Evaluating Long-Term Outcomes in STEMI Patients with New Left Bundle Branch Block: The Impact of Modifiable Risk Factors.

Background/Objectives: Coronary artery disease, a leading global cause of death, highlights the essential need for early detection and management of modifiable cardiovascular risk factors to prevent further coronary events. Methods: This study, conducted at a major tertiary academic PCI-capable hospital in Romania from 1 January 2011 to 31 December 2013, prospectively analyzed 387 myocardial infarction with ST-segment elevation (STEMI) patients to assess the long-term management of modifiable risk factors. This study particularly focused on patients with new-onset left bundle branch block (LBBB) and compared them with a matched control group without LBBB. Results: During median follow-up periods of 9.6 years for LBBB patients and 9.2 years for those without LBBB, it was found that smoking, obesity, and dyslipidemia were prevalent in 73.80%, 71.42%, and 71.42% of the LBBB group, respectively, at baseline. Significant reductions in smoking were observed in both groups, with the LBBB group's smoking rates decreasing significantly to 61.90% (p = 0.034). Patients with LBBB more frequently achieved low-density lipoprotein cholesterol (LDLc) target levels during the follow-up period (from 71.42% to 59.52%; p = 0.026) compared to the control group (from 66.67% to 71.42%; p = 0.046). Prescription rates for dual antiplatelet therapy (DAPT), angiotensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARBs), beta-blockers, and statins were initially high but then decreased by the follow-up. Statin use was reduced from 97.62% to 69.04% (p = 0.036) in the LBBB group and from 100% to 61.90% (p = 0.028) in the non-LBBB group. This study also highlighted moderate correlations between obesity (r = 0.627, p = 0.040) and subsequent coronary reperfusion in the LBBB group, while dyslipidemia and smoking showed very strong positive correlations across both groups (dyslipidemia: r = 0.903, p = 0.019 for LBBB; r = 0.503, p = 0.048 for non-LBBB; smoking: r = 0.888, p = 0.035 for LBBB; r = 0.517, p = 0.010 for non-LBBB). Conclusions: These findings underscore the crucial need for targeted management of modifiable risk factors, particularly focusing on dyslipidemia and smoking cessation, to improve subsequent coronary reperfusion outcomes post-STEMI, especially in patients with complicating factors like LBBB.

Role of Cardiac Magnetic Resonance in the Assessment of Patients with Premature Ventricular Contractions: A Narrative Review.

Premature ventricular contractions (PVCs) are a common finding in clinical practice, requiring a full diagnostic work-up in order to exclude an underlying cardiomyopathy. Still, in a substantial proportion of patients, these investigations do not identify any substrate, and the PVCs are labelled as idiopathic. Cardiac magnetic resonance (CMR) has proven in the last decades as the method of choice for the exploration of patients with cardiomyopathies, since it can identify subtle changes in the myocardial tissue and help with risk stratification. In patients with idiopathic PVCs and a high PVC burden, several studies report the presence of late gadolinium enhancement (LGE) at CMR, which can offer additional diagnostic and prognostic benefits, as well as assistance in catheter ablation procedures, as the risk for adverse cardiac and risk for arrhythmic events events is higher compared to patients without scar. This paper focuses on the impact of the presence of LGE in patients with idiopathic PVCs, reviewing all the relevant studies published so far, including randomized controlled clinical trials, prospective or retrospective cohort studies, case series and case reports as well as systematic reviews.

Unraveling the Cardiac Matrix: From Diabetes to Heart Failure, Exploring Pathways and Potential Medications.

