Search Results (50)

Mitral annular calcification (MAC) is usually considered an incidental, benign, age-related finding without serious complications in patients evaluated for cardiovascular or pulmonary disease with imaging studies that may result in mitral regurgitation or stenosis when severe. Therefore, it is usually not considered a significant alteration. However, there is accumulating evidence that it is associated with a higher risk of cardiovascular events, such as atherosclerotic coronary artery disease, aortic artery disease, carotid artery disease, peripheral artery disease, stroke, atrial fibrillation, atrioventricular and/or intraventricular conduction disturbance, systemic embolization, infective endocarditis, heart failure and mortality. The presence of MAC also significantly influences the outcome of mitral valve transcatheter and surgical interventions. Several conditions may predispose to MAC. MAC is strongly related to cardiovascular risk factors, such as hypertension, diabetes, smoking and cardiovascular atherosclerosis, and inflammation may also play a role in the pathogenesis of MAC. Also, conditions that increase mitral valve stress, such as hypertension, aortic stenosis and hypertrophic cardiomyopathy, predispose to accelerated degenerative calcification of the mitral annulus area. Congenital disorders, e.g., Marfan syndrome and Hurler syndrome, are also associated with MAC, due to an intrinsic abnormality of the connective tissue composing the annulus. Full article

Emerging research suggests that the intrauterine environment plays a critical role in predisposing individuals to metabolic syndrome (MetS), a constellation of conditions that heightens the risk for heart disease, stroke, and diabetes. Traditionally linked to lifestyle, the risk for MetS is now understood to be also influenced by fetal exposures. The environment in which a child lives offers abundant potential sources that can contribute to an increased risk of developing various diseases, and in some cases, these factors can be avoided. This review integrates findings from both epidemiological and experimental research to underscore the impact of prenatal factors, including maternal nutrition, obesity, gestational diabetes (GDM), and birth size, on the subsequent development of metabolic derangements in offspring, particularly during puberty. The progression of genetic and epigenetic studies has enlightened the pathophysiology of these conditions starting in the intrauterine period and continuing into early life. By examining data and studies, this article elucidates the prenatal influences and underlying mechanisms that contribute to the pathogenesis of MetS. The updated understanding of the link between the intrauterine environment and future health comorbidities will draw attention to intrauterine care and maternal health and contribute to the prevention of serious diseases in adulthood. Full article

Hypertrophic cardiomyopathy (HCM) is a condition characterized by left ventricular hypertrophy, with physiopathological remodeling that predisposes patients to atrial fibrillation (AF). The electrocardiogram is a basic diagnostic tool for evaluating heart electrical activity. Key electrocardiographic features that correlate with AF onset are P-wave duration, P-wave dispersion, and electromechanical delay in left atrium (LA). Clinical markers, including age, body mass index, New York Heart Association functional class, and heart failure symptoms, are also strong predictors of AF in HCM. Risk scores have been created using multiple variables to better predict AF development. Increasing knowledge of genetic subsets in HCM and cardiovascular pathology in general has provided novel insight in this context. Structural and mechanical LA remodeling, including fibrosis, altered LA function, and changes in atrial size, further contribute to AF risk prediction. Cardiovascular magnetic resonance (CMR) and echocardiographic measures provide accurate information about atrial structure and function. Machine learning models are increasingly being utilized to refine risk prediction, incorporating a wide range of variables. This review highlights the multifaceted approach required to understand and predict AF development in HCM. Such an approach is imperative to enhance prognostic accuracy and improve the quality of life of these patients. Further research is necessary to refine patient outcomes and develop customized management strategies for HCM-associated AF. Full article

