Current Cardiology Reviews最新文献

Background: Hypermobile Ehlers-Danlos Syndrome (hEDS) is a connective tissue disorder characterized by joint hypermobility and other systemic manifestations, such as cardiovascular symptoms, musculoskeletal pain, and joint instability. Cardiovascular symptoms, such as lightheadedness and palpitations, and types of dysautonomia, including postural orthostatic tachycardia syndrome (POTS), are frequently reported in adults with hEDS and have been shown to negatively impact quality of life (QoL).

Objective: This brief review will be an overview of co-occurring symptoms in POTS and hEDS to inform potential cardiovascular screening procedures.

Results: While many patients with hEDS report cardiovascular symptoms, few have structural abnormalities, suggesting that dysautonomia is likely responsible for these symptoms. One validated screening measure for dysautonomia symptom burden is the Composite Autonomic Symptom Scale (COMPASS-31). Studies have found that adults with POTS, hEDS, and both POTS and hEDS have higher COMPASS-31 scores than the general population, suggesting a high symptom burden due to dysautonomia, which leads to impaired QoL.

Conclusion: While studies have examined cardiovascular symptoms and the impact of dysautonomia in adults with and without hEDS, there is scant literature on dysautonomia in pediatric patients with hEDS. Therefore, more studies on cardiovascular symptoms and dysautonomia, as they relate to the quality of life in pediatric patients with hEDS, are needed. This brief review summarizes the current literature on dysautonomia and cardiovascular symptoms in pediatric and adult populations with hEDS.

The use of cardioprotective strategies as adjuvants of cardioplegic solutions has become an ideal alternative for the improvement of post-surgery heart recovery. The choice of the optimal cardioplegia, as well as its distribution mechanism, remains controversial in the field of cardiovascular surgery. There is still a need to search for new and better cardioprotective methods during cardioplegic procedures. New techniques for the management of cardiovascular complications during cardioplegia have evolved with new alternatives and additives, and each new strategy provides a tool to neutralize the damage after ischemia/reperfusion events. Researchers and clinicians have committed themselves to studying the effect of new strategies and adjuvant components with the potential to improve the cardioprotective effect of cardioplegic solutions in preventing myocardial ischemia/reperfusion-induced injury during cardiac surgery. The aim of this review is to explore the different types of cardioplegia, their protection mechanisms, and which strategies have been proposed to enhance the function of these solutions in hearts exposed to cardiovascular pathologies that require surgical alternatives for their corrective progression.

Congenital heart defects represent the most common structural anomalies observed in the fetal population, and they are often associated with significant morbidity and mortality. The fetal cardiac axis, which indicates the orientation of the heart in relation to the chest wall, is formed by the angle between the anteroposterior axis of the chest and the interventricular septum of the heart. Studies conducted during the first trimester have demonstrated promising outcomes with respect to the applicability of cardiac axis measurement in fetuses with congenital heart defects as well as fetuses with extracardiac and chromosomal anomalies, which may result in improved health outcomes and reduced healthcare costs. The main aim of this review article was to highlight the cardiac axis as a reliable and powerful marker for the detection of congenital heart defects during early gestation, including defects that would otherwise remain undetectable through the conventional four-chamber view.

Vitamin D hormone is an important regulator of various physiological functions, and its deficiency is characterized by an imbalance in parathyroid hormone and calcium homeostasis. The role of vitamin D in cardiovascular physiology is well demonstrated in animal and humanbased studies. In this context, hyperlipidemia, increased atherogenic plaques, cardiac inflammation, hypertension, myocarditis, myocardial infarction, and heart failure are some of the commonest known conditions connected with vitamin D deficiency. Supplementation of vitamin D is recommended to achieve normal serum vitamin D concentrations, nonetheless, in clinical trials often seen discrepancies concerning the supplementation effects and effectiveness. This review summarizes the data on the role of vitamin D in cardiovascular health along with some recent clinical findings regarding the effects of vitamin D supplementation.

Heart failure (HF) is the fastest-growing cardiovascular condition worldwide. The immune system may play a role in the development of HF since this condition is associated with elevated pro-inflammatory cytokine levels. HF is a life-threatening disease, and there is an increasing demand for diagnostic biomarkers, prognostic factors, and therapeutic agents that can help treat it. Galectin-1 (Gal-1) is the prototype galectin of the lectin family. Multiple signal transduction pathways are regulated by Ras proteins, which act as a molecular switch in cells. Gal-1 regulates T and B cell activation, differentiation, and survival. Gal-1 has been linked to inflammation. Activated T cells produce Gal-1 through an autocrine apoptotic mechanism involving MEK1/ERK and p38 MAPK. In the cardiovascular system, atherosclerosis is facilitated by Gal-1. Heart disease, myocardial infarction, hypertension, and stroke can be caused by atherosclerotic plaque. HF and heart hypertrophy are caused by decreased cardiac L-type Ca2+ channel activity. Deregulation of Gal-1 and CaV1.2 in pathological cardiac hypertrophy suggests a possible target for anti-hypertrophic therapy. Rat hypertrophic cardiomyocytes express Gal-1 and CaV1.2 channels simultaneously. It has been reported that diastolic dysfunction (DD) is associated with elevated Gal-1 levels. The high Gal-1 level in subjects led to the lowest cumulative survival as a composite endpoint. Incidences of HF, DD, and serum Gal-1 levels correlated significantly. The ejection fraction was negatively correlated with Gal-1 and CRP concentrations. Based on two different approaches in mice and humans, Gal-1 was identified as a potential mediator of HF.

