Repetitive ventricular tachycardia triggered by a giant benign cardiac lipomyoma.

Cardiac lipomyomas are tumors that may produce various signs and symptoms, including life threatening ventricular tachycardia (VT), often requiring surgical resection and/or catheter ablation. Here we report on a 35-year-old female patient with longstanding repetitive VT in the setting of a large cardiac lipomyoma. Diagnostic testing included non-invasive approaches including ECG, echocardiography and CMR. She then underwent electroanatomic mapping, which provided additional information. The patient ultimately underwent partial resection of the tumor. Postoperatively, long term ambulatory ECG showed VT suppression without anti-arrhythmic or catheter ablation for VT.

Cardiac-Specific Overexpression of Silent Information Regulator 1 Protects Against Heart and Kidney Deterioration in Cardiorenal Syndrome via Inhibition of Endoplasmic Reticulum Stress.

BACKGROUND/AIMS: Increased endoplasmic reticulum (ER) stress contributes to development of cardiorenal syndrome (CRS), and Silent Information Regulator 1 (SIRT1), a class III histone deacetylase, may have protective effects on heart and renal disease, by reducing ER stress. We aimed to determine if SIRT1 alleviates CRS through ER stress reduction. METHODS: Wild type mice (n=37), mice with cardiac-specific SIRT1 knockout (n=29), or overexpression (n=29), and corresponding controls, were randomized into four groups: sham MI (myocardial infarction) +sham STNx (subtotal nephrectomy); MI+sham STNx; sham MI+STNx; and MI+STNx. To establish the CRS model, subtotal nephrectomy (5/6 nephrectomy, SNTx) and myocardial infarction (MI) (induced by ligation of the left anterior descending (LAD) coronary artery) were performed successively to establish CRS model. At week 8, the mice were sacrificed after sequential echocardiographic and hemodynamic studies, and then pathology and Western-blot analysis were performed. RESULTS: Neither MI nor STNx alone significantly influenced the other healthy organ. However, in MI groups, STNx led to more severe cardiac structural and functional deterioration, with increased remodeling, increased BNP levels, and decreased EF, Max +dp/dt, and Max -dp/dt values than in sham MI +STNx groups. Conversely, in STNx groups, MI led to renal structural and functional deterioration, with more severe morphologic changes, augmented desmin and decreased nephrin expression, and increased BUN, SCr and UCAR levels. In MI+STNx groups, SIRT1 knockout led to more severe cardiac structural and functional deterioration, with higher Masson-staining score and BNP levels, and lower EF, FS, Max +dp/dt, and Max -dp/dt values; while SIRT1 overexpression had the opposite attenuating effects. In kidney, SIRT1 knockout resulted in greater structural and functional deterioration, as evidenced by more severe morphologic changes, higher levels of UACR, BUN and SCr, and increased desmin and TGF-ß expression, while SIRT1 overexpression resulted in less severe morphologic changes and increased nephrin expression without significant influence on BUN or SCr levels. The SIRT1 knockout but not overexpression resulted in increased myocardial expression of CHOP and GRP78. Cardiac-specific SIRT1 knockout or overexpression resulted in increased or decreased renal expression of CHOP, Bax, and p53 respectively. CONCLUSIONS: Myocardial SIRT1 activation appears protective to both heart and kidney in CRS models, probably through modulation of ER stress.

All-optical imaging and manipulation of whole-brain neuronal activities in behaving larval zebrafish.

All-optical interrogation of population neuron activity is a promising approach to deciphering the neural circuit mechanisms supporting brain functions. However, this interrogation is currently limited to local brain areas. Here, we incorporate patterned photo-stimulation into light-sheet microscopy, allowing simultaneous targeted optogenetic manipulation and brain-wide monitoring of the neuronal activities of head-restrained behaving larval zebrafish. Using this system, we photo-stimulate arbitrarily selected neurons (regions as small as ~10-20 neurons in 3D) in zebrafish larvae with pan-neuronal expression of a spectrally separated calcium indicator, GCaMP6f, and an activity actuator, ChrimsonR, and observe downstream neural circuit activation and behavior generation. This approach allows us to dissect the causal role of neural circuits in brain functions and behavior generation.

A preliminary investigation of computed tomographic angiography in the assessment of coronary artery distensibility.

OBJECTIVE: To test 2 hypotheses: first, that coronary distensibility can be measured noninvasively using 64-slice computed tomographic angiography (CTA); and second, that the extent of coronary artery disease (CAD) in any individual patient is related to the degree of distensibility detected by CTA. MATERIALS AND METHODS: Computed tomographic angiography was performed in 30 healthy adults and in 30 patients. All subjects were younger than 55 years. The main lesion located in the left anterior descending branch in patients with CAD. The cross-sectional coronary area of the left main and the left anterior descending arteries were measured in each phase (5%-95%, 10% each), and any change in the ratio was quantified. A distensibility value (D value) was determined for each artery. RESULTS: Compared with healthy subjects, the coronary area of the patients with CAD was significantly decreased in 65% to 85% (P < 0.05). There was a significant difference in the D value between healthy subjects and patients with both single-vessel and 2-vessel disease (P < 0.05). CONCLUSIONS: Coronary artery distensibility can be measured noninvasively using data obtained from CTA. The distensibility of the coronary artery decreased with the increasing number of involved pathological coronary vessels. The distensibility of the coronary artery correlated with the extent of CAD.

