Racial Differences in the Coronary Microcirculation

May 12, 2016 updated by: National Heart, Lung, and Blood Institute (NHLBI)
To study mechanisms of excess coronary ischemia secondary to alterations in autoregulation and arteriolar vasoreactivity in Black Americans with hypertension, varying degree of left ventricular hypertrophy, and angiographically normal or mildly diseased coronary arteries.

Study Overview

Status

Completed

Conditions

Detailed Description

BACKGROUND:

Although studies in 1992 with a sufficient number of minority patients were sparse, those available suggested that Black Americans had a higher case fatality from coronary heart disease, but lesser amounts of atherosclerotic coronary artery disease. A possible explanation for this apparent paradox was that myocardial ischemia might be more prevalent with less coronary artery atherosclerosis in Black Americans because of comorbid diseases or differences in coronary physiology. This could be secondary to excess hypertension and left ventricular hypertrophy in Black Americans but might also have been related to intrinsic or acquired differences in coronary artery autoregulation and vasoreactivity leading to depression in coronary blood flow and reserve.

DESIGN NARRATIVE:

The intracoronary Doppler flow velocity guidewire together with quantitative coronary angiography was used to study changes in coronary blood flow in blacks secondary to pharmacologic provocateurs known to induce arteriolar vasodilation. White Americans with similar demographic characteristics and equivalent amount of ventricular hypertrophy and coronary disease were similarly studied in a parallel fashion for comparison. A control group of normal white and Black Americans were studied to detect unexpected intrinsic differences. Both endothelium dependent and independent induction of coronary arteriolar vasodilation were studied. In 25 percent of patients with endothelium dependent defects in arteriolar vasodilation, retesting was performed after intracoronary infusion of L-arginine, the precursor of endothelium dependent relaxing factor. Finally, the possibility of a rightward shift in coronary artery autoregulation in chronic hypertension was investigated. This finding would necessitate that the lower limit of autoregulation occurred at higher diastolic pressures, resulting in a drop-off of coronary perfusion at normal physiologic pressures and ischemia.

The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.

Study Type

Observational

Participation Criteria

Researchers look for people who fit a certain description, called eligibility criteria. Some examples of these criteria are a person's general health condition or prior treatments.

Eligibility Criteria

Ages Eligible for Study

No older than 100 years (Child, Adult, Older Adult)

Accepts Healthy Volunteers

No

Genders Eligible for Study

Male

Description

No eligibility criteria

Study Plan

This section provides details of the study plan, including how the study is designed and what the study is measuring.

How is the study designed?

Collaborators and Investigators

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Sponsor

National Heart, Lung, and Blood Institute (NHLBI)

Publications and helpful links

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General Publications

Study record dates

These dates track the progress of study record and summary results submissions to ClinicalTrials.gov. Study records and reported results are reviewed by the National Library of Medicine (NLM) to make sure they meet specific quality control standards before being posted on the public website.

Study Major Dates

Study Start

September 1, 1992

Study Completion (Actual)

August 1, 1998

Study Registration Dates

First Submitted

May 25, 2000

First Submitted That Met QC Criteria

May 25, 2000

First Posted (Estimate)

May 26, 2000

Study Record Updates

Last Update Posted (Estimate)

May 13, 2016

Last Update Submitted That Met QC Criteria

May 12, 2016

Last Verified

July 1, 2000

More Information

Terms related to this study

Additional Relevant MeSH Terms

Other Study ID Numbers

  • 4267
  • R01HL050262 (U.S. NIH Grant/Contract)

This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.

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