Surgical resection versus biopsy in the treatment of primary central nervous system lymphoma: a systematic review and meta-analysis.

PURPOSE: Despite the improvement in treatment and prognosis of primary central nervous system lymphoma (PCNSL) over the last decades, the 5-year survival rate is approximately 30%; thus, new therapeutic approaches are needed to improve patient survival. The study's aim was to evaluate the role of surgical resection of PCNSL. METHODS: Primary outcomes were the overall survival (OS) and progression-free survival (PFS) of patients with PCNSL who underwent surgical resection versus biopsy alone. The meta-analysis was conducted to calculate pooled hazard ratios (HRs) under a random-effects model for the time-to-event variables. The odds ratios (ORs) were calculated for binary, secondary outcome parameters. RESULTS: Seven studies (n = 1046) were included. We found that surgical resection was associated with significantly better OS (HR 0.63 [95% CI 0.51-0.77]) when compared with biopsy. PFS was also significantly improved (HR 0.64 [95% CI 0.49-0.85]) in patients who underwent resection compared with those who underwent biopsy. The heterogeneity for OS and PFS was low (I2 = 7% and 24%, respectively). We also found that patients who underwent biopsy more often had multiple (OR 0.38 [95% CI 0.19-0.79]) or deep-seated (OR 0.20 [95% CI 0.12-0.34]) lesions compared with those who underwent surgical resection. There were no significant differences in chemotherapy or radiotherapy use or the occurrence of postoperative complications between the two groups. CONCLUSION: In selected patients, surgical resection of PCNSL is associated with significantly better overall survival and progression-free survival compared with biopsy alone.

[Hypertrophic cardiomyopathy with midventricular obstruction of the left ventricle (MVO)--case report]. / Kardiomiopatia przerostowa ze sródkomorowym zawezaniem lewej komory (MVO)--opis przypadku.

A 76-year old woman with a history of stage 3 arterial hypertension, paroxysmal atrial fibrillation, hypercholesterolemia and type 2 diabetes mellitus. Ventricular tachycardia was the first clinical manifestation of the disease. Echocardiography revealed hypertrophic cardiomyopathy with a high intraventricular gradient of 47 mmHg and midventricular obstruction at the level of the papillary muscles (the lumen of the left ventricle was 1-2 mm during systole). No ventricular aneurysm was found but the ventricle was elongated and dilated in the periapical part where systolic function was decreased but synchronized in time. Coronary angiograms showed no narrowing of coronary arteries. A single-chamber cardioverter-defibrillator (ICD, implantable cardioverter-defibrillator) was implanted to prevent sudden cardiac death. Modified-release metoprolol and amiodarone were administered in antiarrhythmic therapy. This case represents a rare kind of hypertrophic cardiomyopathy in an elderly woman which is characterized by midventricular obstruction.

[The influence of antihypertensive treatment on arterial stiffness, shear stress and activity of chosen matrix metalloproteinases]. / Wplyw 1ecenia przeciwnadcisnieniowego na sztywnosc tetnic, stres scinajacy i aktywnosc wybranych metaloproteinaz macierzy zewnatrzkomórkowej.

UNLABELLED: The aim of the study was to compare therapeutic effects of chosen antihypertensive drugs on arterial stiffness, shear stress in carotid arteries and metalloproteinases activity, moreover analysis of relationship of these variables in the course of treatment. METHODS: 95 patients with essential arterial hypertension stage 1 or 2 were randomized to 6 months monotherapy with: quinapril, amlodipine, hydrochlorothiazide, losartan or bisoprolol. Each therapeutic group consisted of 19 patients (N=19). Before and then after 1, 3 and 6 months of treatment carotid-femoral pulse wave velocity (PWV) by using a Complior device, ultrasound of carotid arteries were performed. Blood samples for the measurement of whole blood viscosity were taken during each visit. Shear stress (SS) was calculated using measured variables: blood viscosity and velocity of blood flow. Serum concentration of metalloproteinase 3 (MMP-3) and plasma concentration of tissue inhibitor of metalloproteinase I (TIMP-1) were measured at the initial visit and after 6 months of treatment. RESULTS: ANOVA for repeated measurements revealed for all groups significant decrease of PWV (ΔPWV) and MMP-3 (ΔMMP-3) concentration and increase of shear stress in carotid artery and TIMP-1 (ΔTIMP-1) concentration (p<0.05). No between groups differences appeared in above effects (p>0.05). The multiple regression analysis for the change of PWV (ΔPWV) in the study group considering all investigated variables at R2 = 0,27 revealed its significant relation to PWV at first visit, ΔTIMP-1, ΔMMP-3 and Δ shear stress counted for the maximum flow velocity in common carotid artery. Conclusion: Irrespectively of chosen drug we observed similar effect for PWV drop. Reduction of arterial stiffness as a result of antihypertensive therapy is strongly connected with shear stress increase that is secondary to blood flow velocity growth and changes in connective tissue metabolism.

