Cardiology Research最新文献

Atrial fibrillation (AF) is a common arrhythmia in critically ill patients. The objective of this narrative review is to evaluate the characteristics of patients who develop new-onset atrial fibrillation (NOAF) because of sepsis, current management of NOAF in sepsis patients, special consideration in different populations that developed NOAF, health economic and quality of life of patients. We conducted a literature search on PubMed to find research related to NOAF, sepsis and critical illness. Nineteen studies were analyzed for risk factors and outcomes. The incidence rate ranges from 0.53% to 43.9% among these studies. There were numerous risk factors that had been reported from these articles. The most reported risk factors included advanced age, male sex, White race, and cardiovascular comorbidities. The management of septic patients is significantly challenging because of the unfavorable cardiovascular consequences and thromboembolic hazards associated with NOAF. There are comprehensive guidelines available for managing AF, but the effectiveness and safety of therapies in patients with sepsis are still uncertain. Various approaches for managing newly diagnosed AF have been explored. Sinus rhythm can be restored through either pharmacological or non-pharmacological intervention or combination of both. In addition, thromboembolism is a complication that can occur in patients with AF and can have a negative impact on the prognosis of sepsis patients. The use of anticoagulation to prevent stroke after NOAF in sepsis patients is still controversial. Extensive prospective investigations are required to have a deeper understanding of the necessity for anticoagulation following NOAF in sepsis. Beside the treatment of NOAF, early detection of NOAF in sepsis plays a critical role. The prompt initiation of rhythm control medication following a clinical diagnosis of AF can enhance cardiovascular outcomes and reduce mortality in patients with AF and cardiovascular risk factors. Additionally, NOAF in the intensive care unit can prolong hospital stays, increasing hospitalization costs and burdening the hospital. Therefore, preventing and managing NOAF effectively not only benefit the patients but also the hospital in financial aspect. Lastly, to address the existing gaps in knowledge, future research should focus on developing machine learning models that can accurately anticipate risks, establish long-term follow-up protocols, and create complete monitoring systems. The focus is on early intervention and personalized approaches to improve outcomes and quality of life.

Background: This study evaluated the safety and efficacy of BioMime sirolimus-eluting stent (SES) system, with an ultra-low strut thickness (65 µm), in real-world all-comers population with coronary artery stenosis (CAD).

Methods: This was a post-marketing, multicenter, single-arm, observational clinical registry among patients undergoing intervention for CAD. Patients were clinically followed up at 1, 9, 12, and 24 months after the index percutaneous coronary intervention. Four major indications, namely long stents of > 30 mm, stents with diameters of 4 and 4.5 mm, bifurcation subgroup, and chronic total occlusion (CTO) were evaluated as pre-specified subsets.

Results: A total of 771 patients (1,079 treated lesions) from 23 sites were included in this study. The mean length and diameter of the implanted stents were 25.57 ± 9.35 mm and 3.00 ± 0.44 mm, respectively. The mean minimum lumen diameter before and after the procedure was 1.00 ± 1.69 mm and 2.96 ± 1.35 mm, respectively. The cumulative rates of major adverse cardiovascular events (MACEs) and stent thrombosis (ST) at 1, 9, 12, and 24 months were 1.05%, 3.13%, 4.04%, 5.64% and 0%, 0.13%, 0.28%, 0.28%, respectively. In a subset with > 30 mm long stents, the cumulative rate of MACEs was 0.4%, 4.6%, 5.12%, and 7.01% at 1, 9, 12, and 24 months, respectively. The corresponding rates of ST were 0%, 0.42%, 0.43%, and 0.44%, indicating constant rate of ST after 9 months. In a subset of 4 and 4.5 mm diameter stents, the cumulative rate of MACEs was high (0%, 6.25%, 6.25%, and 10.41%) at 1, 9, 12, and 24 months, respectively. However, there was no case of ST until 24 months. In patients with bifurcation lesions, the cumulative rates of MACEs and ST were 2.46%, 6.32%, 11.53%, 16.21% and 0%, 1.27%, 1.28%, 1.35% at 1, 9, 12, and 24 months follow-up. In patients with chronic total occlusion, the cumulative rates of MACEs and ST were 0.79%, 5.04%, 6.83%, 7.07% and 0%, 0.84%, 0.85%, 0.88% at 1, 9, 12, and 24 months, respectively, indicating constant rate of ST after 9 months.

