Pediatrician, Pediatric Specialist
7 years of experience
Video profile
Accepting new patients
Grand View
Cook Children's Medical Center
1500 Cooper St
Fort Worth, TX 76104
682-885-2140
Locations and availability (9)

Education ?

Medical School Score Rankings
University of Iowa (2003)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Associations
American Board of Pediatrics

Affiliations ?

Dr. Muyskens is affiliated with 16 hospitals.

Hospital Affilations

Score

Rankings

  • Texas Health Harris Methodist Hospital Azle
    Cardiology
    108 Denver Trl, Azle, TX 76020
    • Currently 4 of 4 crosses
    Top 25%
  • Denton Hospital
    Cardiology
    3000 N Interstate 35, Denton, TX 76201
    • Currently 3 of 4 crosses
    Top 50%
  • Cook Children's Medical Center
    801 7th Ave, Fort Worth, TX 76104
    • Currently 2 of 4 crosses
  • Texas Health Presbyterian Hospital Of Dallas
  • Medical Center Of Arlington
  • Texas Health Denton
  • Texas Health Harris Methodist Hospital Fort Worth
  • Texas Health Harris Methodist Hospital Southwest Fort Worth
  • Harris Methodist - Springwood
    1608 Hospital Pkwy, Bedford, TX 76022
  • Texas Health HEB
  • Texas Health Southwest Fort Worth
  • Texas Health Arlington Memorial Hospital
  • Texas Health Flower Mound
  • Harris Methodist H E B
  • Texas Health Fort Worth
  • Harris Continued Care Hospital
    1301 Pennsylvania Ave, Fort Worth, TX 76104
  • Publications & Research

    Dr. Muyskens has contributed to 3 publications.
    Title Endovascular Stent Placement for Right Ventricle to Pulmonary Artery Conduit Stenosis in the Norwood with Sano Modification.
    Date August 2008
    Journal Congenital Heart Disease
    Excerpt

    OBJECTIVE: Conduit obstruction is increasingly recognized as a complication of the Sano modified Norwood procedure. We report our experience with stent placement to ameliorate conduit stenoses and prevent premature surgical intervention. DESIGN: Records for all patients having undergone a Sano modified Norwood between September 2003 and December 2006 were reviewed. All patients with Sano conduit obstruction requiring stent placement were included. Sites of obstruction, method of stenting, pre- and poststent oxygen saturations, reinterventions, age at next surgery, and complications were collected and reviewed. RESULTS: Forty-one patients underwent a Sano modified Norwood procedure, and 9 patients had stents deployed for conduit stenoses. The patients presented a median of 52 days following Norwood palliation. Twelve stents were successfully placed in 9 patients. In 8 patients, saturations improved from a median of 67.5% to 81% after stent placement (P = .0005). Arterial saturations were unavailable in 1 patient requiring extracorporeal membrane oxygenation. No patients required reintervention after stent placement. The median age at their next surgery was 144 days. Seven patients underwent a successful bidirectional Glenn, 1 patient underwent a modified Blalock-Taussig shunt, and 1 expired. Complications included hypotension during stent deployment and 1 episode of transient complete heart block. CONCLUSIONS: Transcatheter treatment of Sano conduit obstruction can be performed safely and results in immediate improvement in oxygenation, thereby allowing substantial delay of the cavo-pulmonary shunt.

    Title Combined Endothelial Nitric Oxide Synthase Upregulation and Caveolin-1 Downregulation Decrease Leukocyte Adhesion in Pial Venules of Ovariectomized Female Rats.
    Date February 2002
    Journal Stroke; a Journal of Cerebral Circulation
    Excerpt

    BACKGROUND AND PURPOSE: We recently found that chronic estrogen depletion enhances leukocyte adhesion in pial venules in the female rat, while estrogen repletion decreases it. Estrogen-associated repression of inflammation may be due to upregulation of the endothelial isoform of nitric oxide synthase (eNOS) and concomitant downregulation of the endogenous inhibitor of eNOS, caveolin-1 (CAV-1). In this study we examined the effects of estrogen-independent eNOS upregulation (via simvastatin) and/or CAV-1 downregulation (antisense) on pial venular leukocyte adhesion in ovariectomized (OVX) rats. METHODS: Intact and OVX rats were prepared with closed cranial windows. Adherent rhodamine 6G-labeled leukocytes were viewed by intravital microscopy. To demonstrate the importance of pial venular eNOS in the resistance to leukocyte adhesion, intact female rats were treated with a nonselective (N(G)-nitro-L-arginine) or a neuronal NOS-selective (7-nitroindazole) inhibitor. In OVX females, leukocyte adhesion was compared in the following groups: (1) untreated; (2) treated with simvastatin; (3) treated with simvastatin plus CAV-1 antisense; (4) treated with simvastatin plus CAV-1 missense; (5) treated with CAV-1 antisense; and (6) treated with CAV-1 missense. RESULTS: In intact females, pial venular leukocyte adhesion was increased when total NOS activity, but not neuronal NOS activity alone, was blocked. In OVX rats, basal leukocyte adhesion, measured as the percentage of venular area occupied by adherent leukocytes, was attenuated (by approximately equal 60%) only in the presence of combined simvastatin plus CAV-1 antisense treatment. CONCLUSIONS: Present findings demonstrate that eNOS-derived NO plays an important role in limiting cerebral venular leukocyte adhesion in female rats. These data also suggest that simvastatin-induced upregulation of eNOS expression in OVX rats will not restore eNOS function, as measured by decreased leukocyte adhesion, unless CAV-1 levels are reduced as well.

    Title Percutaneous Closure of a Complex Posttraumatic Muscular Ventricular Septal Defect.
    Date
    Journal Catheterization and Cardiovascular Interventions : Official Journal of the Society for Cardiac Angiography & Interventions
    Excerpt

    We report the percutaneous closure of a complex traumatic ventricular septal defect resulting from a stab wound to the anterior chest. The patient presented with heart failure 3 months after the initial trauma. Evaluation revealed a new large ventricular septal defect with diminished cardiac function. Closure was accomplished with a combination of an Amplatzer muscular ventricular septal defect occluder and two Amplatzer vascular plugs.

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