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Find video protocols related to scientific articles indexed in Pubmed.
[Clock genes and circadian rhythm of blood pressure].
Nippon Rinsho
PUBLISHED: 08-30-2014
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Cardiovascular function such as blood pressure and heart rate exhibits circadian oscillation. The circadian rhythmicity had been supposed to be regulated by an internal biological. The identification and characterization of mammalian clock genes revealed that the biological clock is composed of feedback loops of transcription factors. Previous studies reported that night shift workers had high risk of ischemic heart disease, suggesting a close association between cardiovascular diseases and circadian rhythm. In addition, recent studies obtained from the genetically engineered mice with disrupted circadian rhythm have revealed that the circadian clock is closely related to the pathogenesis of cardiovascular diseases including hypertension. Understanding the biological relevance of the internal clock in cardiovascular diseases will provide a novel chronotherapeutic approaches to the prevention and treatment of cardiovascular diseases.
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Longitudinal strain of right ventricular free wall by 2-dimensional speckle-tracking echocardiography is useful for detecting pulmonary hypertension.
Life Sci.
PUBLISHED: 06-05-2014
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Echocardiography is widely used for screening pulmonary hypertension (PH). More recently developed two-dimensional speckle-tracking echocardiography (2D-STE) can assess regional deformation of the myocardium and is useful for detecting left ventricular dysfunction. However, its usefulness to assess right ventricular (RV) dysfunction is not clear. Therefore, the aim of this study was to investigate the ability of peak systolic strain (PSS) and post-systolic strain index (PSI) at the RV free wall determined by 2D-STE to detect PH.
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Effects of moderate-to-severe obstructive sleep apnea on the clinical manifestations of plaque vulnerability and the progression of coronary atherosclerosis in patients with acute coronary syndrome.
Eur Heart J Acute Cardiovasc Care
PUBLISHED: 05-24-2014
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It is unclear whether obstructive sleep apnea (OSA) increases the recurrence of acute coronary syndrome (ACS) in patients with acute myocardial infarction (MI). We hypothesized that moderate-to-severe OSA increased the number of adverse cardiovascular events in patients who underwent primary percutaneous coronary intervention (PCI).
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Successful treatment of a ruptured spontaneous dissecting coronary artery pseudoaneurysm with a covered stent in a patient with cardiac tamponade.
Intern. Med.
PUBLISHED: 05-16-2014
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The rupture of spontaneous dissecting coronary artery pseudoaneurysms is rare, and no standard therapy has yet been established for this condition. This report describes a case of a ruptured spontaneous dissecting coronary artery pseudoaneurysm in a patient with cardiac tamponade that was successfully treated with emergent implantation of a covered stent.
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Adipose-derived regenerative cell therapy inhibits the progression of monocrotaline-induced pulmonary hypertension in rats.
Life Sci.
PUBLISHED: 04-26-2014
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Functional and structural changes in pulmonary vasculature characterize pulmonary arterial hypertension (PAH) and the prognosis of advanced PAH remains poor despite progress in pharmacotherapy. Adipose-derived regenerative cells (ADRCs) promote cell regeneration at pathological sites and comprise a novel therapy for ailments of various organs. We investigated the effects of ADRC therapy in rat models of monocrotaline (MCT)-induced pulmonary hypertension (PH) and the underlying mechanisms.
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Sodium channelopathy underlying familial sick sinus syndrome with early onset and predominantly male characteristics.
Circ Arrhythm Electrophysiol
PUBLISHED: 04-24-2014
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Sick sinus syndrome (SSS) is a common arrhythmia often associated with aging or organic heart diseases but may also occur in a familial form with a variable mode of inheritance. Despite the identification of causative genes, including cardiac Na channel (SCN5A), the pathogenesis and molecular epidemiology of familial SSS remain undetermined primarily because of its rarity.
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Cardiac diastolic dysfunction predicts in-hospital mortality in acute ischemic stroke with atrial fibrillation.
J. Neurol. Sci.
PUBLISHED: 03-17-2014
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The aim of this study was to identify whether diastolic dysfunction predicts in-hospital death in ischemic stroke patients with atrial fibrillation.
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Plasma pentraxin 3 is a more potent predictor of endothelial dysfunction than high-sensitive C-reactive protein.
Int Heart J
PUBLISHED: 03-14-2014
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An inflammatory response is a key event for endothelial dysfunction. Pentraxin 3 (PTX3) is an inflammatory protein produced at inflammation sites such as leukocytes and vascular endothelial cells. Here, we compared the relationships between endothelial function assessed by flow-mediated dilation (FMD), and the levels of plasma PTX3 and high-sensitive C-reactive protein (hsCRP), another inflammatory protein of the pentraxin family. Levels of FMD, PTX3 and hsCRP were measured twice within 6 to 8 months and retrospectively analyzed in 36 patients with coronary artery disease. We examined the associations between the values of FMD and the levels of PTX3 and hsCRP at the first measurement, and between the change ratios (second value/first value) of these parameters. Univariate linear regression analysis showed significantly negative correlations between FMD values and PTX3 and hsCRP levels at the first measurement, and significant associations with taking statins or calcium antagonists. Multivariate linear stepwise regression analysis identified PTX3 levels and taking statins and calcium antagonists as independent factors for endothelial function. The change ratio of FMD correlated more closely with that of PTX3 than of hsCRP (r = -0.446, P = 0.006 versus r = -0.330, P = 0.050). Significantly more patients with decreased FMD values had increased levels of PTX3 than those of hsCRP at the second measurement compared with the fi rst measurement. Furthermore, the ratio of patients with increased PTX3, but not increased hsCRP, was significantly reduced among those with increased, rather than decreased, FMD values. Endothelial dysfunction might be more accurately predicted by plasma PTX3 levels than by serum hsCRP levels.
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Right bundle branch block without overt heart disease predicts higher risk of pacemaker implantation: the study of atomic-bomb survivors.
Int. J. Cardiol.
PUBLISHED: 02-14-2014
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We investigated the clinical course of complete right bundle branch block (RBBB) or RBBB with axis deviation (AD) in terms of subsequent pacemaker implantation for high-degree atrioventricular (AV) block or sick sinus syndrome (SSS).
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Cyclophosphamide-induced cardiotoxicity with a prolonged clinical course diagnosed on an endomyocardial biopsy.
Intern. Med.