Myocardial infarction (MI) often leads to heart failure (HF) through acute or chronic maladaptive remodeling processes. This establishes coronary artery disease (CAD) and HF as significant contributors to cardiovascular illness and death. Therefore, treatment strategies for patients with CAD primarily focus on preventing MI and lessening the impact of HF after an MI event. Myocardial fibrosis, characterized by abnormal extracellular matrix (ECM) deposition, is central to cardiac remodeling. Understanding these processes is key to identifying new treatment targets. Recent studies highlight SGLT2 inhibitors (SGLT2i) and GLP-1 receptor agonists (GLP1-RAs) as favorable options in managing type 2 diabetes due to their low hypoglycemic risk and cardiovascular benefits. This review explores inflammation's role in cardiac fibrosis and evaluates emerging anti-diabetic medications' effectiveness, such as SGLT2i, GLP1-RAs, and dipeptidyl peptidase-4 inhibitors (DPP4i), in preventing fibrosis in patients with diabetes post-acute MI. Recent studies were analyzed to identify effective medications in reducing fibrosis risk in these patients. By addressing these areas, we can advance our understanding of the potential benefits of anti-diabetic medications in reducing cardiac fibrosis post-MI and improve patient outcomes in individuals with diabetes at risk of HF.

Casting Light on The Hidden Prevalence: A Novel Perspective on Hypoplastic Coronary Artery Disease.

Background and Objectives: Coronary artery anomalies (CAAs) represent a group of rare cardiac abnormalities with an incidence of up to 1.2%. The aim of this retrospective study was to conduct a comprehensive epidemiological assessment of the prevalence of hypoplastic coronary arteries using coronary computed tomography angiography (CCTA) in patients with diagnosed CAAs and individuals presenting with cardiovascular manifestations in the north-eastern region of Romania. This study was motivated by the limited investigation of the CAAs conducted in this area. Methods: We analyzed data collected from 12,758 coronary computed tomography angiography (CCTA) records available at the "Prof. Dr. George I.M. Georgescu" Cardiovascular Diseases Institute, spanning the years 2012 to 2022. Results: Among 350 individuals with CAAs (2.7% of the total cohort), 71 patients (20.3% of the anomaly presenting group and 0.5% of the entire CCTA cohort) exhibited at least one hypoplastic coronary artery. The mean age of individuals diagnosed with hypoplastic coronary artery disease (HCAD) was 61 years, while the age distribution among them ranged from 22 to 84 years. Nearly equal cases of right and left dominance (33 and 31, respectively) were observed, with only 7 cases of co-dominance. Conclusions: HCAD may be considered underexplored in current published research, despite its potentially significant implications ranging to an increased risk of sudden cardiac arrest. The specific prevalence of HCAD among CAAs might be higher than previously reported, possibly reflecting better diagnostic accuracy of CCTA over classic coronary imaging. The absence of standard diagnostic and therapeutic protocols for HCAD underscores the necessity of a personalized approach for such cases.

Electrocardiogram Features in Non-Cardiac Diseases: From Mechanisms to Practical Aspects.

Despite the noteworthy advancements and the introduction of new technologies in diagnostic tools for cardiovascular disorders, the electrocardiogram (ECG) remains a reliable, easily accessible, and affordable tool to use. In addition to its crucial role in cardiac emergencies, ECG can be considered a very useful ancillary tool for the diagnosis of many non-cardiac diseases as well. In this narrative review, we aimed to explore the potential contributions of ECG for the diagnosis of non-cardiac diseases such as stroke, migraine, pancreatitis, Kounis syndrome, hypothermia, esophageal disorders, pulmonary embolism, pulmonary diseases, electrolyte disturbances, anemia, coronavirus disease 2019, different intoxications and pregnancy.

Genetic Characterization of Dilated Cardiomyopathy in Romanian Adult Patients.

