Current Cardiology Reviews最新文献

Introduction: Percutaneous atrial septal defects (ASD) closure with fluoroscopy guidance is the standard procedure. However, fluoroscopy poses stochastic and deterministic risks for small infants and children. Zero fluoroscopy ASD closure is an alternative, yet its feasibility and safety compared to fluoroscopy remain unclear. Therefore, this study compares outcomes using standardized fluoroscopy and zero fluoroscopy methods for transcatheter ASD closure.

Methods: Four databases (PubMed, ProQuest, Google Scholar, Wiley) were used to search literature published before July 2023. The main results were the success rate and the complications. Outcomes were processed using the DerSimonian-Laird random-effects model of proportional meta-analysis to determine the overall proportion.

Results: A total of 68 cohort studies (8,989 patients) were included in this meta-analysis. Overall, percutaneous ASD closure was successfully performed in 97% of patients (95%CI: 96-98%) based on 59 studies (8,989 patients), of which fluoroscopy accounted for 97% (95%CI: 96- 98%) based on 51 studies (7,760 patients) and non-fluoroscopy for 98% (95%CI: 96-100%)] based on 8 studies (1,229 patients). Device embolization, AV block, and other arrhythmias did not differ significantly between the two groups. However, the percentage difference in residual leaks between the two groups was quite vast, with 5% in the non-fluoroscopy group and 12% in the fluoroscopy group.

Conclusion: Percutaneous ASD closure with zero fluoroscopy is safe and effective, as evidenced by the high success rate, and is non-inferior to the standardized fluoroscopy method.

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: Our final cohort included 8,801 hospitalizations with NICM and CRT-D 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 CRTP 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.

Chronic ischemic heart failure (CIHF), caused by myocardial injury and cell loss, is a growing public health concern. Despite substantial investments in pharmaco- and device therapies for acute myocardial infarction and CIHF over the past decades, long-term prognosis has shown little improvement. There is a clear need to develop novel therapeutic strategies capable of attenuating progression from acute to chronic myocardial damage, reducing adverse myocardial remodeling, and enhancing myocardial contractility. Cell-based approaches are an important direction in basic and clinical research. Nevertheless, candidate cell types tested to-date in experimental and human studies show several fundamental limitations, including insufficient quantities and potency, poor myocardial uptake, immunogenicity and/or risk of tumorigenicity. Human umbilical cord matrix is a rich source of mesenchymal stem cells (Wharton's jelly mesenchymal stem cells, WJMSCs). WJMSCs are naturally low-immunogenic, demonstrate high plasticity and proliferation capacity, and exhibit an absence of tumorigenic potential. Moreover, by producing specific anti-inflammatory cytokines and chemokines, they reduce the inflammatory response (hence their use in graft-versus-host disease) and have pro-angiogenic, antiapoptotic, and anti-fibrotic properties, making them a natural player in myocardial repair and regeneration. Furthermore, WJMSCs can be expanded ex vivo with high genomic stability and full clonogenic potential and can be standardized as an "off-the-shelf" next-generation advanced therapy medicinal product (ATMP). This review aggregates essential, contemporary information on the properties and fundamental mechanisms of WJMSCs, addressing the process of infarct healing and chronic myocardial injury. It discusses outcomes from pre-clinical studies, such as improvements in myocardial function and reductions in fibrosis in animal models, paving the way for human ATMP trials.

Introduction/objective: Outcomes of iron deficiency (ID) in heart failure (HF) with preserved ejection fraction (HFpEF) or in samples with mixed heart failure subtypes are variably described. Hence, we investigated the prevalence and adverse outcomes of ID in a sample of mixed heart failure subtypes.

Methods: Adult patients admitted with HF over a six-month period were retrospectively studied. ID was defined as serum ferritin<100mcg/L, or serum ferritin 100-300mcg/L with serum transferrin saturation<20%. For each case of ID, sex- and age-matched (within five years) controls were selected. The primary outcome was the composite of all-cause mortality or readmissions up to 12 months post-index admission.

Results: Of the 245 patients admitted with HF [HFpEF: 83 (70.3%), HFrEF: 35 (29.6%)], 233 met the inclusion criteria. Iron studies were available for 131 patients and 59 (45%) had ID. ID had a significant univariate association with the primary outcome (OR: 3.80, 95% CI: 1.42- 10.18, P=0.008), and it remained significant after controlling for age, anaemia, comorbidities, and frailty (OR: 6.04, 95% CI: 1.18-30.85, P=0.031). ID also had a significant independent association with readmissions (OR: 4.61, 95% CI: 1.15-18.43, P=0.03), but not with mortality (OR: 1.17, 95% CI: 0.67-4.35, P=0.257). In post-hoc analysis, ID exhibited a significant association with primary outcome in patients with HFrEF (OR: 14.12, 95% CI: 1.7-0-117.33, P=0.014), but not in patients with HFpEF (OR: 1.8, 95% CI: 0.71-4.58, P=0.214).