PUBLISHED: 10-16-2013
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A 31-year-old woman with primary mediastinal large B-cell lymphoma refractory to conventional chemotherapy was treated with high-dose chemotherapy containing cyclophosphamide (CY). Subsequently, she was treated with auto peripheral blood stem cell transplantation. Although a complete remission was obtained, heart failure developed two months later. Echocardiography showed an impaired systolic function with pericardial effusion. A biopsy of the endomyocardial region from the left ventricle demonstrated spotty myocardial hemorrhage and myocardial fibrosis with disruption and aggregation of mitochondrial cristae. Based on these findings, CY-induced cardiotoxicity was diagnosed. The patient was treated with conventional therapy for heart failure, which required approximately one year to improve her condition.
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Melatonin ameliorates angiotensin II-induced vascular endothelial damage via its antioxidative properties.
J. Pineal Res.
PUBLISHED: 05-14-2013
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Melatonin is well known to have a beneficial effect on the cardiovascular system, but it remains to be elucidated whether melatonin has a therapeutic effect on the vascular damage induced by the potential vasoactive substance angiotensin II (Ang II). In this study, the effects of melatonin on Ang II-induced vascular endothelial damage were investigated. In cultured vascular endothelial cells, Ang II stimulation increased ROS generation and inhibited eNOS phosphorylation (Ser1177), both of which were clearly restored by pretreatment with melatonin. The translocation of p47(phox) subunit of NADPH oxidase from the cytosol to plasma membrane was promoted in Ang II-treated vascular endothelial cells, which was canceled by melatonin pretreatment. In Ang II-infused rats, increased ROS generation in the aortic wall and impaired endothelial function of the aortic ring were observed, which were rescued by coadministration of melatonin. In vasculature, melatonin receptor agonist ramelteon had the antioxidative effect in the same manner as melatonin by itself. These findings suggest that melatonin directly ameliorates Ang II-induced vascular endothelial damage partly via its antioxidative properties, providing with us the potential rationale for clinical application of melatonin to the prevention from cardiovascular diseases.
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Angiotensin II impairs endothelial nitric-oxide synthase bioavailability under free cholesterol-enriched conditions via intracellular free cholesterol-rich membrane microdomains.
J. Biol. Chem.
PUBLISHED: 04-02-2013
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Vascular endothelial function is impaired in hypercholesterolemia partly because of injury by modified LDL. In addition to modified LDL, free cholesterol (FC) is thought to play an important role in the development of endothelial dysfunction, although the precise mechanisms remain to be elucidated. The aim of this study was to clarify the mechanisms of endothelial dysfunction induced by an FC-rich environment. Loading cultured human aortic endothelial cells with FC induced the formation of vesicular structures composed of FC-rich membranes. Raft proteins such as phospho-caveolin-1 (Tyr-14) and small GTPase Rac were accumulated toward FC-rich membranes around vesicular structures. In the presence of these vesicles, angiotensin II-induced production of reactive oxygen species (ROS) was considerably enhanced. This ROS shifted endothelial NOS (eNOS) toward vesicle membranes and vesicles with a FC-rich domain trafficked toward perinuclear late endosomes/lysosomes, which resulted in the deterioration of eNOS Ser-1177 phosphorylation and NO production. Angiotensin II-induced ROS decreased the bioavailability of eNOS under the FC-enriched condition.
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Successful treatment of heart failure in an adult patient with Prader-Willi syndrome.
Intern. Med.
PUBLISHED: 04-01-2013
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Prader-Willi Syndrome (PWS) is a rare genetic disorder characterized by physical, psychological and physiological abnormalities. Obesity and related cardiovascular diseases are a common problem in adult patients with PWS. This report describes a case of adult PWS with heart failure associated with marked obesity and sleep-disordered breathing that was successfully treated with oxygen therapy, adaptive servoventilation, medications, diet therapy and rehabilitation.
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Elevated levels of systemic pentraxin 3 are associated with thin-cap fibroatheroma in coronary culprit lesions: assessment by optical coherence tomography and intravascular ultrasound.
JACC Cardiovasc Interv
PUBLISHED: 03-27-2013
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This study sought to determine whether systemic levels of pentraxin 3 (PTX3), a novel inflammatory marker, are associated with thin-cap fibroatheroma (TCFA).
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Differences in body temperature variability between subjects with and without diabetes and predictive value for cardiovascular events.
Circ. J.
PUBLISHED: 03-27-2013
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Differences in regulating factors and the clinical implications of body temperature variability (BTV) between subjects with and without diabetes have not been clarified to date.
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VEGF-A induces its negative regulator, soluble form of VEGFR-1, by modulating its alternative splicing.
FEBS Lett.
PUBLISHED: 03-25-2013
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Vascular endothelial growth factor-A (VEGF-A) is one of the major angiogenic factors, and its actions are primarily mediated through its two membrane receptors, VEGFR-1 and VEGFR-2. A soluble form of VEGFR-1 (sVEGFR-1) sequesters the free form of VEGF-A, and acts as a potent anti-angiogenic factor. While sVEGFR-1 is synthesized as a splice variant of VEGF-R1 gene, the interactions between VEGF-A and sVEGFR-1 remain largely unknown. Here, we show that VEGF-A upregulates sVEGF-R1 expression in human vascular endothelial cells but leaves full-length VEGF-R1 expression unchanged, and that this induction was dependent on the VEGFR-2-protein kinase C-MEK signaling pathway. The VEGF-A-induced sVEGFR-1 upregulation can operate as a negative feedback system, which if modulated can become a novel therapeutic target for regulating pathological angiogenesis.
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Impairment of flow-mediated dilation correlates with aortic dilation in patients with Marfan syndrome.
Heart Vessels
PUBLISHED: 02-26-2013
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Marfan syndrome is an inherited disorder characterized by genetic abnormality of microfibrillar connective tissue proteins. Endothelial dysfunction is thought to cause aortic dilation in subjects with a bicuspid aortic valve; however, the role of endothelial dysfunction and endothelial damaging factors has not been elucidated in Marfan syndrome. Flow-mediated dilation, a noninvasive measurement of endothelial function, was evaluated in 39 patients with Marfan syndrome. Aortic diameter was measured at the aortic annulus, aortic root at the sinus of Valsalva, sinotubular junction and ascending aorta by echocardiography, and adjusted for body surface area (BSA). The mean value of flow-mediated dilation was 6.5 ± 2.4 %. Flow-mediated dilation had a negative correlation with the diameter of the ascending thoracic aorta (AscAd)/BSA (R = -0.39, p = 0.020) and multivariate analysis revealed that flow-mediated dilation was an independent factor predicting AscAd/BSA, whereas other segments of the aorta had no association. Furthermore, Brinkman index had a somewhat greater influence on flow-mediated dilation (R = -0.42, p = 0.008). Although subjects who smoked tended to have a larger AscAd compared with non-smokers (AscA/BSA: 17.3 ± 1.8 versus 15.2 ± 3.0 mm/m(2), p = 0.013), there was no significant change in flow-mediated dilation, suggesting that smoking might affect aortic dilation via an independent pathway. Common atherogenic risks, such as impairment of flow-mediated dilation and smoking status, affected aortic dilation in subjects with Marfan syndrome.
