Cardiology Discovery
Volume 02 · Issue 02 · 2022
Cardiol Discov
- Sections
- Original Article
- State of the Art
- Hot Topic
- Case Report
Coronavirus disease 2019 (COVID-19) exists as a pandemic. Mortality during hospitalization is multifactorial, and there is urgent need for a risk stratification model to predict in-hospital death among COVID-19 patients. Here we aimed to construct a risk score system for early identification of COVID-19 patients at high probability of dying during in-hospital treatment.
In this retrospective analysis, a total of 821 confirmed COVID-19 patients from 3 centers were assigned to developmental (n = 411, between January 14, 2020 and February 11, 2020) and validation (n = 410, between February 14, 2020 and March 13, 2020) groups. Based on demographic, symptomatic, and laboratory variables, a new Coronavirus estimation global (CORE-G) score for prediction of in-hospital death was established from the developmental group, and its performance was then evaluated in the validation group.
The CORE-G score consisted of 18 variables (5 demographics, 2 symptoms, and 11 laboratory measurements) with a sum of 69.5 points. Goodness-of-fit tests indicated that the model performed well in the developmental group (H = 3.210, P = 0.880), and it was well validated in the validation group (H = 6.948, P= 0.542). The areas under the receiver operating characteristic curves were 0.955 in the developmental group (sensitivity, 94.1%; specificity, 83.4%) and 0.937 in the validation group (sensitivity, 87.2%; specificity, 84.2%). The mortality rate was not significantly different between the developmental (n = 85,20.7%) and validation (n = 94, 22.9%, P = 0.608) groups.
The CORE-G score provides an estimate of the risk of in-hospital death. This is the first step toward the clinical use of the CORE-G score for predicting outcome in COVID-19 patients.
Cardiac damage is commonly reported in patients with coronavirus disease 2019 (COVID-19) but its prevalence and impact on the long-term survival of patients remain uncertain. This study aimed to explore the prevalence of myocardial injury and assess its prognostic value in patients with COVID-19.
A single-center, retrospective cohort study was performed at the Affiliated Hospital of Jianghan University. Data from 766 patients with confirmed COVID-19 who were hospitalized from December 27, 2019 to April 25, 2020 were collected. Demographic, clinical, laboratory, electrocardiogram, treatment data and all-cause mortality during follow-up were collected and analyzed.
Of the 766 patients with moderate to critically ill COVID-19, 86 (11.2%) died after a mean follow-up of 72.8 days. Myocardial injury occurred in 94 (12.3%) patients. The mortality rate was 64.9% (61/94) and 3.7% (25/672) in patients with and without myocardial injury, respectively. Cox regression showed that myocardial injury was an independent risk factor for mortality (hazard ratio: 8.76, 95% confidence interval: 4.76-16.11, P < 0.001). Of the 90 patients with myocardial injury with electrocardiogram results, sinus tachycardia was present in 29, bundle branch block in 26, low voltage in 10, and abnormal T-wave in 53.
COVID-19 not only involves pneumonia but also cardiac damage. Myocardial injury is a common complication and an independent risk factor for mortality in COVID-19 patients.
Microchannels are associated with the progression of atherosclerotic vulnerable plaques. However, in patients with culprit optical coherence tomography (OCT)-defined plaque erosion, the knowledge of microchannels and culprit lesion vulnerability is limited. The aim of this study was to investigate culprit lesion characteristics in patients with ST-segment elevated myocardial infarction (STEMI) caused by plaque erosion with and without microchannels using OCT.
In all, 348 STEMI patients with plaque erosion who underwent OCT of the culprit lesion at the 2nd Affiliated Hospital of Harbin Medical University (Harbin, China) from August 2014 to December 2017 were included and divided into the microchannel group (n= 116, 33.3%) and no-microchannel group (n = 232, 66.7%). The clinical characteristics and OCT-derived plaque features were compared between both groups.
Among the 348 STEMI patients with plaque erosion, culprit lesions with microchannels had higher incidence of lipid plaque (59.5% vs. 45.3%, P= 0.012); calcification (41.4% vs. 24.6%, P= 0.002); spotty calcification (30.2% vs. 18.1%, P= 0.014); macrophages accumulation (72.4% vs. 45.7%, P < 0.001); and cholesterol crystals (32.8% vs. 14.2%, P < 0.001) than those without microchannels. In addition, minimal lumen area was smaller ((1.9 ± 0.9) mm2vs. (2.8 ± 2.3) mm2, P < 0.001) and lumen area stenosis was greater ((71.3% ± 13.4%) vs. (65.3% ± 19.3%), P= 0.001) in the microchannel group than in the no-microchannel group.
In patients with STEMI caused by plaque erosion, one-third manifested typical microchannel characteristics, and those with microchannels were associated with more severe luminal stenosis and more vulnerable plaque features than those without microchannels.
Pressure overload-induced myocardial apoptosis is a critical pathologically initiated process leading to heart failure (HF). Growth differentiation factor 15 (GDF15) dramatically increases during cardiac hypertrophy and dysfunction, but its functions and mechanisms are barely known. This study aims to elucidate the role and mechanism of GDF15 in HF.