Cardiovascular consequences of aircraft noise exposure.

The results from epidemiological studies suggest that environmental noise including aircraft, railway, road traffic, wind turbine, and leisure-related noise is a growing public health concern. According to the WHO, at least 100 million people in the European Union are affected by traffic noise levels above the WHO-recommended thresholds. Environmental noise can adversely affect physical and mental health, as well as wellbeing. Chronic low-level noise exposure typical for most environmental sources is associated with psychophysiological stress causing non-auditory or indirect noise effects leading ultimately to cardiovascular diseases. Among all environmental noise sources, aircraft noise is considered the most annoying, and its leading mechanism of action is autonomic system activation such as increases in heart rate and blood pressure. Previously, we observed that long-term exposure to aircraft noise was associated with increased diastolic blood pressure, arterial stiffness (as assessed by pulse wave velocity), and impaired left ventricular diastolic function. All mentioned above effects are early, subclinical, and potentially reversible changes which preceded late noise effects in the cardiovascular system, that is, established cardiovascular diseases such as myocardial infarction, stroke, and heart failure. However, even a short-term reduction in aircraft noise exposure as observed during the COVID-19 lockdown may reverse these negative effects on arterial stiffness and blood pressure and may decrease the prevalence of insomnia. In this review, we aimed to critically discuss our obtained results considering recent studies on the influence of aircraft noise (and other traffic noises) on cardiovascular diseases in the context of the WHO Environmental Noise Guidelines for the European Region.

Blood Pressure and Arterial Stiffness in Association With Aircraft Noise Exposure:Long-Term Observation and Potential Effect of COVID-19 Lockdown.

In a cross-sectional analysis of a case-control study in 2015, we revealed the association between increased arterial stiffness (pulse wave velocity) and aircraft noise exposure. In June 2020, we evaluated the long-term effects, and the impact of a sudden decline in noise exposure during the coronavirus disease 2019 (COVID-19) lockdown, on blood pressure and pulse wave velocity, comparing 74 participants exposed to long-term day-evening-night aircraft noise level >60 dB and 75 unexposed individuals. During the 5-year follow-up, the prevalence of hypertension increased in the exposed (42% versus 59%, P=0.048) but not in the unexposed group. The decline in noise exposure since April 2020 was accompanied with a significant decrease of noise annoyance, 24-hour systolic (121.2 versus 117.9 mm Hg; P=0.034) and diastolic (75.1 versus 72.0 mm Hg; P=0.003) blood pressure, and pulse wave velocity (10.2 versus 8.8 m/s; P=0.001) in the exposed group. Less profound decreases of these parameters were noticed in the unexposed group. Significant between group differences were observed for declines in office and night-time diastolic blood pressure and pulse wave velocity. Importantly, the difference in the reduction of pulse wave velocity between exposed and unexposed participants remained significant after adjustment for covariates (-1.49 versus -0.35 m/s; P=0.017). The observed difference in insomnia prevalence between exposed and unexposed individuals at baseline was no more significant at follow-up. Thus, long-term aircraft noise exposure may increase the prevalence of hypertension and accelerate arterial stiffening. However, even short-term noise reduction, as experienced during the COVID-19 lockdown, may reverse those unfavorable effects.

The relation of nocturnal exposure to aircraft noise and aircraft noise-induced insomnia with blood pressure.