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Effect of pimobendan in addition to standard therapy for heart failure on prevention of readmission in elderly patients with severe chronic heart failure.
Geriatr Gerontol Int
PUBLISHED: 02-24-2013
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AIM: We evaluated the effect of pimobendan, a positive inotropic agent, in elderly patients with frequent readmission as a result of heart failure despite conventional therapy. METHODS: Pimobendan was given to five male patients with severe chronic heart failure (New York Heart Association class III-IV) (age range 69-89 years; mean 78?±?8 years; ischemic cardiomyopathy in three cases, dilated cardiomyopathy in two cases) who required repeated admission for heart failure despite conventional therapy with angiotensin inhibitors, beta-blockers, diuretics and anti-arrhythmic agents. After the addition of pimobendan at a dose of 1.25-3.75?mg/day, we evaluated serum levels of brain natriuretic peptide (BNP), left ventricular ejection fraction (LVEF), septal e and left ventricular end-diastolic diameter (LVDD) by echocardiography, as well as readmission rates for more than 2 years. RESULTS: The serum level of BNP significantly decreased after treatment with pimobendan, although its level returned to pretreatment levels after 2 years. LVEF significantly improved after the treatment, with the improvement continuing beyond the 2 years, although LVDD did not change after treatment. Septal e significantly improved after the treatment, although its level returned to pretreatment levels at 2 years after the treatment. Readmission rates significantly decreased for 2 years after the treatment, although one patient required cardiac resynchronization therapy for severe heart failure, and another patient required cardiac pacemaker implantation for sick sinus syndrome 2 years after adding pimobendan. CONCLUSIONS: Pimobendan in conjunction with conventional therapy for heart failure decreases the readmission rate in elderly patients with severe heart failure for at least 2 years. Geriatr Gerontol Int 2013; ??: ??-??.
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Effects of nasal continuous positive airway pressure on the glomerular filtration rate in patients with obstructive sleep apnea syndrome.
Intern. Med.
PUBLISHED: 02-01-2013
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Previous studies have shown a possible role for obstructive sleep apnea syndrome (OSAS) in the development and/or progression of chronic kidney disease (CKD). However, the impact of treatment for OSAS on CKD has not been clarified. The aim of this study was to investigate the influence of OSAS and the short-term effects of nasal continuous positive airway pressure (CPAP) on the estimated glomerular filtration rate (eGFR).
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Obstructive sleep apnoea increases the incidence of morning peak of onset in acute myocardial infarction.
Eur Heart J Acute Cardiovasc Care
PUBLISHED: 01-23-2013
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There exists a discrepancy regarding the relationship between obstructive sleep apnoea (OSA) and circadian variation during the onset of acute myocardial infarction (MI). We hypothesized that OSA patients show a characteristic circadian variation and that the severity of OSA significantly affects this variation.
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Successful blood sampling through azygos continuation with interrupted inferior vena cava. A case report and review of the literature.
Int Heart J
PUBLISHED: 10-20-2011
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Interrupted inferior vena cava (IVC) with azygos continuation is a rare congenital anomaly, and is frequently associated with other cardiovascular malformations and situs anomalies, such as left isomerism. These patients usually develop deep vein thrombosis (DVT), and asymptomatic patients above 60 years of age are very rare. Here we report a case of interrupted IVC which we diagnosed in a 72-year-old woman. She was admitted to our hospital suffering from heart failure and supraventricular tachycardia. Echocardiography detected secundum atrial septal defect (ASD). An abnormal paravertebral pleural line on the chest X-rays indicated the existence of venous anomaly. Anatomical images obtained by Multidetector Computed Tomography (MDCT) helped us to successfully perform right heart catheterization procedures through azygos continuation including blood sampling from pulmonary veins. Even in elderly patients, a careful examination of chest X-rays can indicate undiagnosed venous anomalies; thus, it is critically important before planning surgical or interventional procedures.
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Cardiac rehabilitation decreases plasma pentraxin 3 in patients with cardiovascular diseases.
Eur J Prev Cardiol
PUBLISHED: 09-13-2011
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Inflammatory markers such as serum C-reactive protein (CRP), serum amyloid A (SAA), and plasma pentraxin 3 (PTX3), which belong to the pentraxin superfamily, increase due to various inflammatory diseases. Some studies demonstrated that serum CRP and SAA are predictors of cardiovascular diseases, and cardiac rehabilitation (CR) induces anti-inflammatory effects. In the present study, we investigated the effects of CR on pentraxins (serum CRP, SAA, and plasma PTX3) in patients with cardiovascular diseases.
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Incidence and prognostic value of early repolarization pattern in the 12-lead electrocardiogram.
Circulation
PUBLISHED: 06-06-2011
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Early repolarization pattern is a common ECG finding characterized by J-point elevation and QRS notching or slurring in the inferior and/or lateral leads, yet little is known about its incidence and long-term prognosis in Asian populations.
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Low glomerular filtration rate is associated with high prevalence of vasospastic angina.
Circ. J.
PUBLISHED: 05-11-2011
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Although chronic kidney disease is associated with a high prevalence of cardiovascular disease, the relationship between coronary artery spasm and renal dysfunction has not been elucidated.
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Negatively charged low-density lipoprotein is associated with atherogenic risk in hypertensive patients.
