B a c k g r o u n d: A novel paradigm of diastolic heart failure with preserved ejection fraction (HFpEF) proposed the induction of coronary microvascular dysfunction by HFpEF comorbidities via a systemic pro-infl ammatory state and associated oxidative stress. Th e consequent nitric oxide deficiency would increase diastolic tension and favor fi brosis of adjacent myocardium, which implies not only left ventricular (LV), but all-chamber myocardial stiff ening. Our aim was to assess relations between low-grade chronic systemic infl ammation and left atrial (LA) pressure-volume relations in real-world HFpEF patients.

Me t h o d s: We retrospectively analyzed medical records of 60 clinically stable HpEFF patients in sinus rhythm with assayed high-sensitive C-reactive protein (CRP) during the index hospitalization. Subjects with CRP >10 mg/L or coexistent diseases, including coronary artery disease, were excluded. LV and LA diameters and mitral E/E’ ratio (an index of LA pressure) were extracted from routine echocardiographic 46 Cyrus M. Sani, Elahn P.L. Pogue, et al. records. A surrogate measure of LA stiff ness was computed as the averaged mitral E/e’ ratio divided by LA diameter.

R e s u l t s: With ascending CRP tertiles, we observed trends for elevated mitral E/e’ ratio (p <0.001), increased relative LV wall thickness (p = 0.01) and higher NYHA functional class (p = 0.02). Th e LA stiffness estimate and log-transformed CRP levels (log-CRP) were interrelated (r = 0.38, p = 0.003). On multivariate analysis, the LA stiff ness index was independently associated with log-CRP (β ± SEM: 0.21 ± 0.07, p = 0.007) and age (β ± SEM: 0.16 ± 0.07, p = 0.03), which was maintained upon adjustment for LV mass index and relative LV wall thickness.

C o n c l u s i o n s: Low-grade chronic infl ammation may contribute to LA stiff ening additively to age and regardless of the magnitude of associated LV hypertrophy and concentricity. LA stiff ening can exacerbate symptoms of congestion in HFpEF jointly with LV remodeling.

Common variable immunodeficiency (CVID) is a primary immunodeficiency disorder related to recurrent infections, as well as a range of non-infectious manifestations including autoimmune and inflammatory disorders. We hypothesized that patients with CVID and different clinical phenotypes would demonstrate alterations in lymphocyte T subsets, including T lymphocytes expressing programmed cell death protein 1 (PD-1), and regulatory T lymphocytes. We performed flow cytometry in two CVID groups: group 1 with infections only, and group 2 with infections and concomitant noninfectious manifestations. Patients were 18–59 years old (mean 35.8 years of age). Increased proportions of CD8+PD-1+ T cells and reduced regulatory T cells were associated with lymphadenopathy. Amount of regulatory T cells correlated with CD8+PD-1+ T lymphocytes (r = 0.54; p = 0.013), and with CRP (r = –0.64; p = 0.004). Forty percent of patients expressed manifestations in addition to infections (group 2), and they had reduction in number of regulatory T cells [8 (3–12) vs. 24 (11–26)/μl; p = 0.034), naive CD4+ T lymphocytes [36 (27–106) vs. 149 (81–283)/μl; p = 0.034], and elevated C-reactive protein (CRP) [5.33 (3.15–8.82) vs. 1 (1–2.16) mg/l; p = 0.003] in comparison to group 1. In conclusion, the amount of CD8+ T cells expressing PD-1 is associated with lymphadenopathy and number of regulatory T cells in patients with CVID. Patients with CVID and non-infectious complications have increased level of inflammation and alterations in regulatory T cells.