Huai-Min Chen

Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways.

BackgroundLysophosphatidylcholine (lysoPC), a metabolite from membrane phospholipids, accumulates in the ischemic myocardium and plays an important role in the development of myocardial dysfunction ventricular arrhythmia. In this study, we investigated if baicalein, a major component of Huang Qui, can protect against lysoPC-induced cytotoxicity in rat H9c2 embryonic cardiomyocytes.MethodsCell viability was detected by the MTT assay; ROS levels were assessed using DCFH-DA; and intracellular free calcium concentrations were assayed by spectrofluorophotometer. Cell apoptosis and necrosis were evaluated by the flow cytometry assay and Hoechst staining. Mitogen-Activated Protein Kinases (MAPKs), which included the ERK, JNK, and p38, and the apoptotic mechanisms including Bcl-2/Bax, caspase-3, caspase-9 and cytochrome c pathways were examined by Western blot analysis. The activation of MAPKs was examined by enzyme-linked immunosorbent assay.ResultsWe found that lysoPC induced death and apoptosis of H9c2 cells in a dose-dependent manner. Baicalein could prevent lysoPC-induced cell death, production of reactive oxygen species (ROS), and increase of intracellular calcium concentration in H9c2 cardiomyoctes. In addition, baicalein also inhibited lysoPC-induced apoptosis, with associated decreased pro-apoptotic Bax protein, increased anti-apoptotic Bcl-2 protein, resulting in an increase in the Bcl-2/Bax ratio. Finally, baicalein attenuated lysoPC-induced the expression of cytochrome c, casapase-3, casapase-9, and the phosphorylations of ERK1/2, JNK, and p38. LysoPC-induced ERK1/2, JNK, and p38 activations were inhibited by baicalein.ConclusionsBaicalein protects cardiomyocytes from lysoPC-induced apoptosis by reducing ROS production, inhibition of calcium overload, and deactivations of MAPK signaling pathways.

Labedipinedilol-A prevents lysophosphatidylcholine-induced vascular smooth muscle cell death through reducing reactive oxygen species production and anti-apoptosis

OBJECTIVE Labedipinedilol-A, a novel calcium antagonist, has been previously demonstrated to have pleiotropic protective effects in the cardiovascular system. This study aimed to investigate its cytoprotective effects in rat vascular smooth muscle cells (VSMCs) treated with lysophosphatidylcholine (lysoPC), a key lipid component mediating atherogenesis. METHODS AND RESULTS VSMCs were incubated with lysoPC with or without labedipinedilol-A pretreatment to determine its effects on lysoPC-induced cell death, Ca(2+) influx, oxidative stress, MAPK signaling and apoptosis. Labedipinedilol-A attenuated lysoPC-induced cell death and Ca(2+) influx. It also reduced reactive oxygen species (ROS) production evoked by lysoPC and down-regulated expressions of NAD(P)H oxidase subunits, Nox1 and Rac1. Moreover, it inhibited lysoPC-induced phosphorylation of MAPK including ERK1/2, JNK, and p38. It mitigated the dissipation of mitochondrial transmembrane potential induced by lysoPC. Lastly, labedipinedilol-A inhibited lysoPC-induced apoptosis with attenuation of caspase-3/-9 activations and modulation of Bax/Bcl-2 protein expressions. CONCLUSION Labedipinedilol-A can suppress lysoPC-induced VSMCs death via reducing ROS production and anti-apoptosis. These protective effects are potentially mediated through the inhibition of Ca(2+) influx, down-regulation of the NAD(P)H oxidase subunits (Nox1/Rac1) and MAPK signaling, and attenuation of mitochondrial depolarization. Thus, labedipinedilol-A may have a valuable role in the preventing atherosclerosis associated with hyperlipidemia.

Acute aortic dissection type A with acute coronary involvement: a novel classification.

BACKGROUND Acute coronary involvement (ACI) due to acute aortic dissection (AAD) type A is potentially fatal. We examined selected patients with AAD type A, which had evolved over 14 years, and acute coronary involvement. The purpose of this study was to determine the characteristics of patients with ACI due to AAD type A. METHODS Between 1997 and 2011, we recruited 20 patients (14.1%) with ACI (14 men, 6 women; mean age: 51.8 ± 11.8 years; age range: 35-79 years) from 142 patients who had undergone surgical repair of AAD type A. RESULTS We propose a novel 4-category classification scheme based on the surgical pathological findings. The right coronary artery was involved in 15 patients, and the left was involved in 5 patients. Fourteen patients had preoperative myocardial ischemia. In the other 6 patients, acute coronary involvement was found intraoperatively. Patients with ACI were significantly younger than those without ACI (51.8 ± 11.8 vs. 61.0 ± 11.8; p = 0.001), a lower prevalence of intramural hematoma (5.0% vs. 32.8%; p = 0.011), a higher aortic regurgitation rate (95.0% vs. 53.5%; p = 0.001). Patients presenting with ACI had an in-hospital mortality rate of 20.0% (4/20), while those without ACI had an in-hospital mortality rate of 19.7% (24/122). CONCLUSIONS Acute coronary involvement due to AAD type A is not always associated with coronary malperfusion. Patients with ACI were much younger, had a higher aortic regurgitation rate, and, less commonly, had intramural hematoma. This new classification scheme would make it more convenient for surgeons to decide on treatment options for this special cohort.

