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BACKGROUND: Balloon pulmonary angioplasty (BPA) is a promising therapy for patients with chronic thromboembolic pulmonary hypertension (CTEPH) who are ineligible for pulmonary endarterectomy. AIMS: The present study aimed to evaluate the safety and efficacy of BPA for CTEPH using the first multicentre registry of a single European country. METHODS: Data were obtained from the Database of Pulmonary Hypertension in the Polish Population (NCT03959748), a prospective, multicentre registry of adult and paediatric pulmonary arterial hypertension (PAH) and CTEPH, for a total of 236 patients with confirmed CTEPH (124 women; mean age 67 years) who underwent 1,056 BPA procedures at eight institutions in Poland. RESULTS: In 156 patients who underwent follow-up assessments after a median of 5.9 (IQR: 3.0-8.0) months after final BPA, the mean pulmonary arterial pressure decreased from 45.1±10.7 to 30.2±10.2 mmHg (p

Ultrasound-assisted, catheter-directed, low-dose thrombolysis (USAT) at an average alteplase dose of 20 mg infused over 12 to 24 hours reversed right ventricular disfunction and improved pulmonary hemodynamics in intermediate-high-risk pulmonary embolism patients. As bleeding risk increases with the thrombolytic dose, establishing a minimal effective USAT dosing regimen is of clinical importance. We aimed to investigate hemodynamic effects and safety of a very low-alteplase-dose USAT of 10 mg administered within 5 hours. We included 12 consecutive intermediate-high-risk pulmonary embolism patients with symptoms duration of14 days and proximal thrombi location in pulmonary arteries. Pulmonary Embolism Response Team decision-based fixed, bilateral ultrasound-assisted alteplase infusions at the rate of 1mg/hour/catheter for 5 hours through EKOS system catheters were made. The primary efficacy measure was the change in invasive systolic and mean pulmonary arteries pressure, and in cardiac index from USAT start to termination. Safety measures were 180-day all-cause death or cardiopulmonary decompensation and bleeding complications. The systolic pulmonary arteries pressure and mean pulmonary arteries pressure decreased from 53 (45.5 to 59) to 37.5 (27.5 to 40.5) mm Hg (p = 0.02) and from 29.5 (27.5 to 32) to 21.5 (15.5 to 25) mm Hg (p = 0.02), respectively. The cardiac index increased from 1.6 (1.5 to 1.8) to 2.2 (1.9 to 2.4) l/min/m

Chronic thromboembolic pulmonary hypertension (CTEPH) results from an obstruction of pulmonary arteries (PAs) by organized thrombi. The stenosed PAs are targeted during balloon pulmonary angioplasty (BPA). We aimed to evaluate the mechanism of BPA in inoperable patients with CTEPH. We analyzed stenosed PAs with intravascular grey-scale ultrasound (IVUS) to determine the cross-sectional area (CSA) of arterial lumen and of organized thrombi. The composition of organized thrombi was assessed using virtual histology. We distinguished two mechanisms of BPA: Type A with dominant vessel stretching, and type B with dominant thrombus compression. PAs were assessed before (n = 159) and after (n = 98) BPA in 20 consecutive patients. Organized thrombi were composed of dark-green (57.1 (48.0&ndash, 64.0)%), light-green (34.0 (21.4&ndash, 46.4)%), red (6.4 (2.9&ndash, 11.7)%, ) and white (0.2 (0.0&ndash, 0.9)%) components. The mechanism type depended on vessel diameter (OR = 1.09(1.01&ndash, 1.17), p = 0.03). In type B mechanism, decrease in the amount of light-green component positively correlated with an increase in lumen area after BPA (r = 0.50, p = 0.001). The mechanism of BPA depends on the diameter of the vessel. Dilation of more proximal PAs depends mainly on stretching of the vessel wall while dilation of smaller PAs depends on compression of the organized thrombi. The composition of the organized thrombi contributes to the effect of BPA.

Introduction Metabolic alterations have been recently associated with onset and progression of idiopathic pulmonary arterial hypertension (IPAH). We aimed to determine the prevalence and prognostic role of cardiovascular risk factors in patients with IPAH. Material and methods Between February 2009 and January 2015 we recruited consecutive IPAH patients. Clinical assessment included medical history, fasting glucose, lipid profile, N-terminal pro-brain natriuretic peptide concentration, 6-minute walk test distance, WHO functional class and hemodynamic evaluation. Patients' risk was estimated based on the Swedish PAH Register grading system. Results The study group included 61 IPAH patients, and the control group included 2413 Polish residents. When compared to the general population, IPAH patients had lower low-density lipoprotein cholesterol (LDL-C) and a higher triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio. Female patients were characterized by elevated glucose level, higher prevalence of diabetes and lower HDL-C than controls. PAH severity grade correlated positively with age and TG/HDL-C ratio (R = 0.29, p = 0.02) and inversely with LDL-C (R = -0.28, p = 0.03) and HDL-C (R = -0.39, p = 0.02) concentrations. After a follow-up of 48 (23-79) months we recorded 28 deaths in the IPAH group. In the regression analysis lower LDL-C (p = 0.002) and HDL-C (p = 0.0002) levels, and higher TG/HDL-C ratio (p = 0.003) and glucose level (p = 0.003) were associated with all-cause mortality after adjustment for age, sex or PAH severity grade. Conclusions Patients with IPAH are characterized by an altered profile of lipid and glucose metabolism. Lowered levels of LDL-C and HDL-C and increased TG/HDL-C ratio correlate with disease severity and together with elevated plasma glucose level predict poor survival in IPAH.

