Current Cardiology Reviews最新文献

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.

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: 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.

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.

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.

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.

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.

Background: Pericardial effusion is associated with amyloidosis, specifically amyloid light chain (AL) and transthyretin (ATTR) subtypes. However, the patients might present with different clinical symptoms.

Objective: To determine the characteristics and associations of patients with pericardial effusion owing to either AL or ATTR amyloidosis.

Methods: This study reviewed 26 studies from databases such as PubMed, MEDLINE, Web of Science, Google Scholar and CINAHL databases after protocol registration. The data were analyzed in IBM SPSS 21. Many statistical tests, such as Student t- and the Mann-Whitney U tests, were used. Multivariate logistic regression analysis was also performed. A p-value< 0.05 was considered significant.

Results: A total of 531 patients with pericardial effusion secondary to amyloidosis were included. The mean age was 58.4±24.5 years. Most of the patients were male (72.9%). Common co-morbid conditions included hypertension (16.8%) and active smoking (12.9%). The most common time from symptom onset to the clinical presentation was less than 1 week (45%). ATTR amyloidosis was more common in older patients (p<0.05). Abdominal and chest discomfort were commonly associated with AL and ATTR amyloidosis, respectively (p<0.05). Patients with AL amyloidosis had a higher association with interventricular septal thickening and increased posterior wall thickness (p<0.05). First-degree atrioventricular block, left bundle branch block (LBBB), and atrial fibrillation (AF) were more associated with ATTR amyloidosis (p<0.05).

Conclusion: Pericardial effusion in patients with AL amyloidosis was associated with hypertrophic remodeling, while conduction abnormalities were associated with ATTR amyloidosis.

Ischemic heart disease (IHD) is a pathology of global interest because it is widespread and has high morbidity and mortality. IHD pathophysiology involves local and systemic changes, including lipidomic, proteomic, and inflammasome changes in serum plasma. The modulation in these metabolites is viable in the pre-IHD, during the IHD period, and after management of IHD in all forms, including lifestyle changes and pharmacological and surgical interventions. Therefore, these biochemical markers (metabolite changes; lipidome, inflammasome, proteome) can be used for early prevention, treatment strategy, assessment of the patient's response to the treatment, diagnosis, and determination of prognosis. Lipidomic changes are associated with the severity of inflammation and disorder in the lipidome component, and correlation is related to disturbance of inflammasome components. Main inflammasome biomarkers that are associated with coronary artery disease progression include IL-1β, Nucleotide-binding oligomerization domain- like receptor family pyrin domain containing 3 (NLRP3), and caspase-1. Meanwhile, the main lipidome biomarkers related to coronary artery disease development involve plasmalogen lipids, lysophosphatidylethanolamine (LPE), and phosphatidylethanolamine (PE). The hypothesis of this paper is that the changes in the volatile organic compounds associated with inflammasome and lipidome changes in patients with coronary artery disease are various and depend on the severity and risk factor for death from cardiovascular disease in the time span of 10 years. In this paper, we explore the potential origin and pathway in which the lipidome and or inflammasome molecules could be excreted in the exhaled air in the form of volatile organic compounds (VOCs).