2021 Vol. 18, No. 4
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2021, 18(4): 245-251.
doi: 10.11909/j.issn.1671-5411.2021.04.001
Abstract:
BACKGROUND Cognitive decline is common among older patients with cardiovascular disease (CVD) and can decrease their self-management abilities. However, the instruments for identifying mild cognitive impairment (MCI) are not always feasible in clinical practice. Therefore, this study evaluated whether MCI could be detected using the Japanese version of the Rapid Dementia Screening Test (RDST-J), which is a simple screening tool for identifying cognitive decline. METHODS This retrospective single-center study included patients who were ≥ 65 years old and hospitalized because of CVD. Patients with a pre-hospitalization diagnosis of dementia were excluded. Each patient’s cognitive function had been measured at discharge using the RDST-J and the Japanese version of the Montreal Cognitive Assessment (MoCA-J), which is a standard tool for MCI screening. The correlation between the two scores was evaluated using Spearman’s rank correlation coefficient. Receiver operating characteristic (ROC) analysis was also to evaluate whether the RDST-J could identify MCI, which was defined as a MoCA-J score of ≤ 25 points. RESULTS The study included 78 patients (mean age: 77.2 ± 8.9 years). The RDST-J and MoCA-J scores were strongly correlated (r = 0.835, P < 0.001). The ROC analysis revealed that an RDST-J score of ≤ 9 points provided 75.4% sensitivity and 95.2% specificity for identifying MCI, with an area under the curve of 0.899 (95% CI: 0.835−0.964). The same cut-off value was identified when excluding patients with a high probability of dementia (RDST-J score of ≤ 4 points). CONCLUSIONS The RDST-J may be a simple and effective tool for identifying MCI in older patients with CVD.
2021, 18(4): 252-260.
doi: 10.11909/j.issn.1671-5411.2021.04.007
Abstract:
OBJECTIVE To investigate a new noninvasive method for calculating left ventricular diastolic time constant (Tau) through a continuous-wave aortic regurgitation Doppler spectrum. METHODS According to ultrasound guidance, twenty-four animal models (beagles) of aortic regurgitation and acute ischemic left ventricular diastolic dysfunction were created. The left ventricular diastolic function was manipulated with dobutamine or esmolol and fifty-nine hemodynamic stages were achieved. Raw audio signals of the continuous-wave Doppler spectra were collected, and new aortic regurgitation Doppler spectra were built after reprocessing by a personal computer. The updating time of the spectral line was 0.3 ms. The new Doppler spectra contour line was automated using MATLAB (MATrix LABoratory, MathWorks, Natick, MA, USA), and two time intervals, (t2–t1) and (t3–t1) were measured on the ascending branch of the aortic regurgitation Doppler spectrum. Then, the two time intervals were substituted into Bai’s equations, and Doppler-derived Tau (Tau-D) was resolved and compared with catheter-derived Tau (Tau-c). RESULTS There is no significant difference between Tau-D and Tau-c (45.95 ± 16.90 ms and 46.81 ± 17.31 ms, respectively; P > 0.05). Correlation analysis between Tau-c and Tau-D suggested a strong positive relationship (r = 0.97, P = 0.000). A Bland-Altman plot of Tau-c and Tau-D revealed fair agreement. CONCLUSIONS This new calculation method is simple, convenient, and shows a strong positive relationship and fair agreement with the catheter method.
2021, 18(4): 261-270.
doi: 10.11909/j.issn.1671-5411.2021.04.005
Abstract:
BACKGROUND The efficacy and safety of proprotein convertase subtilisin/kexin type 9 (PCSK-9) inhibitors were confirmed by several clinical trials, but its effectiveness in routine clinical practice in China has not been evaluated. This study aims to describe the real world effectiveness of PCSK-9 inhibitors combined with statins compared with statins-based therapy among patients with very high risk of atherosclerotic cardiovascular disease (ASCVD). METHODS This is a multi-center observational study, enrolled patients from 32 hospitals who underwent percutaneous coronary intervention (PCI) from January to June in 2019. There are 453 patients treated with PCSK-9 inhibitors combined with statins in PCSK-9 inhibitor group and 2,610 patients treated with statins-based lipid lowering therapies in statins-based group. The lipid control rate and incidence of major adverse cardiovascular events (MACE) over six months were compared between two groups. A propensity score-matched (PSM) analysis was used to balance two groups on confounding factors. Survival analysis using Kaplan-Meier methods was applied for MACE. RESULTS In a total of 3,063 patients, 89.91% of patients had received moderate or high-intensity statins-based therapy before PCI, but only 9.47% of patients had low-density lipoprotein cholesterol (LDL-C) levels below 1.4 mmol/L at baseline. In the PSM selected patients, LDL-C level was reduced by 42.57% in PCSK-9 inhibitor group and 30.81% (P < 0.001) in statins-based group after six months. The proportion of LDL-C ≤ 1.0 mmol/L increased from 5.29% to 29.26% in PCSK-9 inhibitor group and 0.23% to 6.11% in statins-based group, and the proportion of LDL-C ≤ 1.4 mmol/L increased from 10.36% to 47.69% in PCSK-9 inhibitor group and 2.99% to 18.43% in statins-based group (P < 0.001 for both). There was no significant difference between PCSK-9 inhibitor and statins-based treatment in reducing the risk of MACE (hazard ratio = 2.52, 95% CI: 0.49−12.97, P = 0.250). CONCLUSIONS In the real world, PCSK-9 inhibitors combined with statins could significantly reduce LDL-C levels among patients with very high risk of ASCVD in China. The long-term clinical benefits for patients received PCSK-9 inhibitor to reduce the risk of MACE is still unclear and requires further study.
