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Dipyridamole and Nifedipine—Studies on Their Protective Effects for Heart Graft Arterial Stenosis

Department of Surgery, Saitama Medical School

Ahvie Herskowitz

Department of Medicine, The Johns Hopkins Medical Institutions

Thomas A. Pearson

Department of Medicine, The Johns Hopkins Medical Institutions

John M. Dillman

Department of Medicine, The Johns Hopkins Medical Institutions

Masako Suzuki

Department of Pathology, Saitama Medical School, Saitama, Japan

Hideo Adachi

Department of Surgery, Saitama Medical School

Ryozo Omoto

Department of Surgery, Saitama Medical School

William A. Baumgartner

Department of Cardiac Surgery, The Johns Hopkins Medical Institutions, Baltimore, Maryland

Bruce A. Reitz

Department of Cardiac Surgery, The Johns Hopkins Medical Institutions, Baltimore, Maryland

The etiology of accelerated graft coronary arterial stenosis (CAS) was stud ied in a rat heterotopic heart transplantation model. Spontaneously hyperten sive rats (SHR), Wistar rats (WR), and Lewis rats (LEW) were used. Thirty-four recipients rats fed a hypercholesterol diet (HCD) and saline for eight weeks were divided into six groups. Group 1 and 2 (5 rats each) were hypertensive isograft models (SHR to SHR), group 2 being treated with cyclos porine (CsA: 10mg/kg/day orally). The other 4 groups (6 rats each) represented the allograft models. Group 3 (LEW to WR) was the CsA-treated normotensive model, and Groups 4, 5, and 6 (LEW to SHR) were CsA-treated hypertensive models. Additionally, group 5 was treated by dipyridamole (DP; 25mg/kg/day orally) and group 6 was by nifedipine (NF; 3mg/kg/day orally). The coronary stenosis index (CSI) was calculated in each case and the proportion of arteries affected (AR, %) was estimated in each group. AR and CSI were 6.1% and 0.53 ± 0.76 in group 1, 3.6 % and 0.50 ± 0.71 in group 2, 23.7 % and 1.85±0.52 in group 3, 58.2 % and 2.45 ±0.18 in group 4, 32.3% and 2.25 ±0.29 in group 5, and 27.7% and 1.93 ± 0.48 in group 6. AR and CSI were significantly increased in group 3 vs group 1 (p < 0.05) and in group 4 vs group 3 (p < 0.05). AR was reduced in groups 5 and 6 vs group 4 (p < 0.05), and CSI was also reduced in group 6 vs group 4(p < 0.05). In conclusion, hypercholesterolemia and hyper tension were recognized as risk factors for CAS aggravation in allografts but failed to affect the coronary arteries of isografts. Both antiatherogenic agents reduced the number of affected vessels, but only NF reduced the degree of CAS. However, neither controlled graft CAS completely.

Vascular and Endovascular Surgery, Vol. 24, No. 5, 326-334 (1990)
DOI: 10.1177/153857449002400505


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