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AIMS: Left bundle branch area pacing (LBBaP) upgrade can improve cardiac function and clinical outcomes in patients with pacing-induced cardiomyopathy (PICM), but the specific value of LBBaP upgrade, especially compared with the cardiac function level before right ventricular pacing (RVP) in patients with PICM and non-pacing-induced cardiomyopathy-related upgrade status (Non-PICMUS) is still unknown. METHODS: This study retrospectively enrolled 70 patients with LBBaP upgrade (38 patients with PICM and 32 patients with Non-PICMUS). All upgrade patients experienced three stages: before RVP (Pre-RVP), before LBBaP upgrade (Pre-LBBaP), and after LBBaP upgrade (Post-LBBaP). QRS duration (QRSd), lead parameters, echocardiographic indicators, and clinical outcomes evaluation were recorded at multiple time points. RESULTS: At the follow-up of 12 months, for PICM patients, left ventricular ejection fraction (LVEF) significantly increased from 36.6% ± 7.2% to 51.3% ± 8.7% Post-LBBaP (p < .001), and left ventricular end-diastolic diameter (LVEDD) significantly decreased from 61.5 ± 6.4 mm to 55.2 ± 6.5 mm Post-LBBaP (p < .001), but they both failed to restore the level Pre-RVP (both p < .001). For PICM patients, New York Heart Association (NYHA) classification, the number of moderate-to-severe heart failure (NYHA III-IV), and diuretics using rate after the LBBaP upgrade also could not restore to the level Pre-RVP (all p < .001). At the follow-up of 12 months, Non-PICMUS patients after the LBBaP upgrade had no significant improvement in LVEF, LVEDD, and NYHA classification (all p > .05). CONCLUSION: LBBaP upgrade effectively improved the cardiac function and clinical outcomes in PICM patients, but its effectiveness seemed to be limited as the deteriorated cardiac function cannot be completely reversed. For Non-PICMUS patients, the cardiac function and clinical outcomes Post-LBBaP had no significant improvement.
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Cardiomiopatias , Septo Interventricular , Humanos , Estudos Retrospectivos , Volume Sistólico , Função Ventricular Esquerda , Estimulação Cardíaca Artificial/efeitos adversos , Eletrocardiografia , Cardiomiopatias/etiologia , Cardiomiopatias/terapia , Resultado do Tratamento , Fascículo AtrioventricularRESUMO
Nutritional risk is closely related to the poor prognosis of hospitalized patients. However, the association of pre-procedural nutritional risk with periprocedural myocardial infarction (PMI) after percutaneous coronary intervention (PCI) remains unclear.A total of 22,267 patients who underwent elective PCI were enrolled in this retrospective cross-sectional study. Nutritional risk was evaluated by three nutritional risk assessment tools, namely, controlling nutritional status (CONUT), prognostic nutritional index (PNI), and geriatric nutritional risk index (GNRI). PMI after PCI was defined as elevation of cardiac troponin I (cTnI) values > 5 × 99th percentile upper reference limit. Linear regression analysis was performed to explore the association of nutritional risk assessment tools with cTnI fold elevation. Log-binomial regression analysis was conducted to determine the association of nutritional risk assessment tools with PMI.The average age of the enrolled patients was 66.4 years old, and 2,647 of them (11.9%) suffered PMI after PCI. Multivariable linear regression analysis determined a linear association between nutritional risk assessment tools and cTnI fold elevation (CONUT: ß = 0.220, 95% CI [0.088-0.352], P = 0.001; PNI: ß = -0.105, 95% CI [-0.146 to -0.065], P < 0.001; GNRI: ß = -0.090, 95% CI [-0.122 to -0.057], P < 0.001). Log-binomial regression analysis showed that nutritional risk assessment tools were strongly associated with PMI after PCI (CONUT [4-12 versus 0-1]: RR = 1.168, 95% CI [1.054-1.295], P = 0.003; PNI [< 44 versus ≥ 52]: RR = 1.168, 95% CI [1.038-1.315], P = 0.010; GNRI [< 98 versus ≥ 108]: RR = 1.128, 95% CI [1.006-1.264], P = 0.039).Pre-procedural nutritional status, assessed by CONUT, PNI, and GNRI, was significantly and strongly associated with PMI in patients undergoing elective PCI.
