Key result
FIBFAR phenotype linked to ~8.6-fold higher odds of subclinical 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 in patients with cardiometabolic risk.
Is the low-flow, high-systemic vascular resistance hemodynamic-inflammatory phenotype (FIBFAR) associated with the presence of subclinical carotid plaque in outpatients with cardiometabolic risk?
Cross-Sectional (n=243)
No
Is the low-flow, high-systemic vascular resistance hemodynamic-inflammatory phenotype (FIBFAR) associated with the presence of subclinical carotid plaque in outpatients with cardiometabolic risk?
Answers are grounded in this paper and cite their sources.
Integrating noninvasive hemodynamic parameters (low cardiac index and high systemic vascular resistance) with systemic inflammation (elevated hs-CRP) into the FIBFAR phenotype strongly identifies subclinical carotid atherosclerosis in patients with hypertension and diabetes or prediabetes.
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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Chong et al. (2026) conducted a cross-sectional in Cardiometabolic risk (hypertension and diabetes mellitus or prediabetes) (n=243). FIBFAR phenotype (low-flow, high-systemic vascular resistance hemodynamic-inflammatory phenotype: hs-CRP >=2.5 mg/L, cardiac index <2.5 L/min/m2, and SVR >1600 dynes·s·cm-5) vs. Non-FIBFAR phenotypes (adaptive, inflammatory vasoconstrictor, or indeterminate) was evaluated on Presence of subclinical carotid plaque assessed by Doppler ultrasound (OR 8.60, 95% CI 4.39-17.70, p=<0.001). The FIBFAR hemodynamic-inflammatory phenotype was independently associated with subclinical carotid plaque in patients with cardiometabolic risk (adjusted OR 8.60; 95% CI 4.39-17.70; p<0.001).
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