Left ventricular ejection fraction is associated with intraoperative circulatory collapse during transcatheter aortic valve implantation.

BACKGROUND: Intraoperative hemodynamic collapse during transcatheter aortic valve implantation (TAVI) is a devastating complication that requires mechanical support. In this study, we sought to analyze our early experience in using cardiopulmonary bypass (CPB) support to circumvent circulatory compromise during TAVI. METHODS: Between January 2018 and December 2020, 102 consecutive patients (54 males; mean age, 71.2±8.9 years) received TAVI at Tianjin Chest Hospital, and an emergency CPB device was used in 6 of these patients (5.9%). The clinical data of the CPB and no-CPB groups were analyzed to identify the factors associated with intraoperative hemodynamic collapse requiring CPB. RESULTS: All 6 patients who needed emergency CPB support were successfully weaned from the device. This group had a higher Society of Thoracic Surgeons Score [4.09 (2.02, 6.85) vs. 7.47 (5.07, 23.46); P=0.030], more patients with a left ventricular ejection fraction (LVEF) ≤30% [4 (66.7%) vs. 2 (2.1%); P=0.000], a larger right ventricle anteroposterior diameter [20.50 (19.75, 21.25) vs.19.00 (17.00, 20.00); P=0.016], and a higher degree of aortic regurgitation [4.50 (2.75, 5.00) vs. 2.00 (1.00, 4.00); P=0.018] compared to the no-CPB group. The CPB group also had a higher in-hospital mortality rate than did the no-CPB group (16.7% vs. 4.7%; P=0.026). Multivariable analysis determined that the presence of lower pre-TAVI LVEF was associated with intraoperative hemodynamic collapse. CONCLUSIONS: Our results indicate that LVEF is an independent risk factor for requiring emergency CPB during the TAVI procedure. The need for emergency CPB support was associated with higher in-hospital mortality.

Low-dose dobutamine stress myocardial contrast echocardiography for the evaluation of myocardial microcirculation and prediction of overall cardiac function recovery.

The study aimed to investigate the role of low-dose dobutamine stress myocardial contrast echocardiography (MCE) in evaluating myocardial local microcirculation and predicting cardiac function recovery in patients with myocardial infarction. A total of 50 patients with acute myocardial infarction (AMI) were enrolled in the present study. Positron emission tomography was used as a gold standard to determine viable/non-viable myocardial segments in infarcted myocardial region. MCE and dobutamine stress MCE were carried out 72 h after PCI. MCE was carried out again to evaluate myocardial condition at 6 months after PCI. As compared with normal myocardial segments, resting MCE revealed a significant decrease of the values of A (the peak intensity of the time-perfusion intensity curve, reflecting the myocardial blood volume), ß (the slope of the curve, reflecting the myocardial blood flow (MBF) velocity) and A x ß (reflecting MBF) of viable and non-viable myocardial segments. After being challenged by dobutamine, the values of A, ß and A x ß of normal coronary blood supply areas were significantly increased; while the segments A and A x ß of viable myocardium were markedly decreased. Patients were further divided into two groups based on the changes in the contrast-enhanced index (CSI) following dobutamine loading. In the dobutamine stress echocardiography-positive group (the CSI increased or decreased by >0.2), the left ventricular ejection fraction was significantly increased and pro-B-type natriuretic peptide significantly decreased at 6 months following intervention. Low-dose dobutamine stress MCE was indicated to be an effective method to evaluate myocardial microcirculation perfusion in patients with AMI following PCI. In addition, CSI, as a simple semi-quantitative index, may predict left ventricular function in patients with AMI.

[Evaluating the left ventricular diastolic function of diabetes mellitus patients using dual-gate Doppler].

To evaluate the value of left ventricular diastolic function in type 2 diabetes mellitus (DM) using dual-gate Doppler and relative factors, we included 50 non-obesity and hypertension-free DM patients into the controlled group in the study along with 48 age-and-gender-matched healthy volunteer subjects. The peak early diastolic velocity (E), peak later diastolic velocity (A), deceleration time (DT), anterior mitral annulus diastolic peak velocity (e') , isovolumic relaxation time (IVRT), E/A, E/e', Tei index and T(E-e), were measured with dual-gate Doppler. 20 subjects were randomly selected for repetitive analysis. Study showed statistical difference in E/A, DT, e', E/e', IVRT, Tei index and T(E-e), between the two groups (P < 0.05). Linear regression analysis showed positive correlation between T(E-e), and IVRT, course of DM patients and T(E-e), (Beta = 0.295, P = 0.020), and HbA1c control level and T(E-e), (Beta = 0.399, P = 0.010). Repeated analysis showed good reproducibility for both within and between groups. Dual-gate Doppler has clinical value in evaluating left ventricular diastolic function in type 2 diabetes mellitus patients. The course of type 2 diabetes mellitus patients and HbA(1C) control level were both closely related with left ventricular diastolic function.

The effect of myocardial infarct size on cardiac reserve in rhesus monkeys.

