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The application of unattended blood pressure measurement (uAOBPM) for resting heart rate (RHR) assessment is unknown. To assess the agreement between RHR measured during uAOBPM and other methods, the authors conducted a comparability study with office blood pressure measurement (OBPM), ambulatory blood pressure monitoring (ABPM), and electrocardiogram (ECG) in a group of 110 participants referred for ABPM. RHR measured with uAOBPM (70.8 ± 12.5 bpm) was significantly lower than OBPM (72.8 ± 12.6 bpm) but higher than measured by 24 h ABPM (67.5 ± 10.2 bpm). There was no significant difference was found between RHR measured by uAOBPM and daytime ABPM (70.3 ± 11.2 bpm) or ECG (69.1 ± 11.6 bpm). Using Bland-Altman statistics, the authors discovered a small difference in agreement between RHR measured by uAOBPM and daytime ABPM (bias: 0.4 with 95% confidence interval: -0.8 to 1.6 bpm), with a poorer agreement with OBPM (bias -2 with 95% confidence interval: -2.8 to -1.3 bpm) and ECG (bias 1.6 with 95% confidence interval: 0.5 to 2.7 bpm). The authors found significant agreement between uAOBPM and ECG in identifying subjects with RHR > 80 bpm OBPM, with Cohen's kappa coefficients of 0.783 and 0.671, respectively. Their findings indicate that RHR measured with uAOBPM remains in acceptable agreement with OBPM, ABPM, and ECG, the best agreement obtained with RHR from daytime ABPM., (© 2024 The Author(s). The Journal of Clinical Hypertension published by Wiley Periodicals LLC.)

Background: The guidelines recommend intensive blood pressure control. Randomized trials have focused on the relevance of the systolic blood pressure (SBP) lowering, leaving the safety of the diastolic blood pressure (DBP) reduction unresolved. There are data available which show that low DBP should not stop clinicians from achieving SBP targets; however, registries and analyses of randomized trials present conflicting results. The purpose of the study was to apply machine learning (ML) algorithms to determine, whether DBP is an important risk factor to predict stroke, heart failure (HF), myocardial infarction (MI), and primary outcome in the SPRINT trial database. Methods: ML experiments were performed using decision tree, random forest, k-nearest neighbor, naive Bayesian, multi-layer perceptron, and logistic regression algorithms, including and excluding DBP as the risk factor in an unselected and selected (DBP < 70 mmHg) study population. Results: Including DBP as the risk factor did not change the performance of the machine learning models evaluated using accuracy, AUC, mean, and weighted F-measure, and was not required to make proper predictions of stroke, MI, HF, and primary outcome. Conclusions: Analyses of the SPRINT trial data using ML algorithms imply that DBP should not be treated as an independent risk factor when intensifying blood pressure control.

Adequate control of blood pressure (BP) is essential to prevent complications in pregnant women with a history of eclampsia or pre-eclampsia. However, the importance of office (OBPM), home (HBPM), and ambulatory (ABPM) BP measurements for proper control and prognosis in high-risk pregnancy is unknown. The present study aimed to compare BP values obtained during these three different BP measurements in women with a history of eclampsia or pre-eclampsia. This study included 79 pregnant women with chronic hypertension and a documented history of eclampsia or pre-eclampsia in previous pregnancy/pregnancies. Every fifth week of the study, all participants underwent ABPM, HBPM and OBPM. BP values from the 10th, 25th, and 37th weeks of pregnancy were evaluated. Therapy was intended to meet the ABPM treatment goal of <130/80 mmHg. Day, night, and 24 h ABPM systolic BP values were lower than HBPM and OBPM values at each study visit. Night and 24 h ABPM diastolic BP values were lower than HBPM and OBPM values, while day 24 h ABPM values were slightly higher than HBPM and OBPM values. ABPM provides different BP values than OBPM and HBPM. Target BP for ABPM in high-risk pregnancy hypertension should be estimated based on the predictive value of adverse pregnancy outcomes.

The association between elevated resting heart rate (RHR) as a cardiovascular risk factor and lowering of systolic blood pressure (SBP) to currently recommended values remain unknown. Systolic Blood Pressure Intervention Trial (SPRINT) data obtained from the NHLBI were used to describe the relationship between RHR and SBP reduction to <120 mmHg compared to SBP reduction to <140 mmHg. The composite clinical endpoint (CE) was defined as myocardial infarction, acute coronary syndrome, decompensation of heart failure, stroke, or cardiovascular death. Increased RHR was associated with a higher CE risk compared with low RHR in both treatment arms. A more potent increase of risk for CE was observed in subjects who were allocated to the SBP < 120 mmHg treatment goal. A similar effect of intensive and standard blood pressure (BP) reduction ( p for interaction, 0.826) was observed in subjects with RHR in the 5th quintile (hazard ratio, 0.78, with 95% confidence interval (CI), 0.55-1.11) and in other quintiles of baseline RHR (hazard ratio, 0.75, with 95% CI, 0.62-0.90). Lower in-trial than baseline RHR was associated with reduced CE risk (hazard ratio, 0.80, with 95% CI, 0.66-0.98). We concluded that elevated RHR remains an essential risk factor independent of SBP reduction.