Dilated cardiomyopathy (DCM) represents a group of disorders affecting the structure and function of the heart muscle, leading to a high risk of heart failure and sudden cardiac death (SCD). DCM frequently involves an underlying genetic etiology. Genetic testing is valuable for risk stratification, treatment decisions, and family screening. Romanian population data on the genetic etiology of DCM are lacking. We aimed to investigate the genetic causes for DCM among Romanian adult patients at tertiary referral centers across the country. Clinical and genetic investigations were performed on adult patients presenting to tertiary hospitals in Romania. The genetic investigations used next-generation sequencing panels of disease-associated DCM genes. A total of 122 patients with DCM underwent genetic testing. The mean age at DCM diagnosis was 41.6 ± 12.4 years. The genetic investigations identified pathogenic or likely pathogenic variants in 50.8% of participants, while 25.4% had variants of unknown significance. Disease-causing variants in 15 genes were identified in people with DCM, with 31 previously unreported variants. Variants in TTN, LMNA, and DSP explained 75% of genetic causes for DCM. In total, 52.4% of patients had a family history of DCM/SCD. Left ventricular ejection fraction of <35% was observed in 41.9% of patients with disease-causing variants and 55% with negative or uncertain findings. Further genotype-phenotype correlations were explored in this study population. The substantial percentage (50.8%) of disease-causing variants identified in patients with DCM acknowledges the importance of genetic investigations. This study highlights the genetic landscape in genes associated with DCM in the Romanian population.

Phospholamban p.Leu39* Cardiomyopathy Compared with Other Sarcomeric Cardiomyopathies: Age-Matched Patient Cohorts and Literature Review.

Hypertrophic cardiomyopathy (HCM) is a heterogeneous genetic disorder, most often caused by sarcomeric gene mutations, with a small proportion due to variants in non-sarcomeric loci. Phospholamban (PLN) is a phosphoprotein associated with the cardiac sarcoplasmic reticulum, a major determinant of cardiac contractility and relaxation. We conducted a retrospective study to determine the prevalence, phenotypical spectrum and clinical course of patients carrying the PLN p.Leu39* variant. A cohort including 11 PLN patients was identified among all patients with HCM (9/189, 4.8%) and DCM (2/62, 3.2%) who underwent genetic testing from two tertiary centers and five more were detected through cascade screening. Complete phenotyping was performed. PLN p.Leu39* variant-driven cardiomyopathy presented mostly as hypertrophic, with frequent progression to end-stage dilated HCM. We proceeded to compare these results to a similar analysis of a control cohort consisting of age-matched individuals that inherited pathogenic or likely pathogenic variants in common sarcomeric genes (MYBPC3/MYH7). Overall, the clinical characteristics and examination findings of patients carrying PLN p.Leu39* were not different from patients with cardiomyopathy related to sarcomeric mutations except for the presence of pathological Q waves and the incidence of non-sustained ventricular arrhythmias, which were higher in PLN patients than in those with MYBPC3/MYH7-related diseases.

Cardiac and Renal Fibrosis, the Silent Killer in the Cardiovascular Continuum: An Up-to-Date.

Cardiovascular disease (CVD) and chronic kidney disease (CKD) often coexist and have a major impact on patient prognosis. Organ fibrosis plays a significant role in the pathogenesis of cardio-renal syndrome (CRS), explaining the high incidence of heart failure and sudden cardiac death in these patients. Various mediators and mechanisms have been proposed as contributors to the alteration of fibroblasts and collagen turnover, varying from hemodynamic changes to the activation of the renin-angiotensin system, involvement of FGF 23, and Klotho protein or collagen deposition. A better understanding of all the mechanisms involved has prompted the search for alternative therapeutic targets, such as novel inhibitors of the renin-angiotensin-aldosterone system (RAAS), serelaxin, and neutralizing interleukin-11 (IL-11) antibodies. This review focuses on the molecular mechanisms of cardiac and renal fibrosis in the CKD and heart failure (HF) population and highlights the therapeutic alternatives designed to target the responsible pathways.

Cardiac Device Therapy in Patients with Chronic Kidney Disease: An Update.