Cardiovascular diseases (CVD) constitute a leading cause of global mortality. Inflammation and oxidative stress are key molecular underpinnings of CVD pathogenesis. This comprehensive review explores the multifaceted role of nutrients in cardiovascular health beyond their impact on cardiac events. The manuscript examines the influence of macronutrients such as fats and carbohydrates, as well as micronutrients including vitamins and folate, on CVD. Additionally, the interplay between dietary supplements and CVD risk reduction is investigated. The purpose of this manuscript is to provide a comprehensive overview of the diverse mechanisms through which nutrients contribute to cardiovascular well-being, addressing both cardioprotective effects and their broader implications. Through an analysis of pertinent studies, we illuminate the complex relationship between nutrition, lifestyle, and cardiovascular health, underscoring the significance of a holistic approach to CVD prevention and management.

Over 750,000 individuals suffer from stroke annually in the United States, with 87% of these strokes being ischemic in nature. Roughly 40% of ischemic strokes occur in individuals 60 years of age or under. A quarter of all ischemic strokes have no identifiable cause despite extensive workup and are deemed cryptogenic in nature. Patent Foramen Ovales (PFO) has been postulated in stroke causation by either paradoxical embolization or platelet activation in the tunnel of the defect. The incidence of PFO is reported to be 15-25% in the general population but rises to 40% in patients with cryptogenic stroke. While the initial trials evaluating PFO closures were non-revealing, subsequent long-term follow-ups, as well as recent trials evaluating PFO closures in cryptogenic stroke patients 60 years of age or under, demonstrated the superiority of percutaneous closure compared to medical therapy alone, leading to FDA approval of PFO closure devices. In this review, we review the diagnosis of PFO, postulated stroke mechanisms, literature supporting PFO closure, patient selection for percutaneous closure, procedural considerations, and associated procedural complications.

Background: Cardiac remodelling could be a key mechanism in aldosteronemediated cardiovascular morbidity and mortality. Experimental and clinical evidence has demonstrated that aldosterone causes cardiac structural remodelling and dysfunction by its profibrotic and pro-hypertrophic effects, which result mainly from the direct effects on myocardial collagen deposition, inflammation, and oxidative stress. Clinical studies have investigated the aldosterone effects on the heart in different clinical conditions, including general population, essential hypertension, primary aldosteronism, heart failure, and atrial fibrillation. Robust findings indicate that aldosterone or the activation of the cardiac mineralocorticoid receptor can cause damage to myocardial tissue by mechanisms independent of the blood pressure, leading to tissue hypertrophy, fibrosis, and dysfunction.

Conclusion: Aldosterone-mediated cardiovascular morbidity and mortality mainly result from cardiac structural and functional alterations. In different clinical settings, aldosterone can induce cardiac structural remodelling and dysfunction via several pathological mechanisms, including cardiac fibrosis, inflammation, and oxidative stress. Aldosterone antagonists could effectively decrease or reverse the detrimental aldosterone-mediated changes in the heart.

Background: Previous publications in 2011, 2016, and 2022 have presented lists of drugs associated with takotsubo cardiomyopathy (TCM). This review aims to provide updated drug lists that have been reported as potential causes of TCM.

Methods: Following the same methodology employed in previous reviews, a detailed investigation was carried out in the PubMed/Medline database from June 2022 to July 2023 to identify drug-induced TCM (DITC) case reports. Various search terms related to the drug-induced transient left ventricular ballooning syndrome, ampulla cardiomyopathy, apical ballooning syndrome, drug-induced broken heart syndrome, drug triggered takotsubo cardiomyopathy, takotsubo cardiomyopathy, and iatrogenic takotsubo cardiomyopathy were utilized. Filters for fulltext availability, case reports, human studies, and English language were applied. Articles reporting drugs associated with TCM development were included in the analysis.

Results: Foremost 192 case reports were initially identified, with 75 drugs meeting the inclusion criteria after a thorough review. The latest revision identified seven drugs that might lead to TCM, with four drugs (57.14%) already reported in previous reviews and three drugs (42.86%) newly identified. Consequently, the updated drug list potentially triggering TCM in 2023 comprises a sum of 75 drugs.

Conclusion: The recent 75 drugs provided additional evidence linking to TCM development. The updated list predominantly includes drugs that induce sympathetic overstimulation, although some drugs on the list have unclear associations with sympathetic nervous system activation.