Introduction: Optimal diastolic blood pressure (DBP) during antihypertensive treatment in patients without a history of cardiovascular disease (CVD) remains unknown., Objectives: This post‑hoc analysis of the SPRINT (Systolic Blood Pressure Intervention Trial) data aimed to determine the optimal DBP evaluated using automated office blood pressure measurements (AOBPM) in hypertensive patients without a history of CVD., Patients and Methods: Data of 1470 patients with CVD and 7117 patients without CVD were used. Clinical composite endpoint (CE) was defined as the occurrence of myocardial infarction, acute coronary syndrome other than myocardial infarction, decompensation of heart failure, stroke, or cardiovascular death. Two different approaches based on the hazard ratio plot were used to identify the optimal DBP range. The first approach was to determine the 10 mm Hg-wide DBP range with the lowest risk for CE. In the second approach, it was assumed that the hazard ratio of CE at the boundary points of the optimal DBP range should be the same in patients with and without CVD., Results: Two ranges of on-treatment DBP were proposed: 73.7 to 83.7 mm Hg (first approach) and 63.6 to 95.8 mm Hg (second approach). The risk for CE was increased by 3% and 20% at the boundary points of the range, respectively, depending on the method of DBP determination., Conclusions: Due to the fact that the range determined by the second method was wide and substantially different from the one recommended by the European Society of Cardiology (70-79 mm Hg), we have concluded that a DBP range of 73.7 to 83.7 mm Hg, measured using AOBPM, should be considered optimal in patients without CVD.

Introduction: Cancer therapies are currently more efficient at increasing the survival of patients (pts) with cancer. Unfortunately, the cardiovascular (CV) complications of cancer therapies may adversely affect improving results of treatment. The aim of the study was to evaluate the prevalence of classical CV risk factors among pts with de novo diagnosis of cancer and thus identify the cohort of pts with potentially increased future risk of CV complications., Material and Methods: The analysis is based on the database of the multicentre ONCOECHO study. Pts before systemic treatment (chemotherapy or targeted therapy) were included. The diagnostic datasets of resting electrocardiogram, blood samples, and transthoracic echocardiogram were analysed in 343 consecutive pts who were free from any cardiovascular disease that could adversely affect the introduced treatment., Results: Our cohort included 4.4% of pts with kidney cancer, 7.3% with colorectal cancer, 26.5% with haematological malignancies (HM), and 61.8% with breast cancer. The risk estimated by SCORE was 4.56 ±5.07%. Breast cancer pts had lower cardiovascular risk than those with HM ( p = 0.001) and kidney cancer ( p = 0.002). Additionally, the HM group had much higher levels of natriuretic peptides ( p < 0.001) and creatinine ( p = 0.008) than pts with breast cancer. The comparison with the NATPOL population data showed that our pts were more often smokers, hypertensives, and diabetics, but less frequently presented with hypercholesterolaemia., Conclusions: Patients with new diagnosis of cancer, who are candidates for potentially cardiotoxic medical treatment, have increased prevalence of significant cardiovascular risk factors and therefore should be followed by a multidisciplinary team during the therapeutic process., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2020 Termedia & Banach.)

Introduction: Polycythemia vera (PV) is a rare myeloproliferative disease associated with an increased prevalence of hypertension and increased risk of cardiovascular complications. However, the precise mechanisms leading to the elevation of blood pressure (BP) and secondary target organ damage remain poorly understood., Objectives: The study aimed to evaluate BP profile, assess the activity of the sympathetic nervous system and the renin‑angiotensin system, and provide a comprehensive assessment of subclinical target organ damage in patients with PV., Patients and Methods: Twenty consecutive patients with newly diagnosed PV and 20 control subjects were included. The following were assessed: BP, levels of catecholamines, urinary and plasma O‑methylated catecholamine metabolites, concentrations of aldosterone and renin. We also assessed microneurography sympathetic nervous system activity (MSNA) and baroreflex control of heart rate as well as subclinical target organ damage., Results: At similar levels of BP, BP variability was decreased in the PV group (mean [SD] 24‑hour systolic BP, 9 [3] vs 12 [3] mm Hg; P = 0.003). Patients with PV had lower norepinephrine excretion (mean [SD], 16.54 [6.32] vs 25.46 [12.88] μg/d; P = 0.03) as well as decreased MSNA as assessed by microneurography compared with controls (mean [SD] MSNA, 30.7 [8.7] bursts/min vs 38.7 [5.4] bursts/min; P = 0.007 and MSNA 51.8 [11] bursts/100 beats vs 61.1 [11.3] bursts/100 heart beats; P = 0.04). Baroreflex control of HR was unaltered in the PV group. Increased hemoglobin levels and red blood cell count correlated with decreased retinal capillary flow in patients with PV., Conclusions: Patients with PV, characterized by high hemoglobin concentrations and hematocrit levels had lower sympathetic nervous activity and decreased BP variability as compared with controls. There was no relationship between hemoglobin plasma concentration, hematocrit level, and target organ damage.

