Browsing by Author "Dobric, Milan (23484928600)"

Background and Objectives: ACS presents an acute manifestation of coronary artery disease and its treatment is based on timely interventional diagnostics and PCI. It has been known that the treatment and the outcomes are not the same for all the patients with ACS during the working day, depending on the availability of the procedures and staff. The aim of the study was to explore the differences in clinical characteristics and outcomes in patients admitted for ACS during on- and off-hours. Materials and Methods: The retrospective study included 1873 consecutive ACS patients admitted to a tertiary, university hospital that underwent coronary angiography and intervention. On-hours were defined from Monday to Friday from 07:30 h to 14:30 h, while the rest was considered off-hours. Results: There were more males in the off-hours group (on-hours 475 (56%) vs. off-hours 635 (62%); p = 0.011), while previous MI was more frequent in the on-hours group (on 250 (30%) vs. off 148 (14%); p < 0.001). NSTEMI was more frequent during on-hours (on 164 (19%) vs. off 55 (5%); p < 0.001), while STEMI was more frequent during off-hours (on 585 (69%) vs. off 952 (93%); p < 0.001). Patients admitted during on-hours had more multivessel disease (MVD) (on 485 (57%) vs. off 489 (48%); p = 0.006), as well as multivessel PCI (on 187 (22%) vs. off 171 (16%); p = 0.002), while radial access was preferred in off-hours patients (on 692 (82%) vs. off 883 (86%); p = 0.004). Left main PCI was performed with similar frequency in both groups (on 37 (4%) vs. off 35 (3%); p = 0.203). Death occurred with similar frequency in both groups (on 17 (2.0%) vs. off 26 (2.54%); p = 0.404), while major adverse cardio-cerebral events (MACCEs) were more frequent in the on-hours group (on 105 (12.4%) vs. off 70 (6.8%); p = 0.039) probably due to the more frequent repeated PCI (on 49 (5.8%) vs. off 27 (2.6%); p = 0.035). Conclusions: Patients admitted for ACS during working hours in a tertiary hospital present with more complex CAD, have more demanding interventions, and experience more MACCEs during follow-up mostly due to myocardial infarctions and repeated procedures. © 2023 by the authors.

This study evaluated additive prognostic value of the SYNTAX score over GRACE, TIMI, ZWOLLE, CADILLAC and PAMI risk scores in patients with STsegment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI). All six scores were calculated in 209 consecutive STEMI patients undergoing pPCI. Primary end-point was the major adverse cardiovascular event (MACE-composite of cardiovascular mortality, non-fatal myocardial infarction and stroke); secondary end point was cardiovascular mortality. Patients were stratified according to the SYNTAX score tertiles (≤12; between 12 and 19.5; >19.5). The median follow-up was 20 months. Rates of MACE and cardiovascular mortality were highest in the upper tertile of the SYNTAX score (p<0.001 and p = 0.003, respectively). SYNTAX score was independent multivariable predictor of MACE and cardiovascular mortality when added to GRACE, TIMI, ZWOLLE, and PAMI risk scores. However, the SYNTAX score did not improve the Cox regression models of MACE and cardiovascular mortality when added to the CADILLAC score. The SYNTAX score has predictive value for MACE and cardiovascular mortality in patients with STEMI undergoing primary PCI. Furthermore, SYNTAX score improves prognostic performance of well-established GRACE, TIMI, ZWOLLE and PAMI clinical scores, but not the CADILLAC risk score. Therefore, long-term survival in patients after STEMI depends less on detailed angiographical characterization of coronary lesions, but more on clinical characteristics, myocardial function and basic angiographic findings as provided by the CADILLAC score.

