Key result
FIBFAR phenotype linked to ~8.6-fold higher odds of carotid plaque in cardiometabolic risk.
Why the study?
Systemic inflammation and hemodynamic alterations are complementary mechanisms in cardiovascular disease, and identifying integrative phenotypes using noninvasive tools could better characterize subclinical atherosclerosis. The association between the FIBFAR hemodynamic-inflammatory phenotype and carotid plaque in patients with cardiometabolic risk required evaluation.
Is the FIBFAR hemodynamic-inflammatory phenotype associated with the presence of subclinical carotid plaque in patients with hypertension and diabetes or prediabetes?
Cross-Sectional (n=243)
Is the FIBFAR hemodynamic-inflammatory phenotype associated with the presence of subclinical carotid plaque in patients with hypertension and diabetes or prediabetes?
Identifies a noninvasively measured low-flow, high-resistance, pro-inflammatory phenotype (FIBFAR) that is strongly associated with subclinical carotid atherosclerosis in patients with hypertension and dysglycemia.
Answers are grounded in this paper and cite their sources.
FIBFAR may indicate higher subclinical atherosclerosis risk in cardiometabolic patients; hypothesis-generating and requires prospective validation before clinical use.
Background: Systemic inflammation and hemodynamic alterations represent complementary pathophysiological mechanisms involved in cardiovascular disease.The identification of integrative phenotypes using noninvasive tools could contribute to better characterization of subclinical atherosclerosis.Objective: To evaluate the association between the low-flow, high-systemic vascular resistance hemodynamic-inflammatory phenotype (FIBFAR) and the presence of carotid plaque in patients with cardiometabolic risk, defined by the presence of hypertension and diabetes or prediabetes.Methods: An observational, analytical, cross-sectional study based on a retrospective analysis of 243 outpatients aged ≥18 years with hypertension and diabetes mellitus or prediabetes.Clinical, biochemical, and hemodynamic variables were analyzed, including high-sensitivity C-reactive protein (hs-CRP), cardiac index (CI), and systemic vascular resistance (SVR) measured by impedance cardiography.Carotid plaque was assessed using Doppler ultrasound.The association between FIBFAR (hs-CRP ≥2.5 mg/L, CI <2.5 L/min/m², and SVR >1600 dynes•s•cm -5 ) and carotid plaque was assessed using multivariate logistic regression.Results: The median age was 58 years (IQR 49-67), and 64.0% were male.The prevalence of carotid plaque was 37.0%.The FIBFAR phenotype was present in 23.0% of the cohort and was independently associated with carotid plaque (OR 8.60; 95% CI: 4.39-17.70;p < 0.001), along with age ≥65 years (OR 1.94; 95% CI: 1.01-3.72;p = 0.047).The model showed appropriate calibration (Hosmer-Lemeshow p = 0.374) and moderate discriminatory power (AUC = 0.73; 95% CI: 0.66-0.79;p < 0.001).Conclusions: In patients with cardiometabolic risk, the FIBFAR phenotype was independently associated with subclinical carotid atherosclerosis.Given the cross-sectional design, these findings should be interpreted as statistical associations and require prospective validation before their clinical application can be considered.
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Velázquez et al. (2026) conducted a cross-sectional in Cardiometabolic risk (hypertension and diabetes mellitus or prediabetes) (n=243). FIBFAR hemodynamic-inflammatory phenotype (hs-CRP ≥2.5 mg/L, cardiac index <2.5 L/min/m², and systemic vascular resistance >1600 dynes•s•cm⁻⁵) vs. Absence of FIBFAR phenotype was evaluated on Presence of carotid plaque assessed using Doppler ultrasound (OR 8.60, 95% CI 4.39-17.70, p=<0.001). The FIBFAR hemodynamic-inflammatory phenotype was independently associated with carotid plaque in patients with cardiometabolic risk (OR 8.60; 95% CI 4.39-17.70; p<0.001).
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