Case report: A 56-year-old woman presenting with torsades de pointes and cardiac arrest associated with levosimendan administration and underlying congenital long QT syndrome type 1.

Torsades de Pointes (TdP) is a malignant polymorphic ventricular tachycardia with heart rate corrected QT interval (QTc) prolongation, which may be attributed to congenital and acquired factors. Although various acquired factors for TdP have been summarized, levosimendan administration in complex postoperative settings is relatively uncommon. Timely identification of potential causes and appropriate management may improve the outcome. Herein, we describe the postoperative case of a 56-year-old female with initial normal QTc who accepted the administration of levosimendan for heart failure, suffered TdP, cardiac arrest, and possible Takotsubo cardiomyopathy, further genetically confirmed as long QT syndrome type 1 (LQT1). The patient was successfully treated with magnesium sulfate, atenolol, and implantable cardioverter defibrillator implantation. There should be a careful evaluation of the at-risk populations and close monitoring of the electrocardiograms, particularly the QT interval, to reduce the risk of near-fatal arrhythmias during the use of levosimendan.

Research on clinical characteristics and prognostic analysis of heparin-induced thrombocytopenia after surgery for acute type a aortic dissection.

PURPOSE: The present study aimed to explore the clinical characteristics of heparin-induced thrombocytopenia (HIT) after surgery for acute type A aortic dissection and perform a relevant prognostic analysis. METHODS: After continuous observation and analysis of 204 patients who underwent acute type A aortic dissection, we found that blood platelets decreased significantly after surgery and that these patients can be suspected to suffer HIT based on relevant 4Ts scores. For these suspected HIT patients, a latex particle-enhanced immunoturbidimetric assay was conducted to detect heparin-induced antibodies. Perioperative clinical data of patients in HIT and non-HIT groups were recorded as were blood platelet counts, HIT antibody test results, 4Ts scores, thromboembolic complications, clinical prognosis and outcomes. RESULTS: In the present study, 38 suspected HIT patients, 16 HIT patients and 188 non-HIT patients were selected in the clinical setting. Among them, HIT patients were found to have prolonged cardiopulmonary bypass time (223 min on average vs. 164 min) and delayed aortic cross-clamp time (128 min on average vs. 107 min), and these differences between HIT patients and non-HIT patients were significant (P < 0.05). Additionally, the HIT group required longer operation time and higher dose of heparin, but showing no statistical differences (P > 0.05). The transfusions of blood platelets in the HIT group and non-HIT group were 18.7 ± 5.0u and 15.6 ± 7.34 u, respectively. In the HIT group, the mechanic ventilation time and the length of ICU stay were longer comparing the non-HIT group(P < 0.05), though no significant differences in total length of stay or In-hospital mortality were observed (P > 0.05). The incidence of continuous renal replacement therapy in HIT group was higher than the non-HIT group (P < 0.05). Additionally,there were no significant differences in 24-h postoperative drainage or reoperation for bleeding in both group(P > 0.05). However, the HIT antibody titer in the HIT group was significantly higher than that in the Suspected HIT group (2.7 ± 0.8 U/mL vs. 0.3 ± 0.2 U/mL) (P < 0.05). Among patients diagnosed with HIT, the incidence of thromboembolism reached 31.5%.For example, two HIT patients newly developed thromboembolism in both lower extremities,and three patients experienced cerebral infarction. CONCLUSIONS: After surgery for acute type A aortic dissection, HIT patients developed postoperative complications, the duration of ventilatory support and length of ICU stay were extended, and the incidence of thromboembolism increased. HIT antibody detection and risk classification should be implemented for high-risk patients showing early clinical characteristics.

Changes in Coagulation and Fibrinolysis Systems During the Perioperative Period of Acute Type A Aortic Dissection.

BACKGROUND: Acute type A aortic dissection (ATAAD) has a high risk of perioperative bleeding and often requires extensive blood product infusions. Analysis of the changes in coagulation and fibrinolysis is both helpful for proper treatment and an improved prognosis. The present study investigated the changes in the coagulation and fibrinolysis systems during the perioperative period of ATAAD. METHODS: Twenty-two patients with ATAAD were included in this study. After diagnosis, all patients underwent ascending aorta replacement, aortic arch replacement, and implantation of a special stented endovascular graft. The control group included 25 patients undergoing elective aortic surgery. Baseline preoperative, intraoperative, and postoperative data were collected in both groups. Venous blood samples of all subjects were collected at five time points, after admission (T1), before surgery (T2), after protamine reversal (T3), postoperative 6 h (T4), and postoperative 24 h (T5), measuring the concentrations of platelet factor 4 (PF4), prothrombin fragment 1 + 2 (F1+2), tissue factor (TF), tissue factor pathway inhibitor (TFPI), plasminogen activator (PA), plasminogen activator inhibitor-1 (PAI-1) and thrombin antithrombin complex (TAT) by enzyme-linked immunosorbent assays (ELISAs). RESULTS: The average age of the ATAAD group was 49.9±12.5 years old, while that of the control group was 57.0±12.1 years old. There were more patients with a smoking history, and the cardiopulmonary bypass time, aortic cross-clamp time, and preoperative left ventricular ejection fraction were higher in the ATAAD group than in the control group (P < 0.05). Additionally, preoperative fibrin degradation products (FDP) and preoperative D-dimer were higher in the ATAAD group than in the control group (P < 0.05). However, time from onset to operation, intraoperative core temperature, preoperative B-type natriuretic peptide (BNP), and left ventricular end-diastolic diameter in the ATAAD group were lower than those in the control group (P < 0.05). In contrast, however, the proportion of abnormal bicuspid aortic valves in the control group was higher (P < 0.05). TF in the ATAAD group was significantly higher at T1 (7.9±3.7 ng/mL versus 0.9±0.7 ng/mL, P < 0.05). The TFPI in the ATAAD group was higher than that in the control group at T1 and T2 (P < 0.05). Additionally, PA in the ATAAD group was higher than that in the control group at T1, T2, T3, and T5 (P < 0.05), while PA in the control group was significantly higher at T3 than at T1 (P < 0.05). There was no significant difference in PAI-1 between the two groups before surgery (P > 0.05). Nevertheless, both groups reached their peak value at T3. The platelet count and fibrinogen (FBG) in the ATAAD group decreased significantly from T1 to T2 and continued to decrease after cardiopulmonary bypass. F1+2 and TAT in the ATAAD group were higher than in the control group (P < 0.05); however, they peaked at T3. The PF4 in the ATAAD group slightly increased at T1, while PF4 at T3 was significantly higher than at T1 (P < 0.05). CONCLUSION: The changes in coagulation and fibrinolysis in the ATAAD group before surgery were very significant, which caused a large amount of fibrinogen and platelet consumption. Cardiopulmonary bypass (CPB) and a lower intraoperative core temperature exacerbated the coagulation and fibrinolysis disorder, and the pro-coagulant function of the platelets was activated after surgery. Maintaining the normal concentration of fibrinogen was helpful to correct the coagulation function disorder.

