Increase In Systolic Pressure Research Articles

RV in COPD - The complicated matters of the heart - Correlation of ECHO and biomarker with COPD severity and outcome.

Patients with chronic obstructive pulmonary disease (COPD) have an increased risk of cardiovascular involvement, which is among the leading causes of morbidity and mortality worldwide. Echocardiography (ECHO) could be a reliable, non-invasive tool for predicting the risk of cardiovascular modalities in patients with COPD. Combining the ECHO parameters with highly selective cardiac troponin could predict the severity and outcome of patients with COPD. This prospective observational study was conducted at a tertiary care hospital in South India. All patients who met the criteria were included. Patients with other concomitant chronic lung diseases were excluded. An echocardiographic examination was performed, and blood samples for hs-Tnt were taken on admission for patients admitted with COPD. Categorical variables were analyzed using Pearson's Chi-square test, and the T-test was used to compare the means. One-way analysis of variance (ANOVA) followed by the Bonferroni multiple comparison tests was done to compare different echo parameters concerning COPD severity. The mean tricuspid annulus plane systolic excursion (TAPSE) and right ventricle (RV) fraction area change (FAC) values were lower with the increase in the disease severity (P < 0.001). There was a significant increase in the mean systolic pressures in the right atrium and ventricle in patients with severe COPD (P < 0.001). The mean hs-TnT values were significantly higher in patients with severe COPD (18.86 ± 18.12) and correlated well with the increase in the severity of the disease (P < 0.001). Changes in the echo parameters, such as mean TAPSE and RV FAC values, negatively correlated with COPD severity. There was an increase in systolic pressure in both atria and ventricles with the progression of COPD. Troponin helped predict mortality during hospitalization. Comprehensive echocardiographic parameters, such as TAPSE and RV FAC, help assess the disease's severity, predict mortality, and evaluate whether the proper ventricular function is reliable. Troponin is a valuable adjunct that is an independent and strong predictor of overall mortality in patients with COPD.

Persistent iatrogenic atrial septal defect after cryoballoon ablation for atrial fibrillation

Aims: Pulmonary vein isolation (PVI) by cryoballoon ablation (CB) technology is effective and safe treatment option for atrial fibrillation (AF). CB is performed by large diameter, 15Fr (4.95mm) transseptal sheath that may lead to creation of iatrogenic atrial septal defect (iASD). The objective of this study was to assess the incidence of iASD in patients who had undergone CB. Methods: Patients with AF having undergone Arctic Front® CB ablation and a subsequent transesophageal echocardiography (TEE) examination during post-ablation follow up period were consecutively enrolled. During all CB procedures, 15Fr transseptal sheath (Flex Cath, Medtronic, Minneapolis, MN) was utilized via single transseptal puncture (TsP). Results: Twenty-eight patients (15 females, mean age 55.8+15.5) with paroxysmal (n=24) or persistent (n=4) AF formed study group. iASD was present 11 (39.3%) of them after mean follow-up time of 17.3+6.2 months. The procedural time is significantly longer in patient with iASD (119.0+8.8 minutes, p=0.01). No patients died or suffered from any clinically significant cerebral ischemic event. There was no sign of increase in systolic pulmonary arterial pressure (sPAP). Conclusion: iASD after CB was found to be present in 39.3% of patient during a mean follow-up time of 17.3+6.2 months. The prolonged CB procedural time was the only factor that predicted iASD in our study. No adverse clinic events that might be related to iASD was observed during follow-up period.

GLI1+ Cells Contribute to Vascular Remodeling in Pulmonary Hypertension.

The precise origin of newly formed ACTA2+ (alpha smooth muscle actin-positive) cells appearing in nonmuscularized vessels in the context of pulmonary hypertension is still debatable although it is believed that they predominantly derive from preexisting vascular smooth muscle cells (VSMCs). Gli1Cre-ERT2; tdTomatoflox mice were used to lineage trace GLI1+ (glioma-associated oncogene homolog 1-positive) cells in the context of pulmonary hypertension using 2 independent models of vascular remodeling and reverse remodeling: hypoxia and cigarette smoke exposure. Hemodynamic measurements, right ventricular hypertrophy assessment, flow cytometry, and histological analysis of thick lung sections followed by state-of-the-art 3-dimensional reconstruction and quantification using Imaris software were used to investigate the contribution of GLI1+ cells to neomuscularization of the pulmonary vasculature. The data show that GLI1+ cells are abundant around distal, nonmuscularized vessels during steady state, and this lineage contributes to around 50% of newly formed ACTA2+ cells around these normally nonmuscularized vessels. During reverse remodeling, cells derived from the GLI1+ lineage are largely cleared in parallel to the reversal of muscularization. Partial ablation of GLI1+ cells greatly prevented vascular remodeling in response to hypoxia and attenuated the increase in right ventricular systolic pressure and right heart hypertrophy. Single-cell RNA sequencing on sorted lineage-labeled GLI1+ cells revealed an Acta2high fraction of cells with pathways in cancer and MAPK signaling as potential players in reprogramming these cells during vascular remodeling. Analysis of human lung-derived material suggests that GLI1 signaling is overactivated in both group 1 and group 3 pulmonary hypertension and can promote proliferation and myogenic differentiation. Our data highlight GLI1+ cells as an alternative cellular source of VSMCs in pulmonary hypertension and suggest that these cells and the associated signaling pathways represent an important therapeutic target for further studies.