Heart Vessels
PUBLISHED: 03-18-2011
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Negatively charged low-density lipoprotein (LDL), generated via multiple processes such as oxidation, acetylation, or glycosylation, plays a key role in the initiation and progression of atherosclerosis and related diseases. Anion-exchange high-performance liquid chromatography (AE-HPLC) can subfractionate LDL into LDL-1, LDL-2, and LDL-3 based on LDL particle charge, but the clinical significance of LDL subfractions has not yet been elucidated. The aim of this study was to determine the clinical significance of these fractions with particular regard to atherogenic risk in hypertensive patients. Ninety-eight patients with essential hypertension (age 67.0 ± 10.7 years; 54 males) were enrolled in the present study. The relationships between LDL subfractions and atherogenic risk factors, including lipid profiles, blood pressure and plasma 8-isoprostane as a marker of oxidative stress, were examined. LDL-1 levels were significantly and negatively correlated with body mass index (r = -0.384, p < 0.001), systolic blood pressure (r = -0.457, p < 0.001), non-high-density lipoprotein cholesterol levels (r = -0.457, p < 0.001) and 8-isoprostane levels (r = -0.415, p < 0.001). LDL-3, which is the most negatively charged fraction of total LDL, was significantly and positively correlated with these parameters (r = 0.267, 0.481, 0.357, and 0.337, respectively). LDL-1 levels were significantly lower (p < 0.001), and LDL-2 and LDL-3 levels were significantly higher (each p < 0.001) in patients with poorly controlled hypertension than in patients with well-controlled hypertension. In addition, an increase in the total number of traditional risk factors at time of study participation, but not previous diagnosis, was associated with a decrease in LDL-1 levels and increases in LDL-2 and LDL-3 levels. These data suggest that LDL subfractions are associated with multiple atherogenic risk factors and that treatment to modify these risk factors could result in changes in LDL subfraction levels. In conclusion, LDL subfractions isolated by AE-HPLC may represent a marker of atherogenic risk in patients with hypertension.
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Ezetimibe and vascular endothelial function.
Curr Vasc Pharmacol
PUBLISHED: 03-11-2011
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Hypercholesterolemia is a major risk factor for cardiovascular diseases that has been managed mostly with 3-hydroxy-3-methyl glutaryl coenzyme A reductase inhibitors (statins) that suppress de novo cholesterol synthesis in the liver. Statins also have beneficial pleiotropic effects on the atherosclerotic process that are independent of their ability to lower lipid values. However, the levels of low-density lipoprotein cholesterol (LDL-C) in most hypercholesterolemic patients at high risk for cardiovascular disease do not reach the goals proposed by guidelines even when prescribed with statins. Ezetimibe is a new lipid-lowering agent that blocks the intestinal absorption of dietary and biliary cholesterol and reduces LDL-C levels, especially when combined with statins. However, its effect on cardiovascular events remains unknown. We reviewed the effects of ezetimibe on cardiovascular diseases, in particular, vascular endothelial function, which is initially impaired during the atherogenetic process and is an important predictor of cardiovascular events. The simultaneous inhibition of cholesterol synthesis by statin and of cholesterol absorption by ezetimibe might retard the atherogenetic process. These effects are considered to be mainly mediated by lipid lowering. However, further studies should elucidate the mechanism of the anti-atherosclerotic effects induced by ezetimibe; for instance, whether or not it directly affects atherogenesis independently from its lipid-lowering effects.
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Circadian clock and cardiovascular disease.
J Cardiol
PUBLISHED: 02-20-2011
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Both the physiological and pathological functions of cardiovascular organs are closely related to circadian rhythm, an endogenously driven 24-h cycle. Heart rate, blood pressure, and endothelial function show diurnal variations within a day. The onset of cardiovascular disorders such as acute coronary syndrome, atrial arrhythmia, and subarachinoid hemorrhage also exhibits diurnal oscillation. Recent progress in studying the functions and molecular mechanisms of the biological clock brought forth the idea that intrinsic circadian rhythms are tightly related to cardiovascular pathology. The center of the biological clock exists in the suprachiasmatic nucleus in the hypothalamus. In addition to this central clock, each organ has its own biological clock system, termed the peripheral clock. Each cardiovascular tissue or cell, including heart and aortic tissue, cardiomyocyte, vascular smooth muscle cell, and vascular endothelial cell also has intrinsic biological rhythm. Until recently, little was known about the roles of peripheral clocks in cardiovascular organs. However, studies using genetically engineered mice revealed their contributions during the process of disease progression. Loss of synchronization between the internal clock and external stimuli can induce cardiovascular organ damage. Discrepancy in the phases between the central and peripheral clocks also seems to contribute to progression of the disorders. Elucidation of the precise roles of biological clocks in cardiovascular organs will provide us with more profound insights into the relevance of the circadian rhythm in cardiac pathology. Moreover, identification of the modalities with which we can manipulate the phase of each peripheral clock will enable us to establish a novel chronotherapeutic approach. This time-of-day based strategy may innovate a new paradigm in the prevention and treatment of cardiovascular disorders.
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Culprit segments identified by optical coherence tomography in patients with acute myocardial infarction: two case reports.
Cardiovasc Interv Ther
PUBLISHED: 02-14-2011
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The high resolution of optical coherence tomography (OCT) provides detailed information about coronary plaque morphology, which enables the mechanism of acute myocardial infarction to be evaluated. We describe two patients with acute myocardial infarction in whom culprit segments were identified by OCT, but not by either coronary angiography or intravascular ultrasound.
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Increased Akt-mTOR signaling in lung epithelium is associated with respiratory distress syndrome in mice.
Mol. Cell. Biol.
PUBLISHED: 12-28-2010
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Pregnancy in women with diabetes is associated with a higher risk of perinatal complications. In particular, infants of diabetic mothers frequently suffer from respiratory distress syndrome (RDS), which is a leading cause of death in preterm infants and is considered to be primarily due to hyperinsulinemia in infants in response to maternal hyperglycemia. To elucidate the mechanism of how insulin signaling induces RDS, bronchoalveolar epithelium-specific Akt1 transgenic (TG) mice were generated. Akt1 overexpression in fetal lung epithelium resulted in RDS in preterm infants born by Caesarean section at embryonic day 18.5 (E18.5). The expression levels of hypoxia-inducible factor 2? (HIF-2?) and its target vascular endothelial growth factor (VEGF) were downregulated in the lung of Akt1 TG mice. Inhibition of the Akt-mammalian target of rapamycin (mTOR) signaling axis by rapamycin restored the expression of VEGF and improved the lung pathology of Akt1 TG pups. Rapamycin also attenuated the RDS phenotype in wild-type mice delivered preterm at E17.5. In cultured lung epithelial cells, insulin reduced VEGF expression and transcriptional activity of HIF-2 on VEGF promoter in an mTOR-dependent manner. Thus, aberrant activation of the Akt-mTOR pathway in lung epithelium plays a causal role in the pathogenesis of infant RDS, presumably through downregulation of HIF-2-dependent VEGF expression in the lung.
