Jakub Stępniewski

Atrioventricular Conduction Delay Predicts Impaired Exercise Capacity in Patients with Heart Failure with Reduced Ejection Fraction

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 <35%, sinus rhythm, and QRS ≥120 ms. PR interval and peak oxygen consumption (VO2 peak) were specifically investigated. Multiple regression analysis was used to adjust the association between PR interval and VO2 peak for possible confounders. Results Most (57.5%) of the 40 included patients [20% female, aged 63±12, 47.5% of ischemic etiology (IHD)] were in NYHA class III. Mean PR interval was 196±38.1 ms. There were 26 (65%) patients with PR interval ≤200 ms and 14 (35%) with >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.

Rare cardiovascular diseases: from European legislations to classification and clinical practice

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Right Ventricular Epicardial Vascularisation in Patients With Pulmonary Arterial Hypertension

BACKGROUND 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. METHODS 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. RESULTS 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], p<0.001) and increased RCAB_sum (9.4 [8.2-10.5] vs. 7.3 [6.6-7.40] mm; p<0.001) 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 R2=0.65; p<0.0001). CONCLUSIONS Right 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.