A mathematical model to assess the effects of COVID-19 on the cardiocirculatory system

Impaired cardiac function has been described as a frequent complication of COVID-19-related pneumonia. To investigate possible underlying mechanisms, we represented the cardiovascular system by means of a lumped-parameter 0D mathematical model. The model was calibrated using clinical data, recorded in 58 patients hospitalized for COVID-19-related pneumonia, to make it patient-specific and to compute model outputs of clinical interest related to the cardiocirculatory system. We assessed, for each patient with a successful calibration, the statistical reliability of model outputs estimating the uncertainty intervals. Then, we performed a statistical analysis to compare healthy ranges and mean values (over patients) of reliable model outputs to determine which were significantly altered in COVID-19-related pneumonia. Our results showed significant increases in right ventricular systolic pressure, diastolic and mean pulmonary arterial pressure, and capillary wedge pressure. Instead, physical quantities related to the systemic circulation were not significantly altered. Remarkably, statistical analyses made on raw clinical data, without the support of a mathematical model, were unable to detect the effects of COVID-19-related pneumonia in pulmonary circulation, thus suggesting that the use of a calibrated 0D mathematical model to describe the cardiocirculatory system is an effective tool to investigate the impairments of the cardiocirculatory system associated with COVID-19.

Effects of fecal microbiota transfer on blood pressure in animal models: A systematic review and meta-analysis.

Numerous recent studies have found a strong correlation between intestinal flora and the occurrence of hypertension. However, it remains unclear whether fecal microbiota transfer might affect the blood pressure of the host. This study aimed to quantify both associations. An electronic search was conducted in PubMed, EMBASE, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), WanFang database, Weipu, Embase, and SinoMed to retrieve relevant studies. The final search was completed on August 22, 2022. Two authors independently applied the inclusion criteria, extracted data, and assessed the risk of bias assessment. All data were analyzed using RevMan 5.4. A total of 5 articles were selected for final inclusion. All studies were assessed as having a high risk of bias according to the SYRCLE risk of bias tool. The meta-analysis results showed that transplantation of fecal bacteria from the hypertensive model can significantly improve the host's systolic pressure (MD = 18.37, 95%CI: 9.74~26.99, P<0.001), and diastolic pressure (MD = 17.65, 95%CI: 12.37~22.93, P<0.001). Subgroup analyses revealed that the increase in systolic pressure in the hypertension model subgroup (MD = 29.56, 95%CI = 23.55-35.58, P<0.001) was more pronounced than that in the normotensive model subgroup (MD = 12.48, 95%CI = 3.51-21.45, P<0.001). This meta-analysis suggests a relationship between gut microbiota dysbiosis and increased blood pressure, where transplantation of fecal bacteria from the hypertensive model can cause a significant increase in systolic pressure and diastolic pressure in animal models.

Usefulness of cardiopulmonary exercise test combined with exercise stress echocardiography in mild chronic thromboembolic pulmonary disease.

Chronic thromboembolic pulmonary disease (CTEPD) can lead to exercise limitations even without right ventricular (RV) dysfunction or pulmonary hypertension at rest. Combining exercise stress echocardiography with cardiopulmonary exercise testing (ESE-CPET) for RV function and pressure changes combined measuring overall function may be useful for CTEPD evaluation. This study aims to investigate CPET and ESE results to elucidate the mechanisms of exercise limitation in mild CTEPD cases. Among our CTEPD registry, 50 patients who performed both right heart catheterization data of mild disease (less than 30mm Hg of mean pulmonary arterial pressure (mPAP)) and ESE-CPET were enrolled.Echocardiography and CPET-derived parameters were compared with hemodynamic parameters measured through right heart catheterization. Peak VO2 (maximal oxygen consumption) was decreased in overall population (71.3±16.3% of predictive value). Peak VO2 during exercise was negatively correlate with mPAP and pulmonary vascular resistance at rest. A substantial increase in RV systolic pressure (RVSP) was observed during exercise (RVSP: pre-exercise 37.2±11.8mm Hg, postexercise 64.3±24.9mm Hg, p-value<.001). Furthermore, RV function deteriorated during exercise when compared to the baseline (RV fractional area change: 31.5±10.0% to 37.8±7.0%, p-value<.001; RV global longitudinal strain: -17.1±4.2% to -17.7±3.3%, p-value<.001) even though basal RV function was normal. While an excessive increase in RVSP during exercise was noticed in both groups, dilated RV and RV dysfunction during exercise were demonstrated only in the impaired exercise capacity group. CTEPD patients with mild PH or without PH exhibited limited exercise capacity alongside an excessive increase in RVSP during exercise. Importantly, RV dysfunction during exercise was significantly associated with exercise capacity. ESE-CPET could aid in comprehending the primary cause of exercise limitation in these patients.