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Infarto do Miocárdio , Intervenção Coronária Percutânea , Humanos , Idoso , Intervenção Coronária Percutânea/efeitos adversos , Estudos Retrospectivos , Estudos Transversais , Fatores de Risco , Infarto do Miocárdio/epidemiologia , Infarto do Miocárdio/etiologia , Troponina IRESUMO
BACKGROUND: Nutritional risk is prevalent in various diseases, but its association with contrast-induced acute kidney injury (CI-AKI) remains unclear. This study aimed to explore this association in patients undergoing coronary angiography (CAG). METHODS: In this retrospective cross-sectional study, 4386 patients undergoing CAG were enrolled. Nutritional risks were estimated by nutritional risk screening 2002 (NRS-2002), controlling nutritional status (CONUT), prognostic nutritional index (PNI), and geriatric nutritional risk index (GNRI), respectively. CI-AKI was determined by the elevation of serum creatinine (Scr). Multivariable logistic regression analyses and receiver operator characteristic (ROC) analyses were conducted. Subgroup analyses were performed according to age (< 70/≥70 years), gender (male/female), percutaneous coronary intervention (with/without), and estimated glomerular filtration rate (< 60/≥60 ml/min/1.73m2). RESULTS: Overall, 787 (17.9%) patients were diagnosed with CI-AKI. The median score of NRS-2002, CONUT, PNI, and GNRI was 1.0, 3.0, 45.8, and 98.6, respectively. Nutritional risk was proven to be associated with CI-AKI when four different nutritional tools were employed, including NRS-2002 ([3-7 vs. 0]: odds ratio [95% confidence interval], OR [95%CI] = 4.026 [2.732 to 5.932], P < 0.001), CONUT ([6-12 vs. 0-1]: OR [95%CI] = 2.230 [1.586 to 3.136], P < 0.001), PNI ([< 38 vs. ≥52]: OR [95%CI] = 2.349 [1.529 to 3.610], P < 0.001), and GNRI ([< 90 vs. ≥104]: OR [95%CI] = 1.822 [1.229 to 2.702], P = 0.003). This is consistent when subgroup analyses were performed. Furthermore, nutritional scores were proved to be accurate in predicting CI-AKI (area under ROC curve: NRS-2002, 0.625; CONUT, 0.609; PNI, 0.629; and GNRI, 0.603). CONCLUSIONS: Nutritional risks (high scores of NRS-2002 and CONUT; low scores of PNI and GNRI) were associated with CI-AKI in patients undergoing CAG.
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Injúria Renal Aguda , Injúria Renal Aguda/induzido quimicamente , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/epidemiologia , Idoso , Angiografia Coronária/efeitos adversos , Creatinina , Estudos Transversais , Feminino , Humanos , Masculino , Estudos Retrospectivos , Fatores de RiscoRESUMO
BACKGROUND: Inflammation contributes to poor prognosis in cardiovascular diseases. A novel biomarker for systemic inflammation that has garnered attention is the red blood cell distribution width (RDW). This study is designed to explore potential associations between RDW and hemoglobin-to-RDW ratio (HRR) with contrast-associated acute kidney injury (CA-AKI). METHODS: This study retrospectively analyzed 4054 patients undergoing coronary angiography (CAG). Linear regression models were employed to assess the relationships between RDW or HRR and the elevation of serum creatinine (Scr). The associations between RDW or HRR and CA-AKI were explored using restricted cubic spline and log-binomial regression analyses taking into account specific cutoff values and quintiles. Exploratory analyses were also conducted to further investigate these associations. RESULTS: Among enrolled patients, the average age was 66.9 years and 34.3% were female. Notably, patients who developed CA-AKI tended to have higher RDW and lower HRR. Multivariable linear regression models demonstrated that RDW exhibited a positive association with Scr elevation (ß = 2.496, 95% confidence interval [CI] = 1.784-3.208), while HRR displayed a negative association (ß = -3.559, 95% CI = -4.243 to -2.875). Multivariable log-binomial regression models confirmed that both high RDW (RDW ≥ 13.8%) and low HRR (HRR < 8.9) were significantly associated with a higher risk of CA-AKI (RDW [≥13.8% vs. <13.8%]: relative risk [RR] = 1.540, 95% CI = 1.345-1.762; HRR [<8.9 vs. ≥8.9]: RR = 1.822, 95% CI = 1.584-2.096). Exploratory analysis determined that such associations still existed regardless of age, gender, estimated glomerular filtration rate, or anemia. CONCLUSIONS: Elevated preoperative RDW and decreased HRR were significantly associated with CA-AKI in patients undergoing CAG.