Background and Clinical Significance: Renal abscess represents one infectious urological complication with lethal potential. The treatment of this pathology may differ depending on the severity of the symptoms and the size of the infectious collection. Diabetes, immunosuppression, and associated urinary pathologies are most frequently responsible for the development of abscesses. This case report presents the first documented case of a renal abscess associated with Sodium-glucose cotransporter 2 (SGLT2) inhibitors in a person without previous predisposing pathologies. Case Presentation: A 62-year-old patient presented to the emergency department for pain in the right flank, vomiting, and dysuria. The patient’s medical history revealed Heart Failure New York Heart Association (NYHA) Class II, Coronary Artery Disease (CAD) with prior angioplasty, and permanent Atrial Fibrillation. No prior urological or immunosuppressive conditions were detected. The Computed Tomography (CT) evaluation confirmed the ultrasound suspicion of a right renal abscess performed in the emergency room. The only risk factor identified was the initiation of SGLT2 inhibitor therapy for cardiac pathology approximately 2 months before. According to the small dimensions and urine culture, the abscess was successfully treated with antibiotic administration in collaboration with the urology department. The infectious process was remitted within 2 weeks. Conclusions: To our knowledge this is the first documented case of a renal abscess associated with SGLT2 inhibitor administration in a person without previous predisposing risk factors. Despite the relatively low incidence of urinary tract infections (UTIs) associated with SGLT2 inhibitors, their widespread use in the treatment of various socially significant conditions highlights the need for both patients and medical specialists to be aware of all potential risks and pay increased attention to these cases. Full article

As snorkelling and breath-hold diving are conducted in a potentially hostile environment by participants with varying skills and health, fatalities occur. In this study, snorkelling and breath-hold diving fatalities were investigated in Australia from 2000 to 2021 to identify causes and countermeasures. The Australasian Diving Safety Foundation database and the National Coronial Information System were searched to identify snorkelling/breath-hold diving deaths from 2000 to 2021. Relevant data were extracted, recorded, and analysed. The median age of the 317 victims was 48 years, two-thirds were overweight or obese, and almost half had health conditions, including ischaemic heart disease (IHD) and left ventricular hypertrophy (LVH), predisposing them to an arrhythmia-related snorkelling incident. One-third of victims were likely disabled by cardiac arrhythmias and at least 137 deaths were from primary drowning, with 34 following apnoeic hypoxia. Pre-existing health conditions, particularly IHD and LVH, predispose to many snorkelling deaths in older participants and may be somewhat mitigated by targeted health screening. Drownings from apnoeic hypoxia persist in younger breath-hold divers who should avoid pushing their limits without close monitoring. Skills practice in a controlled environment, increased focus on the importance of an effective buddy, and improved supervision are necessary to mitigate risk in the inexperienced. Full article

Heart failure with preserved ejection fraction (HFpEF) is increasing at an alarming rate worldwide, with limited effective therapeutic interventions in patients. Sudden cardiac death (SCD) and ventricular arrhythmias present substantial risks for the prognosis of these patients. Obesity is a risk factor for HFpEF and life-threatening arrhythmias. Obesity and its associated metabolic dysregulation, leading to metabolic syndrome, are an epidemic that poses a significant public health problem. More than one-third of the world population is overweight or obese, leading to an enhanced risk of incidence and mortality due to cardiovascular disease (CVD). Obesity predisposes patients to atrial fibrillation and ventricular and supraventricular arrhythmias—conditions that are caused by dysfunction in the electrical activity of the heart. To date, current therapeutic options for the cardiomyopathy of obesity are limited, suggesting that there is considerable room for the development of therapeutic interventions with novel mechanisms of action that will help normalize sinus rhythms in obese patients. Emerging candidates for modulation by obesity are cardiac ion channels and Ca-handling proteins. However, the underlying molecular mechanisms of the impact of obesity on these channels and Ca-handling proteins remain incompletely understood. Obesity is marked by the accumulation of adipose tissue, which is associated with a variety of adverse adaptations, including dyslipidemia (or abnormal systemic levels of free fatty acids), increased secretion of proinflammatory cytokines, fibrosis, hyperglycemia, and insulin resistance, which cause electrical remodeling and, thus, predispose patients to arrhythmias. Furthermore, adipose tissue is also associated with the accumulation of subcutaneous and visceral fat, which is marked by distinct signaling mechanisms. Thus, there may also be functional differences in the effects of the regional distribution of fat deposits on ion channel/Ca-handling protein expression. Evaluating alterations in their functional expression in obesity will lead to progress in the knowledge of the mechanisms responsible for obesity-related arrhythmias. These advances are likely to reveal new targets for pharmacological modulation. Understanding how obesity and related mechanisms lead to cardiac electrical remodeling is likely to have a significant medical and economic impact. Nevertheless, substantial knowledge gaps remain regarding HFpEF treatment, requiring further investigations to identify potential therapeutic targets. The objective of this study is to review cardiac ion channel/Ca-handling protein remodeling in the predisposition to metabolic HFpEF and arrhythmias. This review further highlights interleukin-6 (IL-6) as a potential target, cardiac bridging integrator 1 (cBIN1) as a promising gene therapy agent, and leukotriene B4 (LTB4) as an underappreciated pathway in future HFpEF management. Full article

