2020 Vol. 17, No. 5
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2020, 17(5): 243-245.
doi: 10.11909/j.issn.1671-5411.2020.05.010
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2020, 17(5): 303-304.
doi: 10.11909/j.issn.1671-5411.2020.05.012
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2020, 17(5): 294-299.
doi: 10.11909/j.issn.1671-5411.2020.05.011
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2020, 17(5): 300-302.
doi: 10.11909/j.issn.1671-5411.2020.05.009
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2020, 17(5): 246-255.
doi: 10.11909/j.issn.1671-5411.2020.05.008
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Objective To describe the long-term antithrombotic management patterns (AMPs) and clinical outcomes of Chinese patients with acute coronary syndrome (ACS). Methods This was an observational, multicenter, longitudinal cohort extension study of Chinese patients who had completed the EPICOR Asia 2-year follow-up study post-hospitalization for an ACS event. Changes in AMP and clinical outcomes for up to 5 years post-ACS event were evaluated. Results Overall, 2334 patients with ACS were enrolled at 49 sites. The mean age was 61.6 years and 76.3% were men. By study end, 2093 patients completed the 3-year follow-up. At baseline (2 years post-ACS event), 72.4% of patents received one antiplatelet (AP) medication, with aspirin being the preferred one. A small proportion of patients (21.5%) was treated with two or more APs (2+ AP), and even fewer patients (6.1%) did not receive any AP medication at baseline. Upon study completion, the proportion of patients without AP therapy increased to 13.6%, while the percentage of patients on one AP and 2+ AP decreased to 69.3% and 17.1%, respectively. Numerically, a higher incidence of clinical events (composite of all-cause mortality, myocardial infarction, stroke) was observed for the 2+ AP (13.2%) subgroup than for the no AP (10.5%) and one AP (8.6%) subgroups. Furthermore, the 2+ AP subgroup exhibited the greatest number of bleeding events, outpatient visits, and hospitalization rates. Unlike myocardial infarction or stroke, bleeding events prompted an adjustment in AMP. Conclusion Most patients in China received at least one AP medication up to 5 years after an ACS event.
Objective To describe the long-term antithrombotic management patterns (AMPs) and clinical outcomes of Chinese patients with acute coronary syndrome (ACS). Methods This was an observational, multicenter, longitudinal cohort extension study of Chinese patients who had completed the EPICOR Asia 2-year follow-up study post-hospitalization for an ACS event. Changes in AMP and clinical outcomes for up to 5 years post-ACS event were evaluated. Results Overall, 2334 patients with ACS were enrolled at 49 sites. The mean age was 61.6 years and 76.3% were men. By study end, 2093 patients completed the 3-year follow-up. At baseline (2 years post-ACS event), 72.4% of patents received one antiplatelet (AP) medication, with aspirin being the preferred one. A small proportion of patients (21.5%) was treated with two or more APs (2+ AP), and even fewer patients (6.1%) did not receive any AP medication at baseline. Upon study completion, the proportion of patients without AP therapy increased to 13.6%, while the percentage of patients on one AP and 2+ AP decreased to 69.3% and 17.1%, respectively. Numerically, a higher incidence of clinical events (composite of all-cause mortality, myocardial infarction, stroke) was observed for the 2+ AP (13.2%) subgroup than for the no AP (10.5%) and one AP (8.6%) subgroups. Furthermore, the 2+ AP subgroup exhibited the greatest number of bleeding events, outpatient visits, and hospitalization rates. Unlike myocardial infarction or stroke, bleeding events prompted an adjustment in AMP. Conclusion Most patients in China received at least one AP medication up to 5 years after an ACS event.
2020, 17(5): 279-283.
doi: 10.11909/j.issn.1671-5411.2020.05.007
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Background Longevity, combined with a higher prevalence of obesity, particularly visceral obesity, has been associated with an increased risk of cardiovascular diseases. Insulin resistance (IR) is an important link between visceral obesity and cardiovascular diseases. An important association has been found between sagittal abdominal diameter, visceral obesity and IR. The objective of this study is to evaluate sagittal abdominal diameter as a marker of visceral obesity and correlate it with IR in older primary health care patients. Methods A cross-sectional study was performed with 389 patients over 60 years of age (70.6 ± 6.9), of whom 74% were female. Their clinical, anthropometric and metabolic profiles were assessed and their fasting serum insulin level was used to calculate the homeostasis model assessment insulin resistance (HOMA-IR). Sagittal abdominal diameter was measured in the supine position at the midpoint between the iliac crest and the last rib with abdominal calipers. Results Sagittal abdominal diameter was significantly correlated with anthropometric measures of general and visceral obesity and with HOMA-IR in both genders. There was no change in the association between sagittal abdominal diameter and HOMA-IR after adjusting for age, sex, diabetes and hypertension. Conclusion It is feasible to use sagittal abdominal diameter in older primary care patients as a tool to evaluate visceral obesity, which is an indicator of cardiovascular risk.