Baicalein Inhibits HMGB1 Release and MMP-2/-9 Expression in Lipopolysaccharide-Induced Cardiac Hypertrophy

Myocardial dysfunction, a common complication after sepsis, significantly contributes to the death of patients with septic shock. In the search for potentially effective drugs to decrease mortality from sepsis, we investigated the cardioprotective effects of baicalein, a flavonoid present in the root of Scutellaria baicalensis, on lipopolysaccharide (LPS)-induced pro-inflammatory cytokine production and matrix metalloproteinase-2 and -9 (MMP-2/-9) expression. We found that baicalein significantly attenuated LPS-induced cardiac hypertrophy and counteracted reactive oxygen species (ROS) generation in neonatal rat cardiomyocytes. In addition, pretreatment with baicalein inhibited LPS-induced early (e.g., tumor necrosis factor-α (TNF-α) and interleukin-6) and late (e.g., high mobility group box 1 (HMGB1) pro-inflammatory cytokine release, inducible nitric oxide synthase (iNOS) expression and NO production. Finally, baicalein also significantly down-regulated the expression of MMP-2/-9 and attenuated HMGB1 translocation from the nucleus to the cytoplasm. These results suggest that baicalein can protect cardiomyocytes from LPS-induced cardiac injury via the inhibition of ROS and inflammatory cytokine production. These cardioprotective effects are possibly mediated through the inhibition of the HMGB1 and MMP-2/-9 signaling pathways.

Double right coronary artery and its clinical implications

Congenital anomalies of the coronary arteries are present in 0.2-1.4% of the general population. These anomalies represent one of the most confusing issues in the field of cardiology and challenges for interventional cardiologists and cardiac surgeons if the anomalies are unrecognised. Double right coronary artery is one of the rarest coronary arteries. Previously, the probability of developing atherosclerotic changes in patients with a double right coronary artery was considered to be equal to that in those without it. In reality, however, a high prevalence of atherosclerotic coronary artery disease was found in patients with a double right coronary artery originating from a single ostium after our comprehensive literature search through the PubMed database. Owing to the fact that double right coronary artery is both a congenital and potentially atherosclerotic coronary artery disease at diagnosis, coronary intervention or cardiac operation is more complicated than previously believed. Individuals with a double right coronary artery may be unaware of its presence until an accidental finding during coronary angiography or cardiac operation and are at risk for unsuspected complications of atherosclerotic coronary artery disease or during cardiac operation. Therefore, it is important to obtain information on the anatomic variants of this congenital coronary anomaly in patients who are undergoing either coronary intervention, aortic root operation or myocardial revascularisation. To our knowledge, this is the first comprehensive article to discuss the anomalies and their clinical implications.

Stable haemodynamics associated with no significant electrocardiogram abnormalities is a good prognostic factor of survival for acute type A aortic dissection repair

OBJECTIVES Acute type A aortic dissection (AAD) is a medical emergency with high mortality even with emergency repair. We explored the prognostic factors of in-hospital mortality for AAD repair. METHODS One hundred and thirty-three consecutive patients operated on for AAD between 1997 and 2011 were enrolled in our study. They were assigned to the in-hospital mortality or the survival group. We evaluated 101 variables to predict in-hospital mortality. All data were collected retrospectively. RESULTS The 30-day mortality, including intraoperative deaths, was 12.8% (17/133 patients) and in-hospital mortality was 18.0% (24/133). Univariate analysis disclosed 10 significant prognostic factors. Multivariate analysis confirmed that preoperative shock or hypotension (odds ratio (OR) = 4.71; P = 0.004), an initial 24 h of bleeding >1500 ml (OR = 5.17; P = 0.01) and age ≥ 75 years (OR = 3.70; P = 0.019) were independent prognostic factors of in-hospital mortality. On the contrary, an electrocardiogram (ECG) showing no abnormalities (OR = 0.22; P = 0.008) is a good prognostic factor for survival. Interestingly, patients with stable haemodynamics without abnormal ECG findings had an excellent result of 1.6% (1/63) in-hospital mortality. CONCLUSIONS Stable haemodynamics and no significant abnormal ECG findings predicted excellent in-hospital survival. Cardiac surgeons and cardiologists should be aware of these positive predictors when treating patients diagnosed with AAD.

