Notes about telocytes and immunity.

The interstitial cells known as telocytes have been described in various organs. Their role in the normal physiology and pathogenesis of numerous diseases is well known. They have been described in the context of various diseases (gallstone disease, endometriosis, uterine myoma, hydronephrosis, myocardial infraction, psoriasis, etc.), while their impact on inflammation, involvement in angiogenesis, and repair highlights their part in local homeostasis. What is known about their relationship with the immune system? Their secretomes, genome, immune profiles, contacts with surrounding cells, and specific localization allow us to give a possible explanation for their involvement in pathological pathways. This review aims to present the roles and features of telocytes in the context of intestinal immunity (the largest in our body), in the spleen, their interactions with immunocytes, and their place in stem cell niches.

Microvascular angina (Cardiac Syndrome X) from a historical overview, epidemiology, pathophysiology to treatment recommendations - a minireview.

Microvascular angina (MVA) is a condition characterized by the presence of angina-like chest pain, a positive response to exercise stress tests, and no significant stenosis of coronary arteries in coronary angiography, with absence of any other specific cardiac diseases. The etiology of this syndrome is still not known and it is probably multifactorial. Coronary microvascular dysfunction is proposed as the main pathophysiological mechanism in the development of MVA. Altered somatic and visceral pain perception and autonomic imbalance, in addition to myocardial ischemia, has been observed in subjects with MVA, involving dynamic variations in the vasomotor tone of coronary microcirculation with consequent transient ischemic episodes. Other theories suggest that MVA may be a result of a chronic inflammatory state in the body that can negatively influence the endothelium or a local imbalance of factors regulating its function. This article presents the latest information about the epidemiology, diagnostics, etiopathogenesis, prognosis, and treatment of patients with MVA.

Cardiotoxicity of Fluoropyrimidines: Epidemiology, Mechanisms, Diagnosis, and Management.

Cancer is a growing public health problem; it is responsible annually for millions of deaths worldwide. Fluoropyrimidines are highly effective and commonly prescribed anti-neoplastic drugs used in a wide range of chemotherapy regimens against several types of malignancies. 5-fluorouracil and its prodrugs affect neoplastic cells in multiple ways by impairing their proliferation, principally through the inhibition of thymidylate synthase. Fluoropyrimidine-induced cardiotoxicity was described more than 50 years ago, but many details such as incidence, mechanisms, and treatment are unclear and remain disputed. Severe cardiotoxicity is not only life-threatening, but also leads to withdrawal from an optimal chemotherapy regimen and decreases survival rate. Differences in the frequency of cardiotoxicity are explained by different chemotherapy schedules, doses, criteria, and populations. Proposed pathophysiological mechanisms include coronary vasospasm, endothelial damage, oxidative stress, Krebs cycle disturbances, and toxic metabolites. Such varied pathophysiology of the cardiotoxicity phenomenon makes prevention and treatment more difficult. Cardiovascular disturbances, including chest pain, arrhythmias, and myocardial infarction, are among the most common side effects of this class of anti-neoplastic medication. This study aims to summarize the available data on fluoropyrimidine cardiotoxicity with respect to symptoms, incidence, metabolism, pathophysiological mechanism, diagnosis, management, and resistance.

Past strong experiences determine acute cardiovascular autonomic responses to acoustic stress.

BACKGROUND: Stress is a major risk factor for cardiovascular (CV) disease. We hypothesized that past strong experiences might modulate acute CV autonomic responses to an unexpected acoustic stimulus. A i m: The study's aim was to compare acute CV autonomic responses to acoustic stress between students with and without a past strong experience associated with the acoustic stimulus. MATERIALS AND METHODS: Twenty five healthy young volunteers - medical and non-medical students - were included in the study. CV hemodynamic parameters, heart rate (HR), and blood pressure (BP) variability were assessed for 10 min at rest and for 10 min after two different acoustic stimuli: a standard sound signal and a specific sound signal used during a practical anatomy exam (so-called "pins"). RESULTS: Both sounds stimulated the autonomic nervous system. The "pins" signal caused a stronger increase in HR in medical students (69 ± 10 vs. 73 ± 13 bpm, p = 0.004) when compared to non-medical students (69 ± 6 vs. 70 ± 10, p = 0.695). Rises in diastolic BP, observed 15 seconds after sound stressors, were more pronounced after the "pins" sound than after the standard sound signal only in medical students (3.1% and 1.4% vs. 3% and 4.4%), which was also reflected by low-frequency diastolic BP variability (medical students: 6.2 ± 1.6 vs. 4.1 ± 0.8 ms2, p = 0.04; non-medical students: 6.0 ± 4.3 vs. 4.1 ± 2.6 ms2, p = 0.06). CONCLUSIONS: The "pins" sound, which medical students remembered from their anatomy practical exam, provoked greater sympathetic activity in the medical student group than in their non-medical peers. Thus, past strong experiences modulate CV autonomic responses to acute acoustic stress.

