Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
LIPOPROTEIN(A) LEVEL DOES NOT PREDICT RESTENOSIS AFTER PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY
Autore:
ALAIGH P; HOFFMAN CJ; KORLIPARA G; NEUROTH A; DERVAN JP; LAWSON WE; HULTIN MB;
Indirizzi:
SUNY STONY BROOK,DEPT MED,DIV HEMATOL,HLTH SCI CTR T15 040 STONY BROOK NY 11794 SUNY STONY BROOK,DEPT MED,DIV HEMATOL,HLTH SCI CTR T15 040 STONY BROOK NY 11794
Titolo Testata:
Arteriosclerosis, thrombosis, and vascular biology
fascicolo: 8, volume: 18, anno: 1998,
pagine: 1281 - 1286
SICI:
1079-5642(1998)18:8<1281:LLDNPR>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
SINGLE-VESSEL DISEASE; SERUM LIPOPROTEIN(A); RISK FACTOR; APOLIPOPROTEIN(A); PROTEIN; PLASMINOGEN; BINDING;
Keywords:
LIPOPROTEIN(A); ANGIOPLASTY; THROMBIN; PLASMIN; ANTIPLASMIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
P. Alaigh et al., "LIPOPROTEIN(A) LEVEL DOES NOT PREDICT RESTENOSIS AFTER PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY", Arteriosclerosis, thrombosis, and vascular biology, 18(8), 1998, pp. 1281-1286

Abstract

The serum lipoprotein(a) [Lp(a)] level is a known risk factor for arteriosclerotic coronary artery disease. However, its association with restenosis after percutaneous transluminal coronary angioplasty (PTCA) is controversial. We hypothesized that the Lp(a) level is a significant risk factor for restenosis after angioplasty through a pathophysiological mechanism leading to excess thrombin generation or inhibition offibrinolysis. We designed a prospective study of the relation of Lp(a) to outcome after PTCA, in which we measured selected laboratory variables at entry and collected clinical, procedural, lesion-related, andoutcome data pertaining to restenosis. Restenosis was defined as >50%stenosis of the target lesion by angiography or as ischemia in the target vessel distribution by radionuclide-perfusion scan. Before the patients underwent PTCA, blood was obtained by venipuncture for measurement of Lp(a), total cholesterol, thrombin-antithrombin (TAT) complex, alpha(2)-antiplasmin-plasmin (APP) complex, and plasminogen activator inhibitor-1 (PAI-1). Evaluable outcome data were obtained on 162 subjects, who form the basis of this report. Restenosis occurred in 61 subjects (38%). The Lp(a) level was not correlated significantly with TAT,APP, PAI-1, or the TAT-APP ratio. Levels of TAT, APP, and PAI-1 were not statistically different in the patients with versus those without restenosis. The median ratio of TAT to APP was 2-fold higher in the restenosis group, and this difference approached statistical significance (P=0.07). Univariate analysis was performed for the association of clinical, lesion-related, and procedural risk factors with restenosis. Lp(a) levels did not differ significantly in the restenosis versus no-restenosis group, whether assessed categorically (>25 mg/dL versus <25mg/dL) or as a continuous variable by Mann-Whitney U test. The numberof lesions dilated and the lack of family history of premature heart disease were significantly associated with restenosis (P=0.002 and P=0.008, respectively). A history of diabetes mellitus was of borderline significance (P=0.055). By multiple logistic regression analysis, the number of lesions dilated was the only variable significantly associated with restenosis (P=0.03). We conclude hat the number of lesions dilated during PTCA is a significant risk factor for restenosis, whereas the serum Lp(a) level was not a significant risk factor for restenosisin our patient population. The TAT to APP ratio merits further study as a possible risk factor for restenosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 23:54:44