Inflammation plays an important role in all stages of atherosclerosis — from endothelial dysfunction, to formation of fatty streaks and atherosclerotic plaque, and its progression to serious complications, such as atherosclerotic plaque rupture. Although dyslipidemia is a key driver of atherosclerosis, pathogenesis of atherosclerosis is now considered interplay between cholesterol and inflammation, with the significant role of the immune system and immune cells. Despite modern therapeutic approaches in primary and secondary cardiovascular prevention, cardiovascular diseases remain the leading cause of mortality worldwide. In order to reduce residual cardiovascular risk, despite the guidelines-guided optimal medical therapy, novel therapeutic strategies are needed for prevention and management of coronary artery disease. One of the innovative and promising approaches in atherosclerotic cardiovascular disease might be inflammation-targeted therapy. Numerous experimental and clinical studies are seeking into metabolic pathways underlying atherosclerosis, in order to find the most suitable pathway and inflammatory marker/s that should be the target for anti-inflammatory therapy. Many anti-inflammatory drugs have been tested, from the well-known broad range anti-inflammatory agents, such as colchicine, allopurinol and methotrexate, to targeted monoclonal antibodies specifically inhibiting a molecule included in inflammatory pathway, such as canakinumab and tocilizumab. To date, there are no approved anti-inflammatory agents specifically indicated for silencing inflammation in patients with coronary artery disease. The most promising results came from the studies which tested colchicine, and studies where the inflammatory-target was NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome/interleukin-1 beta (IL-1β)/interleukin-6 (IL-6)/C-reactive protein (CRP) pathway. A growing body of evidence, along with the ongoing clinical studies, suggest that the anti-inflammatory therapy might become an additional strategy in treating atherosclerotic cardiovascular disease. Herein we present an overview of the role of inflammation in atherosclerosis, the most important inflammatory markers chosen as targets of anti-inflammatory therapy, along with the critical review of the major clinical trials which tested non-targeted and targeted anti-inflammatory drugs in patients with atherosclerotic cardiovascular disease. © 2023 The Author(s). Published by IMR Press.

Chronic total occlusions (CTO) are frequently encountered during coronary angiography, and are generally regarded as the most challenging coronary lesions for percutaneous coronary intervention (PCI). Despite great technical advancements and greatly improved reported procedural success rates during previous years, data on clinical benefit of these procedures still remain scarce and controversial. Data from observational trials suggested that PCI for CTO could be linked to improvements both in symptoms and hard cardiovascular outcomes, while randomized controlled trials showed symptomatic improvement only, without improvement in patient’s prognosis. This is in parallel with findings for non-CTO PCI in patients with stable angina. Having in mind complexity of these interventions, high costs, greater volume of contrast, and radiation exposure, appropriate patient selection is crucial for optimizing treatment effectiveness. There are few important factors that should be taken into consideration before planning and attempting PCI for CTO. These are: severity of patient’s symptoms despite optimal medical therapy, presence of inducible myocardial ischemia and/or viability in the territory of occluded coronary artery. © The Author(s) 2019.

Background: Retrograde approach increases the success rate for percutaneous recanalization of complex chronic total occlusion (CTO) of coronary arteries. Objectives: The purpose of this study was to describe our initial experience of retrograde percutaneous coronary intervention for CTO program, focusing on its safety and feasibility, and long-term clinical follow-up. Methods: The study was a single center retrospective registry which included a total of 40 patients, of 590 CTO treated patients (6.7%), between January 2008 and October 2011, who underwent retrograde approach for CTO recanalization. Results: Mean occlusion duration was 37.8 ± 40.3 months. Overall success recanalization rate was 87.5% (35/40). Septal collaterals were used to access the occlusion in all cases (100%). Retrograde guidewire crossing of collateral channels was successful in 36/40 (90.0%) patients with success rate of CTO recanalization in these patients of 97.2%. Retrograde approach as the primary strategy was applied in 23/40 (57.5%) patients, retrograde approach immediately after antegrade failure attempt was performed in 8/40 (20.0%) patients, and retrograde approach as elective procedure, after previously failed antegrade attempt, was performed in 9/40 (22.5%) patients. The success rate of these strategies was: 87.0% (20/23 patients) for primary, 87.5% (7/8 patients) for retrograde immediately after antegrade failure, and 88.9% (8/9 patients) for retrograde after previous failed antegrade attempt, respectively. Total in-hospital major adverse cardiac events (MACE) rate was 5.0% (2 non-Q-wave myocardial infarctions). The MACE free survival at median follow-up of 20 months was 89% (95% CI: 78-100%). Conclusions: This study has demonstrated that adequate training and international proctorship for this complex and demanding technique is a necessity and prerequisite to achieve high overall success rates, with acceptable complication rates and excellent long-term survival rate. © 2012, Wiley Periodicals, Inc.