Gene expression profiling analysis to investigate the role of remote ischemic postconditioning in ischemia-reperfusion injury in rats.

BACKGROUND: Blood flow restoration is a definitive therapy for salvaging the myocardium following ischemic injury. Nevertheless, the sudden restoration of blood flow to the ischemic myocardium can induce ischemia-reperfusion injury (IRI). RESULTS: Herein, we investigated the cardioprotective effect of remote ischemic postconditioning (RPostC) through our in vivo rat model of myocardial IRI. The study included three groups: the control group, the IRI group, and the IRI + RPostC group. Ischemia-reperfusion treatment led to an increase in the myocardial infarction area, which was inhibited by RPostC. In contrast to that in the control group, the myocardial apoptosis level was enhanced in the IRI group, whereas RPostC treatment decreased IRI-induced cellular apoptosis. Affymetrix Rat Gene 2.0 ST chip data identified a total of 265 upregulated genes and 267 downregulated genes between the IRI and IRI + RPostC groups. A group of differentially expressed noncoding RNAs (ncRNAs), such as MTA_TC0600002772.mm, MTA_TC1300002394.mm, U7 small nuclear RNA (Rnu7) and RGD7543256_1, were identified. Gene Ontology (GO) enrichment analysis indicated that the positive regulation of some molecular functions, such as GTPase activity, GTP binding, cyclic-nucleotide phosphodiesterase activity and cytokine activity, may contribute to the cardioprotective role of RPostC. Moreover, pathway enrichment analysis using the Kyoto Encyclopedia of Genes and Genomes (KEGG) suggested the potential implication of the TNF signaling pathway and Toll-like receptor signaling pathway. Global signal transduction network analysis, co-expression network analysis and quantitative real-time polymerase chain reaction analysis further identified several core genes, including Pdgfra, Stat1, Lifr and Stfa3. CONCLUSION: Remote ischemic postconditioning treatment can decrease IRI-mediated myocardial apoptosis by regulating multiple processes and pathways, such as GTPase activity, cytokine activity, and the TNF and Toll-like receptor signaling pathways. The potential role of the above ncRNAs and core genes in IRI-induced cardiac damage merits further study as well.

Arterial stiffness is associated with target organ damage in subjects with pre-hypertension.

INTRODUCTION: Present study was to evaluate whether increased arterial stiffness was associated with target organ damage in pre-hypertensive subjects. MATERIAL AND METHODS: Pre-hypertensive subjects enrolled and echocardiography was used to evaluate left ventricular hypertrophy (LVH) and the first morning urine was collected to evaluate albumin and creatinine ratio (ALB/Cr ratio). Carotid-femoral pulse wave velocity (cf-PWV) was measured. RESULTS: A total of 420 subjects were recruited and mean age was 42.6 years. Mean systolic/diastolic blood pressure (SBP/DBP) were 130 ±9 mm Hg and 85 ±4 mm Hg. The prevalence of albuminuria and left ventricular hypertrophy was 8.6 % and 11.7 %. Mean cf-PWV was 9.2 ±1.0 m/s, with arterial stiffness prevalence was 8.8%. Subjects with arterial stiffness had higher cf-PWV value (10.6 ±0.4 m/s vs. 8.7 ±0.6 m/s, p < 0.05), and ALB/Cr ratio (28.3 ±13.2 µg/mg vs. 23.1 ± 11.4 µg/mg, p < 0.05). Overall, with multivariate regression analysis, aging and arterial stiffness were significantly associated with pre-hypertension. With stepwise adjusted for potential covariates including age, male gender, fasting plasma glucose, presence of current cigarette smoking, dyslipidemia, statins and SBP, increased cf-PWV remained independently associated with left ventricular hypertrophy and albuminuria, with an increased odds of 41 % and 24 % (p < 0.05), respectively. CONCLUSIONS: In pre-hypertensive subjects, arterial stiffness is independently associated with LVH and albuminuria and cf-PWV may be a useful marker to identify target organ damage in pre-hypertensive subjects.