Cardiovascular diseases (CVDs) and chronic kidney disease (CKD) are frequently interconnected and their association leads to an exponential increase in the risk of both fatal and non-fatal events. In addition, the burden of arrhythmias in CKD patients is increased. On the other hand, the presence of CKD is an important factor that influences the decision to pursue cardiac device therapy. Data on CKD patients with device therapy are scarce and mostly derives from observational studies and case reports. Cardiac resynchronization therapy (CRT) is associated with decreased mortality, reduced heart failure symptoms, and improved renal function in early stages of CKD. Implantable cardioverter defibrillators (ICDs) are associated with a significant reduction in the mortality of CKD patients only for the secondary prevention of sudden cardiac death. Cardiac resynchronization therapy with defibrillator (CRT-D) is preferred in patients who meet the established criteria. The need for cardiac pacing is increased three-fold in dialysis patients. CKD is an independent risk factor for infections associated with cardiac devices.

Patient-Related Factors Predicting Stent Thrombosis in Percutaneous Coronary Interventions.

Over the past four decades, percutaneous coronary intervention (PCI) safety and efficacy have significantly improved, particularly with the advent of the drug-eluting stent (DES). First-generation DESs reduced in-stent restenosis rates and targeted lesion revascularization; however, safety issues emerged, due to high incidences of stent thrombosis (ST) linked to death, myocardial infarction, and repeat revascularization. Second-generation DESs were developed to overcome these issues, reducing late-thrombotic-event risk while maintaining anti-restenosis efficacy. Nevertheless, ST still occurs with second-generation DES use. Stent thrombosis etiology is multifaceted, encompassing lesion-, patient-, procedural-, and stent-related factors. Overall, most early-stent-thrombosis cases are linked to procedural and patient-related aspects. Factors like premature discontinuation of dual antiplatelet therapy, resistance to clopidogrel, smoking, diabetes mellitus, malignancy, reduced ejection fraction or undertaking coronary angioplasty for an acute coronary syndrome can increase the risk of stent thrombosis. The aim of this study is to assess patient-related factors that potentially heighten the risk of stent thrombosis, with the objective of pinpointing and addressing modifiable contributors to this risk. By focusing on both patient- and procedure-related factors, a multifaceted approach to coronary revascularization can help minimize complications and maximize long-term benefits in managing ST.

Changes in Arterial Stiffness in Response to Blood Flow Restriction Resistance Training: A Narrative Review.

Arterial stiffness naturally increases with age and is a known predictor of cardiovascular morbimortality. Blood flow restriction (BFR) training involves decreasing muscle blood flow by applying a strap or a pneumatic cuff during exercise. BFR induces muscle hypertrophy even at low intensities, making it an appealing option for older, untrained individuals. However, BFR use in patients with cardiovascular comorbidities is limited by the increased pressor and chronotropic response observed in hypertensive elderly patients. Furthermore, the impact of BFR on vascular function remains unclear. We conducted a comprehensive literature review according to PRISMA guidelines, summarizing available data on the acute and long-term consequences of BFR training on vascular function. Although evidence is still scarce, it seems that BFR has a mild or neutral long-term impact on arterial stiffness. However, current research shows that BFR can cause an abrupt, albeit transient, increase in PWV and central blood pressure. BFR and, preferably, lower-body BFR, should be prescribed with caution in older populations, especially in hypertensive patients who have an exacerbated muscle metaboreflex pressor response. Longer follow-up studies are required to assess the chronic effect of BFR training on arterial stiffness, especially in elderly patients who are usually unable to tolerate high-intensity resistance exercises.

The Prognostic Value of Creatine Kinase-MB Dynamics after Primary Angioplasty in ST-Elevation Myocardial Infarctions.

BACKGROUND: In STEMIs, the evaluation of the relationship between biomarkers of myocardial injury and patients' prognoses has not been completely explored. Increased levels of CK-MB in patients with a STEMI undergoing primary angioplasty are known to be associated with higher mortality rates, yet the correlation of these values with short-term evolution remains unknown. MATERIAL AND METHODS: The research encompassed a sample of 80 patients diagnosed with STEMIs, and its methodology entailed a retrospective analysis of the data collected during their hospital stays. The study population was then categorized into three distinct analysis groups based on the occurrence or absence of acute complications and fatalities. RESULTS: The findings indicated that there is a notable correlation between rising levels of CK-MB upon admission and peak CK-MB levels with a reduction in left ventricular ejection fraction. Moreover, the CK-MB variation established a point of reference for anticipating complications at 388 U/L, and a cut-off value for predicting death at 354 U/L. CONCLUSION: CK-MB values are reliable indicators of the progress of patients with STEMIs. Furthermore, the difference between the peak and admission CK-MB levels demonstrates a high accuracy of predicting complications and has a significant predictive power to estimate mortality risk.