This study investigates the impact of single prolonged stress (SPS), a model of post-traumatic stress disorder (PTSD), on cardiovascular responses, hypothalamic paraventricular nucleus (PVN) activity, and vascular function to elucidate the mechanisms linking traumatic stress to hypertension. Although SPS did not directly cause chronic hypertension in male Sprague Dawley (SD) rats, it induced acute but transient increases in blood pressure and heart rate and significantly altered the expression of hypertension-associated genes, such as vasopressin, angiotensin II type 1 receptor (AT1R), and FOSL1 in the PVN. Notably, mitochondrial reactive oxygen species (mtROS) were predominantly elevated in the pre-autonomic regions of the PVN, colocalizing with AT1R- and FOSL1-expressing cells, suggesting that oxidative stress may amplify sympathetic activation and stress responses. SPS also increased mRNA levels of pro-inflammatory cytokines (TNFα and IL1β) and inducible nitric oxide synthase (iNOS) in the aorta, and impaired vascular reactivity to vasoconstrictor and vasodilator stimuli, reflecting compromised vascular function. These findings suggest that SPS-sensitize neuroendocrine, autonomic, and vascular pathways create a state of cardiovascular vulnerability that could predispose individuals to hypertension when exposed to additional stressors. Understanding these mechanisms provides critical insights into the pathophysiology of stress-related cardiovascular disorders and underscores the need for targeted therapeutic interventions that address oxidative stress and modulate altered PVN pathways to mitigate the cardiovascular impact of PTSD and related conditions. Full article

Heart failure impairs the heart’s pumping ability and triggers catecholamine production as an adaptive mechanism. Uterine leiomyomas are common tumors of the female reproductive tract. Their growth is promoted by dysregulated angiogenesis and gonadal steroid hormones. Although uterine leiomyomas share risk factors with most cardiovascular diseases, their relationship with heart failure has not been well described. Herein, we present the case of a 45-year-old woman with heart failure who visited the emergency department, where we incidentally discovered a giant uterine leiomyoma. The patient was admitted with progressive dyspnea and abdominal distension. Echocardiography revealed an enlarged right ventricle and a decreased systolic function. Computed tomography revealed cardiomegaly with bilateral pleural effusions and a tumor measuring 18.0 × 12.0 cm in the abdominal cavity with massive ascites. A diagnosis of heart failure in conjunction with a uterine leiomyoma was established, which prompted the prescription and adjustment of heart failure medications according to the patient’s clinical presentation. Three weeks later, given the persistent symptoms of bilateral lower extremities pitting edema and abdominal distension, a total hysterectomy was performed. Postoperatively, echocardiography revealed marked improvement in her heart failure. The patient was discharged in a stable clinical and hemodynamic conditions, and reported good physical condition at the 4-month follow-up. Growth factors and the compression effect of uterine leiomyomas may predispose patients to heart failure and exacerbate its deterioration. Although reports of fibroid-related heart failure are rare, uterine leiomyomas should be considered a potential cause of refractory heart failure. Nevertheless, a direct association requires a longer follow-up period. Full article