INTRODUCTION: Nighttime environmental noise exposure leads to unconscious stress reactions and autonomic arousals. These may disturb overnight sleep and the diurnal blood pressure (BP) profile, contributing to an increased risk of developing hypertension. OBJECTIVES: This study aimed to investigate the effects of chronic nighttime exposure to aviation noise on sleep disturbances and the relationship with annoyance and the BP profile. PATIENTS AND METHODS: Based on acoustic maps, we selected 2 groups of normotensive participants: exposed (n = 48; mean age, 50.9 years; 29 women) and unexposed (n = 50; mean age, 49.7 years; 35 women) to nocturnal aircraft noise. We collected anthropometric and demographic data using a standardized questionnaire. Insomnia symptoms were evaluated using the Athens Insomnia Scale (AIS). In both study groups, we performed office BP measurements and 24­hour ambulatory BP monitoring. RESULTS: Noise­exposed participants showed distinctive sleep disturbances, higher AIS scores (4.3 vs 2.3; P = 0.01), and an increased insomnia risk (odds ratio, 2.62; P = 0.046). With increased noise annoyance, a higher AIS score was observed (PANOVA = 0.02). Noise­exposed individuals had higher diastolic BP at night than those unexposed (64.6 mm Hg vs 61.7 mm Hg; P = 0.03). Insomnia among noise­exposed participants resulted in higher 24­hour (115.2 mm Hg vs 122.2 mm Hg; P = 0.03) and nighttime (103.7 mm Hg vs 112.2 mm Hg; P = 0.02) systolic BP. A significant interaction was noted between aircraft noise exposure and the AIS score. The association of the AIS score with 24­hour systolic BP (P = 0.048) and pulse pressure (P = 0.04) was stronger in the exposed group. CONCLUSIONS: The study results may indicate different pathomechanisms affecting BP in terms of nighttime noise and noise­related insomnia.

Plasma renin activity, serum aldosterone concentration and selected organ damage indices in essential arterial hypertension.

INTRODUCTION: The aim of this study was to assess the relations between plasma renin activity (PRA), serum aldosterone concentration (ALDO) and selected asymptomatic organ damage (AOD) indices in mild primary arterial hypertension (AH). MATERIAL AND METHODS: We measured PRA, ALDO, and selected AOD indices (carotid-femoral pulse wave velocity (cfPWV), central aortic pulse pressure (cPP), estimated glomerular filtration rate (eGFR)) in 122 patients with untreated AH. RESULTS: Patients with high PRA (≥ 0.65 ng/ml/h) were characterized by lower plasma sodium and aldosterone to renin ratio (ARR), higher ALDO, but a similar level of AOD indices compared to patients with low PRA. cfPWV (p = 0.04) and cPP (p = 0.019) increased with ARR, while eGFR decreased with ALDO (p = 0.008). Only eGFR was independently correlated with ALDO. In subjects with simultaneously high PRA and ARR values, we found significantly higher cfPWV (p = 0.02) and cPP (p = 0.04) and lower eGFR (p = 0.02) than in those with high PRA but low ARR values. CONCLUSIONS: Assessment of the influence of the renin-angiotensin-aldosterone system (RAAS) on AOD should include the relationship between renin and aldosterone. The PRA itself has no predictive value for AOD. More advanced arterial stiffness and renal impairment are associated with increased PRA and ARR. The RAAS activity might be useful in AOD prediction and hypertension severity assessment.

Relationship among long-term aircraft noise exposure, blood pressure profile, and arterial stiffness.

OBJECTIVE: To assess the impact of long-term exposure to aircraft noise on blood pressure (BP), prevalence of arterial hypertension, and indices of asymptomatic organ damage. METHODS: Using acoustic maps, we selected and further compared people living (average 35 years) in areas exposed to high, more than 60 dB (n = 101), and low aircraft noise, less than 55 dB (n = 100). Medical history taking, office BP measurement, ambulatory BP monitoring, and echocardiographic and arterial stiffness measurements were performed. RESULTS: Exposure to aircraft noise did not increase the prevalence of arterial hypertension (50%, both groups) but was associated with higher office (88.3 ±â€Š11.4 vs. 79.8 ±â€Š8.6 mmHg, P < 0.001) and night-time DBP (66.6 ±â€Š9.5 vs. 63.6 ±â€Š7.3 mmHg, P < 0.01). Participants exposed to a high aircraft noise level had a higher carotid-femoral pulse wave velocity (PWV) (10.3 ±â€Š1.8 vs. 9.4 ±â€Š1.4 m/s, P < 0.01) and lower early mitral annulus velocity (e') (8.4 ±â€Š2.9 vs. 9.2 ±â€Š3.4 cm/s, P = 0.047). These differences were independent of age, sex, BMI, education, time spent at home, smoking status, alcohol consumption, and antihypertensive treatment. Higher office and night-time DBP, PWV, and e' values were explicitly observed in exposed normotensive participants. PWV in aircraft noise-exposed normotensive participants was equal to that of two decades older unexposed normotensive participants and was significantly associated with noise annoyance. CONCLUSION: Long-term aircraft noise exposure is related to higher office and night-time DBP, more advanced arterial stiffness, and unfavourable left ventricle diastolic function changes. Accelerated arterial stiffening was observed in those exposed to aircraft noise, even normotensive participants, to a degree depending on noise annoyance.