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Injúria Renal Aguda , Índices de Eritrócitos , Humanos , Feminino , Idoso , Masculino , Estudos Retrospectivos , Angiografia Coronária/efeitos adversos , Hemoglobinas , Eritrócitos , Injúria Renal Aguda/induzido quimicamente , Injúria Renal Aguda/diagnóstico , InflamaçãoRESUMO
BACKGROUND: Statins are lipid-lowering drugs with favorable anti-inflammatory effects. This study aimed to explore different statin-based lipid-lowering strategies to reduce high-sensitivity C-reactive protein (hs-CRP). HYPOTHESIS: The hypothesis is that different statin-based lipid-lowering strategies might reduce hs-CRP. METHODS: This retrospective study included 3653 patients who underwent percutaneous coronary intervention (PCI). Three statin-based lipid-lowering strategies were investigated, including different types of statins (atorvastatin vs. rosuvastatin), statin combined with ezetimibe therapy (vs. without), and intensive statin therapy (vs. regular). The hs-CRP levels and blood lipid indicators were measured at baseline and after 1-month lipid-lowering therapy. Multivariable linear regression analysis and structural equation mode analysis were conducted to verify the association between different lipid-lowering strategies, Δhs-CRP (%) and ΔLDL-C (%). RESULTS: Totally, 3653 patients were enrolled with an average age of 63.81 years. Multivariable linear regression demonstrated that statin combined with ezetimibe therapy was significantly associated with decreased Δhs-CRP (%) (ß = -0.253, 95% CI: [-0.501 to -0.005], p = 0.045). The increased ΔLDL-C (%) was an independent predictor of elevated levels of Δhs-CRP (%) (ß = 0.487, 95% CI: [0.15-0.824], p = 0.005). Furthermore, structural equation model analysis proved that statin combined with ezetimibe therapy (ß = -0.300, p < 0.001) and intensive statin therapy (ß = -0.032, p = 0.043) had an indirect negative effect on Δhs-CRP via ΔLDL-C. CONCLUSIONS: Compared with routine statin use, statin combined with ezetimibe therapy and intensive statin therapy could further reduce hs-CRP levels.
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Biomarcadores , Proteína C-Reativa , Doença da Artéria Coronariana , Ezetimiba , Inibidores de Hidroximetilglutaril-CoA Redutases , Intervenção Coronária Percutânea , Humanos , Masculino , Estudos Retrospectivos , Feminino , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Proteína C-Reativa/análise , Proteína C-Reativa/metabolismo , Doença da Artéria Coronariana/sangue , Doença da Artéria Coronariana/tratamento farmacológico , Pessoa de Meia-Idade , Biomarcadores/sangue , Resultado do Tratamento , Intervenção Coronária Percutânea/métodos , Ezetimiba/uso terapêutico , Quimioterapia Combinada , Idoso , Rosuvastatina Cálcica/uso terapêutico , Atorvastatina/uso terapêutico , LDL-Colesterol/sangue , Anticolesterolemiantes/uso terapêutico , Dislipidemias/sangue , Dislipidemias/tratamento farmacológico , Dislipidemias/diagnósticoRESUMO
Aims: Myocardial ischemia can affect traditional right ventricular (RV) pacing parameters, but it is unclear whether coronary artery disease (CAD) impact the pacing parameters and electrophysiological characteristics of left bundle branch area pacing (LBBaP) as a physiological pacing representative. Methods: Patients who underwent coronary angiography (CAG) after/before the LBBaP procedure and underwent percutaneous coronary intervention after LBBaP procedure were divided into CAD group and Non-CAD group according to visual CAG. Pacing parameters and electrophysiological characteristics were recorded at LBBaP implantation. Multivariate logistic regression analysis was implemented to evaluate the association between CAD and higher capture threshold. Sensitivity analyses were conducted to verify result stability. Results: A total of 176 patients met inclusion criteria (115 Non-CAD patients and 61 CAD patients) with a mean age of 71.1 ± 9.0 years. Compared with the Non-CAD patients, CAD patients had the higher capture threshold (0.67 ± 0.22 V vs. 0.82 ± 0.28 V, P < 0.001) and lower R-wave amplitude (12.5 ± 4.8 mV vs. 10.1 ± 2.7 mV, P = 0.001). Moreover, CAD was independently associated with higher capture threshold (adjusted Odds ratio (OR) 3.418, 95% confidence interval (CI): 1.621-7.206, P = 0.001), which was further validated through sensitivity analyses. Conclusion: Patients without CAD might have safer pacing parameters in the LBBaP procedure. Besides, CAD might be the risk factor of capture threshold increase during permanent LBBaP implantation.