Endothelial cell markers are membrane-bound or cytoplasmic molecules expressed by endothelial cells, which help their easier identification and discrimination from other cell types. During vasculogenesis, endothelial cells differentiate from hemangioblasts to form new blood vessels. With the discovery of endothelial progenitor cells (EPC) and their ability to form new blood vessels, the term vasculogenesis is not only reserved for the embryonic development. Possibility of de novo blood vessel formation from EPC is now widely explored in different ischemic conditions, especially in cardiovascular medicine. Numerous clinical trials have tested enhancing tissue vascularization by delivering hematopoietic cells that expressed endothelial markers. This therapeutic approach proved to be challenging and promising, particularly for patients who have exhausted all conventional therapeutic modalities. Angiogenesis, which refers to the formation of new blood vessels from existing vasculature, is indispensable process during tumor progression and metastasis. Blockage of tumor angiogenesis by targeting and inhibiting endothelial cell has emerged as novel safe and efficacious method to control many advanced malignant diseases. Numerous clinical studies are currently testing new antiangiogenic drugs which target and inhibit endothelial cell markers, receptors or molecules which transmit receptor-mediated signals, therefore inhibiting endothelial cell proliferation, migration and vascular tube formation. Many of these drugs are now widely used in clinical settings as first- or second-line chemotherapy in advanced malignant conditions. So far, these therapeutic approaches gave modest, yet encouraging clinical improvements, prolonging survival and improving functional capacity and quality of life for many terminally ill patients. Here we present the most commonly used endothelial cell markers along with their applicability in contemporary clinical practice. © 2017 Elsevier Inc.

Endothelial cell markers are membrane-bound or cytoplasmic molecules expressed by endothelial cells, which help their easier identification and discrimination from other cell types. During vasculogenesis, endothelial cells differentiate from hemangioblasts to form new blood vessels. With the discovery of endothelial progenitor cells (EPC) and their ability to form new blood vessels, the term vasculogenesis is not only reserved for the embryonic development. Possibility of de novo blood vessel formation from EPC is now widely explored in different ischemic conditions, especially in cardiovascular medicine. Numerous clinical trials have tested enhancing tissue vascularization by delivering hematopoietic cells that expressed endothelial markers. This therapeutic approach proved to be challenging and promising, particularly for patients who have exhausted all conventional therapeutic modalities. Angiogenesis, which refers to the formation of new blood vessels from existing vasculature, is indispensable process during tumor progression and metastasis. Blockage of tumor angiogenesis by targeting and inhibiting endothelial cell has emerged as novel safe and efficacious method to control many advanced malignant diseases. Numerous clinical studies are currently testing new antiangiogenic drugs which target and inhibit endothelial cell markers, receptors or molecules which transmit receptor-mediated signals, therefore inhibiting endothelial cell proliferation, migration and vascular tube formation. Many of these drugs are now widely used in clinical settings as first- or second-line chemotherapy in advanced malignant conditions. So far, these therapeutic approaches gave modest, yet encouraging clinical improvements, prolonging survival and improving functional capacity and quality of life for many terminally ill patients. Here we present the most commonly used endothelial cell markers along with their applicability in contemporary clinical practice. © 2017 Elsevier Inc.

Background: Optimizing patient exposure in interventional cardiology is key to avoid skin injuries. Purpose: To establish predictive models of peak skin dose (PSD) during percutaneous coronary intervention (PCI), chronic total occlusion percutaneous coronary intervention (CTO), and transcatheter aortic valve implantation (TAVI) procedures. Material and Methods: A total of 534 PCI, 219 CTO, and 209 TAVI were collected from 12 hospitals in eight European countries. Independent associations between PSD and clinical and technical dose determinants were examined for those procedures using multivariate statistical analysis. A priori and a posteriori predictive models were built using stepwise multiple linear regressions. A fourfold cross-validation was performed, and models’ performance was evaluated using the root mean square error (RMSE), mean absolute percentage error (MAPE), coefficient of determination (R²), and linear correlation coefficient (r). Results: Multivariate analysis proved technical parameters to overweight clinical complexity indices with PSD mainly affected by fluoroscopy time, tube voltage, tube current, distance to detector, and tube angulation for PCI. For CTO, these were body mass index, tube voltage, and fluoroscopy contribution. For TAVI, these parameters were sex, fluoroscopy time, tube voltage, and cine acquisitions. When benchmarking the predictive models, the correlation coefficients were r = 0.45 for the a priori model and r = 0.89 for the a posteriori model for PCI. These were 0.44 and 0.67, respectively, for the CTO a priori and a posteriori models, and 0.58 and 0.74, respectively, for the TAVI a priori and a posteriori models. Conclusion: A priori predictive models can help operators estimate the PSD before performing the intervention while a posteriori models are more accurate estimates and can be useful in the absence of skin dose mapping solutions © The Foundation Acta Radiologica 2021.