Heart failure (HF) is a complex syndrome that requires tailored and patient-centered treatment. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) constitute one of the four pillars of the medical treatment of HF. However, the 2023 ESC guidelines treat HF as a single entity without making clear distinctions in phenotypes according to etiology. This creates a “gap in knowledge”, causing much debate about the applicability of these drugs in peculiar clinical settings that are etiological and/or predisposing clinical conditions for HF. Furthermore, considering the variety of etiologies and different pathophysiological backgrounds of HF, one might question whether the use of SGLT2is is equally beneficial in all types of HF and whether certain drug-related properties may be exploited in different contexts. For example, SGLT2is can improve the metabolic and inflammatory state, which is fundamental in ischemic heart disease. Anti-inflammatory power can also play a paramount role in myocarditis or cardiotoxicity, while improving the congestive state and reducing filling pressure may be even more fundamental in restrictive heart disease or advanced heart disease. This review aims to gather the evidence currently present in the literature concerning the advantages or the disadvantages of using these drugs in these particular clinical settings, with the goal being an optimized and highly personalized treatment for HF. Full article

Background and Objectives: Metabolic syndrome (MetS) is a condition marked by a complex array of physiological, biochemical, and metabolic abnormalities, including central obesity, insulin resistance, high blood pressure, and dyslipidemia (characterized by elevated triglycerides and reduced levels of high-density lipoproteins). The pathogenesis develops from the accumulation of lipid droplets in the hepatocyte (steatosis). This accumulation, in genetically predisposed subjects and with other external stimuli (intestinal dysbiosis, high caloric diet, physical inactivity, stress), activates the production of pro-inflammatory molecules, alter autophagy, and turn on the activity of hepatic stellate cells (HSCs), provoking the low grade chronic inflammation and the fibrosis. This syndrome is associated with a significantly increased risk of developing type 2 diabetes mellitus (T2D), cardiovascular diseases (CVD), vascular, renal, pneumologic, rheumatological, sexual, cutaneous syndromes and overall mortality, with the risk rising five- to seven-fold for T2DM, three-fold for CVD, and one and a half–fold for all-cause mortality. The purpose of this narrative review is to examine metabolic syndrome as a “systemic disease” and its interaction with major internal medicine conditions such as CVD, diabetes, renal failure, and respiratory failure. It is essential for internal medicine practitioners to approach this widespread condition in a “holistic” rather than a fragmented manner, particularly in Western countries. Additionally, it is important to be aware of the non-invasive tools available for assessing this condition. Materials and Methods: We conducted an exhaustive search on PubMed up to July 2024, focusing on terms related to metabolic syndrome and other pathologies (heart, Lung (COPD, asthma, pulmonary hypertension, OSAS) and kidney failure, vascular, rheumatological (osteoarthritis, rheumatoid arthritis), endocrinological, sexual pathologies and neoplastic risks. The review was managed in accordance with the PRISMA statement. Finally, we selected 300 studies (233 papers for the first search strategy and 67 for the second one). Our review included studies that provided insights into metabolic syndrome and non-invasive techniques for evaluating liver fibrosis and steatosis. Studies that were not conducted on humans, were published in languages other than English, or did not assess changes related to heart failure were excluded. Results: The findings revealed a clear correlation between metabolic syndrome and all the pathologies above described, indicating that non-invasive assessments of hepatic fibrosis and steatosis could potentially serve as markers for the severity and progression of the diseases. Conclusions: Metabolic syndrome is a multisystem disorder that impacts organs beyond the liver and disrupts the functioning of various organs. Notably, it is linked to a higher incidence of cardiovascular diseases, independent of traditional cardiovascular risk factors. Non-invasive assessments of hepatic fibrosis and fibrosis allow clinicians to evaluate cardiovascular risk. Additionally, the ability to assess liver steatosis may open new diagnostic, therapeutic, and prognostic avenues for managing metabolic syndrome and its complications, particularly cardiovascular disease, which is the leading cause of death in these patients. Full article

