ABSTRACT
Objectives: Trends in prevalence and treatments of atherosclerotic cardiovascular disease (ASCVD) remains to be documented, with frequent update of relevant guidelines. We aimed to characterize trends in prevalence of ASCVD, and risk factor control and medications among ASCVD adults. Methods: We conducted a cross-sectional analysis of data from 55,081 adults in the National Health and Nutrition Examination Surveys (NHANES) 1999-2018. Results: The age-standardized prevalence of ASCVD did not change significantly from 1999-2002 (7.9 %, 95 % CI 7.1 %-8.7 %) to 2015-2018 (7.5 %, CI 6.8 %-8.3 %) (P for trend =0.18), representing an estimated 19.9 million individuals with ASCVD in 2015-2018. The prevalence of premature ASCVD was 2.0 % (CI, 1.6 %-2.5 %). Over 60.0 % of ASCVD participants were at very-high risk. From 1999-2002 to 2015-2018, the percentage with lipid control (non-high-density lipoprotein cholesterol <100 mg/dL) increased from 7.0 % (CI, 3.5 %-12.3 %) to 26.4 % (CI, 16.2 %-38.9 %). The percentage with blood-pressure control (<130/80 mmHg) increased from 51.2 % (CI, 41.0 %-61.3 %) in 1999-2002 to 57.2 % (CI, 48.4 %-65.6 %) in 2011-2014, but then declined to 52.8 % (CI, 44.4 %-81.3 %) in 2015-2018. The percentage with glycemic control (HbA1c <7.0 %) decreased from 95.0 % (CI, 90.2 %-97.9 %) to 84.0 % (CI, 75.9 %-90.3 %). The percentage who achieved all 3 targets was 18.6 % (CI, 8.2 %-33.8 %) in 2015-2018. The percentage of ASCVD participants who were taking statins increased from 1999-2002 to 2011-2014, but then leveled off. Approximately 60 % of individuals with ASCVD and less than 40 % of those with premature ASCVD were taking statins in 2015-2018. The utilization of blood-pressure-lowering drugs remained largely constant over time, whereas the use of glucose-lowering drugs increased. Conclusions: Based on NHANES data from US adults, the estimated prevalence of ASCVD remained relatively stable between 1999 and 2018. Substantial undertreatment with stains was found in individuals with ASCVD, and the percentage achieving optimal lipid control was low.
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Background: Space-occupying cardiac lesions are uncommon but fatal. Echocardiography can identify diseases quickly in the clinic. This study reviews the clinical data of patients with space-occupying cardiac lesions in the past 10 years and analyzes their echocardiographic features, pathological diagnosis, and prognosis. Methods: We performed a retrospective analysis of 412 patients admitted to Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing from 2011 to 2020. All patients were diagnosed with cardiac masses based on transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE). We compared the diagnostic results of echocardiography and the postoperative pathological diagnosis and analyzed the characteristics of different types of space-occupying cardiac lesions. We also compared the mortality of patients with different types of space-occupying cardiac lesions through follow-up results of postoperative patients. Results: The 412 patients included 189 males and 223 females. Among them, 214 patients had benign tumors (including 176 patients with myxomas), 29 had primary malignant tumors, 32 had metastatic tumors, 41 had thrombi, 92 had infectious neoplasms, and 4 patients had special types of space-occupying lesions. A total of 376 lesions were correctly characterized by TTE, with an accuracy of 91.3%. Patients with benign tumors (9/214), thrombi (4/41), infectious neoplasms (5/92), or special types of space-occupying lesions (0/4) exhibited low rates of mortality or recurrence. In contrast, patients with primary malignant tumors (16/29) or metastatic tumors (16/32) exhibited high mortality rates. Conclusions: Echocardiography is a valuable tool for characterizing space-occupying cardiac lesions. It can provide important preoperative diagnostic information for cardiothoracic surgeons.
