Diagnosis and survival analyses of patients with space-occupying cardiac lesions: a 10-year retrospective single-center study.

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.

Early changes in left ventricular myocardial function by 2D speckle tracking layer-specific technique in neonates with hyperbilirubinemia.

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.

Effect of Traditional Chinese Medicine Poge Heart-Saving Decoction on Cardiac Function in Heart Failure Rat Model.

BACKGROUND: Poge heart-saving decoction (PHSD) has been used as a medicine treating heart failure in China for many years. The study aimed to explore the effect of PHSD on cardiac function in heart failure conditions and its underlying mechanism. METHODS: Adriamycin was used to induce the model of heart failure (HF) in rats. Sixty rats were randomly divided into six groups: blank control group, sham group, 9.33 g/kg group (low-PHSD, test group), 13.995 g/kg group (moderate-PHSD, test group), 18.66 g/kg group (high-PHSD, test group), and fosinopril group (4.67 mg/kg, comparison test group). Cardiac ultrasound was used to evaluate the cardiac function of the rats, and radioimmunoassay was used to measure aldosterone (ALD) and angiotensin II (AngII) levels in the serum. RESULTS: Compared with the blank control group, the left ventricular end-diastolic dimension (LVEDd) and left ventricular end-systolic dimension (LVEDs) in the sham group were increased (1.04 ± 0.12 vs. 0.67 ± 0.13 cm; 0.75 ± 0.13 vs. 0.28 ± 0.10 cm; P < 0.05), and the left ventricular ejection fraction was decreased (36.65 ± 5.74 vs. 76.09 ± 4.23%; P < 0.05). The ejection fraction of HF rats was increased in 9.33 g/kg group, 13.995 g/kg group, and 18.66 g/kg group compared with those of the sham group (57.13 ± 1.63, 58.43 ± 1.98, and 59.21 ± 1.37 vs. 36.65 ± 5.74%; P < 0.05). PHSD also improved cardiac function by reducing the LVEDd and LVEDs (0.88 ± 0.11, 0.75 ± 0.13, and 0.72 ± 0.18 vs. 1.04 ± 0.12 cm; 0.62 ± 0.10, 0.63 ± 0.17, and 0.45 ± 0.11 vs. 0.75 ± 0.13 cm; P < 0.05). The levels of ALD and AngII in the serum of rats in the sham group were significantly higher than those in the blank control group (371.58 ± 39.25 vs. 237.12 ± 17.35 µg/L; 232.18 ± 16.33 vs. 159.44 ± 18.42 pg/L; P < 0.05). The ALD and AngII of the rats in all of the three PHSD groups and the fosinopril group were decreased (276.81 ± 25.63, 277.18 ± 21.35, 268.19 ± 19.28, and 271.47 ± 28.96 vs. 371.58 ± 39.25 µg/L; 169.41 ± 27.53, 168.81 ± 19.78, 164.23 ± 21.34, and 174.27 ± 22.84 vs. 232.18 ± 16.33 pg/L; P < 0.05). The histopathological changes of the myocardium in the sham group showed the disorganized fiber, shaded staining, fracture, and zonation. The fracture of the myocardium was relieved in all groups except the sham group and the blank control group. CONCLUSION: Therefore, PHSD could shorten LVEDd and LVEDs of rats and reverse ventricular remodeling. The mechanism might be related to the inhibition of the activation level of renin-angiotensin-aldosterone system (especially ALD and AngII) and decreasing the postload of the heart.

AMPK-mediated degradation of Nav1.5 through autophagy.

The voltage-gated cardiac sodium channel, Nav1.5, is the key component that controls cardiac excitative electrical impulse and propagation. However, the dynamic alterations of Nav1.5 during cardiac ischemia and reperfusion (I/R) are seldom reported. We found that the protein levels of rat cardiac Nav1.5 were significantly decreased in response to cardiac I/R injury. By simulating I/R injury in cells through activating AMPK by glucose deprivation, AMPK activator treatment, or hypoxia and reoxygenation (H/R), we found that Nav1.5 was down-regulated by AMPK-mediated autophagic degradation. Furthermore, AMPK was found to phosphorylate Nav1.5 at threonine (T) 101, which then regulates the interaction between Nav1.5 and the autophagic adaptor protein, microtubule-associated protein 1 light chain 3 (LC3), by exposing the LC3-interacting region adjacent to T101 in Nav1.5. This study highlights an instrumental role of AMPK in mediating the autophagic degradation of Nav1.5 during cardiac I/R injury.-Liu, X., Chen, Z., Han, Z., Liu, Y., Wu, X., Peng, Y., Di, W., Lan, R., Sun, B., Xu, B., Xu, W. AMPK-mediated degradation of Nav1.5 through autophagy.

Elevated Resting Heart Rate Is Associated with Carotid Atherosclerosis in Middle-Aged and Elderly Chinese Population.

BACKGROUND: Elevated resting heart rate predicts poor cardiovascular and cerebrovascular outcomes. Atherosclerosis may be a mediator linking this relationship. In a Chinese population, we investigated whether resting heart rate was associated with carotid atherosclerosis as indicated by elevated carotid intima-media thickness (CIMT) and presence of carotid plaque. METHODS: A total of 1557 participants older than 50 years old from a community-based population without known cardiovascular diseases were included. All participants provided detailed lifestyle and medical information, and blood samples for biochemical measurements. The participants were categorized according to resting heart rate quartiles (<67, 67-73, 74-81, >81 beats per minute [bpm]). CIMT and presence of carotid plaque were determined using B-mode ultrasonography. Elevated CIMT was defined as the upper quartile of CIMT. RESULTS: We observed positively graded associations between resting heart rate quartiles and carotid atherosclerosis. Participants with resting heart rates higher than 81 bpm had an odds ratio of 2.82 (95% confidence interval 1.92-4.13) for elevated CIMT, and an odds ratio of 2.00 (1.36-2.92) for carotid plaque, compared to participants with resting heart rates lower than 67 bmp. Each 10-bpm increase in resting heart rate was associated with an odds ratio of 1.47 (1.29-1.68) for elevated CIMT and an odds ratio of 1.40 (1.23-1.60) for carotid plaque. The associations were independent of conventional cardiovascular risk factors. CONCLUSIONS: Elevated resting heart rate was strongly and independently associated with carotid atherosclerosis in the middle-aged and elderly Chinese population. Atherosclerosis may be a potential mediator between resting heart rate and adverse cardiovascular outcomes.