BACKGROUND Pulmonary endarterectomy (PEA) is a gold standard therapy that can dramatically reduce pulmonary artery pressure (PAP) and improve the prognosis on chronic thromboembolic pulmonary hypertension (CTEPH). However, residual pulmonary hypertension or persistent symptoms even after PEA are still the clinical issues to be solved. We investigated whether additional balloon pulmonary angioplasty (BPA) after PEA was effective.METHODS Since August 2009 until June 2016, 23 patients underwent PEA at Kobe University Hospital. Seven patients with residual pulmonary hypertension or symptom underwent additional BPA. RESULTSThe period from PEA to additional BPA was 8.3 AE 8.3 months and the number of BPA sessions was 2.4 AE 0.9. In 7 patients who underwent additional BPA after PEA, mean PAP and pulmonary vascular resistance (PVR) had significantly improved by PEA (39.3 AE 6.0 to 27.9 AE 10.1 mmHg p<0.01, 996 AE 447 to 473 AE 255 dyne･sec･cm-5 p¼0.02), and improved further (to 19.9 AE 7.9 mmHg p¼0.01 ,to 183 AE 96 dyne･sec･cm-5 p¼0.01) by additional BPA. Before PEA, 2 patients were NYHA/WHO functional class II and 5 patients were class III. Hybrid therapy improved NYHA/WHO functional class (3 patients classI, 3 patients classII, 1 patients classIII p¼0.05)( Figure). No patient died and had severe complication needed mechanical ventilator and extracorporeal membrane oxygenation during whole study period.CONCLUSION Although PEA for CTEPH had improved pulmonary hemodynamic profiles, additional BPA could improve them further. Additional BPA is an effective and safe treatment for residual pulmonary hypertension or persistent symptom. CATEGORIES ENDOVASCULAR: Peripheral Vascular Disease and InterventionTCT-91 Efficacy of aggressive balloon pulmonary angioplasty on chronic thromboembolic pulmonary hypertension beyond normalized mean pulmonary arterial pressure

Pulmonary arterial hypertension (PAH) is a severe, disabling disease characterized by an increase pressure in the pulmonary artery (PA), an increase pressure in the right atrium, and a decrease of the cardiac output. It combines several diseases: idiopathic pulmonary hypertension, inherited pulmonary hypertension, PAH induced by medication and toxins, PAH associated with systemic diseases of connective tissue, HIV infection, portal hypertension, congenital heart defects, schistosomiasis. In the absence of treatment, PAH quickly leads to insufficiency of the right heart and premature death. An effective PAH therapy did not exist for a long time. However, in 1987 there was established a positive effect of taking large doses of calcium channel blockers in patients, who “responded” to their prescription in the short term, and in recently several groups of specific drugs have been developed and approved for the treatment of this pathology: prostacyclin analogues and prostacyclin receptors agonists, endothelin receptor antagonists, phosphodiesterase type 5 inhibitors and soluble guanylate cyclase stimulators. Modern studies of treatment of PAH are based on the latest data of the molecular transmission mechanisms of intracellular and intercellular signals, the action of hormones and tissue enzymes. The available results of these studies allow to suggest the inclusion to clinical guidelines several new drugs for the pathogenetic treatment of PAH in the near future: receptor tyrosine kinase inhibitors, Rho - kinase inhibitors, immunosuppressants and type 2 activin receptor agonists, protein kinase C inhibitors, aromatase inhibitors and estrogen receptor antagonists, poly-(ADP-ribose)-polymerase inhibitors and bromodomain protein 4, elastase inhibitors. Some of the drugs have already passed the III phase of clinical trials (imatinib), others are at the preclinical stage or at the I-II phase tests (olaparib, enzastaurin, elafin).

No abstract

No abstract

Background Our previous study showed that elevated D-dimer (D-D) level after 1 month of the anticoagulant therapy was an independent predictor of deep vein thrombosis (DVT) recurrences and combined endpoint (DVT recurrence and/or death from any causes) during 18 months. Prognostic value of elevated D-D level after 1 month of the anticoagulant therapy for the long-term venous thromboembolism (VTE) outcomes is unknown. Purpose To estimate the elevated D-D level influence after 1 month of the anticoagulant therapy on the 10-year prognosis in VTE pts. Methods One hundred and twelve pts (77 men) aged 18–76 (mean 54±14) years with DVT and/or pulmonary embolism were included in the study. Pts received unfractionated or low molecular weight heparin for at least 5 days followed by the long-term warfarin therapy (target international normalized ratio 2,0–3,0). D-D level was measured after 1 month from the start of the anticoagulant therapy by a quantitative assay with an estimated cut-off level of 0,5 ug/ml. The follow-up period was 10 years. Endpoints were VTE recurrence and combined endpoint (VTE recurrence and/or death from any causes). Results In all pts, median of follow-up was 2,77 years (min 2 weeks, max 11,61 years, IQR 1,44 to 10,31 years). Seventy seven (69%) pts had ended the 10-year follow-up period completely or achieved the endpoint. In these pts, median of follow-up was 9,23 years (IQR 1,70 to 10,53 years). Thirty-five cases were censored. During 10 years, the VTE recurrences rate was 27,7%, 14 pts died, the combined endpoint rate was 36,6%. Kaplan-Meier analysis showed that pts with elevated D-D level after 1 month of the anticoagulant therapy had higher 10-year cumulative risk for adverse outcomes (chi-square=6,0, p=0,014 for VTE recurrence; chi-square=13,7, p<0,001 for combined endpoint). Cox regression confirmed that elevated D-D level after 1 month of the anticoagulant therapy was associated with a 2,5-fold increase in the 10-year VTE recurrences risk (HR 2,52; 95% CI 1,18–5,42; p=0,018) and a 3,2-fold increase in the 10-year combined endpoint risk (HR 3,21; 95% CI 1,68–6,15; p<0,001) compared pts with normal D-D level after 1 month of the anticoagulant therapy. Conclusions During 10 years, the VTE recurrences rate was 27,7%, combined endpoint rate (VTE recurrence and/or death from any causes) was 36,6%. Elevated (>0,5 ug/ml) D-D level after 1 month of the anticoagulant therapy had a prognostic value and was associated with the 2,5-fold increase in the 10-year VTE recurrences risk and the 3,2-fold increase in the 10-year adverse outcomes risk.