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Background: Cardiac dysfunction is a well-established risk factor for contrast-associated acute kidney injury (CA-AKI). Nevertheless, the relationship between cardiac remodeling, as assessed by echocardiography, and CA-AKI remains uncertain. Method: A total of 3,241 patients undergoing coronary angiography (CAG) with/without percutaneous coronary intervention (PCI) were enrolled in this retrospective study. Collected echocardiographic parameters were normalized by body surface area (BSA) and divided according to quartile, including the left ventricular internal end-diastolic diameter index (LVIDDI), left ventricular internal end-systolic diameter index (LVIDSI), and left ventricular mass index (LVMI). Logistic regression analysis was conducted to ascertain the association between structural parameter changes and CA-AKI. Further investigation was performed in different subgroups. Results: The mean age of the participants was 66.6 years, and 16.3% suffered from CA-AKI. LVIDSI [≥22.9â mm/m2: OR = 1.953, 95%CI (1.459 to 2.615), P < 0.001], LVIDDI [≥33.2â mm/m2: OR = 1.443, 95%CI (1.087 to 1.914), P = 0.011], and LVMI [≥141.0â g/m2: OR = 1.530, 95%CI (1.146 to 2.044), P = 0.004] in quartile were positively associated with CA-AKI risk in general (all P for trend <0.05). These associations were consistent when stratified by age, left ventricular ejection fraction, estimated glomerular filtration rate, and N-terminal brain natriuretic peptide (all P for interaction >0.05). The presence of eccentric hypertrophy [OR = 1.400, 95%CI (1.093 to 1.793), P = 0.008] and the coexistence of hypertrophy and dilation [OR = 1.397, 95%CI (1.091 to 1.789), P = 0.008] carried a higher CA-AKI risk. Conclusion: The presence of cardiac remodeling, assessed by echocardiography, is associated with a higher risk of CA-AKI.
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BACKGROUND: Luteolin, a common flavonoid in our daily diet, has potent anti-diabetic effects. However, its prognostic impact on type 2 diabetes mellitus (T2DM) is still uncertain. This study aimed to clarify this association. METHODS: In this prospective cohort study, 2,461 patients with T2DM were included from the National Health and Nutrition Examination Survey. Dietary luteolin intake was estimated by the type and amount of food consumed in a 24-hour dietary recall. All-cause and cardiac mortality were ascertained by National Death Index Mortality data (as of December 31, 2019). The association of luteolin intake with mortality risk was estimated by Cox proportional hazards model. RESULTS: The median (interquartile range) luteolin intake was 0.355 (0.130, 0.835) mg/day. During the follow-up (median, 8.4 years), 561 all-cause deaths (including 136 cardiac deaths) were documented. Per-unit increment of luteolin intake (natural logarithm transformed) was found to reduce all-cause mortality by 7.0% (P = 0.024) and cardiac mortality by 22.6% (P = 0.001) in patients with T2DM. An inverse dose-response association was identified between luteolin intake (range: 0.005-9.870 mg/day) and mortality risk. The consistent result was also shown when stratified by age, gender, race, body mass index, HbA1c level, and T2DM duration. Moreover, luteolin intake increment was also shown to be associated with a lower C-reactive protein level at baseline (ß =-0.332; 95% CI =-0.541, -0.122). CONCLUSION: The current study confirmed that the dietary luteolin intake increment reduced all-cause mortality (especially cardiac mortality) in patients with T2DM, which may be attributed to the anti-inflammatory property of luteolin.