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A critical role of sympathetic nerve regulation for the treatment of impaired daily rhythm in hypertensive Dahl rats.
Hypertens. Res.
PUBLISHED: 07-29-2010
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There is a deep relationship between impaired circadian rhythm and hypertension. However, the detailed mechanisms between the daily sleep-wake rhythm and cardiovascular disorders have not yet been elucidated. To clarify the mechanism, we examined salt-sensitive Dahl rats that were fed normal chow (n=10), high-salt chow (n=10) and high-salt chow with bisoprolol (n=10). Simultaneous electroencephalogram, electromyogram and locomotor activity were examined to analyze the sleep-wake state. We also examined heart rate, blood pressure and echocardiographic findings to verify the presence of hypertension. Hypertension with impaired ventricular contraction was observed in the rats with high-salt-chow consumption whereas normal-chow rats did not show these disorders. Although rats with the normal diet showed a standard daily rhythm with normal rapid eye movement (REM) sleep duration and locomotor activity, the high-salt-diet group exhibited an impaired daily rhythm with suppressed REM sleep and significant abnormal locomotor activity. Bisoprolol significantly improved the daily sleep-wake rhythm and locomotor activity. We showed that an impaired daily rhythm was closely related to the development of hypertension. Regulation of sympathetic nerve alterations may have a key role in the treatment of hypertension and circadian rhythm disorder.
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Pentraxin3 and high-sensitive C-reactive protein are independent inflammatory markers released during high-intensity exercise.
Eur. J. Appl. Physiol.
PUBLISHED: 07-05-2010
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High-intensity exercise shares similarities with acute phase responses of inflammatory diseases. We investigated the influences of acute exercise on inflammatory markers, plasma pentraxin3 (PTX3) and serum high-sensitive C-reactive protein (CRP) (hsCRP). Nine healthy male subjects (41 ± 3 years old) participated. Each subject performed three types of exercise; ergometer exercise at 70% workload of anaerobic threshold (AT) for 30 min (70% AT exercise), peak ergometer exercise (peak EX, 20 watt increase/min until fatigue) and resistance exercises of 70% 1 RM (70% RE) until exhaustion. We measured plasma PTX3, serum hsCRP, lactate, noradrenaline (NOR), white blood cells (WBC), interleukin-6 (IL-6) and myeloperoxidase (MPO), a marker of neutrophil degranulation. The effects of exercise on intracellular PTX3 and MPO in neutrophils were also investigated, by using flow cytometry analysis. Circulating PTX3 and hsCRP significantly increased immediately after 70% RE and peak EX, while they did not increase after 70% AT exercise. The exercise-induced fold increase in PTX3 and hsCRP relative to the resting level was positively correlated with the changes in WBC, NOR, lactate and MPO. The exercise-induced fold increase in IL-6 was positively correlated with that in NOR, but not with that in PTX3 and hsCRP. Neutrophils isolated immediately after 70% RE, but not 70% AT exercise, exhibited lower mean fluorescence for PTX3 and MPO than those from pre-exercise blood. These results provide the evidence that high-intensity exercises significantly increase circulatory PTX3 as well as hsCRP. The release from peripheral neutrophils is suggested to be involved in the exercise-induced plasma PTX3 increase.
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Circadian clock and vascular disease.
Hypertens. Res.
PUBLISHED: 05-07-2010
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Cardiovascular functions, including blood pressure and vascular functions, show diurnal oscillation. Circadian variations have been clearly shown in the occurrence of cardiovascular events such as acute myocardial infarction. Circadian rhythm strongly influences human biology and pathology. The identification and characterization of mammalian clock genes revealed that they are expressed almost everywhere throughout the body in a circadian manner. In contrast to the central clock in the suprachiasmatic nucleus (SCN), the clock in each tissue or cell is designated as a peripheral clock. It is now accepted that peripheral clocks have their own roles specific to each peripheral organ by regulating the expression of clock-controlled genes (CCGs), although the oscillation mechanisms of the peripheral clock are similar to that of the SCN. However, little was known about how the peripheral clock in the vasculature contributes to the process of cardiovascular disorders. The biological clock allows each organ or cell to anticipate and prepare for changes in external stimuli. Recent evidence obtained using genetically engineered mice with disrupted circadian rhythm showed a novel function of the internal clock in the pathogenesis of endothelial dysfunction, hypertension and hemostasis. Loss of synchronization between the central and peripheral clock also contributes to the pathogenesis of cardiovascular diseases, as restoration of clock homeostasis could prevent disease progression. Identification of CCGs in each organ, as well as discovery of tools to manipulate the phase of each biological clock, will be of great help in establishing a novel chronotherapeutic approach to the prevention and treatment of cardiovascular disorders.
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Fatty liver incidence and predictive variables.
Hypertens. Res.
PUBLISHED: 04-09-2010
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Although fatty liver predicts ischemic heart disease, the incidence and predictors of fatty liver need examination. The objective of this study was to determine fatty liver incidence and predictive variables. Using abdominal ultrasonography, we followed biennially through 2007 (mean follow-up, 11.6+/-4.6 years) 1635 Nagasaki atomic bomb survivors (606 men) without fatty liver at baseline (November 1990 through October 1992). We examined potential predictive variables with the Cox proportional hazard model and longitudinal trends with the Wilcoxon rank-sum test. In all, 323 (124 men) new fatty liver cases were diagnosed. The incidence was 19.9/1000 person-years (22.3 for men, 18.6 for women) and peaked in the sixth decade of life. After controlling for age, sex, and smoking and drinking habits, obesity (relative risk (RR), 2.93; 95% confidence interval (CI), 2.33-3.69, P<0.001), low high-density lipoprotein-cholesterol (RR, 1.87; 95% CI, 1.42-2.47; P<0.001), hypertriglyceridemia (RR, 2.49; 95% CI, 1.96-3.15; P<0.001), glucose intolerance (RR, 1.51; 95% CI, 1.09-2.10; P=0.013) and hypertension (RR, 1.63; 95% CI, 1.30-2.04; P<0.001) were predictive of fatty liver. In multivariate analysis including all variables, obesity (RR, 2.55; 95% CI, 1.93-3.38; P<0.001), hypertriglyceridemia (RR, 1.92; 95% CI, 1.41-2.62; P<0.001) and hypertension (RR, 1.31; 95% CI, 1.01-1.71; P=0.046) remained predictive. In fatty liver cases, body mass index and serum triglycerides, but not systolic or diastolic blood pressure, increased significantly and steadily up to the time of the diagnosis. Obesity, hypertriglyceridemia and, to a lesser extent, hypertension might serve as predictive variables for fatty liver.