Obesity has become a global epidemic, contributing to various metabolic diseases. Despite existing therapies, the need to investigate new molecular targets to combat obesity-associated pathologies persists. Glycogen Synthase Kinase-3 (GSK-3), a serine/threonine kinase with two paralogs (GSK-3α and GSK-3β), has emerged as a critical player in obesity-associated metabolic pathologies such as type 2 diabetes (T2D), and cardiovascular diseases (CVDs). However, its ubiquitous dynamic expression and complex context-dependent signaling pathways present challenges in understanding its precise role in metabolic perturbations. In the present review, we will highlight the specific role and the proposed mechanisms via which the two GSK-3 paralogs impact obesity-associated pathologies such as T2D, diabetic cardiomyopathy (DCM), and cognitive impairment, a hallmark of Alzheimer’s disease (AD). We will also highlight studies delineating the role of GSK-3s using either GSK-3 inhibitors or non-pharmacological compounds to inhibit/taper GSK-3 activity in metabolic diseases. Thus, the primary goal of this review is to highlight recent findings delineating the regulation/dysregulation of GSK-3α/β in tissues such as heart, liver, skeletal muscle, pancreas, brain, and adipose tissue that undergo morphological and metabolic changes with diet-induced obesity which predisposes obese individuals to numerous devastating chronic conditions by GSK-3 overactivity. Full article

Obesity is a significant predisposing factor for heart failure with preserved ejection fraction (HFpEF). Although a substantial proportion of individuals with HFpEF also have obesity, those with obesity are under-represented in clinical trials for heart failure. In turn, current guidelines provided limited recommendations for the medical management of this patient population. Both obesity and diabetes induce a pro-inflammatory state that can contribute to endothelial dysfunction and coronary microvascular impairment, finally resulting in HFpEF. Additionally, obesity leads to increased epicardial and chest wall adiposity, which enhances ventricular interdependence. This condition is further aggravated by plasma and blood volume expansion and excessive vasoconstriction, ultimately worsening HFpEF. Despite the well-documented benefits of GLP-1 receptor agonists in subjects with diabetes, obesity, or both, their role in obesity-related HFpEF remains unclear. In light of the recently published literature, this review aims to investigate the potential mechanisms and synthesize the available clinical evidence regarding the role of GLP-1 receptor agonists in patients with obesity-related HFpEF. Full article

Infective endocarditis (IE) associated with implantable cardiac devices (ICD) is a serious disease with high mortality rates. The increased number of ICD implants has led to increased ICD infection rates. The aim of this study was to characterize clinical, laboratory profiles and the prognosis of cardiac-device-related endocarditis (CDIE), as well as to identify predictors of in-hospital death. A total of 274 patients with IE were included in a prospective cohort (2007–2019). From these, 82 patients (30%) had CDIE (46 pacemakers, 23 cardioverter defibrillators, and 13 cardiac resynchronization therapy devices). Predisposed conditions; clinical, laboratory and echocardiographic parameters; etiologic agents; and in-hospital outcomes were evaluated. The mean age was 55.8 ± 16.4 years, where 64.6% were male. Among the clinical manifestations at diagnosis, the most prevalent were heart failure (67.9%), fever (60.5%), anorexia/hyporexia (44.4%), and heart murmur (37.5%). The median serum C-reactive protein (CRP) level at diagnosis was 63 mg/L (interquartile range [IQR] 20–161). Etiological agents were identified through positive blood cultures in 55% of cases. The main etiologic agents were negative-coagulase staphylococci (19.5%) and Staphylococcus aureus (18.3%). Vegetation was identified in 74 patients (90.1%). In-hospital mortality was 28%. CRP concentrations at diagnosis were identified as markers of disease severity (odds ratio [OR] 1.006; 95%CI 1.001–1.011; p = 0.016), and the worsening of heart failure was associated with unfavorable outcomes (OR 3.105; 95%CI 1.397–6.902; p = 0.005). Unlike what is traditionally accepted, CDIE does not have a better prognosis. Full article

