Current Cardiology Reviews最新文献

Background: Supraventricular tachycardia (SVT) is very common in daily clinical practice, especially in the emergency department, with rapid onset and urgent management. The review highlights the recent genetic predispositions and mechanisms in SVT.

Methods: Through analysis of epidemiology, familial clustering, and gene mutations of the relevant literature, the review elucidates the genetic properties and potential pathophysiology of SVT.

Results: There are many pathophysiological mechanisms related to atrioventricular node reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Currently, there is relatively little research on inappropriate sinus tachycardia (IST), atrial tachycardia (AT), and congenital junctional ectopic tachycardia (CJET). It seems that every type of SVT has gene mutations in ion channels, with three types of SVT having gene mutations in signaling pathways, and others including gene mutations in beta-adrenergic-receptor autoantibodies, autonomic nervous system, and AV node structure.

Conclusion: SVT has certain genetic characteristics and is often associated with other heart diseases. From the analysis of mutated genes in SVT, it appears to be a type of cardiac ion channel disease. Unlike common ion channel diseases, it is more insidious and more susceptible to external factors. The confirmation of the genetic basis of SVT provides direction for future hazard stratification assessment and gene targeted therapy drug research.

Introduction: Non-bacterial Thrombotic Endocarditis (NBTE) is a rare condition characterized by aseptic vegetations of the heart valves, predisposing to valvular dysfunction and end-organ infarction. Lung Cancer (LC) is amongst the most common malignancies associated with NBTE.

Methods: PubMed/MEDLINE was searched from database inception until January 2024, pairing Non-bacterial Thrombotic Endocarditis (NBTE) and related terms with "Lung Cancer (LC)". Reports were included if patients had both NBTE and lung cancer. The risk of bias was assessed using Mixed Methods Analysis Testing (MMAT).

Results and discussion: 32 patients with an average age of 59y +/- 11.6 were included from 31 peer-reviewed publications, with significant findings as below: • The majority (47%) of patients were admitted with stroke. • The most commonly affected valve was aortic (51%), followed by mitral (43%), and tricuspid (5%). • At diagnosis of NBTE, 86% of patients had stage IV cancer. • Multi-organ infarct was common (61%), with the brain most often affected (40%). • Treatment of NBTE included antibiotics (86%), anticoagulation (50%), and cardiac surgery (6%). • Treatment of LC included traditional chemotherapy (30.7%), radiation (16%), tyrosine kinase inhibitors (11.5%), lobectomy (6%), and immunotherapy (3.8%). • Overall mortality rate was 77%. • Mortality rate was 38% in patients treated with chemotherapy and 91% in patients who did not receive chemotherapy. • Mortality rate stratified by anticoagulant: unfractionated heparin (85.7%), DOAC (75%), and LMWH (20%).

Conclusion: High clinical suspicion for NBTE in patients presenting with LC and thromboembolic phenomena can lead to changes in treatment and improved clinical outcomes.

The coexistence of cancer and heart disease, both prominent causes of illness and death, is further exacerbated by the detrimental impact of chemotherapy. Anthracycline-induced cardiotoxicity is an unfortunate side effect of highly effective therapy in treating different types of cancer; it presents a significant challenge for both clinicians and patients due to the considerable risk of cardiotoxicity. Despite significant progress in understanding these mechanisms, challenges persist in identifying effective preventive and therapeutic strategies, rendering it a subject of continued research even after three decades of intensive global investigation. The molecular targets and signaling pathways explored provide insights for developing targeted therapies, emphasizing the need for continued research to bridge the gap between preclinical understanding and clinical applications. This review provides a comprehensive exploration of the intricate mechanisms underlying anthracycline-induced cardiotoxicity, elucidating the interplay of various signaling pathways leading to adverse cellular events, including cardiotoxicity and death. It highlights the extensive involvement of pathways associated with oxidative stress, inflammation, apoptosis, and cellular stress responses, offering insights into potential and unexplored targets for therapeutic intervention in mitigating anthracycline-induced cardiac complications. A comprehensive understanding of the interplay between anthracyclines and these complexes signaling pathways is crucial for developing strategies to prevent or mitigate the associated cardiotoxicity. Further research is needed to outline the specific contributions of these pathways and identify potential therapeutic targets to improve the safety and efficacy of anthracycline-based cancer treatment. Ultimately, advancements in understanding anthracycline-induced cardiotoxicity mechanisms will facilitate the development of more efficacious preventive and treatment approaches, thereby improving outcomes for cancer patients undergoing anthracycline-based chemotherapy.