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Lineage analysis of circulating Trypanosoma cruzi parasites and their association with clinical forms of Chagas disease in Bolivia.
PLoS Negl Trop Dis
PUBLISHED: 03-28-2010
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The causative agent of Chagas disease, Trypanosoma cruzi, is divided into 6 Discrete Typing Units (DTU): Tc I, IIa, IIb, IIc, IId and IIe. In order to assess the relative pathogenicities of different DTUs, blood samples from three different clinical groups of chronic Chagas disease patients (indeterminate, cardiac, megacolon) from Bolivia were analyzed for their circulating parasites lineages using minicircle kinetoplast DNA polymorphism.
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Cardiovascular disease, chronopharmacotherapy, and the molecular clock.
Adv. Drug Deliv. Rev.
PUBLISHED: 03-10-2010
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Cardiovascular functions such as heart rate and blood pressure show 24h variation. The incidence of cardiovascular diseases including acute myocardial infarction and arrhythmia also exhibits diurnal variation. The center of this circadian clock is located in the suprachiasmatic nucleus in the hypothalamus. However, recent findings revealed that each organ, including cardiovascular tissues, has its own internal clock, which has been termed a peripheral clock. The functional roles played by peripheral clocks have been reported recently. Since the peripheral clock is considered to play considerable roles in the processes of cardiac tissues, the identification of genes specifically regulated by this clock will provide insights into its role in the pathogenesis of cardiovascular disorders. In addition, the discovery of small compounds that modulate the peripheral clock will help to establish chronotherapeutic approaches. Understanding the biological relevance of the peripheral clock will provide novel approaches to the prevention and treatment of cardiovascular diseases.
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Androgen receptor-dependent transactivation of growth arrest-specific gene 6 mediates inhibitory effects of testosterone on vascular calcification.
J. Biol. Chem.
PUBLISHED: 01-04-2010
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Recent epidemiological studies have found that androgen deficiency is associated with a higher incidence of cardiovascular disease in men. However, little is known about the mechanism underlying the cardioprotective effects of androgens. Here we show the inhibitory effects of testosterone on vascular calcification and a critical role of androgen receptor (AR)-dependent transactivation of growth arrest-specific gene 6 (Gas6), a key regulator of inorganic phosphate (P(i))-induced calcification of vascular smooth muscle cells (VSMC). Testosterone and nonaromatizable androgen dihydrotestosterone inhibited P(i)-induced calcification of human aortic VSMC in a concentration-dependent manner. Androgen inhibited P(i)-induced VSMC apoptosis, an essential process for VSMC calcification. The effects on VSMC calcification were mediated by restoration of P(i)-induced down-regulation of Gas6 expression and a subsequent reduction of Akt phosphorylation. These effects of androgen were blocked by an AR antagonist, flutamide, but not by an estrogen receptor antagonist, ICI 182,780. We then explored the mechanistic role of the AR in Gas6 expression and found an abundant expression of AR predominantly in the nucleus of VSMC and two consensus ARE sequences in the Gas6 promoter region. Dihydrotestosterone stimulated Gas6 promoter activity, and this effect was abrogated by flutamide and by AR siRNA. Site-specific mutation revealed that the proximal ARE was essential for androgen-dependent transactivation of Gas6. Furthermore, chromatin immunoprecipitation assays demonstrated ligand-dependent binding of the AR to the proximal ARE of Gas6. These results indicate that AR signaling directly regulates Gas6 transcription, which leads to inhibition of vascular calcification, and provides a mechanistic insight into the cardioprotective action of androgens.
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SLCO4C1 transporter eliminates uremic toxins and attenuates hypertension and renal inflammation.
J. Am. Soc. Nephrol.
PUBLISHED: 10-29-2009
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Hypertension in patients with chronic kidney disease (CKD) strongly associates with cardiovascular events. Among patients with CKD, reducing the accumulation of uremic toxins may protect against the development of hypertension and progression of renal damage, but there are no established therapies to accomplish this. Here, overexpression of human kidney-specific organic anion transporter SLCO4C1 in rat kidney reduced hypertension, cardiomegaly, and inflammation in the setting of renal failure. In addition, SLCO4C1 overexpression decreased plasma levels of the uremic toxins guanidino succinate, asymmetric dimethylarginine, and the newly identified trans-aconitate. We found that xenobiotic responsive element core motifs regulate SLCO4C1 transcription, and various statins, which act as inducers of nuclear aryl hydrocarbon receptors, upregulate SLCO4C1 transcription. Pravastatin, which is cardioprotective, increased the clearance of asymmetric dimethylarginine and trans-aconitate in renal failure. These data suggest that drugs that upregulate SLCO4C1 may have therapeutic potential for patients with CKD.
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Kruppel-like factor 2 inhibits hypoxia-inducible factor 1alpha expression and function in the endothelium.
J. Biol. Chem.
PUBLISHED: 06-01-2009
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Hypoxia-inducible factor 1 (HIF-1) is a central regulator of the hypoxic response in many cell types. In endothelial cells, HIF-1 induces the expression of key proangiogenic factors to promote angiogenesis. Recent studies have identified Kruppel-like factor 2 (KLF2) as a potent inhibitor of angiogenesis. However, the role of KLF2 in regulating HIF-1 expression and function has not been evaluated. KLF2 expression was induced acutely by hypoxia in endothelial cells. Adenoviral overexpression of KLF2 inhibited hypoxia-induced expression of HIF-1alpha and its target genes such as interleukin 8, angiopoietin-2, and vascular endothelial growth factor in endothelial cells. Conversely, knockdown of KLF2 increased expression of HIF-1alpha and its targets. Furthermore, KLF2 inhibited hypoxia-induced endothelial tube formation, whereas endothelial cells from mice with haploinsufficiency of KLF2 showed increased tube formation in response to hypoxia. Consistent with this ex vivo observation, KLF2 heterozygous mice showed increased microvessel density in the brain. Mechanistically, KLF2 promoted HIF-1alpha degradation in a von Hippel-Lindau protein-independent but proteasome-dependent manner. Finally, KLF2 disrupted the interaction between HIF-1alpha and its chaperone Hsp90, suggesting that KLF2 promotes degradation of HIF-1alpha by affecting its folding and maturation. These observations identify KLF2 as a novel inhibitor of HIF-1alpha expression and function. Therefore, KLF2 may be a target for modulating the angiogenic response in disease states.