Conclusions: The BioMime SES demonstrated good safety and efficacy outcomes at 24-month follow-up, with low rates of MACEs and ST in patients with CAD in the real-world setting.

Continuous electrocardiographic (ECG) monitoring remains crucial during surgery in infants and children. Although generally uncommon in pediatric-aged patients, ECG changes may occasionally be indicative of a variety of myocardial pathologies including anomalous origin of coronary arteries, ventricular hypertrophy, myocarditis, hypothermia, drug effects, electrolyte abnormalities, acid-base disturbances or conduction system disorders such as Wolff-Parkinson-White and Brugada syndrome. Distinguishing between pathologic and non-pathologic conditions impacting the ECG must be considered so that appropriate interventions are provided to prevent perioperative morbidity and mortality. We report a case of a 2-year-old child who exhibited ST segment depression and increased R wave amplitude during general anesthesia. Although the anesthetic care was uneventful and the patient was otherwise asymptomatic, immediate postoperative workup including echocardiogram revealed previously undiagnosed hypertrophic cardiomyopathy. The occurrence of intraoperative ST-T wave changes in this patient underscores the need for a high index of suspicion for underlying cardiac pathology, even in the absence of overt clinical manifestations. This case highlights the importance of intraoperative ECG monitoring in pediatric patients, explores the causes of ST-T wave changes, reviews similar cases in the literature, and proposes a pathway for perioperative evaluation.

Background: Syncope is a common medical condition. The reflex or neurally mediated syncope (NMS) is the most frequent type. The tilt table test (TTT) helps distinguish syncope from other common causes of complete loss of consciousness, such as epilepsy, define syncope subtypes and guide management. This study aimed to assess the TTT yield in patients with suspected NMS and to compare the nitroglycerin (NTG) and isoproterenol (Isuprel) provocative protocols.

Methods: This study was a retrospective analysis of the data of 426 consecutive patients who underwent TTT at the Heart Center at King Faisal Specialist Hospital and Research Center (KFSH&RC), Riyadh, Saudi Arabia, between January 1, 2006, and March 31, 2017.

Results: The age at referral for TTT ranged from 7 to 84 years (mean 38.4 ± 15.75 years), and 212 (49.8%) were males. The main clinical manifestations were recurrent syncope in 259 patients (60.8%), a single syncopal episode in 60 (14.1%), and pre-syncope or dizzy spells without loss of consciousness in 171(25.1%). The test was positive in 295 patients (69.2%), with type 1 (mixed response) seen in 151 patients (51.19%), type 2a (cardioinhibitory without pause) in 16 (5.4%), type 2b (cardioinhibitory with pause) in 10 patients (3.39%), and type 3 (vasodepressor) in 118 patients (40%). A false positive test was seen in 11 patients (2.6%) and a false negative in 27 patients (6.3%). The overall test sensitivity was 91%, specificity was 89%, positive predictive value (PPV) was 96%, and negative predictive value (NPV) was 79%.

Conclusions: The TTT is beneficial in diagnosing syncope in males and females and patients of young and old ages. A provocative test utilizing NTG provides a shorter, more straightforward test with the same diagnostic accuracy as the isoproterenol test. Lifestyle modification is effective and remains the primary intervention in managing patients with NMS.

An 83-year-old man underwent dual-chamber pacemaker placement for complete atrioventricular block at another hospital. The active-fixation ventricular lead was positioned on the free wall of the anterior right ventricle. Ventricular pacing failure occurred on the day after pacemaker implantation, and fluoroscopy revealed right ventricular (RV) lead perforation. The patient was transferred to our hospital, and chest computed tomography revealed a severe pneumothorax and moderate pneumopericardium. These symptoms were relieved after chest tube drainage, and the patient's hemodynamics stabilized. The RV lead was percutaneously removed using simple traction under fluoroscopic guidance with cardiac surgical backup and was uneventfully refixed to the RV septum. Although there have been several reports of pneumopericardium caused by atrial lead perforation, there are very few cases related to RV lead. Pneumopericardium complicated by pneumothorax due to RV lead perforation can be relieved using chest tube drainage without the need for pericardiocentesis.