Evaluation of cardiac reserve under myocardial infarction in patients is important for prognosis. However, this evaluation is difficult to be done due to high risk for mortality in patients with severe myocardial infarction. The present study was undertaken using non-human primate model as a substitute for humans to investigate the relationship between cardiac reserve and myocardial infarct size. Rhesus monkeys of 2-3 years old (n = 27) were subjected to left anterior descending artery ligation to introduce acute myocardial infarction. By altering the ligation position along the artery, varying sizes of myocardial infarction were generated, from 20 to 58 % of the total myocardium mass. These subjects were divided into 4 groups based on the infarct size: below 25 %, between 25 and 35 %, between 35 and 45 %, and above 45 % of the total mass. Changes in cardiac contractility were determined by echocardiography along with the development of myocardial infarction, and by invasive hemodynamic measurement at the end of the experiment. Correlation analysis revealed that hearts with infarct sizes <25 % of the total mass fully responded to the increase in the load generated by heart rate escalation. Hearts with infarct sizes between 25 and 45 % responded the load increase with gradient decline in the maximum contractility. Hearts with infarct sizes more than 45 % failed to respond to the increase in the load. Therefore, we consider myocardial infarct size <25 % of the total mass as compensable injury, between 25 and 45 % as depleting injury, and more than 45 % as exhausted injury with regard to cardiac reserve. This would serve as a surrogate model for patients with myocardial infarction.

[Cytotoxicity of PFOB nanoparticle coupled with ICAM-1 antibody on cardiomyocytes and its targeted adhesion to injured cardiomyocytes in vitro].

OBJECTIVE: To synthesize perfluorooctylbromide (PFOB) nanoparticle coupled with intercellular adhesion molecule-1 (ICAM-1) monoclonal antibody, and to investigate the characteristics of the nonoparticle and its cytotoxcity on and targeted adhesion to injured cardiomocytes in vitro. METHODS: PFOB nanoparticle (control group) biotinylated PFOB nanoparticle (experimental group) were coupled with biotinylated ICAM-1 antibody. The combination of ICAM-1 antibody and the nanoparticle was detected by immunofluorescent assay. The cytotoxicity of the nanoparticle on rat cardiomyocytes was determined with MTT assay in vitro. The adhesion of the nanoparticle to normal and TNF-alpha injured cardiomyocytes were observed and semiquantified with optical microscope. RESULTS: ICAM-1 antibody was successfully coupled with biotinylated PFOB nanoparticle at a rate around 95%, which showed green fluorescence under the laser Confocal Scanning Microscope, with (385.3 +/- 88.9) nm in size, - (60.3 +/- 6.11) mV in electric potential, and 7.0 x 10(8)/mL in concentrations. No fluorescence was observed with the nonoparticle in the control group. No cytotoxicity of the nonoparticle on rat cardiomyocytes was found. There was limited adhesion of the nanoparticle in the control group to cardiomyocytes, normal or injured. A 10-fold increase in adhesion was detected when the nanopaticle in the experimental group was exposed to the injured cardiomyocytes compared with those exposed to the normal cardiomyocytes [(5.1 +/- 0.22) vs. (0.5 +/- 0.3) nanopaticle per cell, P < 0.05]. CONCLUSION: ICAM-1 monoclonal antibody is successfully coupled with PFOB nanoparticle, which can effectively bind to the cardiomyocytes overexpressing ICAM-1 without showing ctytotoxicity in vitro.

[Targeted combination and anti-inflammatory effects of anti-intercellular adhesion molecule 1 targeted perfluorooctylbromide particles on myocardial ischemia-reperfusion injury in rat model].

OBJECTIVE: To investigate the targeted combination and anti-inflammatory effects of anti-intercellular adhesion molecule 1 (ICAM-1) targeted perfluorooctylbromide (PFOB) particles on myocardial ischemia-reperfusion injury in rat model. METHODS: Seventy-six adult Sprague Dawley rats (male or female, weighing 250-300 g) were selected for experiment. The models of myocardial ischemia-reperfusion injury were established by ligating the left anterior descending coronary artery for 30 minutes in 30 rats. The expression of ICAM-1 protein was detected by immunohistochemistry staining at 6 hours after reperfusion, and the normal myocardium of 10 rats were harvested as control; then the content of interleukin 8 (IL-8) in serum was tested every 6 hours from 6 hours to 48 hours after reperfusion. The other 36 rats were randomly divided into 6 groups (n = 6): ischemia-reperfusion injury model/targeted PFOB particles group (group A), ischemia-reperfusion injury model/untargeted PFOB group (group B), normal control/targeted PFOB particles group (group C), normal control/untargeted PFOB particles group (group D), ischemia-reperfusion injury model/normal saline group (group E), and sham operation group (group F). The ischemia-reperfusion injury models were established in groups A, B, and E; while a thread crossed under the coronary artery, which was not ligated after open-chest in group F. After 6 hours of reperfusion, 1 mL of corresponding PFOB particles was injected through juglar vein in groups A, B, C, and D, while 1 mL of nomal saline was injected in group E. Ultrasonography was performed in groups A, B, C, and D before and after injection. The targeted combination was tested by fluorescence microscope. The content of IL-8 was tested after 6 and 24 hours of reperfusion by liquid chip technology in groups A, B, E, and F. RESULTS: After 6 hours of reperfusion, the expression of ICAM-1 protein significantly increased in the anterior septum and left ventricular anterior wall of the rat model. The content of IL-8 rised markedly from 6 hours after reperfusion, and reached the peak at 24 hours. Ultrasonography observation showed no specific acoustic enhancement after injection of PFOB particles in groups A, B, C, and D. Targeted combination was observed in the anterior septum and left ventricular anterior wall in group A, but no targeted combination in groups B, C, and D. There was no significant difference in the content of IL-8 among groups A, B, and E after 6 hours of reperfusion (P > 0.05), but the content in groups A, B, and E was significantly higher than that in group F (P < 0.05). After 24 hours of reperfusion, no sigificant difference was found in the content of IL-8 between groups A and B (P > 0.05), but the content of IL-8 in groups A and B were significantly lower than that in group E (P < 0.05). CONCLUSION: Anti-ICAM-1 targeted PFOB particles can target to bind and pretect injured myocardium of rat by its anti-inflammation effects.