What is the clinical evidence from this study?

Study design: Observational. Population: Coronary atherosclerosis and NSTEMI (n=96). Intervention: Unstable coronary atherosclerosis vs. Stable coronary atherosclerosis. Primary outcome: Low-flow-mediated constriction (L-FMC) (p=<0.01).

October 29, 2010Open Access

Brachial artery low-flow-mediated constriction is increased early after coronary intervention and reduces during recovery after acute coronary syndrome: characterization of a recently described index of vascular function

Q: What are the key findings of this study?

Brachial artery low-flow-mediated constriction was greater in patients with unstable versus stable coronary atherosclerosis (-1.33% vs -0.03%, P<0.01) and increased acutely following PCI.

Key Result

Brachial artery low-flow-mediated constriction was greater in patients with unstable versus stable coronary atherosclerosis (-1.33% vs -0.03%, P<0.01) and increased acutely following PCI.

Study Design

Type

Observational (n=96)

Structured PICO

How does brachial artery low-flow-mediated constriction (L-FMC) change following PCI and during recovery from NSTEMI?

Population

96 participants, including 86 patients with coronary atherosclerosis and 10 healthy volunteers, assessed for brachial artery low-flow-mediated constriction.

Exposure

Percutaneous coronary intervention (PCI) and recovery from NSTEMI

Comparator

Stable vs. unstable coronary atherosclerosis; before vs. after PCI; acute vs. recovery phase of NSTEMI

Outcome

Changes in brachial artery low-flow-mediated constriction (L-FMC) and flow-mediated dilatation (FMD)surrogate

Brachial artery low-flow-mediated constriction (L-FMC) is a reproducible index of vascular function that dynamically changes, increasing acutely after PCI and decreasing during recovery from NSTEMI.

Main Result

Absolute Event Rate: -1.33% vs -0.03%

p-value: p=<0.01

Abstract

AIMS: The endothelium plays a role in regulating vascular tone. Acute and dynamic changes in low-flow-mediated constriction (L-FMC) and how it changes with regard to traditional flow-mediated dilatation (FMD) have not been described. We aimed to investigate the changes in brachial artery L-FMC following percutaneous coronary intervention (PCI) and during recovery from non-ST-segment elevation myocardial infarction (NSTEMI). METHODS AND RESULTS: FMD was performed in accordance with a previously described technique in patients before and after PCI and in the recovery phase of NSTEMI, but in addition, L-FMC data were acquired from the last 30 s of cuff inflation. About 135 scans were performed in 96 participants (10 healthy volunteers and 86 patients). Measurement of brachial L-FMC was reproducible over hours. L-FMC was greater among patients with unstable vs. stable coronary atherosclerosis (-1.33 ±1.09% vs. -0.03 ± 1.26%, P < 0.01). Following PCI, FMD reduced (4.43 ± 2.93% vs. 1.66 ± 2.16%, P < 0.01) and L-FMC increased (-0.33 ± 0.76% vs. -1.63 ± 1.15%, P = 0.02). Furthermore, during convalescence from NSTEMI, L-FMC reduced (-1.37 ± 1.19% vs. 0.01 ± 0.82%, P = 0.02) in parallel with improvements in FMD (2.54 ± 2.19% vs. 5.15 ± 3.07%, P < 0.01). CONCLUSION: Brachial L-FMC can be measured reliably. Differences were observed between patients with stable and unstable coronary disease. L-FMC was acutely increased following PCI associated with reduced FMD and, in the recovery from NSTEMI, L-FMC reduced associated with increased FMD. These novel findings characterize acute and subacute variations in brachial L-FMC. The pathophysiological and clinical implications of these observations require further study.