Central versus Peripheral CTEPH—Clinical and Hemodynamic Specifications

Abstract

Background and Objectives: Chronic thromboembolic pulmonary hypertension (CTEPH) is a chronic progressive disease, resulting from persistent arterial obstruction combined with small-vessel remodeling. Central and peripheral CTEPH are distinguished, according to the dominant lesion’s location. This is important for surgical or percutaneous interventional assessment or for medical treatment. Material and Methods: Eighty-one patients (51 male/30 female) with confirmed CTEPH were analyzed, while the CENTRAL type included 51 patients (63%) and the PERIPHERAL type 30 patients (37%). Results: A significant difference in CENTRAL type vs. PERIPHERAL type was determined in gender (male 72.5% vs. 46.7%; p = 0.0198). No difference was found in age, functional status, or echocardiographic parameters. Invasive hemodynamic parameters showed a significant difference in mean pulmonary arterial pressure (46 vs. 58 mmHg; p = 0.0002), transpulmonary gradient (34 vs. 47 mmHg; p = 0.0005), and cardiac index (2.04 vs. 2.5 L.min.m2; p = 0.02) but not in pulmonary vascular resistance. Risk factors showed a significant difference only in acute pulmonary embolism (93.8% vs. 60%; p = 0.0002) and malignancy (2% vs. 13.3%; p = 0.0426). Conclusions: Our study showed hemodynamic differences between CENTRAL type vs. PERIPHERAL type CTEPH with a worse hemodynamic picture in CENTRAL form. This may indicate a different pathophysiological response and/or possible additional influences contributing especially to the peripheral pulmonary bed affection.

Notch ratio in pulmonary flow predicts long-term survival after pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension

“…The localization of vessel obstruction, either proximal (central) or distal (peripheral), has an impact on RV function in CTEPH [32]. Significant hemodynamic differences have been observed between central and peripheral forms of CTEPH, with worse hemodynamics in the central form of CTEPH which may reflect a different pathophysiological response of the RV between the two forms of CTPEH [32]. Furthermore, additional influences may contribute to this different response especially to peripheral pulmonary bed affection.…”

Analysis of genes characterizing chronic thrombosis and associated pathways in chronic thromboembolic pulmonary hypertension

“…CTEPH remains an unresolved health problem worldwide due to its high rates of disability and mortality [ 1 ]. It is currently believed that the main pathogenesis of CTEPH is divided into two parts, on the one hand, CTEPH is a distant complication of acute pulmonary thromboembolism (APTE), in which the formation of chronic thrombus in the lumen of the blood vessel leads to vascular obstruction, which in turn leads to pulmonary hypertension [ 2 ]. It is also believed that chronic thrombus is closely related to factors such as the blood system or immune system and fibrinolytic system that cause the thrombus to be difficult to regress [ 3 – 5 ].…”