The Role of Rosmarinic Acid in the Protection Against Inflammatory Factors in Rats Model With Monocrotaline-Induced Pulmonary Hypertension: Investigating the Signaling Pathway of NFκB, OPG, Runx2, and P-Selectin in Heart.

Shortness of breath and syncope are common symptoms of right ventricular failure caused by pulmonary arterial hypertension (PAH), which is the result of blockage and increased pressure in the pulmonary arteries. There is a significant amount of evidence supporting the idea that inflammation and vascular calcification (VC) are important factors in PAH pathogenesis. Therefore, we aimed to investigate the features of the inflammatory process and gene expression involved in VC in monocrotaline (MCT)-induced PAH rats. MCT (60 mg/kg, i.p.) was used to induce PAH. Animals were given normal saline or rosmarinic acid (RA) (10, 15, and 30 mg/kg, gavage) for 21 days. An increase in right ventricular systolic pressure was evaluated as confirming PAH. To determine the level of inflammation in lung tissue, pulmonary edema and the total and differential white blood cell counts in the bronchoalveolar lavage fluid were measured. Also, the expression of NFκB, OPG, Runx2, and P-selectin genes was investigated to evaluate the level of VC in the heart. Our experiment showed that RA significantly decreased right ventricular hypertrophy, inflammatory factors, NFκB, Runx2, and P-selectin gene expression, pulmonary edema, total and differential white blood cell count, and increased OPG gene expression. Therefore, our research showed that RA protects against MCT-induced PAH by reducing inflammation and VC in rats.

Dynamics of Right Ventricle Pressure During Stress Echocardiography in Patients with Heart Failure with Preserved Ejection Fraction

Shortness of breath during physical exertion is a non-specific symptom that can hide such potentially dangerous diseases as structural or functional bronchopulmonary, coronary heart disease, structural cardiac disease, but the frequent cause is left ventricle diastolic dysfunction due to its significant hypertrophy. Pathogenetic mechanisms leading to this symptom require detailed study for the possibility of a comprehensive approach in the treatment of such patients with the aim of maximally improving their prognosis and quality of life. Objective — evaluate changes in right ventricle systolic pressure during stress echocardiography in patients with LV myocardial hypertrophy and clinical manifestations of heart failure, search for other mechanisms leading to clinical symptoms. Materials and methods. The study included 49 patients with shortness of breath during physical exertion, who underwent further diagnostic examination after exclusion of coronary stenotic lesions by invasive coronary and ventricular angiography. Patients were excluded from bronchopulmonary pathology using spirometry and chest radiography, structural heart pathology using echocardiography, microvascular angina using echocardiography with intravenous dipyridamole infusion, and the change in systolic pressure in the right ventricle was investigated using echocardiography during a physical exercise test. Results and discussion. There were no cases of infiltrative lung changes, signs of emphysema, or other manifestations of significant pathology according to X-ray data. Spirometry also showed the absence of significant functional abnormalities. Echocardiography revealed significant hypertrophy of LV myocar­dium (thickness of IVS — on average (14.1 ± 0.5) mm, posterior wall thickness — on average (13.5 ± 0.3) mm) with the presence of LV diastolic dysfunction and echocardiographic signs of increased end-diastolic pressure in the LV, which was confirmed invasively during coronary and ventricular angiography. In 9 (18.4 %) cases, heart wall thickening was due to hypertrophic cardiomyopathy according to cardiac MRI, these patients had LV outflow tract obstruction and mild pulmonary hypertension at rest. Conducting strain imaging showed the presence of signs of myocardial ischemia (segmental contractility disorder) with varying degrees of severity (from 1 to 5 segments), which spread to the IVS, the apex of the heart and, less often, to the anterior wall of the LV. All patients experienced an increase in pulmonary artery systolic pressure during exercise, on average, from (37.4 ± 2.1) to (47.1 ± 1.6) mm Hg. Conclusions. The pathogenic mechanism underlying shortness of breath in patients with LV myocardial hypertrophy involves transient pulmonary hypertension occurring during exercise due to left ventricular diastolic dysfunction. Another contributing factor is the development of myocardial ischemia during physical exertion, which, in the absence of coronary stenosis and microvascular angina, is attributed to inadequate supply of coronary blood flow volume velocity relative to the significant left ventricular hypertrophy.

