Biosketch / Results /

Richard M. Hayes, M.D.

Clinical Assistant Professor;
Department of Medicine (Medicine)
NYU EKG Associates
NYU Cardiac Exercise / Stress Lab

Clinical Addresses

NEW YORK CORE CARDIOLOGY PC
35A EAST 35TH STREET, SUITE 204
NEW YORK, NY 10016
Handicap Access: yes
Phone: 212-696-0020
Fax: 212-696-0022

« Back to Results

Medical Specialties

Cardiology, Internal Medicine

Medical Expertise

Radionuclide Imaging Cardilogy, Acute Myocardial Infarction, Lipid Metabolism, Echocardiogram, Arteriosclerosis, General Cardiology, Valvular Disease

Insurance

AETNA HMO, AETNA INDEMNITY, AETNA MEDICARE, AETNA POS, AETNA PPO, BeechSt, Cigna HMO/POS, Cigna PPO, EBC/BS, Empire NYS Plan, GHI, HIP, HealthNet, Local 1199, MagnaCare, Multiplan, One Health:GW Healthcare, Oxford, PHCS, UPN Elite, United Healthcare

Insurance Disclaimer: Insurance listed above may not be accepted at all office locations. Please confirm prior to each visit. The information presented here may not be complete or may have changed.

« Back to Results

Board Certification

1997 — Cardiovascular Disease (Internal Med)
2004 — Internal Medicine

Education

1986-1990 — New York Medical College, Medical Education
1990-1991 — New York Hospital - Cornell Medical Center (Internal Medicine), Internship
1991-1993 — New York Presbyterian Hospital (Cardiology), Residency Training
1994-1997 — Mount Sinai Medical Center (Cardiology), Clinical Fellowships

« Back to Results

All data from NYU Health Sciences Library Faculty Bibliography — -

Contact:
http://hsl.med.nyu.edu/faculty-bibliography-search#about

Administration of abciximab during percutaneous coronary intervention reduces both ex vivo platelet thrombus formation and fibrin deposition: implications for a potential anticoagulant effect of abciximab
Dangas G; Badimon JJ; Coller BS; Fallon JT; Sharma SK; Hayes RM; Meraj P; Ambrose JA; Marmur JD
1998 Aug;18(8):1342-1349, Arteriosclerosis, thrombosis, & vascular biology
Abciximab (c7E3 Fab, ReoPro), a platelet glycoprotein (GP) IIb/IIIa inhibitor, decreases acute ischemic complications after percutaneous coronary interventions. Recently, abciximab was shown to decrease thrombin generation in vitro in a static system. To assess whether abciximab can decrease fibrin formation in blood from patients, we quantified both platelet thrombi and fibrin deposition by using an ex vivo flow chamber model. We prospectively studied 18 consecutive patients who underwent percutaneous interventions for unstable coronary syndromes. Blood was perfused directly from the patient through an ex vivo perfusion chamber at a high shear rate, thus mimicking mildly stenosed coronary arteries. Perfusion chamber studies were performed when patients were being treated with heparin plus aspirin before the procedure (baseline) and then repeated after the procedure, when patients were on either aspirin plus heparin alone (group 1, no abciximab, control) or aspirin plus heparin plus abciximab (group 2, abciximab treated). Each patient served as his or her own control. Specimens were stained with combined Masson's trichrome-elastin and antibodies specific for fibrinogen, fibrin, and platelet GP IIIa. Total thrombus area and areas occupied by platelet aggregates and fibrin layers were quantified by planimetry. Group 1 demonstrated no significant change in thrombus area before versus after the procedure; in contrast, treatment with abciximab reduced total thrombus area by 48% in group 2 (after the procedure versus baseline, P=0.01). This decline was due to significant reductions in both platelet aggregates (55%, P=0.005) and fibrin layers (45%, P=0.03). The addition of abciximab to heparin and aspirin in patients undergoing coronary interventions significantly decreases ex vivo thrombus formation on an injured vascular surface. Treatment with abciximab appears to reduce both the platelet and the fibrin thrombus components. This finding supports a potential role for GP IIb/IIIa receptor blockade in decreasing fibrin formation in addition to inhibition of platelet aggregation. Thus, potent inhibitors of GP IIb/IIIa may also act as anticoagulants
— id: 66737, year: 1998, vol: 18, page: 1342, stat: Journal Article,