2021, 18(4): 271-280.
doi: 10.11909/j.issn.1671-5411.2021.04.003
Abstract:
BACKGROUND M1 polarization of macrophages is an important pathological process in myocardial ischemia reperfusion injury, which is the major obstacle for the treatment of acute myocardial infarction. Currently, the strategies and mechanisms of inhibiting M1 polarization are poorly explored. This study aims to investigate the role of soluble death receptor 5-Fc (sDR5-Fc) in regulating M1 polarization of macrophages under extreme conditions and explore the mechanisms from the aspect of glycolysis. METHODS Extreme conditions were induced in RAW264.7 cells. Real-time quantitative polymerase chain reaction and western blot were used to detect the expression of mRNA and proteins, respectively. Cell counting kit-8 was used to investigate the proliferation activity of cells. Expression levels of inflammatory cytokines were determined by enzyme-linked immunosorbent assay. RESULTS We found that sDR5-Fc rescues the proliferation of macrophages under extreme conditions, including nutrition deficiency, excessive peroxide, and ultraviolet irradiation. In addition, administration of sDR5-Fc inhibits the M1 polarization of macrophages induced by lipopolysaccharide (LPS) and interferon-gamma (IFN-γ), as the expression of M1 polarization markers CD86, CXC motif chemokine ligand 10, matrix metalloproteinase 9, and tumor necrosis factor-α, as well as the secretion of inflammatory factors interleukin (IL)-1β and IL-6, were significantly decreased. By further investigation of the mechanisms, the results showed that sDR5-Fc can recover the LPS and IFN-γ induced pH reduction, lactic acid elevation, and increased expression of hexokinase 2 and glucose transporter 1, which were markers of glycolysis in macrophages. CONCLUSIONS sDR5-Fc inhibits the M1 polarization of macrophages by blocking the glycolysis, which provides a new direction for the development of strategies in the treatment of myocardial ischemia reperfusion injury.
2021, 18(4): 281-288.
doi: 10.11909/j.issn.1671-5411.2021.04.006
Abstract:
BACKGROUND The role of uric acid (UA) in survival of patients with hypertrophic obstructive cardiomyopathy (HOCM) has not been fully evaluated. This study aimed to determine whether UA could be an independent risk factor of cardiac death in patients with HOCM. METHODS A total of 317 patients with HOCM, who were receiving conservative treatment in Fuwai Hospital from October 2009 to December 2014, all of them completed UA evaluations, were analyzed. Patients were divided into three groups according to the UA levels: Tertile 1 (≤ 318 μmol/L, n = 106), Tertile 2 (319 to 397 μmol/L, n = 105), and Tertile 3 (≥ 398 μmol/L, n = 106). RESULTS During a median follow-up of 45 months, 29 cardiac deaths (9.1%) occurred, including 6 sudden cardiac deaths and 23 heart failure-related deaths. Cardiac death in Tertile 3 (n = 16, 55.2%) was significantly higher than in Tertile 1 (n = 6, 20.7%) and Tertile 2 (n = 7, 24.1%). In univariate model, UA level (continuous value) showed predictive value of cardiac death [hazard ratio (HR) = 1.006, 95% CI: 1.003−1.009, P = 0.009]. Univariate Cox survival analysis had shown a significant higher property of cardiac death in patients of Tertile 3 when compared with those of Tertile 1, but cardiac death in patients of Tertile 2 did not show significant prognositic value compared with those of Tertile 1 (HR = 3.927, 95% CI: 0.666−23.162, P = 0.131). UA was found to be an independent risk factor (HR = 1.005, 95% CI: 1.001−1.009, P = 0.009) of cardiac death in the multivariate regression analysis after the adjustment for age, body mass index, atrial fibrillation, hemoglobin, creatinine, high-sensitivity C-reactive protein, interventricular septum/left ventricular posterior wall ratio, left ventricular outflow tract and left ventricular ejection fraction. CONCLUSIONS UA concentration was found to be independently associated with cardiac death in HOCM patients receiving conservative treatment. Randomized trials of UA-lowering agents for HOCM patients are warranted.