Conclusion: ID is common in patients hospitalised for heart failure and has been found to have a significant association with the composite primary outcome, largely due to its effect on readmissions. ID may have a differential effect on adverse outcomes with respect to heart failure subtypes.

Background: Peripartum Cardiomyopathy (PPCM) is a rare yet fatal cardiac disease associated with pregnancy. PPCM has been shown to have similar etiopathogenesis with hypertensive disorders of pregnancy (HDP). Hence, this study aims to study the association between HDP and the development of PPCM.

Methods: Three databases (PubMed, Scopus, Cochrane Library) were searched and screened based on prespecified inclusion and exclusion criteria. Predictors of PPCM evaluated were HDP (preeclampsia, superimposed preeclampsia, chronic hypertension, and gestational hypertension) and its clinical features (severe preeclampsia, age, parity, serum creatinine, etc.). Data were analyzed using the random effects model of pooled odds ratios (ORs) with the Mantel Haenszel method, and publication bias was assessed with a funnel plot.

Results: A total of 13 observational studies with 11,951 PPCM cases from 7 countries were identified. All types of HDP were associated with significantly increased odds of developing PPCM, and severe preeclampsia was associated with the highest OR of 13.33 (CI: 5.95 - 29.83, p < 0.01). Additionally, superimposed preeclampsia, chronic hypertension, preeclampsia, and lastly gestational hypertension were associated with increased odds of PPCM with OR 5.77, 4.73, 4.70, and 3.13, respectively. Other clinical features being statistically significant for PPCM development included advanced age > 35 years and multiple pregnancies (p < 0.05). No significant difference in creatinine level was found between PPCM and no PPCM group. No publication bias was found based on funnel plot assessment.

Conclusion: HDP, especially severe preeclampsia, is associated with increased odds of PPCM development; hence, a low threshold for PPCM screening in this high-risk group is required.

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.

Method: 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: Thoracic aortic aneurysms (TAAs) are worrisome for their propensity to dissect. Previous studies have demonstrated the potential benefits of statin use, particularly with slowing aortic aneurysm growth. The aim of this meta-analysis was to consolidate existing research to ascertain if statins effectively reduce TAA growth.

Methods: Multiple databases were searched to identify studies assessing TAA growth in patients on statins (cases) and those not on statins (controls). The primary outcome was TAA (ascending/ aortic arch) growth rate per year. Standard mean difference (SMD) and 95% confidence intervals (95% CI) were estimated with a random-effects model using the inverse-variance technique. We assigned I2>50% as an indicator of statistical heterogeneity. P-value <0.05 was considered significant. Data analysis was performed using SPSS v.25.0.

Results: Four studies comprising 757 cases (male 64%, mean age 65±14 years) and 1,696 controls (male 62%, mean age 61±18 years) were included. The baseline diameters of TAA for cases and controls were 40.35±8.75mm and 42.39±12.60mm, respectively. Pooled results suggested statins to be associated with slower growth of TAAs with pooled SMD -0.70 mm/year [95% CI (-1.23 - -0.16); p=0.01]. Heterogeneity statistics among 4 studies was 95%.

Conclusion: This pooled meta-analysis showed statins as associated with slower growth of TAAs. However, given the heterogeneity of the included studies in this meta-analysis, results should be interpreted with caution.

Introduction: Nonbacterial 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: 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.

Background: 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: 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. CHD was prevalent in 86.66% of the cases. Clinical classifications revealed age-related differences, emphasizing the heterogeneity of pediatric HF presentations.

Conclusion: Considering that 86.7% of the 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.

Atherosclerosis stands as the primary cause of CVD, characterized by the accumulation of cholesterol deposits within macrophages in medium and large arteries. This deposition promotes the proliferation of specific cell types within the arterial wall, gradually narrowing the vessel lumen and impeding blood flow. Intra-plaque hemorrhages are recognized as critical events in atherosclerotic plaques, leading to the deposition of red blood cells (RBCs) and the release of hemoglobin (Hb). Approximately 40% of high-risk plaques exhibit intra-plaque hemorrhage. Recent studies have demonstrated that intra-plaque hemorrhage is closely linked to plaque progression and increased vulnerability, establishing it as a critical factor in the development of acute clinical symptoms associated with atherosclerosis. The presence of RBC membranes within atherosclerotic plaques contributes significantly to lipid accumulation, indicating a pivotal role in plaque instability. Upon RBC degradation, cholesterol from both the membrane and its interior can profoundly impact atherosclerotic plaque development. Considering that red blood cells (RBCs) can contribute to the excretion of cholesterol through the hepatobiliary system alongside HDL, and given that elevated cholesterol levels are a risk factor for the development and progression of atherosclerotic plaques, RBCs may play a protective role in cardiovascular health. However, when bleeding occurs within a plaque, RBCs that are trapped in the plaque environment, an environment rich in oxidant compounds, can rupture. The cholesterol released from these ruptured RBCs can significantly promote inflammatory reactions. This study aims to explore the inconsistent role of RBCs and their cholesterol content in the progression of atherosclerotic plaques.