Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA) accounts for 5–15% of all presentations of acute myocardial infarction. The absence of obstructive coronary disease may present a diagnostic dilemma and identifying the underlying etiology ensures appropriate management improving clinical outcomes. Cardiac magnetic resonance (CMR) imaging is a valuable, non-invasive diagnostic tool that can aide clinicians to build a differential diagnosis in patients with MINOCA, as well as identifying non-ischemic etiologies of myocardial injury (acute myocarditis, Takotsubo Syndrome, and other conditions). The role of CMR in suspected MINOCA is increasingly recognized as emphasized in both European and American clinical guidelines. In this paper we review the indications for CMR, the clinical value in the differential diagnosis of patients with suspected MINOCA, as well as its current limitations and future perspectives.
Myocardial infarction (MI) is regarded as a serious ischemic heart disease on a global level. The current study set out to explore the mechanism of the Notch signaling pathway in the regulation of fibrosis remodeling after the occurrence of MI. First, experimental mice were infected with recombination signal binding protein J (RBP-J) shRNA and empty adenovirus vector, followed by the establishment of MI mouse models and detection of cardiac function. After 4 weeks of MI, mice in the sh-RBP-J group were found to exhibit significantly improved cardiac function relative to the sh-NC group. Moreover, knockdown of RBP-J brought about decreased infarct area, promoted cardiac macrophages M2 polarization, reduced cardiac fibrosis, and further decreased transcription and protein expressions of inflammatory factors and fibrosis-related factors. Furthermore, downregulation of cylindromatosis (CYLD) using si-CYLD reversed the results that knockdown of RBP-J inhibited fibrogenesis and the release of inflammatory factors. Altogether, our findings indicated that the blockade of Notch signaling promotes M2 polarization of cardiac macrophages and improves cardiac function by inhibiting the imbalance of fibrotic remodeling after MI.
Non-vitamin K antagonist oral anticoagulants (NOACs) are a therapeutic option to prevent stroke in patients with atrial fibrillation (AF). In fact, NOACs have become the recommended choice by international clinical practice guidelines over vitamin K antagonists (VKA), because of their efficacy and safety profile, especially in newly initiated patients. The more predictable pharmacokinetic and pharmacodynamic profile of this family of drugs allows preventing anticoagulation drug monitoring. Furthermore, NOACs have significantly fewer drug and food interactions in comparison with VKAs. Despite this, there are no studies that compare the effects on the quality of anticoagulation of NOACs with the intake of potential interactions drugs of P-glycoprotein and cytochrome P450 (CYP). This review brings an overview of NOACs pharmacokinetics profile and their potential drug-food interactions. We also briefly discuss the potential role of prebiotics and probiotics in patients under therapy with NOACs.
BackgroundWith the growing burden of non-ST-elevation myocardial infarction (NSTEMI), developing countries face great challenges in providing equitable treatment nationwide. However, little is known about hospital-level disparities in the quality of NSTEMI care in China. We aimed to investigate the variations in NSTEMI care and patient outcomes across the three hospital levels (province-, prefecture- and county-level, with decreasing scale) in China.MethodsData were derived from the China Acute Myocardial Infarction Registry on patients with NSTEMI consecutively registered between January 2013 and November 2016 from 31 provinces and municipalities throughout mainland China. Patients were categorized according to the hospital level they were admitted to. Multilevel generalized mixed models were fitted to examine the relationship between the hospital level and in-hospital mortality risk.ResultsIn total, 8,054 patients with NSTEMI were included (province-level: 1,698 patients; prefecture-level: 5,240 patients; county-level: 1,116 patients). Patients in the prefecture- and county-level hospitals were older, more likely to be female, and presented worse cardiac function than those in the province-level hospitals (P <0.05). Compared with the province-level hospitals, the rate of invasive strategies was significantly lower in the prefecture- and county-level hospitals (65.3, 43.3, and 15.4%, respectively, P <0.001). Invasive strategies were performed within the guideline-recommended timeframe in 25.4, 9.7, and 1.7% of very-high-risk patients, and 16.4, 7.4, and 2.4% of high-risk patients in province-, prefecture- and county-level hospitals, respectively (both P <0.001). The use of dual antiplatelet therapy in the county-level hospitals (87.2%) remained inadequate compared to the province- (94.5%, P <0.001) and prefecture-level hospitals (94.5%, P <0.001). There was an incremental trend of in-hospital mortality from province- to prefecture- to county-level hospitals (3.0, 4.4, and 6.9%, respectively, P-trend <0.001). After stepwise adjustment for patient characteristics, presentation, hospital facilities and in-hospital treatments, the hospital-level gap in mortality risk gradually narrowed and lost statistical significance in the fully adjusted model [Odds ratio: province-level vs. prefecture-level: 1.23 (0.73–2.05), P = 0.441; province-level vs. county-level: 1.61 (0.80–3.26), P = 0.182; P-trend = 0.246].ConclusionsThere were significant variations in NSTEMI presentation and treatment patterns across the three hospital levels in China, which may largely explain the hospital-level disparity in in-hospital mortality. Quality improvement initiatives are warranted, especially among lower-level hospitals.