The hemostatic system is characterized by a delicate balance between pro- and anticoagulant forces, and the smallest alteration can cause serious events such as hemorrhages or thrombosis. Although exercise has been shown to play a protective role in athletes, several factors may increase the risk of developing venous thromboembolism (VTE), including hemoconcentration induced by exertion, immobilization following sports injuries, frequent long-distance flights, dehydration, and the use of oral contraceptives in female athletes. Biomarkers such as D-dimer, Factor VIII, thrombin generation, inflammatory cytokines, and leukocyte count are involved in the diagnosis of deep vein thrombosis (DVT), although their interpretation is complex and may indicate the presence of other conditions such as infections, inflammation, and heart disease. Therefore, the identification of biomarkers with high sensitivity and specificity is needed for the screening and early diagnosis of thromboembolism. Recent evidence about the correlation between the intensity of physical activity and VTE is divergent, whereas the repeated gestures in sports such as baseball, hockey, volleyball, swimming, wrestling, or, on the other hand, soccer players, runners, and martial art training represent a risk factor predisposing to the onset of upper and lower DVT. Anticoagulant therapy is the gold standard, reducing the risk of serious complications such as pulmonary embolism. The aim of this review is to provide a general overview about the interplay between physical exercise and the risk of thromboembolism in athletes, focusing on the main causes of thrombosis in professional athletes and underlying the need to identify new markers and therapies that can represent a valid tool for safeguarding the athlete’s health. Full article

Background: Infective endocarditis (IE) remains a difficult disease to diagnose and treat, with a persistently high mortality rate. There is a lack of recent data on IE in Bulgaria over the last decades. Methods: This study is retrospective, single-centered, and includes 270 patients diagnosed with IE for the period 2005–2021. We compared two periods, 2005–2015 (n = 119) and 2016–2021 (n = 151), to find the characteristics changes. Results: The study included 177 (65.5%) male patients. In the second period, there is a significant increase in age from 62 (44–73) to 67 (53–75), (p = 0.023); in the Charlson comorbidities index (CCI) from 3 (1–4) to 4 (2–6), (p = 0.000); in cases with chronic kidney diseases (CKDs) from 15 (12.6%) to 55 (36.9%), (p = 0.001); coronary arterial diseases (CADs) from 20 (16.85%) to 44 (29.1%), (p = 0.018); and atrial fibrillation (AF) from 13 (10.9%) to 36 (23.8%), (p = 0.006). Ejection fraction decreased significantly in the second period from 63 (56–70) to 59 (51–66), (p = 0.000). Almost half of the patients 123 (45.6%) had no known predisposing cardiac condition, and 125 (46.3%) had an unknown port of entry. IE was community-acquired in 174 (64.4%), healthcare-associated in 72 (26.7%), and injection-drug-use-related IE in 24 (8.9%). The study population included 183 (67.8%) native valve IE, 85 (31.5%) prosthetic IE, and 2 (0.74%) intracardiac-device-related IE. The hemocultures were positive in 159 (59.6%), and the most frequent pathogenic agent was staphylococci—89 (33.3%) (Staphylococcus aureus—44 (16.5%) and coagulase negative staphylococci—45 (16.8%)). Only 54 (20%) of patients underwent early surgery. The all-cause 30-day mortality rate was 67 (24.8%). There is no significant difference between the two periods in terms of the characteristics listed above. Conclusions: The profile of IE in Bulgaria has changed with increasing age and comorbidity, changing predisposing cardiac conditions, and entry door. The most common pathogen was the Staphylococcus spp. The 30-day mortality rate remains high. Full article