Stroke, infective endocarditis and a blood filled cyst

A 16-year-old boy was referred to our emergency department after falling off his motorcycle. He had no past medical history. On examination, he had a right sided hemiplegia and grade 4/6 systolic murmur. Brain MRI showed a left middle cerebral artery infarction (fi gure A). At echocardiography, a vegetation attached to a fl ail anterior mitral leafl et, and severe mitral regurgitation were seen (fi gure B), suggestive of ruptured chordae tendineae caused by infective endocarditis. A 1 cm diameter ring-form cystic lesion was also seen on the anterior leafl et of the mitral valve (fi gure B). Blood cultures grew Streptococcus viridans. We diagnosed our patient with an embolic stroke due to infective endocarditis. Our patient had a mitral valve replacement 4 weeks after presentation. During the operation, the cystic mass and vegetation were removed (fi gure C and D); histological examination showed a blood cyst and infective endocarditis. Cardiac blood cysts are congenital; they are usually asymptomatic, but can predispose to regurgitation, infective endocarditis, and cerebral emboli. However, they usually regress spontaneously and rarely persist into adolescence or adulthood.

Easy Category for Complex Congenital Cardiac Segmental Connections

To clarify the variant complex congenital cardiac defects, Van Praagh introduced a system of segmental sets to classify the majority of congenital heart diseases, but the code system entails some confusion for complete understanding. We attempted to recategorize the variant sets into four subgroups according to the connection of the atrial‐ventricular and ventricular‐arterial segments. This complexity can simply be grouped into four subgroups with regularities. From a simple table so formed, we can quickly ascertain the hemodynamics and the circulatory physiology, and therefore quickly determine the treatment protocol for variant complex hearts.

Fate of distal aorta after acute type A aortic dissection repair: Change and persistency of postoperative false lumen status

BACKGROUND The role of false lumen patency related to aortic growth, re-interventions, and post-discharge mortality in the chronic phase of repaired type A acute aortic dissection (TAAAD) remains controversial. We investigated the role of postoperative false lumen patency during long-term follow-up. METHODS Based on postoperative CT images of 70 candidates, 58 eligible patients without alteration of false lumen status were assigned into three groups: complete patency, partial patency, and complete thrombosis. Aortic growth of 7 levels was analyzed. RESULTS Persistent complete patency in post-operative TAAAD presents faster expansion of aortic diameter (95% CI, 0.35 to 11.52; P=0.038; B=5.935) and more patients with growth rate>5mm/year (P=0.029). The persistent status of false lumen does not predict post-discharge mortality (P=0.479). History of coronary artery disease (CAD) is the only independent predictor of post-discharge mortality. CONCLUSIONS In TAAAD patients without change of postoperative false lumen status, completely patent false lumen presents faster aortic growth and more patients with growth rate>5mm/year. False lumen status does not correlate with late survival. Here we provide an insight into persistent postoperative false lumen in TAAAD patients and may help cast light on aortic dissection in this specific subgroup to improve their late outcomes.

Pyrexia of Postimplantation Syndrome for Patients Undergoing (Thoracic) Endovascular Aortic Repair

OBJECTIVE While a clear definition and explanation to postimplantation syndrome are yet to be clarified, this study aims to investigate its nature by retrospectively analyzing postprocedural fever pattern with patient characteristics, procedure details, and responses to medical treatments. MATERIALS AND METHOD Twenty-three patients undergoing (thoracic) endovascular aortic repair between January 2011 and January 2012 were studied for their postimplantation fever pattern. The demographic information, procedure specifications, and postprocedure care details were collected for statistical analysis to find associations between fever pattern and the above-mentioned parameters. RESULTS None of the postprocedure microbial studies returned positive. Longer fever duration and higher fever frequency are statistically associated with younger age (95% confidence interval [CI] -0.82 to -0.04, p < 0.04 and 95% CI -0.74 to -0.01, p = 0.05 respectively), longer procedure duration (95% CI 0.35-0.90, p < 0.01 and 95% CI 0.02-0.75, p = 0.04 respectively), more entry sites created (95% CI 0.09-0.95 p < 0.03 and 95% CI 0.02-0.88, p < 0.04, respectively), and longer stent grafts implanted (95% CI 0.27-0.89, p < 0.01, fever duration only). Fever pattern and different postprocedure medical treatment did not convey a statistically significant association, but effective and dramatic response to steroids was observed in patients with persistent pyrexia that responded poorly to antibiotics and nonsteroidal anti-inflammatory drugs. CONCLUSION Our findings support the view that postimplantation syndrome is caused by host immune response; none of our cases are related with infection and no benefits were observed from the prolonged use of antibiotics, thus adding to the plausibility of employing steroids as part of the postprocedure care scheme.