The Combination of Pakcoy Juice (Brassica Rapa L.) and Antihypertensive Medication in Reducing Blood Pressure in Pregnant Women with Hypertension

Hypertension in pregnant women ranks as the second highest cause of Chronic Kidney Disease (CKD). Hypertension is defined as a minimum diastolic blood pressure of 90 mmHg and a minimum systolic blood pressure of 140 mmHg, with an increase in diastolic and systolic pressure of at least 15 mmHg and 30 mmHg, respectively. This study aims to evaluate the impact of a combination of Pakcoy juice (Brassica rapa L) and antihypertensive medication on blood pressure in pregnant women with hypertension.Using a quasi-experimental design with a One Group Pre-Test – Post-Test without a control group, the study involved 14 pregnant women with hypertension at the Gunung Sugih Community Health Center from January to June 2023 as the population. The results of data analysis indicate a significant influence (p value 0.000 &lt; α: 0.05) on the reduction of blood pressure after the administration of antihypertensive medication and Pakcoy juice.The discussion emphasizes that Pakcoy juice is effective as a supplement to antihypertensive medication due to its natural content of potassium, calcium, and magnesium, which can reduce blood pressure. Consuming 4,700 milligrams of potassium per day is known to lower blood pressure caused by high sodium intake. In conclusion, the combination of Pakcoy juice and antihypertensive medication has a positive effect of 19% on reducing blood pressure in pregnant women with hypertension at the Gunung Sugih Community Health Center, with a recommendation for health education outreach to prevent hypertension cases in pregnant women.

Prognostic value of blood pressure in the acute period of hemispheric ischemic stroke

Aim. To study changes in blood pressure (BP) in patients with acute hemispheric ischemic stroke (AIS), to correlate BP in patients with AIS with BP in patients with chronic brain ischemia, and to study the association of various BP indices with stroke severity and recovery.Material and methods. We included 235 patients with hemispheric AIS (age 64±11 years; women, 41,3%). BP was assessed 6 times as follows: by patient’s self-measurement during the month before the stroke onset, in the ambulance, in the admission department, in the intensive care unit using 24-hour blood pressure monitoring (BPM), in the neurologic department (BPM), and 90 days after stroke. In patients with chronic cerebral ischemia (178 patients, age 62±13 years, 46,1% women), BP was assessed 3 times: by patient’s self-measurement during the month before hospitalization, in the admission department, and in the neurologic department (BPM).Results. Patients with AIS within the month before stroke had higher systolic and pulse pressure than patients with chronic cerebral ischemia. During the acute stroke period, patients with AIS despite reaching target systolic and diastolic BP had significantly increased variability of systolic and diastolic BP compared to patients with chronic brain ischemia. Systolic BP ≥160 mm Hg recorded consecutively in ambulance, in admission department, and in intensive care unit, as well as pulse pressure ≥60 mm Hg, and systolic BP variability ≥18 mm Hg recorded on day 1-2 and day 9-10, positively correlated with National Institute of Health Stroke Scale (NIHSS) score (r≥0,37, p≤0,0017) on day 10 and with modified Rankin Scale (mRS) score (r≥0,29, p≤0,006) on day 90.Conclusion. Patients with hemispheric AIS had significantly higher systolic BP and pulse pressure within the month before stroke. During the first 10 days of AIS persistent increase in systolic, diastolic, and pulse pressure, and BP variability was associated with more severe stroke and less favorable outcome. These results should be taken into account when administering antihypertensive treatment.

Acute changes in cardiac dimensions, function, and longitudinal mechanics in healthy individuals with and without high-altitude induced pulmonary hypertension at 4559m.