Introduction Pulmonary endarterectomy leads to a decrease in systemic inflammation and improvement in endothelial function in patients with chronic thromboembolic pulmonary hypertension (CTEPH). Balloon pulmonary angioplasty (BPA) improves pulmonary hemodynamics in patients with inoperable CTEPH. Aim To assess changes in systemic inflammation and endothelial dysfunction after a single BPA session and after completion of the treatment. Methods We enrolled consecutive, inoperable CTEPH patients who underwent BPA. Interleukin 6, 10 (IL-6, IL-10), and C-reactive protein (hsCRP) constituted markers of systemic inflammation. Endothelin-1 (ET-1) served as a marker of endothelial dysfunction. Serum concentration of selected markers was assessed in every patient before, 24 hours after the first BPA session and 6 months after completion of the BPA treatment. Age- and sex-matched healthy subjects served as a control group. Results We recruited 20 patients with inoperable CTEPH (6 males [30%]), aged 67 [61–74] years in New York Heart Association class III (n=19 [95%]) and II (n=1 [5%]). BPA treatment was completed with a median of 5 [2–8] BPA sessions per patient. Before starting the treatment CTEPH patients, as compared to controls (n=10), had raised serum level of IL-6 (3.82 [2.75 - 6.03] vs. 2.64 [0.88 - 4.75] pg/ml; p=0.04), hsCRP (2.47 [0.93 - 4.27] vs. 1.23 [0.48–3.21] ng/ml; p=0.02) and ET-1 (2.68 [2.24 - 3.64] vs. 1.47 [1.4 - 1.82] pg/ml; p=0.004). There was no difference in IL-10 level. 24 hours after a BPA session we observed an increased level of IL-6, IL-10 and hsCRP. (Tab.) 6 months after completion of the BPA treatment there was a reduced level of IL-6, hsCRP and ET-1 (Tab.) Table 1. Changes (Δ) in serum concentration of analyzed markers 24 hours after a single BPA session and at 6-months assessment after completion of the BPA treatment (n=20) Initial Δ at 24 hours after single BPA p Δ at 6-months follow-up p ET-1 [pg/ml] 2.68 [2.24; 3.64] −0.2 [−0.5; 0.23] 0.21 −0.47 [−0.96; 0.05] 0.004 IL-6 [pg/ml] 3.82 [2.75; 6.03] 3.67 [1.41; 7.16] 0.008 −0.82 [−3.11; 0.54] 0.04 IL-10 [pg/ml] 0.53 [0.44; 0.58] 0.32 [0.21; 0.87] 0.006 −0.11 [−0.33; 0.14] 0.94 hsCRP [ng/ml] 2.47 [0.93; 4.27] 5.4 [3.96; 10.59] 0.008 −0.36 [−0.94; 0.16] 0.02 ET-1, endothelin 1; hsCRP, C-reactive protein; IL-6, interleukin 6; IL-10, interleukin 10. Conclusions Patients with inoperable CTEPH, as compared to healthy controls, exhibit an increased systemic inflammation and endothelial dysfunction, which both improve after completion of the BPA treatment. At short-term follow-up after single BPA session there is an increase in systemic inflammatory response.

Background: Left ventricular (LV) diastolic dyssynchrony is common in patients with heart failure with reduced ejection fraction (HFREF). Little is known however, about its pathophysiology and clinical effects. Herein is hypothesized that presence of diastolic dyssynchrony at rest or at exercise may importantly contribute to HF symptoms. The aim was to investigate the influence of diastolic dyssynchrony and its exercise-induced changes on exercise capacity in HFREF patients. Methods: Patients with stable, chronic HF, LV ejection fraction < 35%, sinus rhythm and QRS ≥ 120ms were eligible for the study. Rest and cyclo-ergometer exercise echocardiography were performed. Diastolic dyssynchrony was defined as opposing-wall-diastolic-delay ≥ 55 ms measured in tissue-Doppler imaging. Exercise capacity was assessed by peak oxygen consumption (VO 2peak ). Association between diastolic dyssynchrony and VO 2peak was assessed in univariate regression analysis and further adjusted for possible confounders. Results: 48 patients were included (aged 63.7 ± 12.2). Twenty-seven (56.25%) had diastolic dyssynchrony at rest and 13 (27%) at exercise. Twenty-two (46%) experienced a change in diastolic dyssynchrony status during exercise. In univariate models diastolic dyssynchrony at rest or at exercise were associated with lower VO 2peak (beta coefficient = –3.8, p = 0.004; beta coefficient = –3.6, p = 0.02, respectively). However, the ability to restore diastolic synchronicity during exercise was associated with higher VO 2peak (beta coefficient = 3.4, p = 0.04) and remained an important predictor of exercise capacity after adjustment for age and HF etiology. Conclusions: The ability to restore diastolic synchronicity at exercise predicts exercise capacity in patients with HFREF.