Cardiovascular response to different types of acute stress stimulations.

INTRODUCTION: Stress is an ubiquitous phenomenon in the modern world and one of the major risk factors for cardiovascular disease. e aim of our study was to evaluate the effect of various acute stress stimuli on autonomic nervous system (ANS) activity, assessed on the basis of heart rate (HRV) and blood pressure (BPV) variability analysis. MATERIALS AND METHODS: the study included 15 healthy volunteers: 9 women, 6 men aged 20-30 years (23.3 ± 1.8). ANS activity was assessed by HRV and BPV measurement using Task Force Monitor 3040 (CNSystems, Austria). ECG registration and Blood Pressure (BP) measurement was done 10 minutes at rest, 10 minutes a er the stress stimulus (sound signal, acoustic startle, frequency 1100 Hz, duration 0.5 sec, at the intensity 95 dB) and 10 minutes after the cold pressor test. The cold pressor test (CPT) was done by placing the person's hand by wrist in ice water (0-4°C) for 120 s. RESULTS: Every kind of stress stimulation (acoustic startle; the CPT) caused changes of HRV indicator values. The time domain HRV analysis parameters (pNN50, RMSSD) decreased after acoustic stress and the CPT, but were significantly lower after the CPT. In frequency domain HRV analysis, significant differences were observed only after the CPT: (LF-RRI 921.23 ms2 vs. 700.09 ms2; p = 0.009 and HF-RRI 820.75 ms2 vs. 659.52 ms2; p = 0.002). The decrease of LF-RRI and HF-RRI value after the CPT was significantly higher than after the acoustic startle (LF-RRI 34% vs. 0.4%, p = 0.022; HF-RRI 19.7% vs. 7% ms2, p = 0.011). The decreased value of the LF and HF components of HRV analysis are indicative of sympathetic activation. Nonlinear analysis of HRV indicated a significant decrease in the Poincare plot SD1 (p = 0.039) and an increase of DFAα2 (p = 0.001) in response to the CPT stress stimulation. The systolic BPV parameter LF/HF-sBP increased significantly after the CPT (2.84 vs. 3.31; p = 0.019) and was higher than after the acoustic startle (3.31 vs. 3.06; p = 0.035). Significantly higher values of diastolic BP (67.17 ± 8.10 vs. 69.65 ± 9.94 mmHg, p = 0.038) and median BP (83.39 ± 8.65 vs. 85.30 ± 10.20 mmHg, p = 0.039) were observed in the CPT group than in the acoustic startle group. CONCLUSIONS: the Cold Pressor Test has a greater stimulatory effect on the sympathetic autonomic system in comparison to the unexpected acoustic startle stress. Regardless of whether the stimulation originates from the central nervous system (acoustic startle) or the peripheral nervous system (CPT), the final response is demonstrated by an increase in the low frequency components of blood pressure variability and a decrease in the low and high frequency components of heart rate variability.

Association between low-grade chronic inflammation and depressed left atrial compliance in heart failure with preserved ejection fraction: A retrospective analysis.

BACKGROUND: 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-inflammatory state and associated oxidative stress. The consequent nitric oxide deficiency would increase diastolic tension and favor fibrosis of adjacent myocardium, which implies not only left ventricular (LV), but all-chamber myocardial stiffening. Our aim was to assess relations between low-grade chronic systemic inflammation and left atrial (LA) pressure-volume relations in real-world HFpEF patients. METHODS: 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 records. A surrogate measure of LA stiffness was computed as the averaged mitral E/e' ratio divided by LA diameter. RESULTS: 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). The LA stiffness estimate and log-transformed CRP levels (log-CRP) were interrelated (r = 0.38, p = 0.003). On multi- variate analysis, the LA stiffness index was independently associated with log-CRP (ß ± SEM: 0.21 ± 0.07, p = 0.007) and age (ß ± SEM: 0.16 ± 0.07, p = 0.03), which was maintained upon adjustment for LV mass index and relative LV wall thickness. CONCLUSIONS: Low-grade chronic inflammation may contribute to LA stiffening additively to age and regardless of the magnitude of associated LV hypertrophy and concentricity. LA stiffening can exacerbate symptoms of congestion in HFpEF jointly with LV remodeling.