The relationship between plasma renin activity and serum lipid profiles in patients with primary arterial hypertension.

INTRODUCTION:: The aim of the study was to evaluate clinical and biochemical differences between patients with low-renin and high-renin primary arterial hypertension (AH), mainly in reference to serum lipids, and to identify factors determining lipid concentrations. MATERIALS AND METHODS:: In untreated patients with AH stage 1 we measured plasma renin activity (PRA) and subdivided the group into low-renin (PRA < 0.65 ng/mL/h) and high-renin (PRA ⩾ 0.65 ng/mL/h) AH. We compared office and 24-h ambulatory blood pressure, serum aldosterone, lipids and selected biochemical parameters between subgroups. Factors determining lipid concentration in both subgroups were assessed in regression analysis. RESULTS:: Patients with high-renin hypertension ( N = 58) were characterized by higher heart rate ( p = 0.04), lower serum sodium ( p < 0.01) and aldosterone-to-renin ratio ( p < 0.01), and significantly higher serum aldosterone ( p = 0.03), albumin ( p < 0.01), total protein ( p < 0.01), total cholesterol ( p = 0.01) and low-density lipoprotein cholesterol (LDL-C) ( p = 0.04) than low-renin subjects ( N = 39). In univariate linear regression, only PRA in the low-renin group was in a positive relationship with LDL-C ( R2 = 0.15, ß = 1.53 and p = 0.013); this association remained significant after adjustment for age, sex, and serum albumin and aldosterone concentrations. CONCLUSIONS:: Higher serum levels of total and LDL-C characterized high-renin subjects, but the association between LDL-C level and PRA existed only in low-renin primary AH.

The relation between blood pressure components and left atrial volume in the context of left ventricular mass index.

Left atrial enlargement (LAE) is a risk factor for cardiovascular complications and death. In hypertensive patients, LAE is usually due to left ventricular (LV) hypertrophy and diastolic dysfunction. We aimed to identify factors associated with LAE in patients with increased and normal left ventricular mass index (LVMI) with reference to pulsatile and steady components of blood pressure (BP).The study was carried out as a cross-sectional observation. In a group of inhabitants of suburban area of Cracow, Poland, we measured office, ambulatory and central BP, carotid-femoral pulse wave velocity (PWV), as well as echocardiographic indices and gathered anthropometric data, information on habits and relevant medical history. Further, with division according to sex-stratified dichotomised LVMI, we performed correlation analysis to identify possibly significant relations between measures of left atrial volume and other studied parameters. We also fitted regression models in order to assess the respective value of steady and pulsatile BP components as factors related to measures of left atrial volume.The mean age of 205 patients (136 females-66%) was 53.6 ±â€Š8.3 years. We found higher values of PWV, office, ambulatory and central BPs in the group of LVMI above median value. This group had also greater left atrial volume index (LAVI), which correlated with LVMI (r = 0.36, P < .001) and ratio of early diastolic mitral peak flow velocity to early diastolic mitral annulus mean velocity in tissue Doppler imaging (E/e') (r = 0.24, P = .04).In the group of LVMI below the median, LAVI correlated with pulsatile and steady BP components. LAVI was independently predicted by mean arterial pressure (MAP) obtained from both ambulatory (MAP24h, ß= 0.15; P = .045) and office measurements (MAPoffice, ß = 0.35; P = .004), but not by pulse pressure.LV mass and function are the main determinants of LAVI. However, in persons with lower LV mass, LAVI depends on the steady component of blood pressure, but not pulsatile one. Increased LAVI reflects early changes in response to systemic blood pressure elevation.