BACKGROUND Idiopathic pulmonary arterial hypertension (IPAH) patients are characterized by elevated triglyceride (TG)-to-HDL cholesterol (HDL-C) ratio, which has been proposed to be an important prognostic factor in this population. The mechanism of this phenomenon remains unknown. We therefore investigated the potential determinants of increased TG/HDL-C ratio in IPAH patients. MATERIAL AND METHODS We prospectively recruited consecutive clinically stable IPAH patients between January 2016 and February 2017. Patients with diabetes or using statins were excluded. Anthropometric measurements included body mass index (BMI) and skinfold thickness; body fat mass was calculated using age and sex-specific equations. We assessed lipid profile, homeostatic model assessment of insulin resistance (HOMA-IR), serum adipokine levels (adiponectin, resistin, leptin, and visfatin), and circulating cytokines (IL-1β, IL-6, MCP-1, and TNF-α). RESULTS We assessed 47 IPAH patients: 9 of them had been diagnosed with diabetes and 10 were treated with statins; therefore, were excluded them from further analysis. Age, sex distribution, and BMI were similar irrespectively of TG/HDL-C ratio. Patients with increased TG/HDL-C ratio (>3) as compared to patients with TG/HDL-C ≤3 were characterized by higher levels of IL-1β, MCP-1, and IL-6. TG level was correlated with IL-1β (R=0.76, p

Background: Left ventricular (LV) dyssynchrony is common in patients with heart failure with reduced ejection fraction (HFREF). However, various conditions including exercise may alter its presence. LV dyssynchrony at exercise (ExDYS) has been associated with lower cardiac performance and exercise capacity but with higher cardiac resynchronization therapy (CRT) response. Therefore, understanding mechanisms underlying ExDYS may improve patient selection for CRT. Aims: To investigate for predictors of ExDYS among patients with HFREF and prolonged QRS duration. Methods: Consecutive patients with stable, chronic HF, LVEF

Pulmonary arterial hypertension (PAH) leads to a haemodynamic overload and ischaemia of the right ventricle (RV), which are important triggers of an arterial growth. Thus, we aimed to assess whether patients with PAH have altered epicardial vasculature of the RV, and how it corresponds to RV haemodynamic stress.We enrolled consecutive patients with PAH diagnosed in a single pulmonary hypertension centre, who underwent coronary angiography. The control group consisted of patients with normal coronary arteries. Artery branches from segments I-III of the right coronary artery (RCAB) and branches of the left coronary artery (LCAB) were assessed. The sum of the diameters of RCABs (RCAB_sum) was used as a marker of RV epicardial vascularisation. Linear regression models were used to investigate associations between the RCAB_sum and markers of RV dysfunction.We recruited 37 PAH patients (idiopathic, n=25; associated with connective tissue disease, n=12) and 37 control subjects of similar age (56±18 vs. 56±13 years, p=0.99) and sex (73% vs. 73% of women, p=0.99). Pulmonary arterial hypertension patients as compared with control subjects had more RCABs (7 [6-8] vs. 6 [5-7], p0.001) and increased RCAB_sum (9.4 [8.2-10.5] vs. 7.3 [6.6-7.40] mm; p0.001) although comparable LCAB count (4 [4-5] vs. 4 [4-5]; p=0.50). In a stepwise multivariable linear regression model, RA area (β=0.152 [0.062-0.242]; p=0.002) and diastolic wall stress (β=0.025 [0.005-0.045]; p=0.02) were significant predictors of RCAB_sum (model RRight ventricular epicardial vasculature is more extensive in PAH patients as compared with control subjects, and it is in linear relation to potential markers of RV diastolic dysfunction.

Background Atrioventricular conduction delay (AVCD) impairs left ventricular (LV) filling and consequently leads to a reduction of cardiac output. We hypothesized that in patients with severely depressed LV function and coexisting intraventricular conduction disturbances (IVCD), AVCD can affect exercise performance. Therefore, we evaluated the association of AVCD and exercise capacity in patients with heart failure (HFREF) and coexisting IVCD. Material/Methods We included patients with stable, chronic HFREF, LVEF 200 ms. Groups were similar in clinical, laboratory, echocardiographic parameters, QRS morphology, and treatment regimens. VO2 peak was lower in patients with longer PR interval group as compared to shorter PR interval group (12.3±4.1 vs. 17.06±4.4, p=0.002). In the regression model, PR interval, female sex, and IHD remained important predictors of VO2 peak (partial=−0.50, p=0.003; rpartial=−0.48, p=0.005; rpartial=−0.44, p=0.01; R2=0.61). Conclusions Delayed AV conduction contributes to decreased exercise capacity in patients with HFREF and coexisting IVCD.