116 research outputs found
Chronic thromboembolic pulmonary hypertension after an acute pulmonary embolism: fundamental concepts of diagnosis and review of current treatment options
Chronic thromboembolic pulmonary hypertension (CTEPH) is a severe and underdiagnosed disorder that leads to right ventricular failure and, subsequently, to death. The article discusses the fundamental concepts of monitoring patients after a pulmonary embolism (PE) in order to timely detect CTEPH. The pathogenetic processes, risk factors and diagnostic criteria of this complication are described. The role of early diagnosis of CTEPH, which may be important in relation to further outcomes, is emphasized. A modern strategy for monitoring patients after PE is presented in detail, where echocardiography plays a key role. The stepwise diagnostic algorithm for CTEPH includes a comprehensive analysis of the patientβs condition: assessment of clinical status, identification of N-terminal pro-brain natriuretic peptide levels, cardiopulmonary exercise testing, imaging diagnostic procedures (ventilation/perfusion lung scanning, pulmonary angiography) and, finally, right heart catheterization. The article provides an overview of modern treatment options. CTEPH is a unique type of pulmonary hypertension because it is potentially curable with surgery β pulmonary thromboendarterectomy. For patients with inoperable or persistent/ recurrent CTEPH, medication therapy is recommended. Currently, the only drug with a high class of evidence for this group of patients is riociguat. A positive effect on exercise tolerance, functional class, and hemodynamic parameters has been shown in the CHEST-1,2 studies. The favorable safety profile of the drug was also demonstrated in the long-term follow-up in routine clinical practice (EXPERT registry). The presence of various options in the management of patients and development of a multimodal therapy makes it possible to provide high-quality care to patients with CTEPH, and, namely, fast and accurate diagnosis plays a key role in timely treatment
Statins and highly sensitive cardiac troponins: cardiotoxicity or cross-reactivity?
To date, hypolipidemic drugs of the statin group are among the most popular therapeutic agents used for the prevention and treatment of the most common worldwide atherosclerotic cardiovascular diseases (CVD). Therefore, considerable attention of researchers is focused on statins to study the additional effects of these drugs, which is accompanied by the discovery of new mechanisms of action and properties that should be taken into account to optimize the tactics of managing patients with CVD. In addition to the key lipid-lowering effect of statins associated with the inhibition of the ratelimiting enzyme (3-hydroxy-3-methylglutaryl-coenzyme A reductase), researchers report a variety of other properties of these drugs. Important circumstances contributing to the disclosure of new effects of statins are: improvement of research methods, and first of all, their sensitivity and specificity; the discovery of new molecules and molecular pathways that may be affected by statins. In general, the currently established numerous non-lipid effects of statin drugs can be divided into two groups: favorable and side effects, which must be taken into account when managing patients with CVD and comorbid diseases. Thanks to recent studies using modern clinical diagnostic cardiomarkers (highly sensitive cardiac troponins (CT)), molecular genetic and morphological methods, potential cardiotoxic properties of statin group drugs have been identified. Of particular concern are the data on a statininduced increase in the concentration of highly sensitive CT, which are a key and generally recognized criterion for myocardial damage. In this article we discuss possible mechanisms of increasing the concentration of CT and cardiotoxic effects when using statins
Cardioprotective Strategies for Doxorubicin-induced Cardiotoxicity: Present and Future