Background Longevity, combined with a higher prevalence of obesity, particularly visceral obesity, has been associated with an increased risk of cardiovascular diseases. Insulin resistance (IR) is an important link between visceral obesity and cardiovascular diseases. An important association has been found between sagittal abdominal diameter, visceral obesity and IR. The objective of this study is to evaluate sagittal abdominal diameter as a marker of visceral obesity and correlate it with IR in older primary health care patients. Methods A cross-sectional study was performed with 389 patients over 60 years of age (70.6 ± 6.9), of whom 74% were female. Their clinical, anthropometric and metabolic profiles were assessed and their fasting serum insulin level was used to calculate the homeostasis model assessment insulin resistance (HOMA-IR). Sagittal abdominal diameter was measured in the supine position at the midpoint between the iliac crest and the last rib with abdominal calipers. Results Sagittal abdominal diameter was significantly correlated with anthropometric measures of general and visceral obesity and with HOMA-IR in both genders. There was no change in the association between sagittal abdominal diameter and HOMA-IR after adjusting for age, sex, diabetes and hypertension. Conclusion It is feasible to use sagittal abdominal diameter in older primary care patients as a tool to evaluate visceral obesity, which is an indicator of cardiovascular risk.
2020, 17(5): 270-278.
doi: 10.11909/j.issn.1671-5411.2020.05.006
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Background Frailty is a multidimensional syndrome that reflects the physiological reserve of elderly. It is related to unfavorable outcomes in various cardiovascular conditions. We conducted a systematic review and meta-analysis of the association of frailty with all-cause mortality and bleeding after acute myocardial infarction (AMI) in the elderly. Methods We comprehensively searched the databases of MEDLINE and EMBASE from inception to March 2019. The studies that reported mortality and bleeding in AMI patients who were evaluated and classified by frailty status were included. Data from each study were combined using the random-effects, generic inverse variance method of DerSimonian and Laird to calculate hazard ratio (HR), and 95% confidence interval (CI). Results Twenty-one studies from 2011 to 2019 were included in this meta-analysis involving 143,301 subjects (mean age 75.33-year-old, 60.0% male). Frailty status was evaluated using different methods such as Fried Frailty Index. Frailty was statistically associated with increased early mortality in nine studies (pooled HR = 2.07, 95% CI: 1.67-2.56, P I2 = 41.2%) and late mortality in 11 studies (pooled HR = 2.30, 95% CI: 1.70-3.11, P I2 = 65.8%). Moreover, frailty was also statistically associated with higher bleeding in 7 studies (pooled HR = 1.34, 95% CI: 1.12-1.59, P I2 = 4.7%). Conclusion Frailty is strongly and independently associated with bleeding, early and late mortality in elderly with AMI. Frailty assessment should be considered as an additional risk factor and used to guide toward personalized treatment strategies.
Background Frailty is a multidimensional syndrome that reflects the physiological reserve of elderly. It is related to unfavorable outcomes in various cardiovascular conditions. We conducted a systematic review and meta-analysis of the association of frailty with all-cause mortality and bleeding after acute myocardial infarction (AMI) in the elderly. Methods We comprehensively searched the databases of MEDLINE and EMBASE from inception to March 2019. The studies that reported mortality and bleeding in AMI patients who were evaluated and classified by frailty status were included. Data from each study were combined using the random-effects, generic inverse variance method of DerSimonian and Laird to calculate hazard ratio (HR), and 95% confidence interval (CI). Results Twenty-one studies from 2011 to 2019 were included in this meta-analysis involving 143,301 subjects (mean age 75.33-year-old, 60.0% male). Frailty status was evaluated using different methods such as Fried Frailty Index. Frailty was statistically associated with increased early mortality in nine studies (pooled HR = 2.07, 95% CI: 1.67-2.56, P I2 = 41.2%) and late mortality in 11 studies (pooled HR = 2.30, 95% CI: 1.70-3.11, P I2 = 65.8%). Moreover, frailty was also statistically associated with higher bleeding in 7 studies (pooled HR = 1.34, 95% CI: 1.12-1.59, P I2 = 4.7%). Conclusion Frailty is strongly and independently associated with bleeding, early and late mortality in elderly with AMI. Frailty assessment should be considered as an additional risk factor and used to guide toward personalized treatment strategies.
