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BackgroundInformation regarding the impact of cardiovascular disease (CVD) on disease progression among patients with mild coronavirus disease 2019 (COVID-19) is limited.MethodsThis study evaluated the association of underlying CVD with disease progression in patients with mild COVID-19. The primary outcome was the need to be transferred to intensive care due to disease progression. The patients were divided with and without CVD as well as stable and intensive care groups.ResultsOf 332 patients with mild COVID-19, median age was 51 years (IQR, 40-59 years), and 200 (61.2%) were female. Of 48 (14.5%) patients with CVD, 23 (47.9%) progressed to severe disease status and required intensive care. Compared with patients without CVD, patients with CVD were older, and more likely to have fatigue, chest tightness, and myalgia. The rate of requiring intensive care was significantly higher among patients with CVD than in patients without CVD (47.92% vs. 12.4%; PConclusionsPatients with mild COVID-19 complicating CVD in are susceptible to develop severe disease status and requirement for intensive care.Key PointsQuestionWhat is the impact of coexisting cardiovascular diseases (CVD) on disease progression in patients with mild COVID-19?FindingsAlthough most patients with mild COVID-19 were discharged alive from hospital, approximately 47.9% patients with coexisting CVD developed severe disease status and required intensive care. CVD is an independent risk factor of intensive care among patients with mild COVID-19.MeaningCoexisting CVD is associated with unfavorable outcomes among patients with mild COVID-19. Special monitoring is required for these patients to improve their outcome.

Obesity is the most common nutritional disorder worldwide and is associated with dyslipidemia and atherosclerotic cardiovascular disease. The hallmark of dyslipidemia in obesity is low high density lipoprotein (HDL) cholesterol (HDL-C) levels. Moreover, the quality of HDL is also changed in the obese setting. However, there are still some disputes on the explanations for this phenomenon. There is increasing evidence that adipose tissue, as an energy storage tissue, participates in several metabolism activities, such as hormone secretion and cholesterol efflux. It can influence overall reverse cholesterol transport and plasma HDL-C level. In obesity individuals, the changes in morphology and function of adipose tissue affect plasma HDL-C levels and HDL function, thus, adipose tissue should be the main target for the treatment of HDL metabolism in obesity. In this review, we will summarize the cross-talk between adipocytes and HDL related to cardiovascular disease and focus on the new insights of the potential mechanism underlying obesity and HDL dysfunction.

In patients with coronary artery disease (CAD), further increasing the level of high-density lipoprotein (HDL) cholesterol (HDL-C) as an add-on to statins cannot reduce cardiovascular risk. And it has been reported that HDL functional metric—cholesterol efflux capacity (CEC) may be a better predictor of CAD risk than HDL-C. CEC measurement is time-consuming and not applicable in clinical settings. Thus, it is meaningful to explore an easily acquired index for evaluating CEC. Thirty-six CAD patients and sixty-one non-CAD controls were enrolled in this cross-sectional study. All CAD patients had acute coronary syndrome (ACS). CEC was measured using a [3H] cholesterol loading Raw 264.7 cell model with apolipoprotein B-depleted plasma (a surrogate for HDL). Proton nuclear magnetic resonance (NMR) spectroscopy was used to assess HDL components and subclass distribution. CEC was significantly impaired in CAD patients (11.9 ± 2.3%) compared to controls (13.0 ± 2.2%, p = 0.022). In control group, CEC was positively correlated with enzymatically measured HDL-C levels (r = 0.358, p = 0.006) or with NMR-determined HDL-C levels (NMR-HDL-C, r = 0.416, p = 0.001). However, in CAD group, there was no significant correlation between CEC and HDL-C (r = 0.216, p = 0.206) or NMR-HDL-C (r = 0.065, p = 0.708). Instead, we found that the level of high-sensitivity C-reactive protein (hsCRP) was inversely associated with CEC (r = − 0.351, p = 0.036). Multiple regression analysis showed that the hsCRP level was associated with CEC after adjusting other cardiovascular risk factors and HDL-C, although the association would not reach significance if adjusting for multiple testing. NMR spectroscopy showed that HDL particles shifted to larger ones in patients with high hsCRP levels, and this phenomenon was accompanied by decreased CEC. In patients with CAD, the level of HDL-C cannot reflect HDL function. The impaired correlation between HDL-C and CEC is possibly due to an inflammation-induced HDL subclass remodeling. These hypothesis-generating data suggest that hsCRP levels, a marker of acute inflammation, may associate with HDL dysfunction in ACS subjects. Due to the design limited to be correlative in nature, not permitting causal inference and a larger, strictly designed study is still needed.

