Right ventricle-pulmonary artery coupling in pulmonary artery hypertension its measurement and pharmacotherapy.

The right ventricular (RV) function correlates with prognosis in severe pulmonary artery hypertension (PAH) but which metric of it is most clinically relevant is still uncertain. Clinical methods to estimate RV function from simplified pressure volume loops correlate with disease severity but the clinical relevance has not been assessed. Evaluation of right ventricle pulmonary artery coupling in pulmonary hypertensive patients may help to elucidate the mechanisms of right ventricular failure and may also help to identify patients at risk or guide the timing of therapeutic interventions in pulmonary hypertension. Complete evaluation of RV failure requires echocardiographic or magnetic resonance imaging, and right heart catheterization measurements. Treatment of RV failure in PAH relies on decreasing afterload with drugs targeting pulmonary circulation; fluid management to optimize ventricular diastolic interactions; and inotropic interventions to reverse cardiogenic shock. The ability to relate quantitative metrics of RV function in pulmonary artery hypertension to clinical outcomes can provide a powerful tool for management. Such metrics could also be utilized in the future as surrogate endpoints for outcomes and evaluation of response to therapies. This review of literature gives an insight on RV-PA coupling associated with PAH, its types of measurement and pharmacological treatment.

Impact of angiotensin receptor-neprilysin inhibition (ARNI) in improving ejection fraction and left and right ventricular remodeling in heart failure.

Angiotensin receptor neprilysin inhibitors (ARNI), a new therapeutic class of agents acting on the renin angiotensin aldosterone system (RAAS) and neutral endopeptidase system has been developed in treatment of ventricular remodeling and has attracted considerable attention. The first in class is LCZ696, which is a molecule that combines Valsartan (ARB) and Sacubitril (neprilysin inhibitor) within a single substance. Sacubitril-Valsartan is the first angiotensin receptor enkephalin inhibitors (ARNI), which can block angiotensin II type 1 receptor (AT1R) while inhibiting enkephalin (NEP) and effectively reverse ventricular remodeling in heart failure patients. It has been recommended by the European and American authoritative guidelines on heart failure as Class I for the treatment of chronic heart failure particularly as intensive care medicine. Sacubitril-Valsartan demonstrated significant effects in improving left ventricular performance and remodeling in patients with heart failure with reduced ejection fraction. Sacubitril acts on increased levels of circulating natriuretic peptides by preventing their enzymatic breakdown and Valsartan, which acts to lessen the effects of the RAAS. However, not more research has been done on its effects on the right ventricle remodeling. This review aimed to assess the impact of angiotensin receptor neprilysin inhibitors on left and right ventricular remodeling in heart failure patients.

An overview regarding the article 'clinical outcomes and mortality in patients with atrial fibrillation and recently diagnosed lung cancer in oncology outpatient settings'.

Cancer-related inflammation, anti-cancer treatment and other cancer-related comorbidities are proposed to affect atrial remodeling, increasing the susceptibility of lung cancer patients for developing atrial fibrillation. Moreover, cancer is assumed to modify the risk of thromboembolisms and bleeding. An association between AF and malignancy has been reported but incompletely defined. The earliest publications of cancer predisposing to AF came in the 1940s-50s with reports of neoplastic cardiac infiltration or mechanical pressure on the heart, and with oncologic thoracic surgery. Subsequently, multiple studies have reported an increased risk of AF after cancer therapy with surgery (particularly thoracic) and chemotherapy. However, the prevalence of AF appears to be higher in patients with cancer at the time of diagnosis even before undergoing therapy. The emerging field of cardio-oncology has revealed that these seemingly disparate disease processes are intertwined, owing to the cardiovascular sequelae of anticancer therapies, shared risk factors that predispose individuals to both cardiovascular disease and cancer, as well the possible potentiation of cancer growth by cardiac dysfunction. Although direct oral anticoagulants (DOAC) seem to represent a safe and effective option, compared to Vitamin K antagonists (VKA), in this population, this statement is based mainly on observational studies and sub analyses of pivotal trials of the DOAC.

Evaluation of research trends in the incidence of postoperative neurocognitive disorders in patients undergoing cardiac surgery.

Postoperative neurocognitive disorders (PNDs) are a kind of acute central nervous system syndrome, which is a common postoperative complication in cardiac elderly patients. The two most commonly used terms for PNDs are postoperative delirium (POD) and postoperative cognitive dysfunction (POCD). POD often leads to a series of adverse clinical outcomes and even death, so its prevention and treatment has become an important part of perioperative management in elderly patients. In the past decades, research has focused on the mechanism and progress of the pathogenesis of PNDs. Nonetheless, little research has been conducted on the research trends in the relevant field.