High-altitude pulmonary hypertension (HAPH) has a prevalence of approximately 10%. Changes in cardiac morphology and function at high altitude, compared to a population that does not develop HAPH are scarce. Four hundred twenty-one subjects were screened in a hypoxic chamber inspiring a FiO2 =12% for 2h. In 33 subjects an exaggerated increase in systolic pulmonary artery pressure (sPAP) could be confirmed in two independent measurements. Twenty nine of these, and further 24 matched subjects without sPAP increase were examined at 4559m by Doppler echocardiography including global longitudinal strain (GLS). SPAP increase was higher in HAPH subjects (∆=10.2vs. ∆=32.0mm Hg, p<.001). LV eccentricity index (∆=.15vs. ∆=.31, p=.009) increased more in HAPH. D-shaped LV (0 [0%] vs. 30 [93.8%], p=.00001) could be observed only in the HAPH group, and only in those with a sPAP ≥50mm Hg. LV-EF (∆=4.5vs. ∆=6.7%, p=.24) increased in both groups. LV-GLS (∆=1.2vs. ∆=1.1 -%, p=.60) increased slightly. RV end-diastolic (∆=2.20vs. ∆=2.7cm2 , p=.36) and end-systolic area (∆=2.1vs. ∆=2.7cm2 , p=.39), as well as RA end-systolic area index (∆=-.9vs. ∆=.3cm2 /m2 , p=.01) increased, RV-FAC (∆=-2.9vs. ∆=-4.7%, p=.43) decreased, this was more pronounced in HAPH, RV-GLS (∆=1.6vs. ∆=-.7 -%, p=.17) showed marginal changes. LV and LA dimensions decrease and left ventricular function increases at high-altitude in subjects with and without HAPH. RV and RA dimensions increase, and RV longitudinal strain increases or remains unchanged in subjects with HAPH. Changes are negligible in those without HAPH.

Functional Roles of CD26/DPP4 in Bleomycin-Induced Pulmonary Hypertension Associated with Interstitial Lung Disease.

Pulmonary hypertension (PH) with interstitial lung diseases (ILDs) often causes intractable conditions. CD26/Dipeptidyl peptidase-4 (DPP4) is expressed in lung constituent cells and may be related to the pathogenesis of various respiratory diseases. We aimed to clarify the functional roles of CD26/DPP4 in PH-ILD, paying particular attention to vascular smooth muscle cells (SMCs). Dpp4 knockout (Dpp4KO) and wild type (WT) mice were administered bleomycin (BLM) intraperitoneally to establish a PH-ILD model. The BLM-induced increase in the right ventricular systolic pressure and the right ventricular hypertrophy observed in WT mice were attenuated in Dpp4KO mice. The BLM-induced vascular muscularization in small pulmonary vessels in Dpp4KO mice was milder than that in WT mice. The viability of TGFβ-stimulated human pulmonary artery SMCs (hPASMCs) was lowered due to the DPP4 knockdown with small interfering RNA. According to the results of the transcriptome analysis, upregulated genes in hPASMCs with TGFβ treatment were related to pulmonary vascular SMC proliferation via the Notch, PI3K-Akt, and NFκB signaling pathways. Additionally, DPP4 knockdown in hPASMCs inhibited the pathways upregulated by TGFβ treatment. These results suggest that genetic deficiency of Dpp4 protects against BLM-induced PH-ILD by alleviating vascular remodeling, potentially through the exertion of an antiproliferative effect via inhibition of the TGFβ-related pathways in PASMCs.

Показатели суточного мониторинга артериального давления у лиц старческого возраста c хронической сердечной недостаточностью в зависимости от жесткости сосудов

INTRODUCTION: Measurement of arterial pressure (AP) is a standard method for assessing the risk of developing cardiovascular diseases. Analysis of systolic and diastolic pressure, as well as their ratio, can help determine the risk of developing cardiovascular diseases. One of the ways to diagnose elevatedarterial pressure is daily monitoring of arterial pressure (DMAP). An increase in AP in the elderly is usually associated with an increase in the stiffness of the vascular walls. This leads to an increase in systolic arterial pressure (SAP) and pulse pressure (PP), as well as a decrease in diastolic arterial pressure (DAP). Elevated arterial pressure enhances the load on the heart and can lead to its pathological alterations. A decrease in DAP impairs the blood supply to the heart, which can cause ischemia and fibrosis; the result isdevelopment of diastolic dysfunction, which is the main cause of chronic heart failure (CHF). Currently, a promising way to determine the arterial stiffness is measurement of a cardio-ankle vascular index.The prognostic and diagnostic value of this parameter has been confirmed by numerous studies. It is important to study the parameters of the daily AP profile and arterial stiffness in older patients with CHF. This permits to identify malignant forms of elevated blood pressure, which can lead to cardiovascular complications. AIM: To study the characteristics of the parameters of the daily arterial pressure profile in elderly patients with CHF, depending on the vascular stiffness determined by volume sphygmography. MATERIALS AND METHODS: One hundred and twenty elderly patients with CHF undergoing treatment in a cardiology hospital were examined. By the method of volume sphygmography, the patients were divided into groups with ‘vessels of normal stiffness’ (group 1) and ‘stiff vessels’ (group 2), with subsequentDMAP. A statistical analysis of the parameters of the daily AP profile in the groups was performed. RESULTS: In patients of group 1, both daytime and nighttime SAP, DAP and PP, were significantly higher than in patients of group 2. Besides, in group 1, there was a nighttime decrease in SAP and DAP, while the morning rise of SAP was statistically higher in group 2, and no differences were recorded between the groups in the morning rise of DAP. When assessing the ankle-brachial index in patients of group 2, daytime and nighttime SAP and DAP were statistically higher. In group 1 (with probable peripheral atherosclerosis), PP was higher both during the day and at night. The nocturnal decrease in SAP was statistically higher in group 2, while the nocturnal decrease in DAP prevailed in group 1. The morning rise of SAP and DAP was higher in group 1. CONCLUSION: The DMAP data may indicate to some extent the severity of hypertension in patients with CHF, and this probably depends on the ‘stiffness of the vessels’. In elderly patients with CHF with ‘normal stiffness’ of vessels, the parameters of the daily arterial pressure profile were higher than in patients with ‘stiff vessels’. However, the daily range of parameters of the daily arterial pressure profile was greater in the group of patients with ‘stiff vessels’ (group 2).