Background: Cholesterol efflux capacity (CEC), a crucial atheroprotective function of high-density lipoprotein (HDL), has proven to be a reliable predictor of cardiovascular risk. Inflammation can damage CEC, but few studies have focused on the relationship between the systemic inflammation marker high-sensitivity C-reactive protein (hsCRP) and CEC in patients with coronary artery disease (CAD). Methods: Thirty-six CAD patients and sixty-one non-CAD controls were enrolled in this observational, cross-sectional study. CEC was measured using a [3H] cholesterol loading Raw 264.7 cell model with apolipoprotein B-depleted plasma (a surrogate for HDL). Proton nuclear magnetic resonance (NMR) spectroscopy was used to assess HDL components and subclass distribution. hsCRP was measured with a latex particle, enhanced immunoturbidimetric assay.Results: CEC was impaired in CAD patients compared to controls (11.9±2.3% vs. 13.0±2.2%, p=0.022). In the control group, CEC was positively correlated with enzymatically measured HDL cholesterol (HDL-C) levels (r=0.358, p=0.006) or NMR-determined HDL-C levels (r=0.416, p=0.001). However, in the CAD group, the significance of correlation disappeared (enzymatic method: r=0.216, p=0.206; NMR spectroscopy: r=0.065, p=0.708). Instead, we found that the level of hsCRP was negatively correlated with CEC (r=-0.351, p=0.036), and this relationship was not modified by CAD risk factors, HDL-C, and HDL subclasses. NMR showed that HDL particles shifted to larger ones in patients with high hsCRP levels, and this phenomenon was accompanied by decreased CEC. Conclusions: In patients with CAD, the level of HDL-C cannot reflect HDL function, but hsCRP is independently associated with HDL dysfunction. The impaired correlation between HDL-C and CEC is possibly due to an inflammation-induced HDL subclass remodeling. Trial registration: Chinese Clinical Trial Registry, ChiCTR1900020873. Registered on 21 January 2019 - Retrospectivelyregistered.

Background There are a variety of causes of left ventricular aneurysm, but it is rarely due to a disturbance in intraventricular hemodynamics. To the best of our knowledge, there have been no reports of ventricular aneurysm at the left ventricular apex caused by an abnormal left ventricular muscle bundle. Case presentation We report two cases of patients with congenital abnormal left ventricular muscle bundles which caused disturbances in intraventricular hemodynamics. This process eventually led to a left ventricular aneurysm at the apex of the heart. In both cases, transthoracic echocardiography (TTE) and cardiac magnetic resonance imaging (CMR) indicated ventricular aneurysm formation at the apex of the left ventricle. There were also abnormal muscular bundles connecting the ventricular septum and the posterior wall of the left ventricle. The only differences between these two cases were the comorbidities and severity of symptoms. Conclusion Ventricular aneurysm at the apex of the left ventricle is common. However, it is rare for a ventricular aneurysm to form due to intraventricular hemodynamic disturbances caused by an abnormal muscle bundle as opposed to that due to original ventricular wall damage, which is more common. There is currently a lack of relevant studies on the treatment and prognosis of such patients. Whether surgical resection of a ventricular aneurysm leads to a better prognosis remains uncertain.

In the recent outbreak of novel coronavirus infection worldwide, the risk of thrombosis and bleeding should be concerned. We aimed to observe the dynamic changes of D-dimer levels during disease progression to evaluate their value for thrombosis. In this study, we report the clinical and laboratory results of 57 patients with confirmed COVID-19 pneumonia and 46 patients with confirmed community-acquired bacterial pneumonia (CAP). And their concentrations of D-dimer, infection-related biomarkers, and conventional coagulation were retrospectively analyzed. The Padua prediction score is used to identify patients at high risk for venous thromboembolism (VTE). The results found that, on admission, both in COVID-19 patients and CAP patients, D-dimer levels were significantly increased, and compared with CAP patients, D-dimer levels were higher in COVID-19 patients (P < 0.05). Besides, we found that in COVID-19 patients, D-dimer were related with markers of inflammation, especially with hsCRP (R = 0.426, P < 0.05). However, there was low correlation between VTE score and D-dimer levels (Spearman’s R = 0.264, P > 0.05) weakened the role of D-dimer in the prediction of thrombosis. After treatments, D-dimer levels decreased which was synchronous with hsCRP levels in patients with good clinical prognosis, but there were still some patients with anomalous increasing D-dimer levels after therapy. In conclusion, elevated baseline D-dimer levels are associated with inflammation but not with VTE score in COVID-19 patients, suggesting that it is unreasonable to judge whether anticoagulation is needed only according to D-dimer levels. However, the abnormal changes of D-dimer and inflammatory factors suggest that anticoagulant therapy might be needed. Electronic supplementary material The online version of this article (10.1007/s11239-020-02171-y) contains supplementary material, which is available to authorized users.