2020, 17(5): 264-269.
doi: 10.11909/j.issn.1671-5411.2020.05.005
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Background Endothelial dysfunction is the initial stage in atherosclerotic formation and progression and is associated with high serum uric acid (SUA) level. We hypothesized that reactive hyperemia index (RHI), which reflects endothelial function, is associated with SUA levels in elderly individuals with untreated mild hypertension. Methods We recruited 123 patients ≥ 60 years with untreated mild hypertension. The association between SUA level and RHI was analyzed using univariate correlation analysis and multiple regression analysis. The receiver operating characteristic (ROC) curve was performed to validate the cutoff value of SUA that can be used to predict endothelial dysfunction. Results The serum uric acid level significantly increased in the RHI P = 0.006) and the association was still observed after adjusting for factors, such as age, sex, smoking status, and creatinine level (P = 0.014). In the subgroup analysis, a positive association was observed only in men. In the ROC curve analysis, the optimal cutoff values of SUA for predicting endothelial dysfunction was 293.5 μmol/L in elderly mild hypertension patients and 287.0 μmol/L in men. Conclusion A high SUA level was considered an independent predictor of endothelial dysfunction among elderly individuals, particularly men with untreated mild hypertension.
Background Endothelial dysfunction is the initial stage in atherosclerotic formation and progression and is associated with high serum uric acid (SUA) level. We hypothesized that reactive hyperemia index (RHI), which reflects endothelial function, is associated with SUA levels in elderly individuals with untreated mild hypertension. Methods We recruited 123 patients ≥ 60 years with untreated mild hypertension. The association between SUA level and RHI was analyzed using univariate correlation analysis and multiple regression analysis. The receiver operating characteristic (ROC) curve was performed to validate the cutoff value of SUA that can be used to predict endothelial dysfunction. Results The serum uric acid level significantly increased in the RHI P = 0.006) and the association was still observed after adjusting for factors, such as age, sex, smoking status, and creatinine level (P = 0.014). In the subgroup analysis, a positive association was observed only in men. In the ROC curve analysis, the optimal cutoff values of SUA for predicting endothelial dysfunction was 293.5 μmol/L in elderly mild hypertension patients and 287.0 μmol/L in men. Conclusion A high SUA level was considered an independent predictor of endothelial dysfunction among elderly individuals, particularly men with untreated mild hypertension.
2020, 17(5): 284-293.
doi: 10.11909/j.issn.1671-5411.2020.05.004
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Background Myocardial injury caused by microvascular obstruction (MVO) is characterized by persistent ischemia/hypoxia (IH) of cardiomyocytes after microembolization. Autophagy and Egr-1 were closely associated with various cardiovascular diseases, including MVO. Bim and Beclin-1 are the important genes for autophagy and apoptosis. We aimed to explore whether the Egr-1/Bim/Beclin-1 pathway is involved in regulating autophagy and apoptosis in IH-exposed cardiomyocytes. Methods Neonatal rat cardiomyocytes exposed to the IH environment in vitro were transfected with lentivirus expressing Egr-1 or Egr-1 shRNA, or further treated with 3-methyladenine (3-MA). The expressions of autophagy and apoptosis-associated genes were evaluated using RT-qPCR and Western blots assays. Autophagic vacuoles and autophagic flux were detected by transmission electron microscopy (TEM) and confocal microscope, respectively. Cell injury was assessed by lactate dehydrogenase (LDH) leakage, and apoptosis was determined by flow cytometry. Results IH exposure elevated Egr-1 and Bim expressions, and decreased Beclin-1 expression in rat cardiomyocytes. Egr-1 overexpression in IH-exposed cardiomyocytes significantly up-regulated the levels of Egr-1 and Bim, and down-regulated the level of Beclin-1. Egr-1 knockdown resulted in down-regulated expressions of Egr-1 and Bim, as well as up-regulated expression of Beclin-1. In addition, Egr-1 knockdown induced autophagy was suppressed by 3-MA treatments. TEM and autophagic flux experiments also confirmed that Egr-1 inhibited autophagy progression in IH-exposed cardiomyocytes. Egr-1 suppression protected cardiomyocytes from IH-induced injury, as evidenced by the positive correlations between Egr-1 expression and LDH leakage or apoptosis index in IH-exposed cardiomyocytes. Conclusions IH-induced cardiomyocyte autophagy and apoptosis are regulated by the Egr-1/Bim/Beclin-1 pathway, which is a potential target for treating cardiomyocyte injury caused by MVO in the IH environment.