2021, 18(4): 289-296.
doi: 10.11909/j.issn.1671-5411.2021.04.004
Abstract:
Ischemic heart disease (IHD) is known as the leading cause of death in both genders. Moreover, significant sex differences were found in cardiac structure, function, pathophysiology, presentation, treatment, and outcome of IHD. The presence of unique risk factors such as exposure to menarche and pregnancy, more anemia, hypertension, and autoimmune disorders in women have recently received attention. Ischemic symptoms are more indefinite and vague in women compared to men as well as a delay in diagnosis, treatment, and worse outcomes compared to men. Women usually receive less evidence-based treatment and intervention, with less concern on preventive health care. Clinical trials primarily recruit male patients and women are underrepresented. Without any correct diagnosis, treatment, and prevention, these problems are accumulated and continue up to older age. Accordingly, with the belief of longer life in women and the increased prevalence of IHD with aging, it will become an important public health problem and concern in the future. This narrative review aimed to provide an overview of some of the differences between the two genders in terms of IHD with paying more attention to practical points.
Ischemic heart disease (IHD) is known as the leading cause of death in both genders. Moreover, significant sex differences were found in cardiac structure, function, pathophysiology, presentation, treatment, and outcome of IHD. The presence of unique risk factors such as exposure to menarche and pregnancy, more anemia, hypertension, and autoimmune disorders in women have recently received attention. Ischemic symptoms are more indefinite and vague in women compared to men as well as a delay in diagnosis, treatment, and worse outcomes compared to men. Women usually receive less evidence-based treatment and intervention, with less concern on preventive health care. Clinical trials primarily recruit male patients and women are underrepresented. Without any correct diagnosis, treatment, and prevention, these problems are accumulated and continue up to older age. Accordingly, with the belief of longer life in women and the increased prevalence of IHD with aging, it will become an important public health problem and concern in the future. This narrative review aimed to provide an overview of some of the differences between the two genders in terms of IHD with paying more attention to practical points.
2021, 18(4): 297-306.
doi: 10.11909/j.issn.1671-5411.2021.04.002
Abstract:
Atrial fibrillation (AF) and heart failure (HF) are complex clinical entities that occur concomitantly in a significant population of patients, and their prevalence is rising in epidemic proportions. Traditionally, both rate and rhythm control strategies have been regarded as equivalent in the management of dysrhythmia in this AF-HF cohort with escalation of treatment largely guided by symptoms. Both disorders are involved in an elaborate pathophysiological interplay with shared cardiovascular risk factors that contribute to the development and sustenance of both AF and HF. Recent studies and continued development of evidence to support catheter ablation for AF has brought into question the traditional belief in equivalence between rate and rhythm control. Indeed, recent trials, in particular the CASTLE-AF (Catheter Ablation versus Standard Conventional Therapy in Patients with Left Ventricular Dysfunction and Atrial Fibrillation) study, suggest that catheter ablation for AF improves survival and rates of hospitalisation in patients with concomitant HF and AF, threatening a paradigm shift in the management of this patient cohort. The evident mortality benefit from clinical trials suggests that catheter ablation for AF should be considered as a therapeutic intervention in all suitable patients with the AF-HF syndrome as these patients may derive the greatest benefit from restoration of sinus rhythm. Further research is needed to refine the evidence base, especially to determine which subgroup of HF patients benefit most from catheter ablation and what is the optimal timing.
Atrial fibrillation (AF) and heart failure (HF) are complex clinical entities that occur concomitantly in a significant population of patients, and their prevalence is rising in epidemic proportions. Traditionally, both rate and rhythm control strategies have been regarded as equivalent in the management of dysrhythmia in this AF-HF cohort with escalation of treatment largely guided by symptoms. Both disorders are involved in an elaborate pathophysiological interplay with shared cardiovascular risk factors that contribute to the development and sustenance of both AF and HF. Recent studies and continued development of evidence to support catheter ablation for AF has brought into question the traditional belief in equivalence between rate and rhythm control. Indeed, recent trials, in particular the CASTLE-AF (Catheter Ablation versus Standard Conventional Therapy in Patients with Left Ventricular Dysfunction and Atrial Fibrillation) study, suggest that catheter ablation for AF improves survival and rates of hospitalisation in patients with concomitant HF and AF, threatening a paradigm shift in the management of this patient cohort. The evident mortality benefit from clinical trials suggests that catheter ablation for AF should be considered as a therapeutic intervention in all suitable patients with the AF-HF syndrome as these patients may derive the greatest benefit from restoration of sinus rhythm. Further research is needed to refine the evidence base, especially to determine which subgroup of HF patients benefit most from catheter ablation and what is the optimal timing.