The improvement of drugs and protocols of chemotherapeutic treatment has led to improved outcomes and survival in patients with cancer. But along with this, at first glance a positive point, there was another interdisciplinary problem, which is the need for early detection and treatment of developing cardiotoxicity when taking chemotherapy drugs. The study of cardioprotective strategies has recently become increasingly relevant, due to the fact that many patients who have successfully undergone treatment for cancer have a high risk of developing or are at high risk of death from cardiovascular diseases. One of the main drugs for the treatment of a number of oncological diseases is an anthracycline β type antibiotic-doxorubicin. This review briefly examines the risk factors and pathophysiological mechanisms underlying anthracycline cardiotoxicity. The current possibilities of cardioprotection of anthracycline cardiotoxicity are considered in detail, and some promising targets and drugs for improving cardioprotective strategies are discussed
ΠΠΈΠΊΡΠΎΠ ΠΠ: ΡΠΎΠ»Ρ Π² ΠΏΠ°ΡΠΎΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΈΠΈ ΠΏΡΠ΅Π΄ΡΠ΅ΡΠ΄ΠΈΠΉ ΠΈ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΠ°
The aim of the study was to analyze medical literature on the role of microRNA in the pathophysiology of atrial fibrillation and the possibilities of using microRNAs as biomarkers.The analysis of modern medical literature was carried out using the PubMed β NCBI database.Atrial fibrillation (AF) is a common and serious cardiovascular disease. The pathophysiological mechanisms underlying the development of atrial fibrillation are not entirely clear. In addition, there are no optimal biomarkers for early detection and assessment of the prognosis for patients with atrial fibrillation. Recently, the attention of researchers has been directed to the molecules of microRNA. There is a lot of evidence that they are involved in the pathogenesis of neurological, oncological, and cardiovascular diseases. This review examines the role of microRNAs in the pathophysiology of atrial fibrillation. The possibility of using microRNA as a biomarker for the diagnosis and prediction of atrial fibrillation is also discussed.MicroRNAs play a crucial role in the pathophysiology of atrial fibrillation, regulating the mechanisms of atrial remodeling, such as electrical remodeling, structural remodeling, remodeling of the autonomic nervous system, and impaired regulation of calcium levels. The stability of microRNAs and the possibility to study them in various biological fluids and tissues, including blood, make these molecules a promising diagnostic biomarker for various cardiovascular diseases. The presented data clearly indicate that AF is associated with changes in the expression level of various microRNAs, which can be quantified using a polymerase chain reaction. Further research is required to assess the role of microRNAs as biomarkers for atrial fibrillation, in particular to establish precise reference limits.ΠΡΠΎΠ²Π΅Π΄Π΅Π½ Π°Π½Π°Π»ΠΈΠ· ΡΠΎΠ²ΡΠ΅ΠΌΠ΅Π½Π½ΠΎΠΉ ΠΌΠ΅Π΄ΠΈΡΠΈΠ½ΡΠΊΠΎΠΉ Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΡ ΠΏΠΎ Π±Π°Π·Π΅ Π΄Π°Π½Π½ΡΡ
PubMed β NCBI. Π€ΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΈΡ ΠΏΡΠ΅Π΄ΡΠ΅ΡΠ΄ΠΈΠΉ ΡΠ²Π»ΡΠ΅ΡΡΡ ΡΠΈΡΠΎΠΊΠΎ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½Π½ΡΠΌ ΠΈ ΡΠ΅ΡΡΠ΅Π·Π½ΡΠΌ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎ-ΡΠΎΡΡΠ΄ΠΈΡΡΡΠΌ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠ΅ΠΌ. ΠΠ°ΡΠΎΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΡ, Π»Π΅ΠΆΠ°ΡΠΈΠ΅ Π² ΠΎΡΠ½ΠΎΠ²Π΅ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΈΠΈ ΠΏΡΠ΅Π΄ΡΠ΅ΡΠ΄ΠΈΠΉ, Π½Π΅ ΡΠΎΠ²ΡΠ΅ΠΌ ΡΡΠ½Ρ. ΠΡΠΎΠΌΠ΅ ΡΠΎΠ³ΠΎ, ΠΎΡΡΡΡΡΡΠ²ΡΡΡ ΠΎΠΏΡΠΈΠΌΠ°Π»ΡΠ½ΡΠ΅ Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΡ Π΄Π»Ρ ΡΠ°Π½Π½Π΅Π³ΠΎ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΠΈ ΠΎΡΠ΅Π½ΠΊΠΈ ΠΏΡΠΎΠ³Π½ΠΎΠ·Π° ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΈΠ΅ΠΉ ΠΏΡΠ΅Π΄ΡΠ΅ΡΠ΄ΠΈΠΉ.Π ΠΏΠΎΡΠ»Π΅Π΄Π½Π΅Π΅ Π²ΡΠ΅ΠΌΡ Π²Π½ΠΈΠΌΠ°Π½ΠΈΠ΅ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°ΡΠ΅Π»Π΅ΠΉ ΠΏΡΠΈΠ²Π»Π΅ΠΊΠ»ΠΈ ΠΌΠΎΠ»Π΅ΠΊΡΠ»Ρ ΠΌΠΈΠΊΡΠΎΡΠΈΠ±ΠΎΠ½ΡΠΊΠ»Π΅ΠΈΠ½ΠΎΠ²ΠΎΠΉ ΠΊΠΈΡΠ»ΠΎΡΡ (ΠΌΠΈΠΊΡΠΎΠ ΠΠ). ΠΠ°ΠΊΠΎΠΏΠ»Π΅Π½ΠΎ Π½Π΅ΠΌΠ°Π»ΠΎ Π΄Π°Π½Π½ΡΡ
, ΡΠΎΠ³Π»Π°ΡΠ½ΠΎ ΠΊΠΎΡΠΎΡΡΠΌ ΠΎΠ½ΠΈ ΡΡΠ°ΡΡΠ²ΡΠ΅Ρ Π² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π΅ Π½Π΅Π²ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
, ΠΎΠ½ΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎ-ΡΠΎΡΡΠ΄ΠΈΡΡΡΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ. Π Π°ΡΡΠΌΠΎΡΡΠ΅Π½Π° ΡΠΎΠ»Ρ ΠΌΠΈΠΊΡΠΎΠ ΠΠ Π² ΠΏΠ°ΡΠΎΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΈΠΈ ΠΏΡΠ΅Π΄ΡΠ΅ΡΠ΄ΠΈΠΉ. Π’Π°ΠΊΠΆΠ΅ ΠΎΠ±ΡΡΠΆΠ΄Π°Π΅ΡΡΡ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΡ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ ΠΌΠΈΠΊΡΠΎΠ ΠΠ Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ Π±ΠΈΠΎΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² Π΄Π»Ρ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ ΠΈ ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΈΠΈ ΠΏΡΠ΅Π΄ΡΠ΅ΡΠ΄ΠΈΠΉ