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Circadian expressions of cardiac ion channel genes in mouse might be associated with the central clock in the SCN but not the peripheral clock in the heart.
Biol Rhythm Res
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Significant circadian variations exist in the frequency of cardiac arrhythmia, but few studies have examined the relation between cardiac ion channels genes and biological clocks. We investigated this relation using suprachiasmatic nuclei lesion (SCNX) and pharmacological autonomic nervous system block (ANSB) mice. Significant 24-h variations were observed in the expression of clock genes Per2, Bmal1, and Dbp and ion channel genes KCNA5, KCND2, KCHIP2, and KCNK3 in the control mice hearts. In the SCNX mice, all genes examined lost circadian rhythm. In the ANSB mice, the expressions of the three clock genes were dampened significantly but still had circadian rhythm, whereas the four ion channel gene expressions lost rhythm. Heart rate also lost circadian rhythm in both the SCNX and ANSB mice. These results suggest that some ion channel gene expressions might be regulated by the central clock in the SCN through the ANS but not the peripheral clock in the heart.
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Thrombomodulin, a novel molecule regulating inorganic phosphate-induced vascular smooth muscle cell calcification.
J. Mol. Cell. Cardiol.
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Hyperphosphatemia has emerged as a cardiovascular risk factor that stimulates calcification in vessels. We explored molecules that were induced by inorganic phosphate (Pi) at an early stage in vascular smooth muscle cells (VSMC). In the present study, we examined the role of thrombomodulin (TM) in Pi-induced VSMC calcification based on the results of DNA microarray analysis. Both mRNA and protein expression of TM were markedly augmented in Pi-induced calcification. Conversely, knockdown of TM by siRNA significantly inhibited calcification, in addition to Pi-induced apoptosis which plays critical roles in VSMC calcification. We further found that TM suppressed both of mRNA and protein expression of growth arrest-specific gene 6 (Gas6), a key molecule regulating apoptosis. Recombinant extracellular epidermal growth factor (EGF)-repeat domain of TM exaggerated calcification and this effect was abrogated by a neutralizing antibody for EGF receptor, suggesting that the cleaved and secreted form of TM may activate EGF receptor. We also found that downregulation of Gas6 by TM/EGF receptor axis was mediated by ERK in VSMC calcification. In the aorta of adenine-fed rat, a typical medial calcification model with hyperphosphatemia, we found that TM expression was increased. Furthermore, in human calcified aorta, increased TM expression was also observed. These results indicate that TM is a novel molecule that promotes apoptosis and vascular calcification by regulation of Gas6, presumably via EGF receptor/ERK axis.
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Simultaneous heart rate variability monitoring enhances the predictive value of flow-mediated dilation in ischemic heart disease.
Circ. J.
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Endothelial dysfunction and autonomic nervous system imbalance are both risk markers of atherosclerotic vascular damage. The relationship between these 2 factors, however, has not been clarified concisely.
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Seizures and syncope due to complete atrioventricular block in a patient with acute myocarditis with a normal left ventricular systolic function.
Intern. Med.
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A 43-year-old man was admitted to our hospital presenting with seizures and syncope. He had a history of a cold with a fever of 39°C occurring three days earlier. Electrocardiography (ECG) showed complete atrioventricular block (AV block) with a maximum pause of 32 seconds, for which temporary pacing was performed. Echocardiography showed mild hypertrophy of the left ventricle (LV) with a normal ejection fraction of 61%. Coronary angiography showed normal coronary arteries. Then, an endomyocardial biopsy was performed, the results of which indicated a diagnosis of acute myocarditis. After admission, the complete atrioventricular block disappeared together with normalization of the LV wall thickness.
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Effects of nasal continuous positive airway pressure on left ventricular concentric hypertrophy in obstructive sleep apnea syndrome.
Intern. Med.
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Abnormal left ventricular (LV) geometry, especially concentric hypertrophy, is associated with cardiovascular morbidity and mortality. The aim of this study was to evaluate the impact of obstructive sleep apnea syndrome (OSAS) and the effects of nasal continuous positive airway pressure (CPAP) on the LV geometric patterns.
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Cardiogenic shock due to left ventricular outflow obstruction and complete atrioventricular block in a patient with hypertrophic cardiomyopathy with acute myocarditis.
Intern. Med.
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A 67-year-old woman was referred to our hospital with a sudden syncopal attack. She suffered from cardiogenic shock due to left ventricular (LV) outflow stenosis with simultaneous complete atrioventricular (AV) block. An endomyocardial biopsy of the left ventricle demonstrated myocardial disarray and myocardial fibrous and edematous tissue with infiltration of mononuclear cells. Cardiac magnetic resonance imaging (cMRI) detected a damaged septal area that was likely associated with the conduction disturbance. The diagnosis was hypertrophic cardiomyopathy accompanied by acute myocarditis. Although the LV outflow stenosis was transient, the complete AV block was persistent, thus requiring permanent pacemaker implantation.
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Cleft-like formation of the aortic valve in an adult patient with a single coronary artery.
Intern. Med.
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A 51-year-old woman was admitted to our hospital with heart failure due to aortic regurgitation. Examination showed severe aortic regurgitation mainly due to cleft-like deformity of the right coronary cusp and single coronary artery. Aortic valve replacement was performed, and the deformity was seen in all aortic cusps. Histological study showed elongation of the leaflets by myofibrotic and fibrotic hyperplasia without calcification and inflammation in the aortic valve. This deformity likely arose from an acquired modification of a congenitally malformed aortic valve.
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Associations of variations in the MRF2/ARID5B gene with susceptibility to type 2 diabetes in the Japanese population.