Recent studies including the SPRINT trial have shown beneficial effects of intensive systolic blood pressure reduction over the standard approach. The awareness of the J-curve for diastolic blood pressure (DBP) causes some uncertainty regarding the net clinical effects of blood pressure reduction. The current analysis was performed to investigate effects of low on-treatment DBP on cardiovascular risk in the SPRINT population. The primary composite outcome was the occurrence of myocardial infarction, acute coronary syndrome not resulting in myocardial infarction, stroke, acute decompensated heart failure or death from cardiovascular causes. The prevalence of primary outcomes was significantly higher in subjects within low DBP in both standard (44-67 mmHg [10.8%] vs 67-73 mmHg [6.7%] vs 73-78 mmHg [5.1%] vs 78-83 mmHg [4.4%] vs 83-113 mmHg [4.3%], p < 0.001) and intensive treatment (38-61 mmHg [6.7%] vs 61-66 mmHg [4.1%] vs 66-70 mmHg [4.5%] vs 70-74 mmHg [2.7%] vs 74-113 mmHg [3.4%], p < 0.001) arms. After adjusting for covariates, low DBP showed no significant effects on cardiovascular risk. Therefore, while reaching blood pressure targets, low DBP should not be a matter of concern.

Introduction: Repeated measurements of ankle-brachial index (ABI) using Doppler method were shown to be accurate during atrial fibrillation. Oscillometric devices are effective in ABI measurement, but their accuracy during atrial fibrillation is unknown. The purpose of the study was to investigate whether atrial fibrillation influences ABI obtained with the automatic oscillometric method., Material and Methods: Ninety-nine patients with atrial fibrillation (mean age: 66.6 +(SD = 11) years, M/F - 63/36) who underwent electrical cardioversion were investigated (198 lower extremities). The ABI measurements using oscillometric and Doppler methods were performed on both lower extremities before and after procedure., Results: The ABI measured using the oscillometric method on both lower limbs did not change after cardioversion (1.21 (IQR: 1.13-1.27) vs. 1.22 (IQR: 1.14-1.26), p = 0.664, respectively). The ABI measured before and after cardioversion using Doppler and oscillometric methods showed a significant difference (1.14 (IQR: 1.07-1.22) vs. 1.21 (IQR: 1.13-1.27), p < 0.001 and 1.18 (IQR: 1.09-1.13) vs. 1.22 (IQR: 1.14-1.26), p < 0.001 respectively). Both methods showed a weak correlation before ( r = 0.35, p < 0.001) and no correlation after cardioversion ( r = 0.12, p = 0.07). The Bland-Altman plot showed poor agreement between measurements performed with the Doppler and oscillometric methods in sinus rhythm and during atrial fibrillation., Conclusions: The automated oscillometric method of ABI measurements should not replace the reference Doppler method in patients with atrial fibrillation. More research related to the oscillometric measurements is needed in subjects with peripheral artery disease and atrial fibrillation., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2019 Termedia & Banach.)

Automated office blood pressure measurement (AOBPM) is recommended for diagnosing hypertension; however, optimal treatment targets using this method are not established. Discrepancies between automated and office measurements of blood pressure have been described, producing uncertainty regarding the use of AOBPM in clinical practice. The Systolic Blood Pressure Intervention Trial (SPRINT) results improved our understanding of target AOBPM systolic blood pressure (SBP) levels; however, diastolic blood pressure (DBP) targets remain unknown. Therefore, we sought to determine the optimal on-treatment DBP range. The analysis was performed on the participants of the SPRINT trial who had hypertension and prior cardiovascular disease. We analyzed the data of 1470 participants (mean age 70.3 ± 9.3 years, 24.1% female) selected from the SPRINT trial database of National Heart, Lung and Blood Institute. The mean achieved SBP and DBP were 127.9 ± 10.7 and 68.3 ± 9.4 mm Hg, respectively. Most of the participants (57.4%) had a DBP lower than 70 mm Hg, while only 11.7% had DPB ≥80 mm Hg. Clinical composite endpoint was defined as myocardial infarction, acute coronary syndrome not resulting in myocardial infarction, stroke, acute decompensated heart failure or death from cardiovascular causes. There were 159 (10.8%) clinical endpoint events. The participants with on-treatment AOBPM DBP range of 68.6-78.6 mm Hg showed the lowest hazard risk of a clinical composite endpoint. These results correspond to the office DBP range of 70-80 mm Hg recommended in ESC guidelines. This is the first attempt to determine the range of optimal DBP values using population-based AOBPM in patients with prior cardiovascular disease., (©2019 Wiley Periodicals, Inc.)