We here studied the clinical features, cardiac structure, and functional changes and prognosis of hypertrophic cardiomyopathy (HCM) patients with hypertension (HTN). A total of 90 HCM patients with HTN and 172 patients without HTN were divided into a hypertensive group and non-hypertensive group. The clinical characteristics, cardiac structure and function, and prognosis of the two groups were compared. Our study found that HCM patients with HTN had fewer syncope events in their medical histories (8% vs. 22%, P P P P P P = 0.065). In conclusion, we found that the clinical phenotypes of HCM patients with HTN differed from those of patients with HCM alone, suggesting that HTN may play a pathogenic role in the pathogenesis of hypertensive hypertrophic cardiomyopathy patients.

The mechanism for an abnormal pattern of triglyceride (TG) metabolism in response to a meal still needs further investigation. Extensive pieces of evidence have shown that apolipoprotein CIII (apoCIII) is a critical modulator of plasma TG metabolism mostly by inhibiting the hydrolysis of TG. Little is known about the role of apoCIII contained in high density lipoprotein (HDL) in plasma TG metabolism after a meal.Fasting and 4-hour postprandial peripheral venous blood were collected in 91 subjects selected from our hospital. Serum lipid parameters, apoCIII levels and HDL subcomponents were tested by standard laboratory procedures, ELISA, and nuclear magnetic resonance (NMR), respectively. The t-test, and Non-parametric tests were performed to examine differences between groups, Pearson's correlation and multiple regression analysis were used to assess the correlations between apoCIII (HDL-associated or nonHDL-associated) and postprandial TG.There was a significant increase in TG after a meal compared to fasting status [155.40(96.70-251.07) mg/dl.vs.118.53(83.38-173.29)mg/dl, p 0.001]. However, the total apoCIII levels were unchanged before (11.56(7.89-16.22) mg/dl) and after a meal (11.66(7.75-16.02)mg/dl, p = 0.124), while a significant increase in HDL-associated apoCIII (HDL-apoCIII) was observed from fasting (5.25(3.92-7.83)mg/dl) to post-meal (6.46(4.57-8.76)mg/dl, p = 0.001). Unlike nonHDL-apoCIII, HDL-apoCIII was positively correlated with both fasting and postprandial plasma TG in subjects with baseline plasma TG 118.53 mg/dl (R = 0.503, p 0.001 for fasting, R = 0.584, p 0.001 for postprandial). Besides, in the subjects who had an abnormal TG response to a meal, which was defined as postprandial plasma TG increase of30% compared to baseline TG levels, postprandial HDL-apoCIII was also increased significantly [5.37(3.52-7.02)mg/dl.vs.6.64(4.61-8.86)mg/dl, p = 0.001]. The enrichment of apoCIII in HDL led to changes of TG, cholesterol, free cholesterol, phospholipid and apoAII contents in HDL particles defined by NMR.Enrichment of apoCIII in HDL particles potentially plays an independent role in postprandial hypertriglyceridemia.

