Current Cardiology Reviews最新文献

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.

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).

Background: Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality worldwide. Polypills, containing various combinations of medications for primary and secondary CVD prevention, have been developed to enhance medication adherence and reduce the healthcare burden of CVD. However, their effectiveness compared to usual care remains uncertain.

Objective: This meta-analysis aimed to evaluate the effects of polypills on cardiovascular risk factors, major adverse cardiovascular events (MACE), and medication adherence.

Methods: We conducted a comprehensive search for large-scale randomized controlled trials and observational studies comparing the effects of polypills versus usual care on CVD risk factors and events. Outcomes included changes in systolic and diastolic blood pressure (SBP, DBP), lipid profiles, occurrence of MACE, and medication adherence.

Results: The use of polypills led to a statistically significant yet clinically modest reduction in SBP (mean difference -1.47 mmHg, 95% CI: -2.50 to -0.44, p<0.01) and DBP (mean difference- 1.10 mmHg, 95% CI: -1.68 to -0.51, p< 0.01) compared to usual care. Polypills also showed a significant reduction in the risk of MACE (RR: 0.86, 95% CI: 0.77 -0.95, p<0.01). There was a non-significant reduction in LDL and HDL levels. Adherence to medication improved by up to 17% in polypill users compared to those on usual care (p < 0.01). A multivariable metaregression analysis suggested that adherence may be the underlying factor responsible for the observed effect of the polypills on blood pressure.

Conclusion: Polypills were found to significantly reduce SBP, DBP and MACE. An improvement in medication adherence was also observed among polypill users, which might be responsible for the significant reduction in SBP observed users. Future research might benefit from exploring a more personalized approach to the composition of polypills, which could reveal a more clinically significant impact of increased adherence on CVD outcomes.

Hypertrophic cardiomyopathy (HCM) results from gene mutations affecting cardiac sarcomeres and is inherited in an autosomal dominant manner. With a prevalence of 1:200-1:500 in the general population, HCM is characterised by a hypertrophied and non-dilated left ventricle with predominant involvement of the interventricular septum. The myocardium's structural and intracellular factors, combined with triggers such as physical exertion, autonomic dysfunction, and ischemia, can lead to reentry events, and atrial and ventricular arrhythmias, including atrial fibrillation (AF) which is common among HCM patients. To manage the increased risk of mortality arising from congestive heart failure and thromboembolism, in patients with AF long-term anticoagulation and antiarrhythmic drugs are employed. HCM patients may also encounter supraventricular and ventricular arrhythmias, such as nonsustained ventricular tachycardia and ventricular premature beats, which can potentially lead to sudden cardiac death and necessitate treatment with implanted defibrillators. Physicians must comprehensively analyse clinical, anatomical, hemodynamic, rhythmic, functional, and genetic characteristics to identify HCM patients at high risk of sudden death. This article aims to discuss the pathophysiology of arrhythmia in HCM and clinical recommendations for various ventricular and atrial fibrillation including catheter ablation and implantable cardioverter-defibrillator (ICD).

Although there is a continually growing number of patients with congenital heart disease (CHD) due to medical and surgical advances, these patients still have a poorer prognosis compared to healthy individuals of similar age. In patients with heart failure, microvascular dysfunction (MVD) has recently emerged as a crucial modulator of disease initiation and progression. Because of the substantial pathophysiological overlap between CHD and heart failure induced by other etiologies, MVD could be important in the pathophysiology of CHD as well. MVD is believed to be a systemic disease and may be manifested in several vascular beds. This review will focus on what is currently known about MVD in the peripheral vasculature in CHD. Therefore, a search on the direct assessment of the vasodilatory capacity of the peripheral microcirculation in patients with CHD was conducted in the PubMed database. Since there is little data available and the reported studies are also very heterogeneous, peripheral MVD in CHD is not sufficiently understood to date. Its exact extent and pathophysiological relevance remain to be elucidated in further research.

Fractional flow reserve computed tomography (FFRCT) is a novel imaging modality. It utilizes computational fluid dynamics analysis of coronary blood flow obtained from CCTA images to estimate the decrease in pressure across coronary stenosis during the maximum hyperemia. The FFRCT can serve as a valuable tool in the assessment of coronary artery disease (CAD). This non-invasive option can be used as an alternative to the invasive fractional Flow Reserve (FFR) evaluation, which is presently considered the gold standard for evaluating the physiological significance of coronary stenoses. It can help in several clinical situations, including Assessment of Acute and stable chest pain, virtual planning for coronary stenting, and treatment decision-making. Although FFRCT has demonstrated potential clinical applications as a non-invasive imaging technique, it is also crucial to acknowledge its limitations in clinical practice. As a result, it is imperative to meticulously evaluate the advantages and drawbacks of FFRCT individually and contemplate its application in combination with other diagnostic examinations and clinical data.