Harvey J. Weiss

Dr. Harvey J. Weiss is Professor Emeritus of Medicine at the Columbia University Vagelos College of Physicians and Surgeons. He received his A.B. from Harvard in 1951 and his M.D. from the Harvard Medical School in 1955. After completing postgraduate training in internal medicine in New York from 1955–1958, and military service in the U.S. Army from 1959–1962, he began a career in New York devoted to teaching, patient care, and research. Initially at the New York University School of Medicine and the Mt. Sinai School of Medicine, he moved to the Roosevelt Hospital in 1968 to establish the Division Hematology. Dr. Weiss then began his affiliation with the Columbia University College of Physicians and Surgeons, attaining the rank of Professor of Medicine in 1975 before retiring in 1969 after serving as a member and chairman of the Committee on Appointments and Promotion (COAP).

Dr. Weiss’ original contributions have been in the field of hemostasis and thrombosis. His were the first reports of the inhibitory effect of aspirin on platelet aggregation (1, 2) and the demonstration that aspirin could inhibit the formation of platelet thrombi in experimental models of thrombosis (3). These experimental studies provided the basis for the use of aspirin as an antithrombotic agent in cardiovascular disease and its current use in preventing heart attacks and strokes. Dr. Weiss has made important contributions to the field of platelet function disorders. He was the first to report that defects in platelet aggregation, distinct from thrombasthenia, could account for the hemostatic defect in some patients with bleeding disorders (4). With Holm Holmsen, he showed that a decreased content of a specialized, non-metabolic pool of adenosine diphosphate (ADP) stored in platelet dense granules could, in some patients, account for this defect (Storage Pool Deficiency, SPD) (5). Further studies by Dr. Weiss and colleagues identified sub-groups of SPD that were characterized by a deficiency of substances stored in dense granules, alpha granules, or both. The designations δ-SPD, α-SPD, and αδ-SPD respectively are those currently used to define these disorders (6). Dr. Weiss has also described patients whose bleeding disorders are the result of impaired platelet procoagulant activity, including a unique disorder (Scott Syndrome) where collaborative studies with Dutch and American investigators have identified the defect as an inability of activated platelets to translocate phosphatidylserine from the inner to the outer plasma membrane (7, 8, 9).

Dr. Weiss has been a major contributor to the field of von Willebrand factor (VWF) and factor VIII. With Leon W. Hoyer, he showed that VWF could be separated from Factor VIII, providing the initial evidence that these were two separate molecules (10). His laboratory was the first to establish the two major physiological functions of VWF. With Hans R. Baumgartner and Vincent T. Turitto, he demonstrated its shear-rate dependent role in mediating platelet adhesion to subendothelium and the complementary role of the platelet GPIb receptor for VWF (11). With other colleagues, he showed that VWF was the carrier molecule for Factor VIII which serves to stabilize its activity in plasma (12). Dr. Weiss also developed an assay that, with modification, is currently used for measuring VWF in plasma (ristocetin co-factor) (13). He also described several subtypes of von Willebrand Disease (VWD), including heterogeneous defects among Type IIA patients (14), Type I-VWD NY (15), and the platelet disorder known as pseudo-VWD (16).

For Dr. Weiss’ major contributions to medical research, he was elected to the American Society for Clinical Investigation in 1970 and to The Association of American Physicians in 1977. In 1995 he received a Distinguished Career Award from the International Society on Thrombosis and Haemostasis. He has lectured widely in both the United Staes and abroad and has served on many editorial boards, including Blood, the American Journal of Medicine, The Journal of Thrombosis and Haemostasis, and Arteriosclerosis and Thrombosis. Dr. Weiss served on the Committee on Certification in Hematology of the American Board of Internal Medicine, as well as other national and international committees.

Selected Papers (16 of over 200)

1. Weiss HJ, Aledort LM: Impaired platelet-connective tissue reaction in man after aspirin ingestion. Lancet 2:495–497, 1967.