Background Hypertension is the most prevalent and leading risk factor for stroke. SPRINT (The Systolic Blood Pressure Intervention Trial) assessed the effects on cardiovascular event risk of intensive compared with standard systolic blood pressure reduction. In this secondary analysis of SPRINT data, we investigated how low on-treatment diastolic blood pressure ( DBP ) influenced risk for stroke events. Methods and Results For this analysis, we used SPRINT &#95; POP (Primary Outcome Paper) Research Materials from the National Heart, Lung and Blood Institute (NHLBI) Biologic Specimen and Data Repository Information Coordinating Center. Data for 8944 SPRINT participants were analyzed from the period after target blood pressure was achieved until the end of the trial. Overall, there were 110 stroke events, including 49 from the intensive-treatment arm and 61 in the standard-treatment group. In participants with DBP <70 mm Hg, stroke risk was higher than with DBP ≥70 mm Hg (hazard ratio, 1.467; 95% CI 1.009-2.133; P=0.0445). Univariable Cox proportional hazard risk analysis showed that in the whole group, age and cardiovascular and chronic renal diseases were stroke risk factors. These risk factors were related to lower DBP and higher pulse pressure, however, not to study arm. Multivariable Cox proportional hazard analysis revealed that only age, history of cardiovascular disease, current smoking status and on-treatment systolic blood pressure were significantly related to stroke risk. Conclusions Low on-treatment DBP is not related to the risk for the first stroke, in contrast to older age, the history of cardiovascular disease, current smoking status, and on-treatment systolic blood pressure. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT 01206062.

Atrial fibrillation may affect blood pressure measurements. The ankle-brachial index (ABI) is a ratio of systolic blood pressure measured on the lower and upper limbs that may also be affected by arrhythmia. The purpose of the study was to investigate whether atrial fibrillation influenced ABI results. Ninety-nine patients (age 66.6±11 years, 63 males and 36 females) who underwent electrical cardioversion of atrial fibrillation were investigated. ABI measurements using the Doppler method were performed on both lower extremities before and after electrical cardioversion. Measurements were repeated three times and then averaged. The ABI using both lower limbs was lower before electrical cardioversion than after restoration to sinus rhythm (right side: 1.132 (1.065-1.210) during atrial fibrillation vs. 1.179 (1.080-1.242) in sinus rhythm, P=0.019; left side: 1.142 (1.075-1.222) during atrial fibrillation vs. 1.170 (1.098-1.255) in sinus rhythm, P=0.011). However, the upper 95% confidence interval (CI) margins for the median differences in ABI were 0.045 and 0.040 for right and left, respectively, suggesting that the observed difference was clinically insignificant. There was a significant correlation between measurements obtained before and after electrical cardioversion on both lower limbs (r=0.61, P<0.001 and r=0.67, P<0.001). The Bland-Altman plot showed good agreement between measurements performed using the Doppler method during atrial fibrillation and sinus rhythm. Study results showed that atrial fibrillation did not have a clinically important effect on ABI measurements.

Background: Colorectal cancer (CRC) is the second most common cancer in women and the third in men in Poland. The role of chemotherapy (CTX) depends on the stage of CRC: adjuvant CTX is a standard treatment in stage III and should also be considered in stage II with risk factors., Aim: The aim of the paper was to assess the cardiovascular consequences of CTX in CRC enrolled to the ONCOECHO multicentre study (2012-2014). To identify potential cardiotoxicity, we focused on myocardial function, heart rhythm and conduction disorders, and adverse cardiovascular events., Methods: Twenty-five CRC patients (12 women, mean age 61.3 [35-76] years), all receiving six-month adjuvant CTX were included. Thirteen patients received 5-fluorouracil (5FU)-based CTX, and 12 patients received a capecitabine-based scheme. Subjects were assessed at baseline and followed-up three, six, and 12 months after the onset of treatment. In this analysis we focused on conduction abnormalities, systolic and diastolic function of the left ventricle (LV), and cardiovascular events., Results: In 12-month follow-up a decrease of selected tissue Doppler parameters (e.g. S'IVS, S'lat, and E'sept) was observed, and it was significant. LV structural parameters and ejection fraction (EF) remained unaffected. Changes in myocardial performance were not influenced by CTX regimen or treatment with beta-blockers or angiotensin-converting enzyme inhibitors. CTX did not affect LV structural parameters, EF, or conduction system, nor was it associated with cardiovascular events during the 12-month follow-up., Conclusions: CTX in CRC patients does not affect LV structural parameters and EF. It may, however, trigger subtle changes in myocardial performance detectable by tissue Doppler echocardiography after 12 months. Moreover, it causes a transient increase of QT, which resolves after CTX cessation.

