Elevated Baseline Serum Fibrinogen: Effect on 2‐Year Major Adverse Cardiovascular Events Following Percutaneous Coronary Intervention

Abstract

BackgroundElevated fibrinogen is associated with short‐term major adverse cardiovascular events (MACE) after percutaneous coronary intervention, but the relation with late MACE is unknown.Methods and ResultsBaseline demographics and 2‐year MACE were recorded among subjects undergoing nonemergent percutaneous coronary intervention. A total of 332 subjects (66.6±19.5 years, 69.9% male, 25.3% acute coronary syndrome) were enrolled. Two‐year MACE (periprocedural myocardial infarction 9.0%, rehospitalization 6.3%, revascularization 12.7%, non–periprocedural myocardial infarction 4.5%, stent thrombosis 0.9%, stroke 1.8%, and death 0.6%) were associated with higher fibrinogen (352.8±123.4 mg/dL versus 301.6±110.8 mg/dL; P<0.001), longer total stent length (40.1±25.3 mm versus 32.1±19.3 mm; P=0.004), acute coronary syndrome indication (38.7% versus 17.8%; P<0.001), number of bare‐metal stents (0.5±1.1 versus 0.2±0.5; P=0.002), and stent diameter ≤2.5 mm (55.8% versus 38.4%, P=0.003). No relation between platelet reactivity and 2‐year MACE was observed. Fibrinogen ≥280 mg/dL (odds ratio [OR] 3.0, confidence interval [CI], 1.6–5.4, P<0.001), total stent length ≥32 mm (OR 2.2, CI, 1.3–3.8, P<0.001), acute coronary syndrome indication (OR 4.1, CI, 2.3–7.5, P<0.001), any bare‐metal stents (OR 3.2, CI, 1.6–6.1, P<0.001), and stent diameter ≤2.5 mm (OR 2.0, CI, 1.2–3.5, P=0.010) were independently associated with 2‐year MACE. Following a landmark analysis excluding periprocedural myocardial infarction, fibrinogen ≥280 mg/dL remained strongly associated with 2‐year MACE (37.0% versus 17.4%, log‐rank P<0.001).ConclusionsElevated baseline fibrinogen level is associated with 2‐year MACE after percutaneous coronary intervention. Acute coronary syndrome indication for percutaneous coronary intervention, total stent length implanted, and use of bare‐metal stents or smaller‐diameter stents are also independently associated with 2‐year MACE, while measures of on‐thienopyridine platelet reactivity are not.

Fibrinogen is associated with glucose metabolism and cardiovascular outcomes in patients with coronary artery disease

“…Fibrinogen (Fib), as a thromboplastic and inflammatory marker, facilitates blood viscosity, platelet aggregation, fibrin cross-linking, and plays a pivotal role in the progression of atherosclerosis [1,2]. Previous studies showed that Fib was not only an indicator of subclinical cardiovascular diseases, such as coronary artery calcification and intima-media thickness of the carotid artery [3,4], but was also independently associated with the development of coronary artery disease (CAD), hypertension, stroke, as well as adverse cardiovascular events [5][6][7][8][9].…”

D-Dimer to Fibrinogen Ratio as a Novel Prognostic Marker in Patients After Undergoing Percutaneous Coronary Intervention: A Retrospective Cohort Study

“…10,11 Previous studies have shown that fibrinogen was not only independently associated with the development of CAD, hypertension and stroke, but also an independent predictor of long-term prognosis in patients after PCI. [12][13][14] More recently, it has been reported that the D-dimer to fibrinogen ratio (DFR) is a novel predictor for the outcomes of pulmonary thromboembolism (PTE), ischemic stroke and gastrointestinal stromal tumors (GISTs). [15][16][17] However, the relationship between the DFR and prognosis in CAD patients after PCI has not been investigated.…”

Prognostic utility of lipoprotein(a) combined with fibrinogen in patients with stable coronary artery disease: a prospective, large cohort study

“…Unlike apolipoprotein B, apo(a) does not contain lipid domains or transport lipid, but instead, it potentiates atherothrombosis through additional pathways including proin ammatory, and potentially anti brinolytic effects by inhibiting plasminogen activation [10]. As one of the important components of brinolytic system, plasma brinogen (Fib) has been proved to be a pivotal CVD risk factor [11][12][13]. However, little is known about the inter-relationship of Lp(a) and Fib in the CVEs risk prediction in the secondary prevention setting.…”