Cardiovascular disease remains the leading cause of death in the United States and globally. Significant advances have been made throughout the history of cardiology and the treatment of this disease; however, these efforts have not halted the alarming statistics. Emerging approaches, such as artificial intelligence applied to cardiac imaging, genetic testing, and genetic silencing, may offer essential additional steps in treating the disease. Moreover, new pathways of the disease are being identified, which differ from traditional risk factors and offer a fresh, innovative approach. This paper focuses on a novel strategy that includes identifying and treating multiple pathways of the disease using both new and traditional interventions. These interventions include plaque-directed therapy rather than surrogate therapy, with the potential to mitigate consequences and possibly eradicate the disease through personalized, multi-approach treatments similar to those used in cancer treatment.

Background: This study aimed to evaluate the effects of different heart rate fluctuation ranges during aerobic training on outcomes in patients with stable coronary artery disease (CAD).

Methods: Ninety-seven patients diagnosed with stable CAD were enrolled between March 2017 and December 2019. Participants were randomly assigned to three groups: the control (CON) group, the medium-intensity heart rate small range (MIS) group, and the medium-intensity heart rate large range (MIL) group. The CON group received standard care and patient education, while the MIS and MIL groups underwent personalized rehabilitation training with specific heart rate fluctuation targeted ranges, in addition to standard care. Cardiopulmonary function and exercise performances were assessed using resting heart rate (RHR), maximum heart rate (HRmax), heart rate recovery (HRR), and a 6-min walk test (6MWT) at the baseline and after 16 weeks of training.

Results: The MIS group demonstrated a significant reduction in RHR compared to the CON and MIL groups. While both exercise rehabilitation groups exhibited improvement in HRR, only the MIS group achieved a statistically significant improvement compared to the CON group. Post-training HRmax and 6MWT performance increased in both MIS and MIL groups, with only the MIL group presenting statistical significance compared to the CON group.

Conclusion: Exercise rehabilitation with different training regimens can enhance cardiac function in patients with CAD. Different heart rate modulation strategies yielded distinct effects on cardiopulmonary function. Maintenance of a narrower heart rate fluctuation during exercise was observed to significantly enhance the effectiveness of rehabilitation, which could lead to new treatment protocols or optimization of existing strategies for patients with cardiovascular conditions. The combination of 6MWT and power bicycle training may offer an effective method for improving cardiac function in community-based rehabilitation settings.

Background: Coronary artery bypass grafting (CABG) provides superior long-term outcomes to percutaneous coronary intervention (PCI) for complex multivessel coronary artery disease (CAD). People with chronic kidney disease (CKD) have increased prevalence of multivessel CAD, but also increased surgical risk. We investigated whether CKD predicted real-world use of CABG, versus PCI, in patients revascularized for acute coronary syndrome (ACS).

Methods: Embase, MEDLINE, Scopus and CENTRAL were searched to identify articles referring to ACS and invasive coronary intervention in high-income countries (2012 - 2023). Articles were included if CABG rates were reported in ACS patients with and without CKD receiving revascularization. CKD was defined as an estimated glomerular filtration rate < 60 mL/min/1.73 m²; proxy definitions were accepted. Random effect meta-analyses were used to determine the average effect of CKD on odds of CABG, stratified by ACS type and dialysis use.

Results: Searches generated 15,138 articles, of which 13 observational studies were included (n = 1,682,207). Amongst revascularized ACS patients, those with CKD were more likely to receive CABG than those without (pooled odds ratio (OR) = 1.50 (95% confidence interval (CI) = 1.30 - 1.72). This association was stronger following ST-elevation myocardial infarction (STEMI) than non-ST-elevation ACS (NSTE-ACS) (OR: 1.54 (95% CI: 1.23 - 1.93)) versus 1.16 (1.10 - 1.23), respectively).