Background Myocardial injury caused by microvascular obstruction (MVO) is characterized by persistent ischemia/hypoxia (IH) of cardiomyocytes after microembolization. Autophagy and Egr-1 were closely associated with various cardiovascular diseases, including MVO. Bim and Beclin-1 are the important genes for autophagy and apoptosis. We aimed to explore whether the Egr-1/Bim/Beclin-1 pathway is involved in regulating autophagy and apoptosis in IH-exposed cardiomyocytes. Methods Neonatal rat cardiomyocytes exposed to the IH environment in vitro were transfected with lentivirus expressing Egr-1 or Egr-1 shRNA, or further treated with 3-methyladenine (3-MA). The expressions of autophagy and apoptosis-associated genes were evaluated using RT-qPCR and Western blots assays. Autophagic vacuoles and autophagic flux were detected by transmission electron microscopy (TEM) and confocal microscope, respectively. Cell injury was assessed by lactate dehydrogenase (LDH) leakage, and apoptosis was determined by flow cytometry. Results IH exposure elevated Egr-1 and Bim expressions, and decreased Beclin-1 expression in rat cardiomyocytes. Egr-1 overexpression in IH-exposed cardiomyocytes significantly up-regulated the levels of Egr-1 and Bim, and down-regulated the level of Beclin-1. Egr-1 knockdown resulted in down-regulated expressions of Egr-1 and Bim, as well as up-regulated expression of Beclin-1. In addition, Egr-1 knockdown induced autophagy was suppressed by 3-MA treatments. TEM and autophagic flux experiments also confirmed that Egr-1 inhibited autophagy progression in IH-exposed cardiomyocytes. Egr-1 suppression protected cardiomyocytes from IH-induced injury, as evidenced by the positive correlations between Egr-1 expression and LDH leakage or apoptosis index in IH-exposed cardiomyocytes. Conclusions IH-induced cardiomyocyte autophagy and apoptosis are regulated by the Egr-1/Bim/Beclin-1 pathway, which is a potential target for treating cardiomyocyte injury caused by MVO in the IH environment.
2020, 17(5): 256-263.
doi: 10.11909/j.issn.1671-5411.2020.05.003
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Background Coronary artery disease (CAD) remains a leading cause of morbidity and mortality. Cytokines play a potential role in atherosclerosis pathogenesis and progression. We investigated the association between high sensitive C-reactive protein (hsCRP) and severity of CAD. Methods CAD patients were stratified according to hsCRP cut-off value into high levels hsCRP group (≥ 8.4 mg/L) and low levels hsCRP group (Results The mean age was 60.3 ± 11.0 years. The level of hsCRP was increased and ranged from 0.2 to 1020.0 mg/L. Biochemical risk factors and severity of CAD didn't show significant differences between the two groups. In multivariate linear analysis, cardiac troponin I (cTnI) and serum amyloid A (SAA) were predictors of hsCRP. As shown in receiver operating characteristic (ROC) curve analysis performed in patients with ST-segment elevation myocardial infarction (STEMI) and compared to myonecrosis biomarkers, hsCRP (area under the curve (AUC): 0.905; 95%CI: 0.844-0.966; P Conclusions HsCRP levels were not associated with the severity of CAD but could be useful in the evaluation of myocardial necrosis in patients with STEMI.
Background Coronary artery disease (CAD) remains a leading cause of morbidity and mortality. Cytokines play a potential role in atherosclerosis pathogenesis and progression. We investigated the association between high sensitive C-reactive protein (hsCRP) and severity of CAD. Methods CAD patients were stratified according to hsCRP cut-off value into high levels hsCRP group (≥ 8.4 mg/L) and low levels hsCRP group (Results The mean age was 60.3 ± 11.0 years. The level of hsCRP was increased and ranged from 0.2 to 1020.0 mg/L. Biochemical risk factors and severity of CAD didn't show significant differences between the two groups. In multivariate linear analysis, cardiac troponin I (cTnI) and serum amyloid A (SAA) were predictors of hsCRP. As shown in receiver operating characteristic (ROC) curve analysis performed in patients with ST-segment elevation myocardial infarction (STEMI) and compared to myonecrosis biomarkers, hsCRP (area under the curve (AUC): 0.905; 95%CI: 0.844-0.966; P Conclusions HsCRP levels were not associated with the severity of CAD but could be useful in the evaluation of myocardial necrosis in patients with STEMI.