Assessment of Inflammatory Hematological Ratios (NLR, PLR, MLR, LMR and Monocyte/HDL-Cholesterol Ratio) in Acute Myocardial Infarction and Particularities in Young Patients.

Cardiovascular disease, particularly coronary artery disease (CAD), remains a predominant cause of mortality globally. Factors such as atherosclerosis and inflammation play significant roles in the pathogenesis of CAD. The nexus between inflammation and CAD is underscored by the role of immune cells, such as neutrophils, lymphocytes, monocytes, and macrophages. These cells orchestrate the inflammatory process, a core component in the initiation and progression of atherosclerosis. The activation of these pathways and the subsequent lipid, fibrous element, and calcification accumulation can result in vessel narrowing. Hematological parameters derived from routine blood tests offer insights into the underlying inflammatory state. Recent studies have highlighted the potential of inflammatory hematological ratios, such as the neutrophil/lymphocyte ratio, platelet/lymphocyte ratio, monocyte/lymphocyte ratio and lymphocyte/monocyte ratio. These parameters are not only accessible and cost-effective but also mirror the degree of systemic inflammation. Several studies have indicated a correlation between these markers and the severity, prognosis, and presence of CAD. Despite the burgeoning interest in the relationship between inflammatory markers and CAD, there remains a paucity of data exploring these parameters in young patients with acute myocardial infarction. Such data could offer valuable insights into the unique pathophysiology of early-onset CAD and improve risk assessment and predictive strategies.

Distinct Features of Vascular Diseases in COVID-19.

The Coronavirus Disease 2019 (COVID-19) pandemic was declared in early 2020 after several unexplained pneumonia cases were first reported in Wuhan, China, and subsequently in other parts of the world. Commonly, the disease comprises several clinical features, including high temperature, dry cough, shortness of breath, and hypoxia, associated with findings of interstitial pneumonia on chest X-ray and computer tomography. Nevertheless, severe forms of acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) are not limited to the respiratory tract but also may be extended to other systems, including the cardiovascular system. The bi-directional relationship between atherosclerosis and COVID-19 is accompanied by poor prognosis. The immune response hyperactivation due to SARS-CoV-2 infection causes an increased secretion of cytokines, endothelial dysfunction, and arterial stiffness, which promotes the development of atherosclerosis. Also, due to the COVID-19 pandemic, access to healthcare amenities was reduced, resulting in increased morbidity and mortality in patients at risk. Furthermore, as lockdown measures were largely adopted worldwide, the sedentary lifestyle and the increased consumption of processed nutrients or unhealthy food increased, and in the consequence, we might observe even 70% of overweight and obese population. Altogether, with the relatively low ratio of vaccinated people in many countries, and important health debt appeared, which is now and will be for next decade a large healthcare challenge. However, the experience gained in the COVID-19 pandemic and the new methods of patients' approaching have helped the medical system to overcome this crisis and will hopefully help in the case of new possible epidemics.