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BACKGROUND: Hyperbilirubinemia (HBN) can cause myocardial injury in neonates. Advancement in myocardial deformation imaging allows the detection of subclinical changes in myocardial contractility. The present study aimed to evaluate the changes in left ventricular contractility in newborns with hyperbilirubinemia by 2D speckle tracking imaging (STI). METHODS: A group of 134 neonates who reached the diagnostic level of HBN as the HBN group was selected. The control group included 56 healthy newborns. The interventricular septum, anterior partition, anterior wall, sidewall, posterior wall, and inferior wall were separated into the basal, middle, and apical segments. In each segment, speckle tracking analysis was performed in the subintimal, middle, and subadventitial myocardium. The overall longitudinal strain of the myocardium in different ventricular walls and segments and global longitudinal strain (GLS) were computed. At the same time, the laboratory results of blood gas analysis, blood routine tests, liver function, and myocardial enzyme spectrum in HBN neonates were collected and correlated with the left ventricular stratified strain parameters. RESULTS: The gradient of the left ventricular GLS had the same characteristics in both groups of newborns. There was a decreasing trend of longitudinal strain (LS) from the intima to the adventitia (i.e., GLSendo > GLSmid > GLSepi). This gradient was also present in stratified LS in each myocardial segment (P<0.001). The LS showed an increasing trend from the basal to the apical segment (P<0.001). The LS of the ventricular septum, anterior wall (or anterior septum), inferior wall, lateral wall, and posterior wall showed a decreasing trend (P<0.001). Stratified strain parameters of the ventricular wall (i.e., the 3-layer myocardium: LSendo-SEPT, LSmid-SEPT, and LSepi-SEPT) were all significantly lower in the HBN group than in the control group (P=0.019, P=0.019, and P=0.023, respectively). LSedo-ANT, LSmid-ANT, and LSepi-ANT were also reduced, and the difference between LSendo-ANT and LSepi-ANT was statistically significant. The segmental stratified strain parameters (i.e., the apical 3-layer myocardium: LSepi-a, LSmid-a, and LSepi-a) decreased, and the difference in LSepi-a was statistically significant (P=0.043). Overall strain parameters (i.e., the 3-layer myocardial overall strain: GLSendo, GLSmid, and GLSepi) were reduced, but the difference was not statistically significant (P=0.612, P=0.653, and P=0.585, respectively). The subclinical changes in systolic function in the HBN group, reflected by the parameters of longitudinal myocardial strain, correlate to some extent with multiple results of laboratory tests. CONCLUSIONS: 2DSTI stratified strain technology can quantitively evaluate changes in the LS of the left ventricle in different ventricular walls, wall segments, and layers of the myocardium.
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AIM: To assess whether glomerular hyperfiltration (GHF) could result in renal tubular damage in type 2 diabetes mellitus (T2DM) patients. METHODS: Reference value of estimated glomerular filtration rate (eGFR) was determined in 248 healthy individuals based on serum CysC levels. GHF was defined as an eGFR exceeding the sex-specific 97.5th percentile in non-diabetic individuals. In the present study, 30 with GHF, 58 with norm-GFR T2DM, and 24 healthy controls were recruited. Tubular markers, such as urinary N-acetyl-ß-D-glucosaminidase (NAG) and kidney injury molecule 1 (KIM-1), as well as serum and urinary neutrophil gelatinase-associated lipocalin (NGAL), were measured and compared. The correlation of these markers with eGFR was analyzed in the GHF group. RESULTS: The GHF group had higher urinary NGAL and KIM-1 levels but lower serum NGAL level than the norm-GFR and control groups. Slightly decreased serum NGAL and increased urinary NGAL levels were also noted in the norm-GFR group compared with those of the controls. There was no statistical difference in the urinary NAG values among the three groups. Correlation analysis showed that eGFR was positively related to fasting blood glucose (FBG), HbA1c, urinary NGAL, and KIM-1, but negatively with serum NGAL in the GHF group. CONCLUSION: Higher urinary tubular damage markers were found in T2DM patients with GHF than the norm-GFR and control groups, probably a direct proof that GHF is a deleterious factor for diabetic nephropathy.