Introduction: Hyperoxia increases total peripheral resistance by acting locally but also inhibits the activity of carotid body chemoreceptors. We studied the effect of hyperoxia on central pressure in normotensive subjects., Material and Methods: Medical air followed by 100% oxygen was provided to 19 subjects (12/7 female/male, age 28.2 ±1.1 years) for 15 min through a non-rebreather mask. Central blood pressure was then measured using applanation tonometry., Results: After the first 2 min of hyperoxia, heart rate decreased significantly (65 ±2.6 beats/min vs. 61 ±2.1 beats/min, p = 0.0002). Peripheral and central blood pressure remained unchanged, while hemoglobin oxygen saturation and subendocardial viability ratio index increased (97 ±0.4% vs. 99 ±0.2%, p = 0.03; 168 ±8.4% vs. 180 ±8.2%, p = 0.009). After 15 min of 100% oxygen ventilation, heart rate and peripheral and central blood pressures remained unchanged from the first 2 min. The augmentation index, augmentation pressure and ejection duration increased as compared to baseline values and those obtained at 2 min (-5.1 ±2.9% vs. -1.2 ±2.6%, p = 0.005 and -4.6 ±2.7% vs. -1.2 ±2.6%, p = 0.0015; -1.3 ±0.7 mm Hg vs. -0.2 ±1.2 mm Hg, p = 0.003 and -1.1 ±0.7 mm Hg vs. -0.2 ±1.2 mm Hg, p = 0.012; 323 ±3.6 ms vs. 330 ±3.5 ms, p = 0.0002 and 326 ±3.5 ms vs. 330 ±3.5 ms, p = 0.021, respectively)., Conclusions: The present study shows that hyperoxia does not affect central blood pressure in young healthy subjects and may improve myocardial blood supply estimated indirectly from applanation tonometry.

Objective: Beyond lipid-lowering properties, statins decrease sympathetic nervous activity. Due to the limited number of studies and included participants, a meta-analysis of randomized, placebo-controlled studies using microneurography (MSNA) was performed to assess sympatholytic effect of statins., Methods: We conducted a comprehensive search of online databases (Cochrane, Embase, and EBSCO) for published human studies up to April 2014. Randomized controlled trials (parallel and crossover design) were eligible for inclusion if results of statins versus placebo treatments on sympathetic activity were measured with MSNA., Results: Data from five studies with a total number of subjects n = 82 were included into the meta-analysis. MSNA expressed as bursts/min and as bursts/100 heartbeats was lower in the statin group than in the placebo group with a mean difference of -4.37 95% CI (-7.03; -1.70), p < 0.0013 and -5.85 95% CI (-7.56; -4.13), p < 0.0001, respectively. No significant publication bias was observed. Meta-regression revealed no significant effect of baseline total cholesterol or dose of statin. No change in blood pressure and heart rate was observed., Conclusions: Published data show that regardless of type and dose, statins reduce sympathetic activity measured by microneurography. The role of decreased sympathetic outflow during statin therapy on clinical end points needs to be clarified.

The relationship between the sympatholytic effects of statins and their lipid-lowering activity remains unclear. Ezetimibe lowers cholesterol, but its sympatholytic activity is unknown. The purpose of study was to compare the influence of equipotent doses of simvastatin and ezetimibe on sympathetic activity. This randomized double-blinded study was performed in 22 hypertensive patients (age, 45.6 ± 2.2 years; female/male, 2/20) with untreated hypercholesterolemia. The subjects were administered 20 mg/d of simvastatin (n = 11) or 20 mg/d of ezetimibe (n = 11) for 6 weeks. Pre- and post-treatment measurements of muscle sympathetic nerve activity (MSNA), baroreceptor control of heart rate (baroreflex sensitivity), and impedance cardiography were recorded. Simvastatin and ezetimibe produced similar reductions of total (-58.0 ± 23.4 vs. -45.2 ± 17.2 mg/dL; P = .15, respectively) and low-density lipoprotein cholesterol (-52.6 ± 20.9 vs. -37.9 ± 17.6 mg/dL; P = .09, respectively). There was a significant difference in the effect of simvastatin and ezetimibe on muscle sympathetic nerve activity (-8.5 ± 5.1 vs. -0.7 ± 3.5 bursts/min; P = .0005). Simvastatin improved baroreflex sensitivity as compared with ezetimibe (10.0 ± 14.3 vs. -2.8 ± 6.1 ms/mm Hg; P = .01). There was no difference in the effect of both treatments on blood pressure, heart rate, cardiac output, stroke volume, total peripheral resistance, high-density lipoprotein, and triglycerides. Simvastatin reduced sympathetic activity via lipid-independent mechanisms, but ezetimibe exerts no sympatholytic effects.