Comboridity of chronic obstructive pulmonary disease and cardiovascular diseases: general factors, pathophysiological mechanisms and clinical significance
Currently, the comorbidity (combination) of chronic obstructive pulmonary disease (COPD) and cardiovascular diseases (CVD) is an important problem for the health care. This is due to the high prevalence and continuing growth of these pathologies. CVD and COPD have common risk factors and mechanisms underlying their development and progression: smoking, inflammation, sedentary lifestyle, aging, oxidative stress, air pollution, and hypoxia. In this review, we summarize the current knowledge related to the prevalence and frequency of cardiovascular diseases in people with COPD and the mechanisms that underly their coexistence. The implications for clinical practice, in particular the main problems of diagnosis and treatment of COPD/CVD comorbidity, are also discussed
Effect of combined lipid-lowering therapy on atherosclerotic plaque vulnerability in patients with acute coronary syndrome (Combi-LLT ACS): randomized trial protocol
Aim. To study the effect of high-dose combined lipid-lowering therapy (statins + ezetimibe vs statins + PCSK9 inhibitors) on plaque vulnerability assessed using multimodal imaging (coronary computed tomography angiography (CCTA) and optical coherence tomography, as well as biomarkers in patients with acute coronary syndrome (ACS).Material and methods. This open, prospective, randomized, single-center study will include 120 patients admitted urgently with an ACS. All patients will undergo percutaneous coronary intervention of the infarct-related artery, as well as intracoronary imaging using optical coherence tomography of one or two noninfarct-related arteries. During hospitalization, patients will receive standard therapy for ACS according to clinical guidelines, while statins will initially be prescribed at a maximum dosage of atorvastatin 80 mg/rosuvastatin 40 mg.Patients who showed high compliance and did not reach the target low-density lipoprotein cholesterol (LDL-C) values (β€1,4 mmol/l) 1 month after myocardial infarction/unstable angina at the second visit will be randomized into two groups. Patients of group 1 will receive PCSK9 inhibitors (alirocumab 150 mg by subcutaneous injection once every 2 weeks or evolocumab 140 mg by subcutaneous injection once every 2 weeks) in addition to maximum statin therapy (atorvastatin 80 mg/rosuvastatin 40 mg), while group 2 participants will take ezetimibe at a dose of 10 mg in combination with the maximum dose of statins. In addition, at the second visit, patients will undergo CCTA, assess the cardio-ankle vascular index (CAVI) index and laboratory tests (complete blood count (neutrophil-to-lymphocyte ratio NLR), lipid profile, alanine aminotransferase (ALT), aspartate aminotransferase (AST), Troponin I, Galectin-3, high-sensitivity C-reactive protein (hs-CRP), metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase 1 (TIMP-1), neutrophil gelatinase-associated lipocalin (NGAL). Total follow-up will last 52 weeks. At the final visit, patients will undergo CCTA, assessment of the CAVI index and laboratory status (NLR, lipid profile, ALT, AST), Troponin I, Galectin-3, hs-CRP, MMP-9, TIMP-1, NGAL).Primary endpoint: reduction in plaque vulnerability according CCTA in non-infarct-related coronary arteries Secondary endpoints: death, stent thrombosis/restenosis, non-fatal myocardial infarction, readmissions with progressive angina, repeat revascularization; changesΒ of the lipid profile (total cholesterol, LDL-C, high-density lipoprotein cholesterol, triglycerides) against the background of maximum combination therapy with statin + PCSK9 inhibitors or statin + ezetimibe; changes of the biomarkers of cardiac injury (Troponin I), inflammation (NLR, hs-CRP, NGAL, Galectin-3) and matrix remodeling (MMP-9, TIMP-1).Conclusion. Our study will allow for the first time to compare and evaluate the effect of both PCSK9 inhibitors and ezetimibe in combination with high-dose statin therapy on reducing the plaque vulnerability according to CCTA in non-infarction-related coronary arteries in patients with ACS undergoing percutaneous coronary intervention, as well as to evaluate the diagnostic value of inflammatory biomarkers (NLR, hs-CRP, NGAL, Galectin-3) and matrix remodeling (MMP-9, TIMP-1)