Despite great advances in lipid-lowering therapy, the gender-based disparities in lipid goal success among Chinese coronary heart disease (CHD) patients receiving lipid-lowering treatment remained uncharacterized. Furthermore, little is known about potential causes for this gender imbalance. This cross-sectional trial included 25 697 patients treated with lipid-lowering agents from 122 centres between April 2012 and October 2012; data for 9420 participants with CHD were analysed in the present study; all underwent clinical examination and had their latest fasting lipid profiles while on lipid-lowering therapy recorded. Logistic regression was used to explore possible factors associated with gender disparity in goal attainment rates, and to what extent each factor contributes. Of 9420 CHD patients (42.5% women) evaluated, women had a significantly lower overall low-density lipoprotein cholesterol (LDL-C) success rate than men (46.2 vs. 62.7%, P < 0.0001). Among CHD patients with diabetes, only 31.5% of women and 46.4% of men ( P < 0.0001) attained the optional LDL-C target of

Aim: Previous studies have demonstrated that the dysregulated-secretion of adipokines by adipocytes may contribute to obesity-associated atherosclerosis (As) and high density lipoprotein (HDL) may protect against atherogenesis through multiple pathways. This study was to explore the effect of HDL on the oxLDL uptake in inflammatory adipocytes stimulated by endotoxin lipopolysaccharide (LPS) and the possible mechanism. Methods and Results: 3T3-L1 adipocytes were cultured and induced to differentiation and maturation. Acute inflammation in adipocytes was induced by LPS (100 ng/ml) for 6 hours. The adipocytes were pretreated with HDL in various concentrations (10, 50, 100 μg/ml) for 16 hours or with specific PPARγ antagonist (GW9662, 10 μM) or agonist (Rosiglitazone, 10 μM) for 30 min before administration of LPS. The results showed that LPS significantly increased the release of inflammation-related adipokines, such as monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor 1 (PAI-1), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-8 and IL-6, while decreasing the release of leptin and adiponectin. Meanwhile, LPS reduced the uptake and degradation of 125 I-oxLDL, and down-regulated the expression of PPARγ and CD36. Pretreatment with HDL dose-dependently affected the release of IL-8 and IL-6 and the reduced uptake and degradation of oxLDL of adipocytes stimulated by LPS, accompanied with marked upregulation of PPARγ and CD36 expression. Pretreatment with GW9662 markedly inhibited the upregulation of CD36 expression mediated by HDL (100 μg/ml), while the effects of Rosiglitazone were opposite to GW9662. Conclusions: HDL may increase oxLDL uptake of inflammatory adipocytes stimulated by LPS via upregulation of PPARγ/CD36 pathway, which may be a new mechanism of anti-atherosclerosis mediated by HDL.

Exchangeable apolipoproteins play an important role in systemic lipid metabolism, especially for lipoproteins with which they are associated. Recently, emerging evidence has suggested that exchangeable apolipoproteins, such as apolipoprotein A4 (apoA4), apolipoprotein A5 (apoA5), apolipoprotein C3 (apoC3) and apolipoprotein E (apoE), also exert important effects on intracellular lipid homeostasis. There is a close link between lipid metabolism in adipose tissue and liver because the latter behaves as the metabolic sensor of dysfunctional adipose tissue and is a main target of lipotoxicity. Given that the energy balance between these two major lipogenic organs is intimately involved in the pathogenesis of obesity and non-alcoholic fatty liver disease (NAFLD), we here review recent findings concerning the intracellular function of exchangeable apolipoproteins in triglyceride metabolism in adipocytes and hepatocytes. These apolipoproteins may act as mediators of crosstalk between adipose tissue and liver, thus influencing development of obesity and hepatosteatosis. This review provides new insights into the physiological role of exchangeable apolipoproteins and identifies latent targets for therapeutic intervention of obesity and its related disorders.

Introduction: Localized pericardium restriction is a rare disease and likely to be unrecognized owing to the atypical manifestation, even after diagnostic avenues are exhausted. Recognizing the red flags of the disease could timely spark a preliminary suspicion of the disease and thus contribute to the early application of relevant examinations. Case presentation: We will here report a case of a 21-year-old young man with a giant right ventricular outflow tract. He was presented to our hospital for further evaluation of progressive right heart failure which had been previously diagnosed as cardiomyopathy. Unlike patients with right heart failure owing to the restrictive cardiomyopathy, our patient's tissue Doppler revealed an increased early diastolic septal mitral annular velocity. In addition, the disproportion between the severity of right heart failure and the degree of myocardial dysfunction could not be completely explained by other myocardial disease, suggesting that alternative diagnosis of the patient should be sought. Subsequently, cardiac computed tomography, which revealed the focally calcific pericardium encircling the left ventricle, gave us a clue to the diagnosis of localized constrictive pericarditis. Cardiac catheterization, showing the “dip and plateau” sign, further confirmed this diagnosis. The patient underwent successful pericardiectomy. Nowadays, he is able to undertake ordinary physical activity. Conclusion: Localized constrictive pericarditis should be suspected in patients for whom the severity of heart failure and deformity of heart might not be completely explained by valvular heart disease or myocardial disease.