Echocardiographic assessment of left ventricular myocardial strain, as a non-invasive method for diagnosing pulmonary hypertension in patients with end-stage chronic kidney disease

Background. Pulmonary hypertension is a common complication of chronic kidney disease, with incidence of up to 50%. Currently, the prognostic significance of non-invasive diagnostic methods for pulmonary hypertension in patients with chronic kidney disease remains relevant.Aim. To determine the significance of transthoracic echocardiography in diagnosing pulmonary hypertension in patients with end-stage chronic kidney disease.Material and methods. The study group consisted of 53 patients with chronic kidney disease stage 5D who were evaluated for kidney transplantation at the N.V. Sklifosovsky Research Institute for Emergency Medicine in 2022. A control group was represented by 24 healthy volunteers. Transthoracic echocardiography was performed on all patients according to a standard protocol, with determination of left ventricular myocardial strain indices.Results. A statistically significant correlation was found between the left ventricular global longitudinal strain and pulmonary artery systolic pressure r=0.488 (p&lt;0.001), as well as between the left ventricular global circumferential strain and pulmonary artery systolic pressure (r=0.545, p&lt;0.001). Regression analysis showed that an increase in pulmonary artery systolic pressure by 1 mmHg increased the odds of lethal outcome by 13% (Odds ratio: 1.13; 95% Confidence interval: [1.05;1.22], p=0.002).Conclusions. Hemodialysis patients are characterized by the development of pre-capillary pulmonary hypertension, which significantly affects their prognosis. Determination of left ventricular myocardial strain indices based on echocardiography provides additional information on the hemodynamics of the pulmonary circulation without using invasive diagnostic methods.

Exaggerated Systolic Blood Pressure Increase with Exercise and Myocardial Ischemia on Exercise Stress Echocardiography.

Central Illustration : Exaggerated Systolic Blood Pressure Increase with Exercise and Myocardial Ischemia on Exercise Stress Echocardiography ESBPRE: exaggerated systolic blood pressure response to exercise; HR: heart rate; SBP: systolic blood pressure. The association between exaggerated systolic blood pressure response to exercise (ESBPRE) and myocardial ischemia is controversial and little studied in patients with established or suspected chronic coronary syndrome. To verify the relationship between myocardial ischemia and ESBPRE in patients undergoing exercise stress echocardiography (ESE). This is a cross-sectional study with 14,367 patients undergoing ESE, from January 2000 to January 2022, divided into the following 2 groups: G1, composed of patients whose peak systolic pressure increased ≥ 90 mmHg (value corresponding to the 95th percentile of the study population), and G2, patients who did not demonstrate an exaggerated hypertensive response. The groups were compared using Student's t and chi-square tests. P values < 0.05 were considered significant. Logistic regression was also performed to identify independent risk factors for myocardial ischemia, ESBPRE, complaints of typical chest pain prior to the exam, and angina during the test. Of the 14,367 patients, 1,500 (10.4%) developed ESBPRE, and 7,471 (52.0%) were female. The percentages of previous complaints of typical chest pain, angina during the test, and myocardial ischemia in patients with ESBPRE were 5.8%, 2.4% and 18.1%, compared to 7.4%, 3.9%, and 24.2%, in patients without ESBPRE, respectively (p = 0.021,p = 0.004, p < 0.001). In multivariate analysis, ESBPRE was independently associated with a lower probability of myocardial ischemia (odds ratio: 0.73; 95% confidence interval: 0.58 to 0.93; p = 0.009). Exaggerated increase in systolic blood pressure during ESE may be a marker for excluding myocardial ischemia.