Letter regarding the article: Trends, and Outcomes of Transcatheter Aortic Valve Implantation in Aortic Insufficiency; A Nationwide Readmission Database Analysis.

With great interest, we have read the article "Trends, and Outcomes of Transcatheter Aortic Valve Implantation In Aortic Insufficiency; A Nationwide Readmission Database Analysis" by Ullah et al. For its clarity and conciseness, we applaud the author for his extensive research on this delicate topic. The authors have concisely written several scenarios including the current understanding of trends, and potential outcome of aortic insufficiency following transcatheter aortic valve implantation (TAVI). Nonetheless, we thought it would be helpful to add a few more things to the article's conclusion to strengthen it. The inclusion of the pathophysiology of coronary microcirculation disorder, and endothelial dysfunction in patients with aortic stenosis and then examine the impact of TAVI on these conditions can improve the results. Second, echocardiographic data regarding right and left ventricular dimensions and function or tricuspid regurgitation presence and its severity could lead to a better understanding of the mechanism.

Insights Regarding the Article "Exploring Transthyretin Amyloid Cardiomyopathy: A Comprehensive Review of the Disease and Upcoming Treatments".

Transthyretin amyloid cardiomyopathy (ATTR-CM) is an increasingly important but under-recognized cause of heart failure in persons over 60 years of age. Transthyretin amyloid cardiomyopathy (ATTR-CM) occurs when the disease affects the heart with or without the involvement of a more extensive systemic disorder. Both ATTRwt and less frequently hATTR are possibilities. Advances in diagnostics have identified specific populations in whom ATTR-CM is clinically important. The recent emergence of effective therapies that slow disease progression and improve clinical outcomes promises to render ATTR-CM a treatable disease. For such therapies to be most effective, early identification of affected individuals is critical. Treatments have been limited to supportive care, with no guideline-recommended treatment. In patients with transthyretin amyloid cardiomyopathy, tafamidis was associated with reductions in all-cause mortality and cardiovascular-related hospitalizations and reduced the decline in functional capacity and quality of life as compared with placebo. This commentary aims to afford providers the tools required to facilitate earlier diagnosis of ATTR-CM and delineate management strategies.

Feasibility of artificial intelligence its current status, clinical applications, and future direction in cardiovascular disease.

In routine clinical practice, the diagnosis and treatment of cardiovascular disease (CVD) rely on data in a variety of formats. These formats comprise invasive angiography, laboratory data, non-invasive imaging diagnostics, and patient history. Artificial intelligence (AI) is a field of computer science that aims to mimic human thought processes, learning capacity, and knowledge storage. In cardiovascular medicine, artificial intelligence (AI) algorithms have been used to discover novel genotypes and phenotypes in established diseases enhance patient care, enable cost effectiveness, and lower readmission and mortality rates. AI will lead to a paradigm change toward precision cardiovascular medicine in the near future. The promise application of AI in cardiovascular medicine is immense; however, failure to recognize and ignorance of the challenges may overshadow its potential clinical impact. AI can facilitate every stage in cardiology in the imaging process, from acquisition and reconstruction, to segmentation, measurement, interpretation, and subsequent clinical pathways. Along with new possibilities, new threats arise, acknowledging and understanding them is as important as understanding the machine learning (ML) methodology itself. Therefore, attention is also paid to the current opinions and guidelines regarding the validation and safety of AI. This paper provides a outline for clinicians on relevant aspects of AI and machine learning, selection of applications and methods in cardiology to date, and identifies how cardiovascular medicine could incorporate AI in the future. With progress continuing in this emerging technology, the impact for cardiovascular medicine is highlighted to provide insight for the practicing clinician and to identify potential patient benefits.

An editorial regarding the article 'A meta-analysis of atrial septal defect closure in patients with severe pulmonary hypertension: is there a room for poking holes amidst debate?'

Pulmonary arterial hypertension (PAH) related to an atrial septal defect (ASD) poses a challenge to transcatheter closure of an ASD. In patients with untreated ASDs, chronic pulmonary over-circulation due to shunt flow can cause pulmonary vascular remodeling and increased pulmonary vascular resistance. PAH is one of the difficult situations to treat. Complex pathophysiology, association of the multiple comorbidities make clinical scenario challenging. The closure of ASD in patients with PAH improves PAH severity and cardiac functional capacity and reduces atrial arrhythmias. However, some patients show remaining PAH or aggravation of PAH post-ASD closure. PAH is a strong predictor of mortality in older patients who undergo ASD closure. Hence, the decision to opt for ASD closure should be carefully considered in high-risk patients with PAH. As per the American Heart Association/American College of Cardiology 2018 guidelines, ASD with elevated pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) more than two-thirds systemic is considered to be a contraindication for closure. However, it is difficult to determine the outcomes for ASD closure in patients with moderately-to-severely elevated PVR. A "treat and repair strategy" might be an option. In addition, the patient should be carefully selected by the observation of PVR change through vasoreactivity and balloon occlusion tests, and then closure should be considered. For patients with a predictable poor prognosis, research on the risk assessment of ASD closure in patients with PAH will be needed for a more individualized treatment plan.