We present a case of a 40-year old woman diagnosed with a four-place spontaneous paraganglioma-pheochromocytoma syndrome, which was treated surgically. The presence of the succinate dehydrogenase complex subunit D (SDHD) mutation that causes the pheochromocytoma was confirmed but no mutations in the family members were found. After the excision of the paragangliomas located in the areas of the division of carotid arteries, and mediastinum, as well as a tumor on the left site of the celiac trunk, the patient remains asymptomatic and is regularly followed-up.

Stroke is the second most common cause of death worldwide and of adult disability, but in the near future the global burden of cerebrovascular diseases will rise due to ageing and adverse lifestyle changes in populations worldwide. The risk of stroke increases at blood pressure levels above 115/75 mm Hg and high blood pressure (BP) is the most important modifiable risk factor for stroke, associated with 54 % episodes of stroke worldwide. There is strong evidence from clinical trials that antihypertensive therapy reduces substantially the risk of any type of stroke, as well as stroke-related death and disability. The risk attributed to BP is associated not only with absolute values but also with certain parameters describing BP diurnal pattern as well as short-term and long-term variability. Many studies reported that certain features of BP like nocturnal hypertension, morning surge or increased variability predict an increased stroke risk. However, there is no accepted effective modality for correction of these disturbances (chronotherapy, certain classes of antihypertensive drugs). In the elderly, who are mostly affected by stroke, the primary prevention guidelines recommend treatment with diuretics and calcium channel blockers to lower blood pressure to the standard level.

Background: Botulism is an acute form of poisoning caused by one of four types (A, B, E, F) toxins produced by Clostridium botulinum, ananaerobic, spore forming bacillus. Usually diagnosis of botulism is considered in patients with predominant motor symptoms: muscle weakness with intact sensation and preserved mental function., Case Presentation: We report a case of 56-year-old Caucasian female with a history of arterial hypertension, who presented with acute respiratory failure and bilateral ptosis misdiagnosed as brainstem ischemia. She had severe external and internal ophtalmoplegia, and autonomic dysfunction with neither motor nor sensory symptoms from upper and lower limbs. Diagnosis of botulinum toxin poisoning was made and confirmed by serum antibody testing in the mouse inoculation test., Conclusions: Ophtalmoplegia, autonomic dysfunction and respiratory failure can be caused by botulism. Early treatment and intensive care is essential for survival and recovery. The electrophysiological tests are crucial to correct and rapid diagnosis. Botulism (especially type B) should be considered in any case of acute or predominant isolated autonomic dysfunction.

Carotid chemoreceptors provoke an increase in muscle sympathetic nerve activation (MSNA) in response to hypoxia; they are also tonically active during normoxic breathing. The contribution of peripheral chemoreceptors to sympathetic activation in hypertension is incompletely understood. The aim of our study was to investigate the effect of chemoreceptor deactivation on sympathetic activity in untreated patients with hypertension. A total of 12 untreated hypertensive males and 11 male controls participated in this randomized, crossover, placebo-controlled study. MSNA, systolic blood pressure(BP), diastolic BP, heart rate (HR), electrocardiogram, hemoglobin oxygen saturation (Sat%) and respiratory movements were measured during repeated 10-min periods of respiration with 100% oxygen or 21% oxygen in a blinded fashion. Compared with controls, hypertensives had higher resting MSNA (38 ± 10 vs. 29 ± 0.9 burst per min, P<0.05), systolic BP (150 ± 12 vs. 124 ± 10 mm Hg, P< 0.001) and diastolic BP (92 ± 10 vs. 77 ± 9 mm Hg, P<0.005). Breathing 100% oxygen caused significant decrease in MSNA in hypertensive patients (38 ± 10 vs. 26 ± 8 burst per min and 100 ± 0 vs. 90 ± 10 arbitrary units, P<0.05) and no change in controls (29 ± 9 vs. 27 ± 7 burst per min and 100 ± 0 vs. 96 ± 11 arbitrary units). BP, respiratory frequency and end tidal CO(2) did not change during chemoreceptor deactivation with hyperoxia. HR decreased and Sat% increased in both the study groups. These results confirm the role of tonic chemoreceptor drive in the development of sympathetic overactivity in hypertension.