Conclusions: In high-income countries, revascularized ACS patients with CKD receive CABG (versus PCI) more frequently than those without kidney disease. However, accounting for lower use of coronary angiography in the CKD population removed this association following NSTE-ACS. Greater use of invasive angiography in those with NSTE-ACS and CKD might therefore increase access to revascularization, and thereby improve outcomes.

Our understanding of dilated cardiomyopathy (DCM) is evolving as new insights into the underlying pathophysiology become available. Professional organizations and clinical experts are improving definitions of DCM, allowing for more accurate treatment recommendations. This review summarized key published literature describing definitions and/or diagnostic criteria for DCM. Embase was searched from database inception to September 19, 2022 for 1) publications reporting definitions of DCM by major professional organizations and related opinion papers, and 2) clinical studies in DCM and heart failure with reduced ejection fraction. Sixty-eight records were included in this review. Definitions of DCM provided by two major professional organizations (American Heart Association (AHA) and European Society of Cardiology (ESC)) agreed on the clinical presentation of DCM; however, they differed in the classification of DCM within the larger context of cardiomyopathy taxonomies. Both organizations agreed that DCM could be clinically defined by the presence of left ventricular dilation and contractile dysfunction in the absence of abnormal loading conditions and severe coronary artery disease. AHA guidelines divided cardiomyopathies into two major groups (primary and secondary) based on predominant organ involvement. DCM was classified as primary cardiomyopathy with mixed (genetic and/or acquired) etiology. Conversely, ESC published a clinically oriented taxonomy in which cardiomyopathies were grouped into specific morphological and functional phenotypes; each was subclassified into familial or non-familial forms. Opinion papers further elaborated on the complex interplay between genetics and environment in the etiology of DCM. Several articles summarized the importance of the new and updated diagnostic tools, such as cardiac magnetic resonance imaging, electrocardiogram, and other biomarkers, in correctly identifying the etiology of DCM. Within clinical studies, most inclusion criteria used standard definitions proposed by leading professional associations (AHA and ESC). Clinical study investigators sometimes used a narrower definition of DCM using additional criteria for the left ventricular ejection fraction threshold value and left ventricular dilatation. Current efforts in cardiology research are focused on a more granular understanding of DCM etiology and the natural history of the disease. Definitions of DCM found in clinical studies mainly rely on published guidelines, with some studies adding idiosyncratic inclusion criteria refining the broad definitions of DCM.

Chronic coronary syndrome (CCS) is a long-term manifestation of coronary artery disease, marked by stable but recurring chest pain and myocardial ischemia due to the gradual buildup of atherosclerotic plaques in the coronary arteries. It is a metabolic disorder of coronary arteries characterized by oxidative stress, endothelial dysfunction, inflammation, and hyperlipidemia. The imbalance in oxidative-antioxidative status contributes to stable ischemic heart disease. Oxidative stress involves reactive oxygen and nitrogen species, leading to low-density lipoprotein (LDL) oxidation. Endothelial dysfunction, marked by reduced nitric oxide (NO) bioavailability, is an early onset of CCS, affecting vasodilation, cell proliferation, and inflammatory responses. Enzyme myeloperoxidase (MPO), traditionally considered protective, plays a dual role in initiating and progressing inflammatory diseases. MPO interacts with NO, modulating its catalytic activity. Elevated NO levels inhibit MPO through a reversible complex formation, preventing NO-induced inhibition by inducible nitric oxide synthase (iNOS). MPO also inactivates endothelial nitric oxide synthase (eNOS) and reacts with L-arginine, hindering NO synthesis. The interplay between MPO and NO significantly influences inflammation sites, impacting peroxidation rates and oxidation reactions. Peroxynitrite, a reactive species, contributes to nitration of tyrosine residues and lipid peroxidation. Mechanistic pathways suggest MPO enhances iNOS catalytic activity, influencing CCS development. iNOS, implicated in inflammation and atherosclerosis, is connected to NO regulation. This review analyzes the complex interplay of MPO, iNOS, and NO that affects plaque morphology, oxidative stress, and inflammation, contributing to atherosclerosis progression. Therefore, it is possible that the phenotypes of atherosclerotic plaques, focal and diffuse coronary artery disease, could be defined by the relationship between MPO and iNOS.