Baicalin attenuates pulmonary vascular remodeling by inhibiting calpain-1 mediated endothelial-to-mesenchymal transition

BackgroundPrevious studies have demonstrated the beneficial effect of baicalin on pulmonary arterial hypertension (PAH), but the mechanism is unclear. AimThe aim of the present study was to evaluate the effect of baicalin on pulmonary vascular remodeling (PVR) with a focus on calpain-1-mediated endothelial-to-mesenchymal transition (EndMT). MethodsPAH was induced by intraperitoneal injection of monocrotaline (MCT) in rats and hypoxia in calpain-1 gene knockout (Capn1−/−) and wild-type C57BL/6 mice. An in vitro PVR model was established in PASMCs and HPAECs. ResultsThe data showed that baicalin treatment and calpain-1 inhibition alleviated MCT and hypoxia-induced increases in right ventricular systolic pressure (RVSP), prevented right ventricle hypertrophy and PVR, and attenuated cardiopulmonary fibrosis. Moreover, baicalin ameliorated PAH-induced EndMT, as evidenced by the suppressed expression of mesenchymal markers vimentin, and α-SMA and restored expression of endothelial markers CD31, and VE-cadherin. In vitro studies showed that baicalin treatment blocked TGF-β1-induced EndMT in HPAECs and abolished hypoxia-induced PASMC proliferation and migration. All the beneficial effects of baicalin on PVR in vitro and in vivo were accompanied by suppressed calpain-1 expression. Further study demonstrated that baicalin treatment and calpain-1 inhibition inhibited the enhanced expression of PI3K and p-AKT both in vitro and in vivo. ConclusionsIn conclusion, baicalin treatment attenuates PVR by inhibiting calpain-1 and PI3K/Akt-mediated EndMT.

Реакція на дозовану гіпоксію у жінок, що перебували у стані хронічного стресу, зумовленого війною

Military stress has a traumatic effect on mental and physical health, and disrupts the adaptive capabilities of the body, in particular, its ability to adequately respond to hypoxia. However, the specifics of the reaction of the cardiorespiratory system to dosed hypoxia in individuals who experiencing warrelated chronic stress (WRCS) have not yet been elucidated. The peculiarities of the reaction of the cardiorespiratory system to dosed hypoxia in women experiencing WRCS were clarified. It was shown that during breathing of atmospheric air, the blood saturation level, lung ventilation indicators, and hemodynamics did not differ significantly between women exposed to WRCS and those not exposed to it. However, during a controlled hypoxic test (breathing a gas mixture with 12% oxygen for 20 min), women experiencing WRCS experienced a more significant decrease in blood saturation, indicating a lower tolerance to hypoxia. This is also evidenced by a reduced lung ventilation response to controlled hypoxia in the WRCS group, where the increase in ventilation primarily occurred due to an elevation in breathing rate rather than tidal volume. At the same time, the hemodynamic response to hypoxia in women with WRCS was characterized by a more substantial increase in heart rate and systolic arterial pressure. Thus, it was established that in women who were in the state of HCV, the body’s resistance to the effects of hypoxia decreases. At the same time, in conditions of hypoxia, the nature of their breathing changes, and the compensatory growth of pulmonary ventilation decreases, but the growth of hemodynamic indicators increases.

Right ventricular diastolic adaptation to pressure overload in different rat strains

Abstract Background Different rat strains are used in various animal models of pulmonary hypertension and right ventricular (RV) failure. No systematic assessment has been performed to test differences in RV response to pressure overload between rat strains. Purpose We compared RV adaptation to pulmonary trunk banding (PTB) in Wistar, Sprague Dawley, and Fischer344 rats by hemodynamic profiling focusing on diastolic function. Methods Age-matched male rat weanlings were randomized to sham operation (Wistar sham, n=5; Sprague Dawley sham, n=4; Fischer344 sham, n=4) or PTB (Wistar PTB, n=8; Sprague Dawley PTB, n=8; Fischer344 PTB, n=8). RV function was evaluated after five weeks by echocardiography, cardiac MRI, and invasive pressure-volume measurements and RV remodelling assessed by histological analyses. Results At end of study, Fischer344 rats weighed 25 % less than Wistar and Sprague Dawley rats. PTB increased RV systolic pressures four-fold, and RV failure was evident by a decrease in cardiac index (Wistar PTB: 1.8±0.2 mL/s/m2 vs. Wistar sham: 3.9±0.2 mL/s/m2, p&amp;lt;0.0001; Sprague Dawley PTB: 1.7±0.1 mL/s/m2 vs. Sprague Dawley sham: 3.0±0.3 mL/s/m2, p=0.0029; Fischer344 PTB: 2.1±0.2 mL/s/m2 vs. Fischer344 sham: 3.8±0.3 mL/s/m2, p&amp;lt;0.0001). There was a 2.4-fold increase in RV end-systolic volume index in Wistar PTB and Sprague Dawley PTB compared with sham, while Fischer344 PTB rats were less affected with only a 2.0-fold increase in RV end-systolic volume index compared with Fischer344 sham. Diastolic and right atrial impairment were evident by increased end-diastolic elastance, filling pressure, and E/e’ in PTB rats compared with sham, again Fischer344 PTB the least affected. PTB increased RV fibrosis in all groups compared with sham, though Fischer344 PTB showed a trend towards a smaller increase in RV fibrosis (Fischer344 PTB: 9.2±0.4 % vs Wistar PTB: 10.7±0.2 %, p=0.0919). Conclusions PTB caused RV failure in all rats subjected to the procedure including signs of diastolic dysfunction. Despite similar increase in RV systolic pressure, Fischer344 PTB rats showed less RV dilatation and where more able to sustain diastolic function compared with Wistar and Sprague Dawley PTB rats. All three rat strains are suitable for PTB and studies of RV failure.