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Background: Glasgow prognostic score (GPS) is a reliable scoring system reflecting both nutritional and inflammatory factors. The association of inflammation and nutrition with contrast-associated acute kidney injury (CA-AKI) has been validated. This study set out to determine the impact of GPS and its derived scores on CA-AKI incidence. Methods: Populations treated with coronary angiography with/without percutaneous coronary intervention were screened retrospectively. According to C-reactive protein and albumin, three kinds of GPSs were involved: GPS, modified GPS (mGPS), and the cutoff-based GPS (cGPS) which was derived by calculating the optimal cutoff values of two parameters. Primary endpoint was CA-AKI. Pearson' r correlation, linear/logistic regression, receiver operating characteristic curve as well as subgroup analyses were conducted. Results: Totally, 3150 patients were valid for analysis, and the mean age was 67.5 years old, with 66.4 % male. Of these, 610 patients suffered CA-AKI. All three kinds of GPSs were independently associated with the SCr elevation proportion (GPS: ß = 4.850, 95%CI [3.700 to 8.722], P < 0.001; mGPS: ß = 3.450, 95%CI [1.896 to 6.888], P = 0.001; cGPS: ß = 3.992, 95%CI [2.368 to 6.940], P < 0.001). GPS, mGPS and cGPS were proved to be the independent risk factors for CA-AKI risk (all P for trend <0.05). Compared with GPS and mGPS, cGPS was of greater prognostic value for predicting CA-AKI incidence (cGPS: AUC = 0.633; mGPS: AUC = 0.567; GPS: AUC = 0.611). Main findings were also consistent in all subgroup analysis. Conclusion: Preprocedural GPS and its derived scores (mGPS and cGPS), especially cGPS, were correlated with the incidence of CA-AKI, which might assist in clinical decision making in treating CA-AKI.
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Backgrounds and Aims: Nutritional Risk Screening 2002 (NRS-2002) has been widely recommended for identifying the nutritional risk. However, the association between NRS-2002 and the prognosis of heart failure has not been fully addressed. This study aimed to explore the association of NRS-2002 with 1-year re-hospitalization and the length of initial hospital stay in heart failure patients. Methods: This retrospective study included 2,830 heart failure patients. The primary endpoint was 1-year re-hospitalization for heart failure. The secondary endpoint was the length of initial hospital stay. The Log-binomial regression analysis was performed to determine the association between NRS-2002 and re-hospitalization. The Cox regression model was fitted to estimate hazard of discharge. The cumulative incidence curves of discharge were plotted using Kaplan-Meier method and log-rank test was performed. Exploratory analysis was also conducted according to the classification of heart failure and the level of N-terminal pro-B-type natriuretic peptide (NT-proBNP) fold-elevation. Results: Among 2,830 heart failure patients, the mean age was 64.3 years and 66.4% were male. A total of 122 (4.3%) patients were considered at high nutritional risk. Log-binomial regression analysis demonstrated that higher NRS-2002 score was an independent risk factor of re-hospitalization ([1 vs. 0]: relative risks [RR] = 1.383, 95% CI = 1.152 to 1.660; [2 vs. 0]: RR = 1.425, 95% CI = 1.108 to 1.832; [3-7 vs. 0]: RR = 1.770, 95% CI = 1.310 to 2.393). Kaplan-Meier curve showed that the cumulative incidence of discharge was lower in high nutritional risk group (Log rank p < 0.001). Cox regression analysis also found that higher NRS-2002 score (2 or ≥3) was strongly associated with longer length of initial hospital stay ([2 vs. 0]: Hazard ratios [HR] = 0.854, 95% CI = 0.748 to 0.976; [3-7 vs. 0]: HR = 0.609, 95% CI = 0.503 to 0.737). Exploratory analysis showed that such association still remained irrespective of NT-proBNP fold-elevation, but only existed in patients with heart failure with preserved ejection fraction (HFpEF). Conclusion: In patients with heart failure, high NRS-2002 score was strongly and independently associated with the incidence of 1-year re-hospitalization and the length of initial hospital stay.
