Introduction: Right atrium volume index (RAVI) has recently been reported as a quantitative echocardiographic parameter associated with right ventricular systolic dys-function (RVSD) in patients with pulmonary arterial hypertension (PAH) due to chronic obstructive pulmonary disease (COPD).
Aims: The aim of the current study was to assess right atrium remodeling (RAVI) in COPD patients without echocardiographic parameters of RVSD or PAH at rest and to analyse its association with right ventricular diastolic dysfunction (RVDD) at rest and after exercise – stress-induced RVDD.
Methods: The study was conducted in 104 COPD patients. Pulmonary function tests, blood gas analysis, incremental, symptom-limited cardio-pulmonary test (CPET) protocol and detailed echocardiographic examinations before and 2-3 minutes after peak CPET were applied. The cut-offvalues for stress-induced RVDD were E/e’ > 6.0.
Results: Patients were divided into two groups: patients with stress-induced RVDD (82/104 – 78%) and those without stress-RVDD (22/104 – 22%). RAVI was significantly higher in the group with stress-induced RVDD (23,04 ± 2,67 ml/m2 vs 18,02 ± 2,69 ml/m2) in comparison to those without it. Correlation analysis showed that RAVI was associated with stress-induced RVDD (E/e’) and the distance from the 6 minute walk test (6-MWT), but was not an independent predictor for any of them.
Conclusions: RAVI correlates with stress-induced RVDD parameters (E/e’) in non-severe COPD patients without pulmonary arterial hypertension at rest. It corresponds to the diminished distance from the 6-MWT, but was not an independent factor of reduced physical activity.
Introduction: The clinical significance of inflammation (and markers such as resistin, hsCRP) and oxidative stress (e.g. 8-isoprostanes) for microvascular disease (MVD) and coronary artery disease (CAD) is still elusive.
Aims: To determine the role of the markers for inflammation and oxidative stress as independent markers for MVD.
Methods: Ninety consecutive patients were recruited: twenty-five of them had CAD; thirty – MVD and thirty-five were controls. The latter included patients with atypical chest pain, risk factors, lack of coronary artery disease and negative adenosine test. Coronary angiography was performed in all participants. The adenosine test was performed in those without CAD, hs CRP, resistin in plasma and urine 8-isoprostanes were measured. The correlation of all these indicators with CAD and MVD was analyzed.
Results: The 8-isoprostanes showed significant differences between patients with MVD and CAD (0,055/0,52 pg/mmol Cre; p = 0,028). The same trend was found between CAD patients and the control group (0,055/0,003 pg/mmol Cre; p = 0,041); as well as between those with MVD and the control group (0,52/0,003 pg/mmol Cre; p = 0,001). The highest values of 8-isoprostanes were detected in patients with MVD – 0,52 pg/mmol Cre. Markers for inflammation were similar in patients with MVD and CAD (hsCRP- p = 0,091; resistin − p = 0,32).
Conclusions: hs CRP, resistin and 8-isoprostanes are involved in the pathogenesis of both CAD and MVD. However, oxidative stress is probably more important for MVD, therefore 8-isoprostanes can be a part of panel of markers for its detection and analysis.
Apoptosis Gene Expression Profile in Early-Stage non Small Cell Lung Cancer
Non small cell lung cancer (NSCLC) is a highly aggressive malignancy with survival rates limited to some patients in early stages (I and II). Apoptosis resistance is a hallmark of solid tumors that is tightly concerned with their biology. We analyzed the expression of 84 apoptosis-related genes in a group of Bulgarian patients with early-stage NSCLC.
RNA samples extracted from 12 early-stage NSCLC patients [five squamous cell carcinomas (SCC) and seven adenocarcinomas (AC)] and eight adjacent non neoplastic pulmonary tissues were used for gene expression analysis. We applied pathway-focused expression profiling of 84 apoptosis-related genes using real-time PCR.
Apoptosis-related genes down regulated in NSCLC compared to non tumor lung tissue (p <0.05) included representatives of the tumor necrosis factor (TNF) ligand family [TNF superfamily 8 (TNFSF8)], caspase cascade (CASP8 and CASP10) and caspase recruitment domain (CARD) family (BCL10), the positive apoptosis regulator DAPK1 and BCL2 family member MCL1. The potential of apoptosis-related genes as prognostic and predictive markers should be validated in future studies.