A review regarding the article 'Dose-response association between cardiovascular health and mortality in cancer survivors'.

Cardiovascular disease (CVD) and cancer are the two leading causes of morbidity and mortality in the world. The emerging field of cardio-oncology has revealed that these seemingly disparate disease processes are intertwined, owing to the cardiovascular sequelae of anticancer therapies, shared risk factors that predispose individuals to both cardiovascular disease and cancer, as well the possible potentiation of cancer growth by cardiac dysfunction. As a result, interest has increased in understanding the fundamental biological mechanisms that are central to the relationship between CVD and cancer. CVD and cancer frequently coincide in the same patient and often complicate each other. To date, much of the focus in cardio-oncology has been on the cardiovascular complications developed during cancer progression and as a result of cancer treatment. However, the reverse can also be true, and patients with CVD have been shown to be at increased risk of developing cancer (reverse cardio-oncology), as reviewed previously. Recently, the American Heart Association (AHA) updated the Life's Essential 8 (LE8) score, which captures modifiable risk factors, including smoking, body mass index, physical activity, sleep, dietary habits, blood pressure, fasting glucose, and total cholesterol levels, to assess CVH. Many studies have demonstrated a robust association between LE8 and CVD and all-cause mortality in the general population. Beyond assessment and monitoring, using metrics such as LE8 has the unique advantage to identify modifiable risk factors and refers cancer survivors for targeted interventions to manage their CVD risk. Future research in larger study samples is needed to investigate whether the optimal CVD defined by LE8 may differ in population subgroups and implement and evaluate CVD promotion interventions in the high-risk cancer survivor population.

Comment on: Smart Technologies Used as Smart Tools in the Management of Cardiovascular Disease and Their Future Perspective.

With keen interest and seriousness, we have read the article "Smart Technologies used as Smart Tools in the Management of Cardiovascular Disease and their Future Perspective" by Muneeb Ullah et al. and writing to provide a critique. For its clarity and conciseness, we applaud the author for his extensive research on this delicate topic. The authors have concisely written several scenarios of using smart technologies used as smart tools in the management of cardiovascular disease, such as wearable devices, mobile applications,3D printing technologies, artificial intelligence, remote monitoring systems, and electronic health records. Nonetheless, While the study addresses an important topic in the field of cardiology, we believe there are certain aspects that require further consideration and exploration.

A Comment on: Anxiety and Depression in Heart Failure: An Updated Review.

With great interest, we have read the article "Anxiety and depression in heart failure: An updated review" by Sarim Rashid et al. For its clarity and conciseness, we applaud the author for his extensive research on this delicate topic. The authors have concisely written several scenarios including the risk factors that contribute to the development and exacerbation of anxiety and depression in individuals with heart conditions, including biological, psychological, and social factors. Nonetheless, we thought it would be helpful to add a few more things to the article's conclusion to strengthen it. Exploring the pathogenesis and pathophysiology of post-sepsis related depression is of positive significance for reducing the occurrence of long-term depression and improving the prognosis of sepsis patients.

Assessing Right Ventricle Pulmonary Artery Coupling and Uncoupling Using Echocardiography and Cardiopulmonary Exercise Test in Post Operative TOF Patients.

Right ventricular-pulmonary arterial (RV-PA) coupling is an important determinant in the development of right ventricular dilatation. RV-PA coupling is defined as the ratio of pulmonary arterial elastance (an index of arterial load) and right ventricular end-systolic elastance (an index of contractility). A retrospective study of postoperative 135 TOF patients who underwent for pulmonary valve replacement was conducted. RV-PA coupling was calculated noninvasively using Ea/Emax (cardiac magnetic resonance) = ventricular end-systolic volume/ventricular systolic volume, equation and patients were divided into coupling and uncoupling group and compared the results on the basis of echocardiography and cardiopulmonary exercise test. Lower tricuspid annular plane systolic excursion, percentage predictive peak VO2, VE/VCO2 at anaerobic threshold, (AT), VE/VCO2 at peak, Minute ventilation, (VE) Volume of Carbondioxide output, (VCO2) slope, volume of oxygen output (VO2) work rate (WR) slope, and WR at VO2 peak were identified as risk factors for uncoupling of RV-PA. In RV-PA coupling combination of echocardiography and cardiopulmonary exercise test revealed the most important modality to identify risk factor and may be useful for therapeutic decision making by identifying patients of especially high risk for inadequate therapy.