Beyond their hypolipidemic effect, statins reduce cardiovascular risk in hypertensive subjects via various mechanisms; one suggested mechanism is that they reduce sympathetic activity. We investigated the hypothesis that simvastatin decreased muscle sympathetic nerve activity (MSNA) in 31 hypertensive subjects with hypercholesterolemia (aged 38.7 ± 10 years). In this randomized, placebo-controlled, double-blinded study, patients were treated with simvastatin (40 mg day(-1); n=15) or placebo (n=16) for 8 weeks. Before and after treatment, we measured MSNA, blood pressure and heart rate. Baroreceptor control of the heart rate, or baroreceptor sensitivity (BRS), was computed by the sequence method, a cross-analysis of systolic blood pressure and the electrocardiogram R-R interval. Blood samples were tested for plasma levels of catecholamines, neuropeptide Y, aldosterone, endothelin and renin activity. Simvastatin significantly reduced MSNA (from 36.5 ± 5 to 27.8 ± 6 bursts per min, P=0.001), heart rate (from 77 ± 6.7 to 71 ± 6.1 beats per min, P=0.01) and both total and low-density lipoprotein cholesterol (from 249 ± 30.6 to 184 ± 28.3 mg dl(-1), P=0.001 and from 169 ± 30.6 to 117 ± 31.2 mg dl(-1), P=0.01, respectively). Simvastatin also improved BRS (from 10.3 ± 4.1 to 17.1 ± 4.3 ms per mm Hg, P=0.04). No changes were observed in systolic or diastolic blood pressures, or in plasma levels of catecholamines, neuropeptide Y, endothelin, aldosterone and renin activity. After simvastatin therapy, MSNA and BRS were inversely related (r=-0.94, P<0.05). In conclusion, we found that, in patients with hypertension and hypercholesterolemia, simvastatin reduced MSNA, and this was related to increased baroreceptor sensitivity.

Recent case reports provided alarming signals that treatment with bortezomib might be associated with cardiac events. In all reported cases, patients experiencing cardiac problems were previously or concomitantly treated with other chemotherapeutics including cardiotoxic anthracyclines. Therefore, it is difficult to distinguish which components of the therapeutic regimens contribute to cardiotoxicity. Here, we addressed the influence of bortezomib on cardiac function in rats that were not treated with other drugs. Rats were treated with bortezomib at a dose of 0.2 mg/kg thrice weekly. Echocardiography, histopathology, and electron microscopy were used to evaluate cardiac function and structural changes. Respiration of the rat heart mitochondria was measured polarographically. Cell culture experiments were used to determine the influence of bortezomib on cardiomyocyte survival, contractility, Ca(2+) fluxes, induction of endoplasmic reticulum stress, and autophagy. Our findings indicate that bortezomib treatment leads to left ventricular contractile dysfunction manifested by a significant drop in left ventricle ejection fraction. Dramatic ultrastructural abnormalities of cardiomyocytes, especially within mitochondria, were accompanied by decreased ATP synthesis and decreased cardiomyocyte contractility. Monitoring of cardiac function in bortezomib-treated patients should be implemented to evaluate how frequently cardiotoxicity develops especially in patients with pre-existing cardiac conditions, as well as when using additional cardiotoxic drugs.

Background: Increased sympathetic activity might be related to pathogenesis of hypertension as well as to end organ damage. Animal studies suggest that statins decrease sympathetic activity and increase baroreceptor reflex sensitivity (BRS)., Aim: To examine whether atorvastatin decreases muscle sympathetic nerve activity (MSNA) and BRS in hypercholesterolaemic and hypertensive patients., Methods: Ten patients with essential hypertension and untreated hypercholesterolaemia (aged 43 +/- 12 years) and eight healthy subjects (aged 37 +/- 7 years) were enrolled in the study. In both groups the recordings of microneurography, ECG, blood pressure and BRS were performed twice, before and after 8 weeks during which the patients (but not controls) were treated with atorvastatin., Results: Compared with controls, the patients had higher MSNA values (36.0 +/- 6.6 vs. 29.8 +/- 3.7 bursts/minute), mean BP levels (145.1 +/- 10 vs. 124.1 +/- 11.1 mmHg) and total cholesterol concentration (252.6 +/- 22.6 vs. 179.8 +/- 20.7 mg/dl) baseline values. Statin therapy resulted in a decrease of total cholesterol (252.6 +/- 22.0 vs. 173.8 +/- 26.2 mg/dl, p < 0.05) and MSNA (36.0 +/- 6.6 vs. 28.6 +/- 4.8 bursts/min, p < 0.05), whereas BRS values were increased (12.6 +/- 5.6 vs. 18.1 +/- 5.9 ms/mmHg, p < 0.05). Post-treatment BRS was inversely related to post-treatment MSNA (r = -0.73, p < 0.05). In the controls there were no changes in MSNA (29.8 +/- 3.7 vs. 28.9 +/- 2.9 bursts/min), BRS (11.9 +/- 5.0 vs. 13.1 +/- 4.8 ms/mmHg), total cholesterol, BP and heart rate between the first and the second measurement., Conclusion: Atorvastatin reduces MSNA and increases BRS in hypertensive and hypercholesterolaemic patients. Decrease in sympathetic activity may be the result of improvement of baroreceptor function by atorvastatin.