Insulin resistance describes the lack of activity of a known quantity of insulin (exogenous or endogenous) to promote the uptake of glucose and its utilization in an individual, as much as it does in metabolically normal individuals. On the cellular level, it suggests insufficient power of the insulin pathway (from the insulin receptor downstream to its final substrates) that is essential for multiple mitogenic and metabolic aspects of cellular homeostasis. Atherosclerosis is a slow, complex, and multifactorial pathobiological process in medium to large arteries and involves several tissues and cell types (immune, vascular, and metabolic cells). Inflammatory responses and immunoregulation are key players in its development and progression. This paper examines the possible pathophysiological mechanisms that govern the connection of insulin resistance, hyperinsulinemia, and the closely associated cardiometabolic syndrome with atherosclerosis, after exploring thoroughly both in vitro and in vivo (preclinical and clinical) evidence. It also discusses the importance of visualizing and developing novel therapeutic strategies and targets for treatment, to face this metabolic state through its genesis.

Iron deficiency anemia (IDA) is highly prevalent among individuals with heart failure (HF), impacting 40-70% of patients and serving as a significant prognostic indicator. Linked with oxidative metabolism and myocardial cell damage, IDA exacerbates HF symptoms, including reduced exercise capacity, diminished quality of life, and heightened cardiovascular morbidity. This review explores the diagnosis, treatment, clinical outcomes, prognostic indicators, and forthcoming challenges associated with IDA in HF patients. Crucially, addressing IDA in HF is critical for enhancing prognosis, including clinical outcomes, quality of life, hospitalizations, and survival rates. While oral iron therapy shows efficacy in reducing mortality and hospitalizations, it falls short in improving exercise capacity and quality of life, often deterring patients due to side effects. In contrast, intravenous (IV) iron therapy is highly effective in enhancing hematological parameters, functional capacity, and reducing HF hospitalizations. Optimizing IV iron dosing based on individual patient characteristics is essential for balancing treatment efficacy and adverse effects. Emphasizing individualized approaches, with IV iron emerging as a superior option, underscores the necessity for ongoing research to refine dosing strategies and explore novel therapies. Compliance remains paramount for positive outcomes with IDA treatment, with oral supplementation being cost-effective and easily accessible. However, parenteral supplementation proves beneficial for patients intolerant to oral therapy. Addressing IDA through tailored interventions, including oral or parenteral supplementation, is pivotal in averting complications and improving outcomes in HF patients. This paper consolidates insights into the diagnosis, treatment, impact, pathophysiology, clinical outcomes, research gaps, and future directions concerning IDA in HF patients, drawing on extensive literature to offer a comprehensive understanding of this critical issue.

Introduction: Advances in cardiac implanted electronic devices (CIED) have significantly improved outcomes for patients with heart failure. However, there is a bereft of recent real- world data on the relative effectiveness of cardiac resynchronization therapy with pacing and defibrillator (CRT-D) and continuous resynchronization therapy with pacing (CRT-P) in patients with nonischemic cardiomyopathy (NICM). We hypothesized that the addition of defibrillation therapy in patients with NICM would offer no significant benefit.

Methods: We searched the National Readmissions Database (NRD) from 2016-2020 to identify hospitalizations with NICM using appropriate ICD-10 diagnosis and procedure codes. The cohort was further divided into groups with NICM and CRT-D implantation and NICM with CRTP implantation.

Results and discussion: Our final cohort included 8,801 hospitalizations with NICM and CRTD implantation and 3,399 hospitalizations with NICM and CRT-P implantation. Propensity matching was performed using comorbidities through multivariate logistic regression. Two thousand nine hundred seventeen hospitalizations were included in each of the two groups, CRT-D and CRT-P. Analysis of the propensity-matched cohorts at 180 days revealed a trend toward lower heart failure readmission, all-cause readmission, and all-cause mortality rates in the group with CRT-P implantation. However, there was no difference noted in the 180-day hazard ratios of HF readmission [1.08 (0.98-1.19); p = 0.1], all-cause readmission [1.04 (0.87- 1.12); p = 0.23], and all-cause mortality [0.83 (0.58-1.19); p = 0.32].