Apolipoprotein (apo) O is a novel apolipoprotein that is present predominantly in high density lipoprotein (HDL). However, overexpression of apoO does not impact on plasma HDL levels or functionality in human apoA-I transgenic mice. Thus, the physiological function of apoO is not yet known. In the present study, we investigated relationships between plasma apoO levels and high-sensitive C-reactive protein (hs-CRP) levels, as well as other lipid parameters in healthy subjects (n = 111) and patients with established acute coronary syndrome (ACS) (n = 50). ApoO was measured by the sandwich dot-blot technique with recombinant apoO as a protein standard. Mean apoO level in healthy subjects was 2.21 ± 0.83 µg/ml whereas it was 4.94 ± 1.59 µg/ml in ACS patients. There were significant differences in plasma level of apoO between two groups (P < 0.001). In univariate analysis, apoO correlated significantly with lg(hsCRP) (r = 0.48, P < 0.001) in ACS patients. Notably, no significant correlation between apoO and other lipid parameters was observed. Logistic regression analysis showed that plasma apoO level was an independent predictor of ACS (OR = 5.61, 95% CI 2.16–14.60, P < 0.001). In conclusion, apoO increased in ACS patients, and may be regarded as an independent inflammatory predictor of ACS patients.

Studies of the past decade have increased our understanding of the role of adipose tissue dysfunction in obesity and obesity-related insulin resistance and type 2 diabetes. Although adipose tissue is the body's largest pool of free cholesterol, adipocytes have limited activity in cholesterol synthetic pathway. Thus, the majority of adipocyte cholesterol originates from circulating lipoproteins. To maintain cholesterol homeostasis, adipocytes have developed multiple pathways for cholesterol efflux. Several transcriptional factors, such as sterol regulatory element-binding proteins and liver X receptors may be responsible for the regulation of cholesterol homeostasis in adipocytes. Most notably, because altering cholesterol balance profoundly modifies adipocyte metabolism in a way resembling that seen in hypertrophied adipocytes, cholesterol imbalance is recognized as a characteristic for enlarged adipocytes per se in the obese state. In addition, plasma membrane cholesterol normalization by chromium picolinate can fully restore insulin-stimulated glucose transport, further supporting the role of the adipocyte cholesterol imbalance in obesity and insulin resistance.

The proband, a 25-year-old female, was presented to our institution with exertional dyspnoea and oedema in lower extremities. Her electrocardiogram showed prominent dilated atria 2 years ago ( Panel A ), followed by sustained atrial fibrillation 1 year later. Transthoracic echocardiography revealed preserved systolic function, massive biatrial enlargement, and moderate left ventricular hypertrophy (LVH) …

Background Despite clear guideline recommendations, there is a paucity of data regarding the prevalence and type of persistent lipid profile abnormalities in patients on stable lipid-lowering therapy in China. Methods This cross-sectional trial included 25,697 patients treated with lipid-lowering agents from 122 centres between April 2012 and October 2012; all underwent clinical examination and had their latest fasting lipid profiles while on lipid-lowering therapy recorded. Logistic regression was performed to assess predictors for lipid abnormalities classified according to current Chinese guidelines. Findings Overall, 29.1% of patients had no lipid abnormalities, and 38.5% of patients did not achieve the therapeutic goal for low-density lipoprotein cholesterol (LDL-C), either as a single lipid anomaly or associated with low high-density lipoprotein cholesterol (HDL-C), elevated triglycerides, or both. Subjects with low risk were more likely than those with very high and high risk to be at target LDL-C levels. Furthermore, 10.4% of very high-risk patients and 11.1% of high-risk patients who attained the LDL-C goal failed to attain non-HDL-C goals. Diabetes was shown to be a strong predictor of failure in attaining non-HDL-C and both goals (OR 3.03; 3.22, 95% CI 2.58–3.55; 2.73–3.79, respectively). Conclusion Although great improvements have been made over the past decade, the large majority of very high-risk and high-risk patients treated with lipid-lowing agents still had one or more manifestations of dyslipidaemia. Further clinical evidence is needed to clarify whether adding other lipid-lowering agents to a statin will be associated with additional cardiovascular risk reduction.