Background: Optimizing patient exposure in interventional cardiology is key to avoid skin injuries. Purpose: To establish predictive models of peak skin dose (PSD) during percutaneous coronary intervention (PCI), chronic total occlusion percutaneous coronary intervention (CTO), and transcatheter aortic valve implantation (TAVI) procedures. Material and Methods: A total of 534 PCI, 219 CTO, and 209 TAVI were collected from 12 hospitals in eight European countries. Independent associations between PSD and clinical and technical dose determinants were examined for those procedures using multivariate statistical analysis. A priori and a posteriori predictive models were built using stepwise multiple linear regressions. A fourfold cross-validation was performed, and models’ performance was evaluated using the root mean square error (RMSE), mean absolute percentage error (MAPE), coefficient of determination (R²), and linear correlation coefficient (r). Results: Multivariate analysis proved technical parameters to overweight clinical complexity indices with PSD mainly affected by fluoroscopy time, tube voltage, tube current, distance to detector, and tube angulation for PCI. For CTO, these were body mass index, tube voltage, and fluoroscopy contribution. For TAVI, these parameters were sex, fluoroscopy time, tube voltage, and cine acquisitions. When benchmarking the predictive models, the correlation coefficients were r = 0.45 for the a priori model and r = 0.89 for the a posteriori model for PCI. These were 0.44 and 0.67, respectively, for the CTO a priori and a posteriori models, and 0.58 and 0.74, respectively, for the TAVI a priori and a posteriori models. Conclusion: A priori predictive models can help operators estimate the PSD before performing the intervention while a posteriori models are more accurate estimates and can be useful in the absence of skin dose mapping solutions © The Foundation Acta Radiologica 2021.

Background: Patients in chronic phase of myocardial infarction (MI) have decreased coronary flow reserve (CFR) in infarct related artery (IRA) that is proportional to the extent of microvascular/myocardial damage. We proposed a novel model for the assessment of microvascular damage and infarct size using Doppler echocardiography evaluation of CFRs of the IRA (LAD) and reference artery (RCA). Methods: Our study included 34 consecutive patients (28 men, mean age 50 ± 11 years) with first anterior STEMI and single vessel disease successfully treated with primary PCI. All patients underwent SPECT MPI for the assessment of infarct size (expressed as a percentage of myocardium with fixed perfusion abnormalities) and CFR evaluation of LAD and RCA. CFR derived percentage of microvascular damage (CFR PMD) was calculated as: CFR PMD = (CFR RCA - CFR LAD) / (CFR RCA - 1) × 100 (%). Results: CFR PMD correlated significantly with all parameters evaluating the severity of myocardial damage including: peak CK activity (r = 0.632, p < 0.001), WMSI (r = 0.857, p < 0.001), ejection fraction (r = - 0.820, p < 0.001), left ventricular end diastolic (r = 0.757, p < 0.001) and end systolic volume (r = 0.794, p < 0.001). Most importantly, CFR PMD (22 ± 17%) correlated significantly with infarct size by SPECT MPI (21 ± 17%) (r = 0.874, p < 0.001). Conclusions: CFR PMD derived from the proposed model was significantly related to echocardiographic and enzymatic parameters of infarct size, as well as to myocardial damage assessed by SPECT MPI in patients with successfully reperfused first anterior STEMI. © 2012 Elsevier Ireland Ltd. All rights reserved.

The natural progression of bioprosthetic valve degeneration over time requires further interventions for those experiencing symptomatic prosthesis dysfunction. Transcatheter aortic valve replacement (TAVR) emerges as a promising therapeutic option to alleviate symptoms in such patients. The valve-in-valve (ViV) technique eliminates the necessity for repetitive open-heart surgical procedures, offering particular advantages for individuals with higher surgical risks. In this report, we describe the case of a 78-year-old female patient presenting with severe symptomatic aortic restenosis of a biological aortic valve implanted 5 years prior. Given the patient’s high surgical risk, a transcatheter ViV implantation was chosen as the treatment approach. Utilizing a balloon-expandable valve, the intervention resulted in the successful implantation of a functional TAVR, resulting in symptom relief and enabling a fast discharge from the hospital. © The authors