Between January 2017 and August 2018, 57 patients diagnosed with chronic HF (aged >18 years, with left ventricular ejection fraction (LVEF) ≤35%) and 57 non-HF patients (aged >18 years, LVEF >35%) were prospectively enrolled in this study based on the balance of the baseline characteristics. Other acute or chronic diseases and pregnant/lactating women were excluded. The serum concentrations of GDF15 were detected. Isoproterenol (ISO)-induced HF mouse model was established by pumping with ISO (30 mg/(kg·day)) for 4 weeks, and the GDF15 expression in serum and heart tissue was evaluated in vivo. Primary cardiomyocytes were cultured and treated with ISO to induce cardiomyocytes damage. The apoptosis of cardiomyocytes and the effect of GDF15 on ISO-induced cardiomyocytes injury was evaluated in vitro.
After adjusting the baseline characteristic, serum levels of GDF15 were significantly higher in HF subjects than in non-HF patients. Similarly, in the ISO-induced HF mouse model, the significant increase in GDF15 was associated with the process of HF in vivo. Moreover, the elevation of GDF15 occurred prior to heart remodeling in the ISO-induced HF mouse model. Furthermore, using primary cardiomyocytes, we demonstrated that the GDF15 was remarkably enhanced in serum from pathological HF patients and cardiac tissue from the ISO-induced mouse model. Reducing GDF15 exaggerated the ISO-induced cell apoptosis by blocking mitochondrial fusion and increasing oxidative stress. In contrast, the silence of GDF15 aggravated the ISO-induced cardiomyocytes damage.
GDF15 acts as a protective factor against cardiomyocyte apoptosis by improving mitochondria fusion during HF. These findings indicate that GDF15 may be a potential therapeutic target for HF.
Valvular heart disease (VHD) is common in the global population, occupying an heavy disease burden among aging population. Currently, it is the booming era of transcatheter VHD treatment, even with superiority than traditional open heart surgery in some clinical outcomes. We collected data sources mainly derived from published articles and conference presentations, including randomized controlled trials, first-in-man studies, clinical registries, and other single- or multi-center and prospective or retrospective clinical studies. This review summarized the relevant devices and researches of transcatheter aortic valve replacement, transcatheter mitral valve repair and replacement, transcatheter tricuspid valve repair and replacement, and transcatheter pulmonary valve replacement. Moreover, possible challenges of interventional therapy for various VHD in the future were discussed as well.
Assessment of the overall risk of atherosclerotic cardiovascular disease (ASCVD) is the first step in managing dyslipidemia and is an important reference for the target and intensity of treatment. Recently, different guidelines and consensuses on the management of this condition have successively recommended further risk stratification among patients with ASCVD, and a new "extreme risk" category has been proposed to identify patients who may obtain greater benefit from more intensive lipid-lowering therapy. The definition and terminology of extreme risk varies among different guidelines and consensuses; however, they all recommended an aggressive lipid-lowering therapeutic approach and/or a more stringent low-density lipoprotein cholesterol target for patients at extreme risk. Regardless of the definitions, this general approach may have a remarkable effect on the treatment of this condition in clinical practice. To help clinicians and patients to better understand the new strategy for the secondary prevention of ASCVD, this review provides a summary highlighting the necessity of further risk stratification among ASCVD patients, how patients at extreme risk can be identified, and the potential impact of applying the new "extreme risk" category in clinical practice.
Type A aortic aneurysm and dissection secondary to bicuspid aortic valve (BAV) with untreated coarctation of the aorta (CoA) in adults is a rare finding because there are almost no "abnormalities" in these patients’ medical histories. Here, we report on a 47-year-old man with unexplained weakness followed by unconsciousness. He was diagnosed with cardiogenic shock and underwent venoarterial extracorporeal membrane oxygenation (VA-ECMO). BAV, ascending aortic aneurysm and dissection (based on bedside echocardiography) and concomitant CoA (based on computed tomography angiography) were confirmed. The patient then underwent emergency surgery including aortic root replacement with a composite mechanical valve conduit, additional ascending-to-descending aortic bypass, and coronary artery bypass grafting with a saphenous vein graft to the right coronary artery. After treatment, he recovered uneventfully. Thus, here we present a case involving a patient in a critical condition with ascending aortic aneurysm and dissection secondary to complex congenital heart defects, who was successfully treated with composite surgical procedures combined with life-saving VA-ECMO.
Both empyema and type A aortic dissection are life-threatening conditions. The combination, though rare, can cause serious complications and death. There have been rare cases of empyema caused by a co-infection with a Gram-positive bacterium, Granulicatella adiacens, which is difficult to identify, and a Gram-negative bacterium, Escherichia coli. In this case, a 50-year-old man was referred to the emergency department due to sudden chest pain and a suspected diagnosis of type A aortic dissection. The patient was subsequently found to have co-morbid empyema and a fissure in the esophagus when the cause of the disease was investigated. Considering the possibility that the patient’s infection was of digestive origin, a combination of Gram-positive and Gram-negative antibiotics was given immediately. Etiological examination later confirmed the presence of Granulicatella adiacens and Escherichia coli in chest drainage fluid, and the patient was successfully treated with antimicrobial therapy and conservative treatment.
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