J. Hum. Genet.
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Modulator recognition factor-2 (Mrf2/AT-rich interaction domain (Arid)5b) has been revealed to be involved in pathogenesis of atherosclerosis and adipogenesis. Single-nucleotide polymorphisms (SNPs) in the MRF2/ARID5B gene are associated with coronary artery disease (CAD) and has been proposed as a candidate gene for type 2 diabetes (T2D). The study was aimed to determine whether any of the four MRF2/ARID5B SNPs (rs2893880, rs10740055, rs7087507 and rs10761600) associated with susceptibility to CAD are also associated with T2D, and to determine whether SNP genotype influences the levels of adiponectin and other clinical factors. Association of MRF2/ARID5B SNPs was investigated in 500 diabetic patients from the Department of Metabolic Diseases at the University of Tokyo and 243 hospital-based nondiabetic individuals from the Institute for Adult Disease Asahi Life Foundation Hospital and 500 community-based nondiabetic individuals from the Hiroshima Atomic Bomb Casualty Council Health Management Center. Associations of haplotypes of these SNP with levels of adiponectin and other clinical factors were evaluated when the data was available. We found rs2893880C, rs10740055A, rs7087507A and rs10761600T were increasingly associated with T2D in terms of allele/genotype frequencies of each SNP and their haplotype combinations. Individuals with haplotype CAAT indicated an 1.86 times higher prevalence of diabetes compared with individuals with GCGA (OR 1.86 (95% confidence interval (CI) 1.43-2.41)). Furthermore, CAAT significantly associated with adiponectin levels and other clinical factors. In conclusion, polymorphisms on the MRF2/ARID5B gene were associated with susceptibility to T2D as well as adiponectin and other clinical factors, which was in a completely concordant way with their associations with CAD.
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Comparison of the diagnostic power of transthoracic and transesophageal echocardiography to detect ruptured chordae tendineae.
Int Heart J
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Preoperative information concerning the severity and etiology of MR is very important for selecting the most appropriate surgical strategy. Ruptured chordae tendineae (RCT) are one of the most important preoperative findings. We compared the diagnostic power of transesophageal echocardiography (TEE) and transthoracic echocardiography (TTE) to detect RCT in patients with MR. We studied 61 patients with MR (30 men, 31 women; mean age, 61 ± 12 years) who underwent mitral valve repair or replacement. Both TTE and TEE were performed before the operations, and the sensitivity and specificity of TTE and TEE to detect RCT were determined. In addition, other factors that influenced the detection of RCT by these two methods were investigated. At the time of an operation, RCT was confirmed in 39 of 61 cases. Transesophageal echocardiography had a higher sensitivity than TTE (74% versus 44%; P = 0.006) to detect RCT, although the specificity was not significantly different. In patients with a body mass index (BMI) > 22 (P = 0.023) or MR grade 4 (P = 0.026), TEE had a significantly higher diagnostic sensitivity than TTE, although there was no significant difference in patients with BMI < 22 or MR grade ? 3. In the lateral and medial segments of the mitral valve, TEE had a significantly higher diagnostic sensitivity to detect RCT than TTE (P = 0.0012), although there was no significant difference in the middle segments. There was no significant difference between TTE and TEE with respect to the sensitivity to detect RCT in myxomatous mitral valves. Although the sensitivity of TEE was higher than that of TTE to detect RCT, it was affected by BMI, MR grade, the RCT-presenting segments, and the etiology of MR.
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[Sleep rhythm and cardiovascular diseases].
Nippon Rinsho
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Sleep disturbance is a common problem in general adult population. Recent evidence suggests the link between the occurrence of cardiovascular events and several sleep disturbances including sleep apnea syndrome, insomnia and periodic limb movements during sleep. Sleep duration may affect the cardiovascular outcome. Shift work also may increase the risk of ischemic heart disease. Normalization of sleep rhythm has a potential to be a therapeutic target of ischemic heart diseases, although further study is required to evaluate the preventive effect on cardiovascular events. Here we describe the current understandings regarding the roles of sleep disorders during the pathogenesis of cardiovascular events.
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Very late stent thrombosis caused by rupture of lipid-laden neointima in a self-expanding coronary stent.
Int Heart J
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A 60-year-old man was admitted to our hospital due to acute ST-segment elevation myocardial infarction. He had a history of self-expanding stent implantation in the proximal left anterior descending artery due to stable angina pectoris 7 years earlier. Emergent coronary angiography on admission showed occlusion in the distal portion of the previously stented segment, in which observation by optical coherence tomography revealed the existence of a remarkable proliferation of lipid-laden neointimal tissues with rupture and thrombus. This suggests that very late stent thrombosis in a self-expanding stent may occur through the process of atheromatous formation.
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A multicenter study design to assess the clinical usefulness of semi-automatic measurement of flow-mediated vasodilatation of the brachial artery.
Int Heart J
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Flow-mediated vasodilatation of the brachial artery (FMD) is a marker which is related to endothelial nitric oxide bioavailability. Commercially available ultrasound machines equipped with online computer-assisted semi-automatic analysis software to measure FMD have recently become available in Japan. These devices enable more convenient examination, enhanced reproducibility of FMD measurement, and a shortened examination time. Using such devices, in the present multicenter prospective study we propose to: 1) establish standardized FMD values and determine the annual rates of FMD change in healthy subjects; 2) confirm the predictive value of FMD for future cardiovascular events in Japanese subjects; 3) evaluate the potential usefulness of a multimarker strategy, including measurements of FMD, pulse-wave velocity (PWV), ankle-brachial pressure index, biochemical markers, and proteomic biomarkers obtained by mass spectroscopic analysis to assess the prognosis of subjects with coronary artery disease; and 4) clarify the usefulness of FMD measurement to predict the rate of progression of carotid atherosclerosis, arterial stiffness and microalbuminuria in subjects with hypertension or diabetes mellitus. In total, we estimate that approximately 4000 Japanese subjects in 3 different study groups will eventually be enrolled in this prospective observational investigation. We anticipate that the present study will provide important evidence for the usefulness of FMD measurement in the risk stratification for cardiovascular disease.
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Chronic renal artery dissection with aneurysm formation treated by stent implantation with coil embolization with detailed intravascular ultrasound evaluation.
Catheter Cardiovasc Interv
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Treatment options for chronic renal artery dissection, which is a rare cause of renal artery stenosis and renovascular hypertension, such as medical management, percutaneous intervention, and open surgical repair remain controversial. We describe a 55-year-old man with a chronic dissecting aneurysm of a renal artery complicated with renovascular hypertension that was initially diagnosed by computed tomography angiography, evaluated by intravascular ultrasound, and treated by stent implantation with coil embolization.© 2012 Wiley Periodicals, Inc.
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Protective human leucocyte antigen haplotype, HLA-DRB1*01-B*14, against chronic Chagas disease in Bolivia.
PLoS Negl Trop Dis
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Chagas disease, caused by the flagellate parasite Trypanosoma cruzi affects 8-10 million people in Latin America. The mechanisms that underlie the development of complications of chronic Chagas disease, characterized primarily by pathology of the heart and digestive system, are not currently understood. To identify possible host genetic factors that may influence the clinical course of Chagas disease, Human Leucocyte Antigen (HLA) regional gene polymorphism was analyzed in patients presenting with differing clinical symptoms.
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JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.