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Background and Aims: Systemic immune-inflammation index (SII) is an emerging indicator and correlated to the incidence of cardiovascular diseases. This study aimed to explore the association between SII and contrast-induced acute kidney injury (CI-AKI). Methods: In this retrospective cross-sectional study, 4,381 subjects undergoing coronary angiography (CAG) were included. SII is defined as neutrophil count × platelet count/lymphocyte count. CI-AKI was determined by the elevation of serum creatinine (Scr). Multivariable linear and logistic regression analysis were used to determine the relationship of SII with Scr and CI-AKI, respectively. Receiver operator characteristic (ROC) analysis, structural equation model analysis, and subgroup analysis were also performed. Results: Overall, 786 (17.9%) patients suffered CI-AKI after the intravascular contrast administration. The subjects were 67.1 ± 10.8 years wold, with a mean SII of 5.72 × 1011/L. Multivariable linear regression analysis showed that SII linearly increased with the proportion of Scr elevation (ß [95% confidence interval, CI] = 0.315 [0.206 to 0.424], P < 0.001). Multivariable logistic regression analysis demonstrated that higher SII was associated with an increased incidence of CI-AKI ([≥12 vs. <3 × 1011/L]: odds ratio, OR [95% CI] = 2.914 [2.121 to 4.003], P < 0.001). Subgroup analysis showed consistent results. ROC analysis identified a good predictive value of SII on CI-AKI (area under the ROC curve [95% CI]: 0.625 [0.602 to 0.647]). The structural equation model verified a more remarkable direct effect of SII (ß = 0.102, P < 0.001) on CI-AKI compared to C-reactive protein (ß = 0.070, P < 0.001). Conclusions: SII is an independent predictor for CI-AKI in patients undergoing CAG procedures.
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Background: The hemoglobin glycation index (HGI) quantifies interindividual variation in glycation and is positively associated with cardiovascular diseases. However, the association between HGI and contrast-induced acute kidney injury (CI-AKI) remains unclear. Therefore, this study aimed to assess the association of HGI with CI-AKI. Methods: In this observational study, a total of 3,142 patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) were included. The HGI was calculated as the difference between the measured glycated hemoglobin (HbA1c) and predicted HbA1c. CI-AKI was defined as an increase of either 25% or 0.5 mg/dl (44.2 µmol/L) in the serum creatinine (SCr) level within 72 h following the exposure to contrast medium. Piecewise linear regression analysis was conducted to testify the association of HGI with the proportion of SCr elevation. Modified Poisson's regression analysis was performed to determine the association between HGI and CI-AKI. Exploratory analysis was also performed according to the stratification of HbA1c levels. Results: Among 3,142 patients, the average age was 66.9 years and 483 of them (15.4%) suffered CI-AKI. Piecewise linear regression analysis demonstrated the linear association of HGI with the proportion of SCr elevation on both positive and negative sides of HGI [HGI <0: ß = -9.537, 95% CI (-12.057 to -7.017), p < 0.001; HGI ≥0: ß = 1.655, 95% CI (0.125 to 3.186), p = 0.034]. Modified Poisson's regression analysis showed that the higher absolute value of HGI was strongly associated with higher incidence of CI-AKI [(<-1.0 vs. -0.2 to 0.2): aRR = 1.897, 95% CI [1.467 to 2.452], p < 0.001 (≥1.0 vs. -0.2 to 0.2): aRR = 1.545, 95% CI (1.171 to 2.037), p = 0.002]. Furthermore, the results in exploratory analysis showed that such association still remained irrespective of HbA1c levels. Conclusion: The higher absolute value of HGI was strongly associated with higher incidence of CI-AKI in patients undergoing CAG and PCI.
