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Clin Cardiol. 2017 May;40(5):300-306. doi: 10.1002/clc.22660. Epub 2016 Dec 22.

Myocardial tissue deformation is reduced in subjects with coronary microvascular dysfunction but not rescued by treatment with ranolazine.

Author information

1
Applied Physiology and Advanced Imaging Laboratory, University of Texas at Arlington, Arlington, Texas.
2
Biomedical Imaging Research Institute, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California.
3
Barbra Streisand Women's Heart Center, Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
4
Biostatistics Core, Cedars-Sinai Medical Center, Los Angeles, California.
5
Emory Women's Heart Center, Emory University School of Medicine, Atlanta, Georgia.
6
Mark S. Taper Imaging Center, Cedars-Sinai Medical Center, Los Angeles, California.
7
Department of Biomedical Engineering, University of Alberta, Edmonton, Alberta, Canada.
8
Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida.

Abstract

BACKGROUND:

Patients with coronary microvascular dysfunction (CMD) often have diastolic dysfunction, representing an important therapeutic target. Ranolazine-a late sodium current inhibitor-improves diastolic function in animal models and subjects with obstructive coronary artery disease (CAD).

HYPOTHESIS:

We hypothesized that ranolazine would beneficially alter diastolic function in CMD.

METHODS:

To test this hypothesis, we performed retrospective tissue tracking analysis to evaluate systolic/diastolic strain, using cardiac magnetic resonance imaging cine images acquired in a recently completed, randomized, double-blind, placebo-controlled, crossover trial of short-term ranolazine in subjects with CMD and from 43 healthy reference controls.

RESULTS:

Diastolic strain rate was impaired in CMD vs controls (circumferential diastolic strain rate: 99.9% ± 2.5%/s vs 120.1% ± 4.0%/s, P = 0.0003; radial diastolic strain rate: -199.5% ± 5.5%/s vs -243.1% ± 9.6%/s, P = 0.0008, case vs control). Moreover, peak systolic circumferential strain (CS) and radial strain (RS) were also impaired in cases vs controls (CS: -18.8% ± 0.3% vs -20.7% ± 0.3%; RS: 35.8% ± 0.7% vs 41.4% ± 0.9%; respectively; both P < 0.0001), despite similar and preserved ejection fraction. In contrast to our hypothesis, however, we observed no significant changes in left ventricular diastolic function in CMD cases after 2 weeks of ranolazine vs placebo.

CONCLUSIONS:

The case-control comparison both confirms and extends our prior observations of diastolic dysfunction in CMD. That CMD cases were also found to have subclinical systolic dysfunction is a novel finding, highlighting the utility of this retrospective approach. In contrast to previous studies in obstructive CAD, ranolazine did not improve diastolic function in CMD.

KEYWORDS:

Coronary microvascular dysfunction; microvascular ischemia; ranolazine; tissue tracking

PMID:
28004395
PMCID:
PMC5436931
DOI:
10.1002/clc.22660
[Indexed for MEDLINE]
Free PMC Article

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