Abstract 16194: Relationship Between Change in Global Longitudinal Strain and Sustained Handgrip Induced Afterload as Assessed Using Invasive Left Ventricular Pressure Measurements and Machine Learning Analytics

Introduction: Global longitudinal strain (GLS) is a sensitive, quantitative measure of left ventricular (LV) systolic function and affected by afterload. We sought to compute the impact of LV systolic pressure (LVP) increase on GLS using handgrip stress during invasive LVP measurements. Methods: Patients undergoing left heart catheterization (n=51; mean age 64+/-11 years; 31% women; Table) for standard of care indications underwent echocardiography during handgrip stress with a catheter in the LV cavity. GLS and LVP were measured simultaneously over 15 seconds of continuous handgrip. GLS and LVP relationships were analyzed using linear regression and machine learning methods. Results: Sustained handgrip (HG) stress significantly increased LVP and reduced GLS. There was no significant correlation between resting and peak HG stress LVP and GLS (p= 0.32 &amp; 0.36, respectively). However, change in GLS was significantly correlated with change in LVP (p&lt;0.0001; Figure) with every 10 unit increase in LVP associated with a 0.6 reduction in GLS. The penalized maximum likelihood machine learning method was used to select key factors associated with the within subject slope of % change in GLS over % change in LVP (median slope -0.53; IQR-0.91 to -0.29). LV ejection fraction was identified as an important predictor of the GLS-LVP slope. LV ejection fraction was significantly associated with the slope (p=0.0005; Figure) with a 10 unit increase in LV ejection fraction corresponding to 0.22 increase in the slope. Conclusions: LV afterload is associated with significant decrements in GLS. LV ejection fraction is an important predictor of the GLS-LVP slope. These data provide the foundation to build models that would account for change in LVP during serial measurements of GLS thus allowing reliable comparison of repeated GLS measurements.

Tumor Necrosis Factor-α-Induced Protein-8-like 2 Transfected Adipose-Derived Stem Cells Regulated the Dysfunction of Monocrotaline Pyrrole-Induced Pulmonary Arterial Smooth Muscle Cells and Pulmonary Arterial Endothelial Cells.

Pulmonary arterial hypertension (PAH) is characterized by pulmonary arterial endothelial cell (PAEC) dysfunction and pulmonary arterial smooth muscle cell (PASMC) activation. For decades, the therapies for PAH based on stem cells have been shown to be effective. Meanwhile, tumor necrosis factor-α-induced protein-8-like 2 (TIPE2) promote the viability of human amniotic mesenchymal stem cells. Therefore, we aimed to explore the role of TIPE2 in adipose-derived stem cells (ADSCs) and the function of TIPE2-transfected ADSCs in the regulation of PAH. We first explored the role and underlying molecular mechanism of TIPE2 in viability and migration of ADSCs. Moreover, the ADSCs transfected with TIPE2 were cocultured with monocrotaline pyrrole (MCTP)-stimulated PASMCs or PAECs. The effects and mechanisms of TIPE2-transfected ADSCs on MCTP-induced PASMCs and PAECs were further investigated. The results showed that TIPE2 overexpression promoted viability and migration of ADSCs by activating the TLR4-ERK1/2 pathway. In addition, TIPE2-transfected ADSCs inhibited the abnormal proliferation and the impaired apoptosis of PASMCs via NF-κB signaling and promoted the conversion of PASMCs from synthetic to contractile. Meanwhile, TIPE2-transfected ADSCs reduced the apoptosis, endothelial-to-mesenchymal transition, and migration of PAECs via PI3K/AKT signaling after MCTP treatment. MCTP-induced oxidative stress and inflammation of PAECs were significantly decreased by TIPE2-transfected ADSCs. In rat model, TIPE2-ADSCs administration further decreased the monocrotaline-induced increase in the right ventricular systolic pressure and ratio of right ventricle weight/left ventricle and septa weight (L + S) and right ventricle weight/body weight compared with the ADSCs group. In conclusion, TIPE2-transfected ADSCs dramatically attenuated the PAH via inhibiting the dysfunction of PASMCs and PAECs.