Background:This study aimed to evaluate the clinical and surgical characteristics of patients who required reoperation after mechanical mitral valve replacement (MVR).Methods:We retrospectively identified 204 consecutive patients who underwent reoperation after mechanical MVR between 2009 and 2018. Patients were categorized according the reason for reoperation (perivalvular leakage, thrombus formation, or pannus formation). The patients' medical and surgical records were studied carefully and the rates of in-hospital complications were calculated.Results:The mean age was 51±12 years and 44% of the patients were male. The reasons for reoperation were perivalvular leakage (117 patients), thrombus formation (35 patients), and pannus formation (52 patients). The most common positions for perivalvular leakage were at the 6–10 o'clock positions (proportions of ≥25% for each hour position). Most patients had an interval of >10 years between the original MVR and reoperation. The most common reoperation procedure was re-do MVR (157 patients), and 155 of these patients underwent concomitant cardiac procedures. There were 10 in-hospital deaths and 32 patients experienced complications. The 10-year survival rate was 82.2 ± 3.9% in general, and the group of lowest rate was patients with PVL (77.5 ± 5.2%). The independent risk factors were “male” (4.62, 95% CI 1.57–13.58, P = 0.005) and “Hb <9g/dL before redo MV operation” (3.45, 95% CI 1.13–10.49, P = 0.029).Conclusion:Perivalvular leakage was the most common reason for reoperation after mechanical MVR, with a low survival rate in long term follow-up relatively.
Anthracycline antineoplastic agents such as doxorubicin are widely used and highly effective component of adjuvant chemotherapy for breast cancer and curative regimens for lymphomas, leukemias, and sarcomas. The primary dose-limiting adverse effect of anthracyclines is cardiotoxicity that typically manifests as cardiomyopathy and can progress to the potentially fatal clinical syndrome of heart failure. Decades of pre-clinical research have explicated the complex and multifaceted mechanisms of anthracycline-induced cardiotoxicity. It is well-established that oxidative stress contributes to the pathobiology and recent work has elucidated important central roles for direct mitochondrial injury and iron overload. Here we focus instead on emerging aspects of anthracycline-induced cardiotoxicity that may have received less attention in other recent reviews: thrombosis, myocardial atrophy, and non-apoptotic programmed cell death.
BackgroundLeft ventricular (LV) mechanics are impaired in patients with severe aortic stenosis (AS). We hypothesized that there would be differences in myocardial mechanics, measured by global longitudinal strain (GLS) recovery in patients with four subtypes of severe AS after transcatheter aortic valve replacement (TAVR), stratified based upon flow and gradient.MethodsWe retrospectively evaluated 204 patients with severe AS who underwent TAVR and were followed post-TAVR at our institution for clinical outcomes. Speckle-tracking transthoracic echocardiography was performed pre- and post-TAVR. Patients were classified as: (1) normal-flow and high-gradient, (2) normal-flow and high-gradient with reduced LV ejection fraction (LVEF), (3) classical low-flow and low-gradient, or (4) paradoxical low-flow and low-gradient.ResultsBoth GLS (−13.9 ± 4.3 to −14.8 ± 4.3, P < 0.0001) and LVEF (55 ± 15 to 57 ± 14%, P = 0.0001) improved immediately post-TAVR. Patients with low-flow AS had similar improvements in LVEF (+2.6 ± 9%) and aortic valve mean gradient (−23.95 ± 8.34 mmHg) as patients with normal-flow AS. GLS was significantly improved in patients with normal-flow (−0.93 ± 3.10, P = 0.0004) compared to low-flow AS. Across all types of AS, improvement in GLS was associated with a survival benefit, with GLS recovery in alive patients (mean GLS improvement of −1.07 ± 3.10, P < 0.0001).ConclusionsLV mechanics are abnormal in all patients with subtypes of severe AS and improve immediately post-TAVR. Recovery of GLS was associated with a survival benefit. Patients with both types of low-flow AS showed significantly improved, but still impaired, GLS post-TAVR, suggesting underlying myopathy that does not correct post-TAVR.
Myocardial infarction (MI) is the most frequent end-point of cardiovascular pathology, leading to higher mortality worldwide. Due to the particularity of the heart tissue, patients who experience ischemic infarction of the heart, still suffered irreversible damage to the heart even if the vascular reflow by treatment, and severe ones can lead to heart failure or even death. In recent years, several studies have shown that microRNAs (miRNAs), playing a regulatory role in damaged hearts, bring light for patients to alleviate MI. In this review, we summarized the effect of miRNAs on MI with some mechanisms, such as apoptosis, autophagy, proliferation, inflammatory; the regulation of miRNAs on cardiac structural changes after MI, including angiogenesis, myocardial remodeling, fibrosis; the application of miRNAs in stem cell therapy and clinical diagnosis; other non-coding RNAs related to miRNAs in MI during the past 5 years.
Objective:The effect of renal denervation (RDN) on heart rate (HR) in patients with hypertension had been investigated in many studies, but the results were inconsistent. This meta-analysis was performed to evaluate the efficacy of RDN on HR control.Methods:Databases, such as PubMed, EMBASE, Cochrane, and ClinicalTrials.gov, were searched until September 2021. Randomized controlled trials (RCTs) or non-RCTs of RDN in hypertensive patients with outcome indicators, such as HR, were selected. Weighted mean difference (WMD) was calculated for evaluating the changes in HR from baseline using fixed-effects or random-effects models. The Spearman's correlation coefficients were used to identify the relationship between the changes of HR and systolic blood pressure (SBP).Results:In the current meta-analysis, 681 subjects from 16 individual studies were included. This study showed that RDN could reduce office HR in patients with hypertension [WMD = −1.93 (95% CI: −3.00 to −0.85, p < 0.001)]. In addition, 24-h HR and daytime HR were decreased after RDN [WMD = −1.73 (95% CI: −3.51 to −0.31, p = 0.017) and −2.67 (95% CI: −5.02 to −0.32, p = 0.026) respectively], but nighttime HR was not significantly influenced by RDN (WMD = −2.08, 95% CI: −4.57 to 0.42, p = 0.103). We found that the reduction of HR was highly related to the decrease of SBP (r = 0.658, p < 0.05).Conclusion:Renal denervation could reduce office, 24-h, and daytime HR, but does not affect nighttime HR. And the effect is highly associated with blood pressure (BP) control.Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO, identifier: CRD42021283065.