Hypertension Clinical Trials

Cedars-Sinai Heart Institute is currently conducting the following hypertension clinical trials:

Barber based intervention for hypertension in black men
• Cocaine and Sympathetic nerve activity in humans: Reversing Cocaine-Induced Cardiovascular Toxicity in Humans

Barber based intervention for hypertension in black men

Principal Investigator: Ronald Victor, MD

IRB Approval Number: 20112

Contact: Julie Groth (310) 248-7641

Status: Data Analysis

Summary: This study addressed an important health disparity – excessive and premature cardiovascular disability and death among African American men from undetected, untreated, or under-treated high blood pressure.  Yet few previous health promotion studies have specifically addressed blood pressure control in this high-risk group.  We have conducted a careful scientific evaluation of an innovative high blood pressure outreach program conducted by barbers.  Barbers are uniquely positioned to administer such a program because they are trusted, influential peers whose historical predecessors were barber-surgeons.  This program thus enabled barbers to become health educators and help combat the epidemic of high blood pressure and cardiovascular disease in their community.  We hypothesized that a continuous high blood pressure detection and medical referral program conducted by barbers in a receptive community setting (barbershops) can promote treatment-seeking behavior and thus lower blood pressure among the regular clients with high blood pressure.  To test our hypothesis, a cohort of 17 previously unstudied barbershops went through a group-randomization protocol.  Serial cross-sectional blood pressure surveys were conducted by trained interviewers to obtain accurate snap-shots of blood pressure control in each of the 17 barbershops before and after a 10-month intervention period consisting of either barber-based intervention or distribution of standard health education brochures.  The data analysis of the major outcomes is underway.  The potential for dissemination is high, with tens of thousands of Non-Hispanic Black-owned barbershops nationwide.  More broadly, this novel approach shifts more of the responsibility for disease prevention to the lay community and links shifts more of the responsibility for disease preventions to the lay community and links community health promotion to the healthcare delivery system.  


Cocaine and Sympathetic nerve activity in humans: Reversing Cocaine-Induced Cardiovascular Toxicity in Humans

Principal Investigator: Ronald Victor, MD

IRB Approval Number: 19420 and 19549

Contact: Andrew Kontak (310) 248-7690

Status: Enrolling

Summary: Cocaine is a major cause of life-threatening cardiovascular emergencies (hypertensive crisis, myocardial infarcts. While these emergencies are related to excessive adrenergic stimulation of the cardiovascular system, our understanding of the underlying mechanisms is far from complete and current therapies are unsatisfactory. The prevailing view is that cocaine blocks norepinephrine (NE) reuptake in peripheral sympathetic terminals, thereby increasing [NE].  During the past two grant cycles, our studies in cocaine-naive human subjects have challenged the predominance of this mechanism and demonstrated instead that cocaine stimulates the human cardiovascular system primarily by acting in the brain to increase sympathetic nerve activity (SNA), the neural stimulus to NE release.  We now hypothesize that the central sympatholytic action of alpha2 adrenergic receptor (AR) agonists can be utilized to counter the centrally-driven cardiovascular consequences of cocaine. These agonists could mitigate effects of cocaine by acting on brainstem alpha2 ARs to decrease SNA as well as on presynaptic alpha2 ARs on sympathetic nerve terminals to inhibit NE release. But they also activate post-junctional alpha2 ARs on vascular smooth muscle which might exacerbate cocaine-induced vasoconstriction. Utilizing rigorously-defined cardiovascular phenotypes in a controlled laboratory setting, we will test whether the efficacy of potent alpha2 AR agonist (i.v. dexmedetomidine) to reverse the sympathomimetic actions of cocaine is maintained even under conditions in which either a) the sympatholytic effects of alpha2 ARs might be attenuated (black ethnicity, loss-of-function mutation in alpha2C AR, chronic cocaine exposure) or b) postjunctional alpha2 AR mediated vasoconstriction might be augmented (coronary disease, gain-of-function mutations in the alpha2B AR or post-receptor signaling).