Current Cardiology Reviews最新文献

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.

Cardiac amyloidosis (CA) is an infiltrative disease characterized by the deposition of misfolded proteins in cardiac interstitial tissue. Interest towards studying this pathology has been growing in the last decade, as new epidemiological insights have revealed that it is not as uncommon as previously believed. Likewise, advances in non-invasive diagnostic approaches and the identification of molecules that modify its long-term progression, even in terms of mortality, have also bolstered interest in CA. Despite this global panorama, in Venezuela, limitations remain regarding the diagnosis of CA, partly associated with a lack of knowledge of the disease. Therefore, additional efforts are necessary for clinical cardiologists to hone their diagnostic skills regarding this disease, as opportune identification is an essential step for its effective management.

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.

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: Echocardiography has been proven to be a useful tool for detecting atrial-occupying lesions, ranging from primary or secondary tumors to thrombi. Although the precise diagnosis is important as clinical treatment modalities differ, sometimes differentiating a thrombus from a myxoma is very difficult.

Case report: From January 2019 to December 2022, we retrospectively analyzed the echocardiographic findings of 8 patients who were found to have an interatrial mass. Of the 8 patients, 4 had a right atrial mass, and 4 had a left atrial mass. Based on ultrasonic examination, the initial diagnosis was a thrombus and the second diagnosis was a myxoma for all 8 patients. All masses were finally confirmed to be thrombi. Although an echocardiogram can provide significant information on the nature of atrial masses in many patients, qualitative diagnosis of a small percentage of atrial masses remains difficult.

Conclusion: An atrial thrombus is occasionally difficult to differentiate from an atrial myxoma in patients without atrial fibrillation, especially when it is not attached to the left atrial appendage. Upon review of the echocardiographic findings of the 8 patients described in our study, it is essential to highlight the fact that a thrombus can mimic a myxoma and thereby create a diagnostic conundrum.

Developing a novel risk score for accurate assessment of cardiovascular disease (CVD) morbidity and mortality is an urgent need in terms of early prevention and diagnosis and, thereafter, management, particularly of ischemic heart disease. The currently used scores for the evaluation of cardiovascular disease based on the classical risk factors suffer from severe limitations, including inaccurate predictive values. Therefore, we suggest adding a novel non-classical risk factor, including the level of specific exhaled volatile organic compounds that are associated with ischemic heart disease, to the SCORE2 and SCORE2-OP algorithms. Adding these nonclassical risk factors can be used together with the classical risk factors (gender, smoking, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, diabetes mellitus, arterial hypertension, ethnicity, etc.) to develop a new algorithm and further program to be used widely.

The association between cryptogenic stroke (CS) and patent foramen ovale (PFO) with or without atrial septal aneurysm (ASA) has been a debate for decades in terms of pathophysiologic processes and clinical courses. This issue has become more interesting and complex, because of the concerns associating the CS with so-called normal variant pathologies of interatrial septum, namely ASA and PFO. While there is an anatomical pathology in the interatrial septum, namely PFO and ASA, the embolic source of stroke is not clearly defined. Moreover, in patients with PFO and CS, the risk of recurrent stroke has also been associated with other PFOunrelated factors, such as hyperlipidemia, body mass index, diabetes mellitus, and hypertension, leading to the difficulty in understanding the pathophysiologic mechanism of CS in patients with PFO and/or ASA. Theoretically, the embolic source of cryptogenic stroke in which PFO and/or ASA has been involved can be categorized into three different anatomical locations, namely PFO tissue and/or ASA tissue itself, right or left atrial chambers, and venous vascular territory distal to the right atrium, i.e., inferior vena cava and lower extremity venous system. However, the possible role of paroxysmal atrial fibrillation associated with PFO and/or ASA as a source of cryptogenic stroke has never been mentioned clearly in the literature. This review aims to explain the association of cryptogenic stroke with PFO and/or ASA in a comprehensive manner, including anatomical, clinical, and mechanistic aspects. The potential role of paroxysmal atrial fibrillation and its contribution to clinical course have been also discussed in a hypothetical manner to elucidate the pathophysiology of CS and support further treatment modalities.