Short acting nitrates are commonly used to prevent the anginal pain. The purpose of the study was to compare antianginal efficacy of Pentaerythritol compositum (20 mg of pentaerythritol tetranitrate and 0.5 mg of nitroglicerine) and 0,5 mg of nitroglycerine. Twenty patients aged 45-75 years with stable angina were enrolled. Antianginal effectiveness was evaluated during treadmill test. Time to ischemic pain and/or electrocardiographic parameters of ischemia were measured. It was found that Pentaerythritol compositum was superior to nitroglycerine in preventing angina with the difference disappearing 60 minutes after drug administration. Both drugs were well tolerated. Achieved results show that Pentaerythritol compositum can be effective as antianginal drug in patients with stable angina.

Respiratory failure coincides frequently with the occurrence of gastric ulceration. In advanced respiratory insufficiency hypoxemia is often accompanied by hypercapnia, which is the stimulus for central chemoreceptors as well as for carotid body chemoreceptors. The purpose of the work was to investigate the reflex effect of stimulation of central chemoreceptors on gastric mucosal blood flow (GMBF) in the rat. Central chemoreceptors were stimulated by a gas mixture composed of 10% carbon dioxide, 50% oxide and 40% nitrogen. In artificially ventilated and spontaneously breathing animals, the stimulation of central chemoreceptors caused a significant increase in gastric mucosal vascular resistance, accompanied by a marked decline in blood flow. We hypothesize that in patients with respiratory insufficiency accompanied by hypercapnia, the reflex impairment of GMBF may contribute to gastric ulceration.

The cardiovascular effects of the stimulation of arterial chemoreceptors are different in spontaneously breathing and artificially ventilated animals. Respiratory failure and long term sojourn at high altitude coincide frequently with the occurrence of gastric ulceration. In both these situations a profound stimulation of arterial chemoreceptors is present. The purpose of the paper was to investigate the reflex effect of stimulation carotid chemoreceptors on gastric mucosal blood flow in the rat. Arterial chemoreceptors were stimulated by two methods (I) substitution gas mixture of 10% oxygen in nitrogen for room air and (II) direct injection of acid saline ( 0.05 ml, pH = 6.8) into the distal part of left common carotid artery. In artificially ventilated rats stimulation of arterial chemoreceptors caused significant increase in gastric mucosal vascular resistance, accompanied by marked decline in blood flow. This effect was mediated by adrenergic mechanism. On the contrary to artificially ventilated rats, decline of gastric mucosal vascular resistance with concomitant increase in blood flow was found in spontaneously breathing animals. This effect was not abolished either by phentolamine or atropine. As vasodilatatory effect of arterial chemoreceptors stimulation was abolished by bilateral vagotomy, we postulate that non adrenergic and non cholinergic vagal fibers mediate observed vascular changes in gastric mucosa in spontaneously breathing rats. We hypothesize that in artificially ventilated patients with respiratory failure stimulation of arterial chemoreceptors by hypoxemia and or acidosis may contribute to the development of gastric mucosal lesions.

An introduction of laser flow meters for a continuous measurements of a tissue blood flow has opened new avenues for an accurate assessment blood flow in peripheral nerves. The aim of our study was: 1) to carry out a functional verification of anatomical sources of a sciatic nerve blood supply in the rat; 2) develop a measurement technique to facilitate standardisation of results; 3) to determine the role of nerve fibres tonic activity in the maintenance of a resting blood flow in the sciatic nerve. Based on results of the present study the following conclusions have been drawn out: 1) in order to obtain a real values of the blood flow through the sciatic nerve it is necessary to remove its muscular fascia; 2) an uninjured epineurium plays a crucial role in maintaining the resting blood flow; 3) major blood supply of sciatic nerve comes from inferior gluteal and popliteal arteries; 4) the tonic neural activity plays a role in the maintenance of the resting sciatic nerve blood flow in anaesthetised rats.

It has been recognised that high haemoglobin oxygen capacity is essential for the development of high blood pressure in spontaneously hypertensive rats. In the present study we have found increased concentration of 2,3 diphosphoglycerate (2,3-DPG) in red blood cells of spontaneously hypertensive rats (SHR) of Okamoto-Aoki strain. As 2,3-DPG is the major factor decreasing haemoglobin affinity to oxygen, our finding suggests that at given value of pO2 oxygen delivery to the tissue of SHR would be increased. Therefore increased concentration of 2,3-DPG in red blood cells of SHR would be of the pathophysiological meaning by promoting autoregulatory increase in total vascular resistance in this strain of rats. The mechanism responsible for enhanced synthesis of 2,3-DPG in SHR remains unclear. Intracellular alkalosis due to either hypocapnia and/or an enhanced activity of Na+/H+ antiporter occurring in SHR are the most plausible explanations for the above finding.