An Update on MYBPC3 Gene Mutation in Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is the most prevalent genetically inherited cardiomyopathy that follows an autosomal dominant inheritance pattern. The majority of HCM cases can be attributed to mutation of the MYBPC3 gene, which encodes cMyBP-C, a crucial structural protein of the cardiac muscle. The manifestation of HCM's morphological, histological, and clinical symptoms is subject to the complex interplay of various determinants, including genetic mutation and environmental factors. Approximately half of MYBPC3 mutations give rise to truncated protein products, while the remaining mutations cause insertion/deletion, frameshift, or missense mutations of single amino acids. In addition, the onset of HCM may be attributed to disturbances in the protein and transcript quality control systems, namely, the ubiquitin-proteasome system and nonsense-mediated RNA dysfunctions. The aforementioned genetic modifications, which appear to be associated with unfavorable lifelong outcomes and are largely influenced by the type of mutation, exhibit a unique array of clinical manifestations ranging from asymptomatic to arrhythmic syncope and even sudden cardiac death. Although the current understanding of the MYBPC3 mutation does not comprehensively explain the varied phenotypic manifestations witnessed in patients with HCM, patients with pathogenic MYBPC3 mutations can exhibit an array of clinical manifestations ranging from asymptomatic to advanced heart failure and sudden cardiac death, leading to a higher rate of adverse clinical outcomes. This review focuses on MYBPC3 mutation and its characteristics as a prognostic determinant for disease onset and related clinical consequences in HCM.

Gastro-Esophageal Reflux Disease and Paroxysmal Atrial Fibrillation Ablation.

Patients undergoing ablation for atrial fibrillation may be at increased risk of developing gastroesophageal reflux disease. We prospectively studied the presence of symptomatic gastroesophageal reflux disease in naïve patients who underwent atrial fibrillation ablation. METHODS: The presence of typical symptoms suggestive of gastroesophageal reflux disease was clinically assessed by the gastroenterologist at baseline and at 3 months after ablation. In addition to that, all patients underwent upper gastrointestinal endoscopy. RESULTS: Seventy-five patients were included in two groups: 46 patients who underwent atrial fibrillation ablation (study group) and 29 patients without ablation (control group). Patients with atrial fibrillation ablation were younger (57.76 ± 7.66 years versus 67.81 ± 8.52 years; p = 0.001), predominantly male (62.2% versus 33.3%; p = 0.030) and with higher body mass index (28.96 ± 3.12 kg/m2 versus 26.81 ± 5.19 kg/m2; p = 0.046). At three months after the ablation, in the study and control groups, there were 88.9% and 57.1% patients in sinus rhythm, respectively, (p = 0.009). Symptomatic gastroesophageal reflux disease was not more frequent in the study group (42.2% versus 61.9%; p = 0.220). There was no difference in terms of sinus rhythm prevalence in patients with versus without symptomatic gastroesophageal reflux disease (89.5% versus 88.5%; p = 0.709). CONCLUSION: In this small prospective study, typical symptoms suggestive of gastroesophageal reflux disease were not more frequent three months following atrial fibrillation ablation.

Long-Term Adherence in Overweight Patients with Obstructive Sleep Apnea and Hypertension-A Pilot Prospective Cohort Study.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular risk, sedentarism, depression, anxiety and impaired quality of life. The long-term effectiveness of positive airway pressure (PAP) is insufficiently studied and limited by poor patient compliance. The aim of this pilot prospective cohort study was to evaluate long-term adherence in overweight patients with moderate-severe OSA and hypertension and to analyze changes in weight, sleepiness and quality of life. We performed a prospective study that included overweight patients with moderate-severe OSA and hypertension who had not undergone previous PAP therapy. All subjects received a standard physical examination, education regarding lifestyle changes and free PAP therapy for 2 months. After five years, the patients were invited to participate in a telephone-based interview regarding PAP compliance and completed standard questionnaires assessing adherence to medication, physical activity, diet, anxiety and quality of life (QoL). Only 39.58% of the patients were adherent to PAP 5 years (58.42 ± 3.70 months) after being diagnosed with moderate-severe OSA. Long-term PAP use results in sustained weight loss; improved blood pressure control, sleepiness and QOL; and lower anxiety and depression scores. PAP compliance was not associated with a higher level of daily physical activity or a healthier diet.

Connection between Cardiac Fibrosis Biomarkers and Echocardiography Parameters in Advanced Chronic Kidney Disease Patients.

