Key result
Pulmonary sarcoidosis in clinical remission was associated with an unfavorably altered thrombin generation profile, including a 16% higher endogenous thrombin potential compared to matched controls.
Why the study?
Sarcoidosis carries an epidemiologically associated cardiovascular risk that suggests an underlying prothrombotic state and endothelial dysfunction, which are currently understudied.
Does non-active sarcoidosis associate with a prothrombotic state, endothelial injury, and echocardiographic changes compared to matched controls?
Case-Control (n=119)
Does non-active sarcoidosis associate with a prothrombotic state, endothelial injury, and echocardiographic changes compared to matched controls?
Despite clinical remission, sarcoidosis is associated with prothrombotic plasma properties, signs of endothelial injury, and subclinical echocardiographic changes, which may contribute to a higher risk of cardiovascular events.
Answers are grounded in this paper and cite their sources.
May warrant CV risk vigilance in remitted sarcoidosis; leaves open whether thrombin changes predict events in prospective cohorts.
Sarcoidosis is a multisystem inflammatory granulomatous disease of unknown cause that most commonly affects lungs and lymph nodes, with frequent yet asymptomatic cardiac involvement. The epidemiologically associated cardiovascular risk suggests an underlying prothrombotic state and endothelial dysfunction, currently understudied in the available literature. Therefore, we aimed to investigate prothrombotic plasma properties together with selected echocardiographic and laboratory biomarkers of cardiovascular injury in that disease. N = 53 patients with pulmonary sarcoidosis in clinical remission and N = 66 matched controls were assessed for inflammatory and endothelial injury biomarkers, plasma thrombin generation profile, and echocardiographic and lung function parameters. Sarcoidosis cases had impaired systolic and diastolic left ventricular function, higher concentrations of inflammatory markers, D-dimer and factor VIII activity compared to the controls. The coexistence of extrapulmonary disease was associated with elevated circulating vascular cell adhesion molecule 1, while cases with hypercalcemia had higher thrombomodulin concentration. Sarcoidosis was characterized by the unfavorably altered thrombin generation profile, reflected by the 16% higher endogenous thrombin potential (ETP), 24% increased peak thrombin concentration, and 12% shorter time to thrombin peak in comparison to the control group. ETP was higher in cases with proxies of pulmonary restriction, extrapulmonary-extracutaneous manifestation, and need for corticosteroids use. Despite the clinical remission, sarcoidosis is related to prothrombotic plasma properties and signs of endothelial injury, likely contributing to the higher risk of cardiovascular events. In addition, subclinical cardiac involvement may play an additional role, although further clinical and experimental studies are needed to verify these findings.
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Siwiec-Koźlik et al. (2022) conducted a case-control in Pulmonary sarcoidosis (n=119). Pulmonary sarcoidosis in clinical remission vs. Matched controls was evaluated on Prothrombotic plasma properties, inflammatory and endothelial injury biomarkers, plasma thrombin generation profile, and echocardiographic parameters. Pulmonary sarcoidosis in clinical remission was associated with an unfavorably altered thrombin generation profile, including a 16% higher endogenous thrombin potential compared to matched controls.
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