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Background: Identifying high-risk patients for contrast-associated acute kidney injury (CA-AKI) helps to take early preventive interventions. The current study aimed to establish and validate an online pre-procedural nomogram for CA-AKI in patients undergoing coronary angiography (CAG). Methods: In this retrospective dataset, 4,295 patients undergoing CAG were enrolled and randomized into the training or testing dataset with a split ratio of 8:2. Optimal predictors for CA-AKI were determined by Least Absolute Shrinkage and Selection Operator (LASSO) and Random Forest (RF) algorithm. Nomogram was developed and deployed online. The discrimination and accuracy of the nomogram were evaluated by receiver operating characteristic (ROC) and calibration analysis, respectively. Clinical usefulness was estimated by decision curve analysis (DCA) and clinical impact curve (CIC). Results: A total of 755 patients (17.1%) was diagnosed with CA-AKI. 7 pre-procedural predictors were identified and integrated into the nomogram, including age, gender, hemoglobin, N-terminal of the prohormone brain natriuretic peptide, neutrophil-to-lymphocyte ratio, cardiac troponin I, and loop diuretics use. The ROC analyses showed that the nomogram had a good discrimination performance for CA-AKI in the training dataset (area under the curve, AUC = 0.766, 95%CI [0.737 to 0.794]) and testing dataset (AUC = 0.737, 95%CI [0.693 to 0.780]). The nomogram was also well-calibrated in both the training dataset (P = 0.965) and the testing dataset (P = 0.789). Good clinical usefulness was identified by DCA and CIC. Finally, this model was deployed in a web server for public use (https://duanbin-li.shinyapps.io/DynNomapp/). Conclusion: An easy-to-use pre-procedural nomogram for predicting CA-AKI was established and validated in patients undergoing CAG, which was also deployed online.
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BACKGROUND: Increased plaque vulnerability and higher lipid variability are causes of adverse cardiovascular events. Despite a close association between glucose and lipid metabolisms, the influence of elevated glycated hemoglobin A1c (HbA1c) on plaque vulnerability and lipid variability remains unclear. METHODS: Among subjects undergoing percutaneous coronary intervention (PCI) from 2009 through 2019, 366 patients received intravascular optical coherence tomography (OCT) assessment and 4,445 patients underwent the scheduled follow-ups within 1 year after PCI. Vulnerability features of culprit vessels were analyzed by OCT examination, including the assessment of lipid, macrophage, calcium, and minimal fibrous cap thickness (FCT). Visit-to-visit lipid variability was determined by different definitions including standard deviation (SD), coefficient of variation (CV), and variability independent of the mean (VIM). Multivariable linear regression analysis was used to verify the influence of HbA1c on plaque vulnerability features and lipid variability. Exploratory analyses were also performed in non-diabetic patients. RESULTS: Among enrolled subjects, the pre-procedure HbA1c was 5.90 ± 1.31%, and the average follow-up HbA1c was 5.98 ± 1.16%. By OCT assessment, multivariable linear regression analyses demonstrated that patients with elevated HbA1c had a thinner minimal FCT (ß = -6.985, P = 0.048), greater lipid index (LI) (ß = 226.299, P = 0.005), and higher macrophage index (ß = 54.526, P = 0.045). Even in non-diabetic patients, elevated HbA1c also linearly decreased minimal FCT (ß = -14.011, P = 0.036), increased LI (ß = 290.048, P = 0.041) and macrophage index (ß = 120.029, P = 0.048). Subsequently, scheduled follow-ups were performed during 1-year following PCI. Multivariable linear regression analyses proved that elevated average follow-up HbA1c levels increased the VIM of lipid profiles, including low-density lipoprotein cholesterol (ß = 2.594, P < 0.001), high-density lipoprotein cholesterol (ß = 0.461, P = 0.044), non-high-density lipoprotein cholesterol (ß = 1.473, P < 0.001), total cholesterol (ß = 0.947, P < 0.001), and triglyceride (ß = 4.217, P < 0.001). The result was consistent in non-diabetic patients and was verified when SD and CV were used to estimate variability. CONCLUSION: In patients undergoing elective PCI, elevated HbA1c increases the atherosclerotic plaque vulnerability and the visit-to-visit variability of lipid profiles, which is consistent in non-diabetic patients.
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Korotkoff sounds (K-sounds) have been around for over 100 years and are considered the gold standard for blood pressure (BP) measurement. K-sounds are also unique for the diagnosis and treatment of cardiovascular diseases; however, their efficacy is limited. The incidences of heart failure (HF) are increasing, which necessitate the development of a rapid and convenient pre-hospital screening method. In this review, we propose a deep learning (DL) method and the possibility of using K-methods to predict cardiac function changes for the detection of cardiac dysfunctions.