[Impact of multifactor intensive intervention on self management, risk factor control and outcome of post percutaneous transluminal coronary intervention patients].

OBJECTIVE: To test the efficacy of multifactor intensive intervention for post percutaneous transluminal coronary intervention (post-PCI) outpatients on self management, risk factor control and outcome. METHODS: A total of 263 patients with coronary heart disease (CAD) discharged from our cardiac center were randomized into usual care (4 CAD lectures focusing on the 2(nd) CAD prevention and patients-oriented outpatient visit) and intensive intervention (4 CAD lectures focusing on the 2(nd) CAD prevention, CAD outpatient visit twice a month, monthly telephone instructions on risk factor control and optimal medication). Patients were followed for 12 months and 250 patients completed follow-up. RESULTS: There were more patients achieved a LDL-C level of less than 2.6 mmol/L in intensive intervention group than in usual care group (71.2% vs. 48.3%, P < 0.01). The percentages of patients taking dietary control (55.3% vs. 26.2%, P < 0.01) and physical exercises (64.4% vs. 39.0%, P < 0.01), receiving beta-adrenergic receptor blocker (75.0% vs. 50.8%, P < 0.01) and statins (72.0% vs. 54.2%, P < 0.01) were significantly higher while cardiovascular event rate (5.9% vs. 0%, P = 0.005)was significantly lower in intensive intervention group than in usual care group. CONCLUSION: Multifactor intensive intervention is helpful on improving the second prevention for post-PCI coronary heart disease patients.

Regulation of Nogo-B expression in the lesion of aortic aneurysms.

1. Our previous study showed that Nogo-B was highly expressed in endothelial cells and downregulated in endothelial cells following induction by lysophosphatidylcholine, which contributed to atherosclerotic lesions. However, the role of Nogo-B in the development of aortic aneurysms remains unclear. 2. In the present study, segments of thoracic aortic aneurysms (TAA) and adjacent normal thoracic aortic tissues (NTA) without aneurysmal changes were obtained from 31 patients undergoing graft surgery. The mRNA and protein expression levels of Nogo-B were measured with semiquantitative reverse transcription-polymerase chain reaction, western blotting and immunohistochemistry. 3. The results demonstrate that Nogo-B mRNA expression levels in TAA lesions decreased to 45% compared with levels in NTA lesions and that protein levels in TAA decreased to 35%. Tissue Nogo immunohistochemical staining in aortic specimens suggested the involvement of Nogo in neovascularization and smooth muscle cell proliferation. The weaker brown staining of endothelial cells in TAA lesions suggested the lower expression of Nogo-B in TAA lesions. 4. These results demonstrate that Nogo-B mRNA and protein expression are downregulated in TAA lesions. It is concluded that the reduction of Nogo-B protein expression in TAA lesions is closely correlated to the formation of aneurysm and that Nogo-B may play a protective role in the pathological process of aneurysms.

Different expressions of Nogo-B1 and Nogo-B2 in mouse heart microvascular endothelial cell dysfunction induced by lysophosphatidylcholine.

To investigate Nogo-B expression changes in mouse heart microvascular endothelial H5V cell line induced by lysophosphatidylcholine. Cells were incubated with different concentrations of lysoPC for the same incubation time and with 10 micromol/l lysoPC at different incubation times. Protein and mRNA expression levels of Nogo-B1 and Nogo-B2 were measured with Western blotting and semiquantitative RT-PCR, respectively. Nogo-B1 protein was detected in normal H5V cells by Western blotting. When H5V cells were incubated with lysoPC, Nogo-B1 protein level decreased, and the lowest point fell to 20% of the original level induced by 20 micromol/l lysoPC for 24 h. Incubation of H5V cells with lysoPC of different concentrations or at different time points caused little change in Nogo-B1 mRNA expression level, except for a 50% decrease in 20 micromol/l lysoPC at 24 h, while a transient change was observed in Nogo-B2 mRNA level. These results demonstrate that Nogo-B1 protein expression could be down-regulated with increasing concentrations of lysoPC and lapse of incubation time, though no mRNA transcription down-regulation occurred. However, mRNA expression level of Nogo-B2 showed a transient up-regulation induced by lysoPC. We conclude that the two subtypes of Nogo-B may play different roles in the endothelial cell injury process.