Conclusion: It was found that NICM patients with CRT-D have a trend towards higher HF readmissions, all-cause readmission, and all-cause mortality compared to those with CRT-P, but no significant difference was noted in hazard ratios. The findings of our study raise further questions about the need for defibrillator therapy in patients with NICM and merit further studies to better select candidates for each of these therapies.

Introduction: Pediatric heart failure (HF) poses diagnostic challenges, especially in emergency settings, where misdiagnoses are common.

Aim: This study aimed to investigate the causes of HF in children with congenital heart disease (CHD) and provide insights into age-related disparities and clinical classifications.

Methods: A prospective observational cohort study was conducted on 402 pediatric patients with CHD during the years 2019-2020. Ultimately, 45 pediatric patients diagnosed with HF by two pediatric cardiologists based on clinical symptoms and radiographic changes were included in the study. Information from the patients' files, including epidemiological findings, clinical examinations, paraclinical findings, and interventions performed, was recorded. Etiological factors and clinical classifications were analyzed using statistical tests.

Results and discussion: Among 402 pediatric patients with CHD, 45 (11.19%) were diagnosed with HF, with a median age of 7.5 months. The predominant etiological factors included ventricular septal defect (VSD), atrial septal defect (ASD), and cardiomyopathy. Analysis of etiological factors revealed that single structural defects accounted for 71.11% of HF cases, while concurrent defects contributed to a significant portion of the remaining cases. Clinical classifications revealed age-related differences, emphasizing the heterogeneity of pediatric HF presentations.

Conclusion: Given that all patients with HF in our study had CHD, more investigations into the causes and mechanisms of this issue are necessary, which will be possible with genetic studies. A significant difference was observed between Class II and Class IV, with Class II patients being older and heavier, and having a lower heart rate compared to those in Class IV. This aligns with the classifications, where Class II indicates mild symptoms during ordinary activity, while Class IV signifies severe symptoms at rest.

Introduction: Reducing the risk of atherosclerotic cardiovascular disease is the aim of lipid-lowering therapy (ASCVD). It is commonly acknowledged that low-density lipoprotein (LDL) is a major cause of ASCVD. Several online databases and search engines, such as Pub- Med and the Cochrane Library, were used to conduct a thorough search.

Methods: This study included RCTs assessing the effect of PCSK9 inhibitors on cardiovascular events. The RevMan 5.4 software was used to conduct the meta-analysis. This analysis included nine RCTs in total.

Results: Meta-analysis of the included studies showed that the levels of total cholesterol, LDL, and triglycerides were reduced after the use of PCSK9 inhibitors, and HDL levels were increased, which is good cholesterol. Most adverse cardiac events (MACE) were reduced after the use of PCSK9 inhibitors.

Conclusion: In conclusion, ezetimibe, a PCSK9 inhibitor added to statin therapy, further reduces MACE risk without affecting all-cause mortality, even though statins already significantly reduce major adverse cardiovascular events (MACE) and mortality.

Background/introduction: The misdiagnosis of seizure disorders in patients with cardiogenic syncope and tachy-bradyarrhythmias is a significant diagnostic challenge as the differentials for altered mental status and syncope are broad and can mimic other clinical conditions. This case report presents a unique case of an elderly male with life-threatening ventricular arrhythmia, initially misdiagnosed as a seizure disorder associated with syncope and treated with anti-epileptics for a neurogenic cause, before an ambulatory cardiac monitor revealed a sinister cardiogenic etiology.

Case presentation: An 87-year-old man with ischemic cardiomyopathy (LVEF 20%) and persistent atrial fibrillation presented for implantable cardioverter-defibrillator (ICD) evaluation following a ventricular fibrillation (VF) arrest. He had a history of recurrent syncope accompanied by muscle jerking and was initially treated with anti-epileptic drugs. However, further evaluation with mobile telemetry revealed ventricular arrhythmias, including nonsustained VT, VF, and asystole. Anti-epileptic medications were discontinued, and the patient was started on amiodarone. A cardiac resynchronization therapy defibrillator (CRT-D) was implanted, which successfully resolved his symptoms. Post-treatment, he remained asymptomatic, with no new VT/VF episodes detected at one week and three months during follow-up device checks.

Conclusion: This case underscores the importance of considering cardiogenic causes in patients with syncope and seizure-like symptoms. Therefore, a multidisciplinary approach is essential for accurate diagnosis and management.