BACKGROUND: Myocardial fibrosis represents a mainstay pathway in the pathophysiology of uremic cardiomyopathy. This process leads to structural and functional changes in the heart, which can be detected by echocardiography. The purpose of our study was to determine the association between four echocardiographic parameters (ejection fraction (EF), global longitudinal strain (GLS), mean E/e' ratio, and left atrial volume indexed) and biomarkers associated with cardiac fibrosis, such as procollagen type I carboxy-terminal propeptide (PICP), procollagen type III N-terminal peptide (P3NP), and galectin-3 (Gal-3) in patients with end-stage renal disease (ESRD). METHODS: 140 patients with ESRD were enrolled and investigated by echocardiography and the serum levels of the aforementioned biomarkers were determined at baseline. RESULTS: The mean EF was 53.63 ± 8%, the mean GLS was -10.2 ± 5.3%, the mean E/e' ratio was 9.8 ± 4.3, and the mean left atrial volume indexed (LAVI) was 45.8 ± 14.2 mL/m2. The average levels for PICP, P3NP, and Gal-3 were 457.2 ± 240 µg/L, 242 ± 199.9 µg/L, and 10.7 ± 3.7 ng/mL, respectively. In regression analysis, PICP was strongly associated with all four echocardiographic parameters (EF: p = 0.0002, R2 = 0.69; GLS: p = 0.00001, R2 = 0.81; mean E/e': p = 0.00002; R2 = 0.89; LAVI: p = 0.003; R2 = 0.73). P3NP and Gal-3 were only associated with the EF (p = 0.01, R2 = 0.31 and p = 0.02; R2 = 0.35, respectively). CONCLUSION: Our study evidenced that PICP, a collagen-derived biomarker, is associated with important echocardiography parameters, suggesting that it can serve as an indicator of the presence of subclinical systolic and diastolic dysfunction in patients with advanced CKD.

Role of arterial hypertension and angiotensin II in chronic kidney disease (Review).

Chronic kidney disease (CKD) is a major public health issue, due to its effect on the quality of life of patients and by the huge costs incurred in treating this disease. It is an irreversible process, characterized by the progressive loss of functional nephrons. CKD ultimately requires the support of renal function by dialysis or even renal transplantation. It has a multiple etiology, but the most common causes remain arterial hypertension and diabetes. High arterial blood pressure affects the target organs (kidneys) and this leads to a vicious circle involved in maintaining high blood pressure. Arterial hypertension is closely related to the renal pathology of CKD. The result of excessive activation of the renin angiotensin system (RAS) is increased angiotensin II (Ang II), which acts upon the systemic circulation and especially upon the kidneys. The outcome is high blood pressure and also the stimulation of proinflammatory and profibrotic effects in the kidneys. Collectively these ultimately lead to CKD. The aim of this review was to provide a brief overview of the pathophysiological associations between CKD, arterial hypertension, and Ang II.

A Systematic Review on the Risk Modulators of Myocardial Infarction in the "Young"-Implications of Lipoprotein (a).

The presence of a myocardial infarction at a younger age is of special interest, considering the psychological and socioeconomic impact, as well as long-term morbidity and mortality. However, this group has a unique risk profile, with less traditional cardiovascular risk factors that are not well studied. This systematic review aims to evaluate traditional risk factors of myocardial infarction in the "young", highlighting the clinical implications of lipoprotein (a). We performed a comprehensive search using Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) standards; we systematically searched the PubMed, EMBASE, and Science Direct Scopus databases, using the terms: "myocardial infarction", "young", "lipoprotein (a)", "low-density lipoprotein", "risk factors". The search identified 334 articles which were screened, and, at the end, 9 original research articles regarding the implications of lipoprotein (a) in myocardial infarction in the "young" were included in the qualitative synthesis. Elevated lipoprotein (a) levels were independently associated with an increased risk of coronary artery disease, especially in young patients, where this risk increased by threefold. Thus, it is recommended to measure the lipoprotein (a) levels in individuals with suspected familial hypercholesterolaemia or with premature atherosclerotic cardiovascular disease and no other identifiable risk factors, in order to identify patients who might benefit from a more intensive therapeutic approach and follow-up.