High calcium score in an 83-year-old patient with non-ST elevation acute coronary syndrome and nonobstructive coronary artery disease: a case report
Currently, multi-slice computed tomography (MSCT) coronary angiography is a leader in the diagnosis of coronary artery disease in patients with non-ST elevation acute coronary syndrome of low or moderate risk. High coronary calcium score (CCS) obtained by MSCT indicate a high probability of obstructive coronary artery disease. In the presented case of an 83-year-old patient with unstable angina, the CCS was 1394, and hemodynamically significant stenoses were detected. However, according to selective coronary angiography, no hemodynamically significant coronary lesions were found. High CCS suggests poor image quality in MSCT coronary angiography. High CCS is detected in most people over 70 years of age. Obviously, in this patient, a high CCS is mainly determined by age. Most studies on CCS did not include patients over 80 years of age. When deciding whether to perform MSCT coronary angiography, it is necessary to take into account the individual characteristics of a particular patient, which may affect the interpretation of results
Cardiorenal relationships in the focus of risks of atrial fibrillation in patients after acute ST-elevated myocardial infarction (observational program FAKEL)
Aim. To study markers of renal dysfunction in relation to the likelihood of atrial fibrillation (AF) in patients after ST-segment elevated myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).Material and methods. The study was conducted with the inclusion of 1 52 patients discharged for outpatient monitoring after STEMI. There were 4 visits:Β V1 - inclusion visit, V2 - in 12 months, V3 - in 18 months, V4- in 24 months with determination of plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP), cystatin C, erythropoietin, galectin-3, von Willebrand factor (fW), left ventricular ejection fraction. Endpoint: new cases of AF, cardioembolic stroke, deaths.Results. After 24 months 35 patients (23.0%) were diagnosed with AF, 6 of them (3.9%) - developed cardioembolic stroke. The multivariate model of risk factors for AF included indicators: cystatin C (odds ratio [OR] 1.31; 95% confidence interval [95%CI] 1.03-1.67), NT-ProBNP (OR 1.11; 95%CI 1.03-1.19), galectin-3 (OR 0.71; 95%CI 0.55-0.91), fV (OR 0.71; 95%CI 0.55-0.91).Conclusion. The prognostic significance of cystatin C in relation to the risk of AF was established, which should be considered when assessing the prognosis in patients after STEMI
Validation of the SIRENA score for assessing the risk of inhospital mortality in patients with acute pulmonary embolism in an independent sample
Aim. To validate the SIRENA scoreΒ in assessing the risk of inhospital mortality in patients with pulmonary embolism (PE) in an independent sample.Material and methods. This retrospective, single-center study was based on the Samara Regional Cardiology Center. The risk of inhospital mortality was assessed using the SIRENA score, which includes such parameters as left ventricular ejection fraction <40%,Β immobilization in prior 12 months, creatinine clearance <50 ml/min, syncope, cyanosis on admission. For each positive sign, 1 point is assigned. Low risk is set at score of 0-1, high β β₯2.Results. The study included 452 patients with PE hospitalized from 2004 to 2019, of which 221 (48,9%) were men (mean age, 60,0 years (50,5-70,0)).Β With SIRENA score of 0, 1, 2, 3, and 4, inhospital mortality was 4,1%, 10,8%, 18,8%, 40,0%, and 100%, respectively. Mortality at SIRENA low risk (<2) was 7,1%, and at high risk (β₯2) β 20,5% (odds ratio (OR), 3,34; 95% confidence interval (CI), 1,74-6,43; p<0,001).Β The predictive sensitivity and specificity for inhospital mortality for the SIRENA score were 70,5% and 60,8%, respectively. Area under the ROC-curve for the SIRENA score was 0,71 (95% CI, 0,63-0,79), while for Simplified Pulmonary Embolism Severity Index (sPESI) β 0,69 (95%Β CI, 0,60-0,77).Β With high risk on both scales (sPESI and SIRENA), inhospital mortality was 24,2% (OR, 4,09, 95% CI, 2,07-8,09; p<0,001).Conclusion. On an independent sample, the SIRENA scoreΒ showedΒ a high predictive ability in predicting adverse outcomes in patients with PE with a sensitivity of 70,5% and a specificity of 60,8% (AUC=0,71, 95% CI, 0,63-0,79), comparable with the sPESI
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