2. Weiss HJ, Aledort LM, Kochwa S: The effect of salicylates on the hemostatic properties of platelets in man. J Clin Invest 47:2169–2180, 1968.

3. Weiss HJ, Tschopp TB, Baumgartner HR: Impaired interaction (adhesion-aggregation) of platelets with the subendothelium in storage-pool disease and after aspirin ingestion – a comparison with von Willebrand's disease. N Eng J Med 293:619–723, 1975.1967.

4. Weiss HJ: Platelet aggregation, adhesion and ADP release in thrombopathia (platele factor 3 deficiency) – a comparison with Glanzmann's thrombasthenia and von Willebrand's disease. Am J. Med 43:570–578,

5. Holmsen H, Weiss HJ: Further evidence for a deficient storage pool of adenine nucleotides in platelets from some patients with thrombocytopathia – “storage pool disease.” Blood 39:197–209, 1972.

6. Weiss HJ, Witte LD, Kaplan KL, Lages BA, Chernoff A, Nossel HL, Goodman DeWS, Baumgartner HR: Heterogeneity in storage pool deficiency: Studies on granule-bound substances in 18 patients including variants deficient in a-granules, platelet factor 4, b-thromboglobulin and platelet-derived growth factor. Blood 54:1296–1319, 1979

7. Weiss HJ, Vicic WJ, Lages BA, Rogers J: Isolated deficiency of platelet procoagulant activity. Am J Med 67:206–213, 1979.

8. Rosing J, Bevers EM, Comfurius P, Hemker HC, von Dieijen G, Weiss HJ, Zwaal RFA: Impaired factor X and prothrombin activation associated with decreased phospholipid exposure in platelets from a patient with a bleeding disorder. Blood 65:1557–1561, 1985.

9. Weiss HJ: Scott syndrome: a disorder of platelet coagulant activity (PCA). Sem Hemat 31:312–319, 1994.

10. Weiss HJ, Hoyer LW: von Willebrand factor: dissociation from antihemophilic factor procoagulant activity. Science 182:1149–1151, 1973.

11.Weiss HJ, Turitto VT, Baumgartner HR: Effect of shear rate on platelet interaction with subendothelium in citrated and native blood. Shear-dependent decrease of adhesion in von Willebrand’s disease and the Bernard-Soulier syndrome. J Lab Clin Med 92:750–764, 1978.

12. Weiss HJ, Sussman II, Hoyer L: Stabilization of factor VIII in plasma by the von Willebrand factor: Studies on post-transfusion and dissociated factor VIII and in patients with von Willebrand’s disease. J Clin Invest 60:390–404, 1977.

13. Weiss HJ, Hoyer LW, Rickles FR, Varma A, Rogers J: Quantitative assay of a plasma factor, deficient in von Willebrand’s disease, that is necessary for platelet aggregation – relationship to decreased factor VIII procoagulant activity and antigen content. J Clin Invest 52:2708–2716, 1973.

14. Weiss HJ, Pietu G, Meyer D, Rabinowitz R, Girma JP, Rogers J: Heterogeneous abnormalities in the multimeric structure, antigenic properties, and plasma/platelet content of FVIII/vWf in classical (Type I) and three sub-types of variant (Type II) von Willebrand's disease. J Lab Clin Med 101:411–425, 1983.

15. Weiss HJ, Sussman II: A new von Willebrand variant (Type I, New York): Increased ristocetin-induced platelet aggregation and plasma von Willebrand factor containing the full range of multimers. Blood 68:149–156, 1986.

16. Weiss HJ, Meyer D, Rabinowitz R, Pietu G, Girma JP, Vicic WJ, Rogers J: Pseudo von Willebrand’s disease: an intrinsic platelet defect with aggregation by unmodified human factor VIII/von Willebrand factor and enhanced adsorption of its high molecular weight multimers. N Eng J Med 306:326–333, 1982.

Updated August 28, 2024