonstrates signals of efficacy on both cardiac and upper limb function for up to 12 months. Thus, future clinical research on CAP-1002 treatment of DMD cardiac and skeletal myopathies is warranted. CLASSIFICATION OF EVIDENCE: This phase I/II study provides Class II evidence that for patients with DMD, intracoronary CAP-1002 is feasible and appears safe and potentially effective.