Early experimental and clinical reports on glycogen phosphorylase BB (GPBB) kinetics following myocardial ischemic injury suggested that it could be a useful diagnostic marker for early detection of acute myocardial infarction (AMI). After more than two decades of investigation, there is now overwhelming body of evidence that do not support the use of GPBB measurement in diagnosis of acute AMI in patients presenting with acute chest pain. Currently, GPBB cannot be recommended as a diagnostic marker of AMI either as a stand-alone test or as an addition to (high-sensitive) troponin testing. It should be noted that these considerations apply to the early diagnosis of AMI, not to the prognostic stratification, which is also suggested but it warrants further investigation. The aim of this review is to summarize available evidence of GPBB measurement in early diagnosis of myocardial infarction. © 2014 Elsevier B.V.

Early experimental and clinical reports on glycogen phosphorylase BB (GPBB) kinetics following myocardial ischemic injury suggested that it could be a useful diagnostic marker for early detection of acute myocardial infarction (AMI). After more than two decades of investigation, there is now overwhelming body of evidence that do not support the use of GPBB measurement in diagnosis of acute AMI in patients presenting with acute chest pain. Currently, GPBB cannot be recommended as a diagnostic marker of AMI either as a stand-alone test or as an addition to (high-sensitive) troponin testing. It should be noted that these considerations apply to the early diagnosis of AMI, not to the prognostic stratification, which is also suggested but it warrants further investigation. The aim of this review is to summarize available evidence of GPBB measurement in early diagnosis of myocardial infarction. © 2014 Elsevier B.V.

Background: Glycogen phosphorylase BB (GPBB) is released from cardiac cells during myocyte damage. Previous studies have shown contradictory results regarding the relation of enzyme release and reversible myocardial ischemia. The aim of this study was to determine the plasma kinetics of GPBB as a response to the exercise stress echocardiographic test (ESET), and to define the relationship between myocardial ischemia and enzyme plasma concentrations. Methods: We studied 46 consecutive patients undergoing ESET, with recent coronary angiography. In all patients, a submaximal stress echo test according to Bruce protocol was performed. Concentration of GPBB was measured in peripheral blood that was sampled 5 min before and 10, 30 and 60 min after ESET. Results: There was significant increase of GPBB concentration after the test (p = 0.021). Significant increase was detected 30 min (34.9% increase, p = 0.021) and 60 min (34.5% increase, p = 0.016) after ESET. There was no significant effect of myocardial ischemia on GPBB concentrations (p = 0.126), and no significant interaction between sampling intervals and myocardial ischemia, suggesting a similar release profile of GPBB in ischemic and non-ischemic conditions (p = 0.558). Patients in whom ESET was terminated later (stages 4 or 5 of standard Bruce protocol; n = 13) had higher GPBB concentrations than patients who terminated ESET earlier (stages 1, 2 or 3; n = 33) (p = 0.049). Baseline GPBB concentration was not correlated to any of the patients' demographic, clinical and hemodynamic characteristics. Conclusions: GPBB plasma concentration increases after ESET, and it is not related to inducible myocardial ischemia. However, it seems that GPBB release during ESET might be related to exercise load/duration.

Background: Glycogen phosphorylase BB (GPBB) is released from cardiac cells during myocyte damage. Previous studies have shown contradictory results regarding the relation of enzyme release and reversible myocardial ischemia. The aim of this study was to determine the plasma kinetics of GPBB as a response to the exercise stress echocardiographic test (ESET), and to define the relationship between myocardial ischemia and enzyme plasma concentrations. Methods: We studied 46 consecutive patients undergoing ESET, with recent coronary angiography. In all patients, a submaximal stress echo test according to Bruce protocol was performed. Concentration of GPBB was measured in peripheral blood that was sampled 5 min before and 10, 30 and 60 min after ESET. Results: There was significant increase of GPBB concentration after the test (p = 0.021). Significant increase was detected 30 min (34.9% increase, p = 0.021) and 60 min (34.5% increase, p = 0.016) after ESET. There was no significant effect of myocardial ischemia on GPBB concentrations (p = 0.126), and no significant interaction between sampling intervals and myocardial ischemia, suggesting a similar release profile of GPBB in ischemic and non-ischemic conditions (p = 0.558). Patients in whom ESET was terminated later (stages 4 or 5 of standard Bruce protocol; n = 13) had higher GPBB concentrations than patients who terminated ESET earlier (stages 1, 2 or 3; n = 33) (p = 0.049). Baseline GPBB concentration was not correlated to any of the patients' demographic, clinical and hemodynamic characteristics. Conclusions: GPBB plasma concentration increases after ESET, and it is not related to inducible myocardial ischemia. However, it seems that GPBB release during ESET might be related to exercise load/duration.