Role and Interaction Between ACE1, ACE2 and Their Related Genes in Cardiovascular Disorders.

Cardiovascular disease is the greatest health care burden and one of the most common causes of death worldwide. Less is known about the genetic factors that are responsible for predisposition to cardiovascular disease thus; the molecular and genetic mechanisms underlying cardiovascular diseases remain obscure. One important regulator of blood pressure homeostasis is the renin-angiotensin system. The protease renin cleaves angiotensinogen into the inactive decameric peptide angiotensin I (Ang I). Angiotensin-converting enzyme (ACE) catalyzes the cleavage of the Ang I into the active octomer angiotensin II (Ang II). In humans, can ACE polymorphism has been associated with determinants of renal and cardiovascular function and pharmacological inhibition of ACE and Ang II receptors are effective in lowering blood pressure and preventing kidney disease. In addition, inhibition of ACE and Ang II receptors has beneficial effects in heart failure. A homologue of ACE, termed ACE2, has been identified; it is predominantly expressed in the vascular endothelial cells of the kidney and heart. Unlike ACE, ACE2 functions as a carboxypeptidase, cleaving a single residue from AngI, generating Ang1-9, and a single residue from AngII to generate Ang1-7. Nevertheless, the in vivo role of ACE2 in the cardiovascular system and the renin-angiotensin system is not known.

Gene Silencing of Transcription Factor TEAD4 Inhibits Esophageal Cancer Cells by Regulating TCF7.

Background: The procancer effect of TEA domain transcription factor 4 (TEAD4) has been gradually discovered. However, its expression in esophageal cancer (EC) cells and its effect on proliferation and apoptosis have not been reported. In this study, we investigated the possible role of TEAD4 in EC cells. Materials and Methods: TEAD4 messenger RNA and protein expression were assessed in EC cell lines by real-time quantitative-PCR and Western blot. Gene silencing approach was employed to investigate the potential role of TEAD4 in cellular growth, proliferation, migration, and invasion in EC cells. The interaction between TEAD4 and transcription factor 7 (TCF7) was verified by co-immunoprecipitation reaction. The cell apoptosis rates of KYSE-30 cells were detected by flow cytometry. Meanwhile, the expression of apoptosis-related proteins in KYSE-30 cells was detected by Western blot analysis. Results: TEAD4 was significantly increased in EC cell lines, interference of TEAD4 inhibited EC cell viability, invasion, and migration, and promotes apoptosis. TCF7 was found when using STRING website to interact with TEAD4 proteins and TCF7 was significantly increased in EC and knockdown expression of TEAD4 hindered biological function of KYSE-30 cells and this effect was reversed by overexpression of TCF7. Conclusions: The findings concluded that TEAD4 is highly expressed in EC cells and gene silencing of TEAD4 inhibits proliferation and promotes apoptosis of EC cells by regulating TCF7. These findings suggested that TEAD4 might be a novel therapeutic target for the prevention of EC.

Mechanism and Prevention of Atrial Remodeling and Their Related Genes in Cardiovascular Disorders.

Atrial fibrillation (AF) is associated with profound structural and functional changes in the atrium. Inflammation mediated atrial fibrosis is one of the key mechanisms in the pathogenesis of AF. The collagen deposition in extracellular matrix (ECM) is mainly mediated by transforming growth factor ß1 (TGF-ß1) which promotes AF via controlling smads mediated-collagen gene transcription and regulating the balance of metalloproteinases (MMPs)/ tissue inhibitor of metalloproteinases (TIMPs). Although many processes can alter atrial properties and promote AF, animal models and clinical studies have provided insights into 2 major forms of atrial remodeling: Atrial tachycardia remodeling (ATR), which occurs with rapid atrial tachyarrhythmia's such as AF and atrial flutter, and atrial structural remodeling (ASR), which is associated with CHF and other fibrosis-promoting conditions. The mechanism of atrial remodeling such as atrial enlargement, ultra-structural changes of atrial muscle tissue and myocardial interstitial fibrosis in AF is still unclear. At present, many studies focus on calcium overload, renin angiotensin aldosterone system and transforming growth factor ß1, that effect on atrial structural remodeling. Recent experimental studies and clinical investigations have provided structural remodeling is important contributor to the AF. This paper reviews the current understanding of the progresses about mechanism of atrial structural remodeling, and highlights the potential therapeutic approaches aimed at attenuating structural remodeling to prevent AF. Now some recent advancements of this area are reviewed in this paper.