Background: Microvascular dysfunction (MVD) is associated with adverse prognosis and may account for abnormal stress tests and angina symptoms in women with cardiac syndrome X (CSX). The aim of our study was to assess MVD by coronary flow velocity reserve (CFVR) and left ventricular (LV) contractile function by LV global longitudinal strain (LVGLS) in CSX patients with respect to presence of slow coronary flow (SCF). It was of additional importance to evaluate clinical status of CSX patients using Seattle Angina Questionnaire. Methods and results: Study population included 70 women with CSX (mean age 61 ± 7 years) and 34 age-matched controls. CSX group was stratified into two subgroups depending on SCF presence: CSX-Thrombolysis In Myocardial Infarction (TIMI) 3- normal flow subgroup (n = 38) and CSX-TIMI 2- SCF subgroup (n = 32) as defined by coronary angiography. LVGLS measurements and CFVR of left anterior descending (LAD) and posterior descending (PD) artery were performed. CFVR-LAD and PD were markedly impaired in CSX group compared to controls (2.34 ± 0.25 vs 3.05 ± 0.21, p < 0.001; 2.32 ± 0.24 vs 3.01 ± 0.13, p < 0.001), and furthermore decreased in CSX-TIMI 2 patients. Resting, peak, and ΔLVGLS were all significantly impaired in CSX group compared to controls (for all p < 0.001), and furthermore reduced in CSX-TIMI 2 subgroup. Strongest correlation was found between peak LVGLS and CFVR LAD (r = −0.784, p < 0.001) and PD (r = −0.772, p < 0.001). CSX-TIMI 2 subgroup had more frequent angina symptoms and more impaired quality of life. Conclusions: MVD in CSX patients is demonstrated by reduction in CFVR and LVGLS values. SCF implies more profound impairment of microvascular and LV systolic function along with worse clinical presentation. © 2020 Japanese College of Cardiology

The objective of the study was to evaluate major adverse cardiovascular events (MACE) after successful versus failed percutaneous coronary intervention for chronic total occlusion (PCI-CTO). Limited data are available on long-term clinical follow-up in the treatment of chronic total occlusion (CTO). Between January 2009 and December 2010 PCI-CTO was attempted in 283 consecutive patients with 289 CTO lesions. Procedural success was 62.3% and clinical follow-up covered 83% (235/283) of the study population with a median follow-up of 66 months (range, 59-74). The total incidence of MACE was 57/235 (24.3%), and was significantly higher in the procedural failure group than in the procedural success group (33/87 (37.9%) versus 24/148 (16.2%), P < 0.001). All-cause mortality was significantly lower in patients with successful PCI-CTO compared to failed PCI-CTO (10.8% versus 20.7%, P < 0.05). Also, the rate of cardiovascular death in the procedural failure group (14.9%) was slightly higher than that in the procedural success group (7.4%, P = 0.066). The rate of TVR was statistically higher in the procedural failure group (P < 0.009). Propensity score-adjusted Cox regression showed that procedural success remained a significant predictor of MACE (adjusted HR 0.402; 95% CI 0.196-0.824; P = 0.013). Our study emphasizes the importance of CTO recanalization in improving long-term outcome including all-cause mortality with a borderline effect on cardiovascular mortality. © 2018, International Heart Journal Association. All rights reserved.

Background: Pleural effusion refractory to diuretic treatment is frequent in advanced heart failure. Therapeutic thoracentesis is a time-honored practice, recently made simpler and safer by guidance with lung ultrasound. To assess the feasibility and clinical impact of lung ultrasound-driven therapeutic thoracentesis in refractory heart failure. Methods and results: In a single-centre retrospective analysis we recruited 373 patients with heart failure with reduced ejection fraction (26 ± 12%), New York Heart Association class ≥3, and pleural effusion ≥ moderate at lung ultrasound. All patients underwent lung ultrasound-guided therapeutic thoracentesis. Total of 462 lung ultrasound-guided therapeutic thoracentesis procedures were successfully performed without complications. Evacuated pleural fluid by passive drainage was 1030 ± 534 mL. The maximal interpleural space was 73.6 ± 15.6 mm before, and 12.4 ± 3.1 mm after therapeutic thoracentesis (p <.001). Therapeutic thoracentesis induced an immediate symptomatic improvement in all patients, with New York Heart Association class decrease from 3.84 ± 0.37 pre- to 2.7 ± 0.55 post-therapeutic thoracentesis (p <.001). The improvement was long-lasting (for weeks/months) in 89% of patients. The 6-min walking test was 52 ± 29 m before, and 287 ± 56 m one month after therapeutic thoracentesis (p <.05). Conclusion: Lung ultrasound-driven therapeutic thoracentesis of pleural effusion in decompensated heart failure patients is feasible, safe, and efficient. Therapeutic thoracentesis induces immediate and substantial symptomatic relief followed by long-lasting improvement. © 2019 Belgian Society of Cardiology.

OBJECTIVE: The aims of this study were to investigate the incidence and parameters associated with myocardial ischemia during mental stress (MS) as measured by echocardiography and to evaluate the relation between MS-induced and exercise-induced myocardial ischemia. METHODS: Study participants were 79 patients (63 men; mean [M] [standard deviation {SD}] age = 52 [8] years) with angiographically confirmed coronary artery disease and previous positive exercise test result. The MS protocol consisted of mental arithmetic and anger recall task. The patients performed a treadmill exercise test 15 to 20 minutes after the MS task. Data of post-MS exercise were compared with previous exercise stress test results. RESULTS: The frequency of echocardiographic abnormalities was 35% in response to the mental arithmetic task, compared with 61% with anger recall and 96% with exercise (p <.001, exercise versus MS). Electrocardiogram abnormalities and chest pain were substantially less common during MS than were echocardiographic abnormalities. Independent predictors of MS-induced myocardial ischemia were: wall motion score index at rest (p =.02), peak systolic blood pressure (p =.005), and increase in rate-pressure product (p =.004) during MS. The duration of exercise stress test was significantly shorter (p <.001) when MS preceded the exercise and in the case of earlier exercise (M [SD] = 4.4 [1.9] versus 6.7 [2.2] minutes for patients positive on MS and 5.7 [1.9] versus 8.0 [2.3] minutes for patients negative on MS). CONCLUSIONS: Echocardiography can be successfully used to document myocardial ischemia induced by MS. MS-induced ischemia was associated with an increase in hemodynamic parameters during MS and worse function of the left ventricle. MS may shorten the duration of subsequent exercise stress testing and can potentiate exercise-induced ischemia in susceptible patients with coronary artery disease. Copyright © 2012 by the American Psychosomatic Society.

OBJECTIVE: The aims of this study were to investigate the incidence and parameters associated with myocardial ischemia during mental stress (MS) as measured by echocardiography and to evaluate the relation between MS-induced and exercise-induced myocardial ischemia. METHODS: Study participants were 79 patients (63 men; mean [M] [standard deviation {SD}] age = 52 [8] years) with angiographically confirmed coronary artery disease and previous positive exercise test result. The MS protocol consisted of mental arithmetic and anger recall task. The patients performed a treadmill exercise test 15 to 20 minutes after the MS task. Data of post-MS exercise were compared with previous exercise stress test results. RESULTS: The frequency of echocardiographic abnormalities was 35% in response to the mental arithmetic task, compared with 61% with anger recall and 96% with exercise (p <.001, exercise versus MS). Electrocardiogram abnormalities and chest pain were substantially less common during MS than were echocardiographic abnormalities. Independent predictors of MS-induced myocardial ischemia were: wall motion score index at rest (p =.02), peak systolic blood pressure (p =.005), and increase in rate-pressure product (p =.004) during MS. The duration of exercise stress test was significantly shorter (p <.001) when MS preceded the exercise and in the case of earlier exercise (M [SD] = 4.4 [1.9] versus 6.7 [2.2] minutes for patients positive on MS and 5.7 [1.9] versus 8.0 [2.3] minutes for patients negative on MS). CONCLUSIONS: Echocardiography can be successfully used to document myocardial ischemia induced by MS. MS-induced ischemia was associated with an increase in hemodynamic parameters during MS and worse function of the left ventricle. MS may shorten the duration of subsequent exercise stress testing and can potentiate exercise-induced ischemia in susceptible patients with coronary artery disease. Copyright © 2012 by the American Psychosomatic Society.