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Clustering of supernumerary centrosomes, which potentially leads to cell survival and chromosomal instability, is frequently observed in cancers. However, the molecular mechanisms that control centrosome clustering remain largely unknown. The centrosomal kinesin KIF24 was previously shown to restrain the assembly of primary cilia in mammalian cells. Here, we revealed that KIF24 depletion suppresses multipolar spindle formation by clustering centrosomes in pancreatic ductal adenocarcinoma (PDAC) cells harboring supernumerary centrosomes. KIF24 depletion also induced hyper-proliferation and improved mitotic progression in PDAC cells. In contrast, disruption of primary cilia failed to affect the proliferation and spindle formation in KIF24-depleted cells. These results suggest a novel role for KIF24 in suppressing centrosome clustering independent of primary ciliation in centrosome-amplified PDAC cells.

In volatile foraging environments, animals need to adapt their learning in accordance with the uncertainty of the environment and knowledge of the hidden structure of the world. In these contexts, previous studies have distinguished between two types of strategies, model-free learning, where reward values are updated locally based on external feedback signals, and inference-based learning, where an internal model of the world is used to make optimal inferences about the current state of the environment. Distinguishing between these strategies during the dynamic foraging behavioral paradigm has been a challenging problem for studies of reward-guided decisions, due to the diversity in behavior of model-free and inference-based agents, as well as the complexities that arise when animals mix between these types of strategies. Here, we developed two solutions that jointly tackle these problems. First, we identified four key behavioral features that together benchmark the switching dynamics of agents in response to a change in reward contingency. We performed computational simulations to systematically measure these features for a large ensemble of model-free and inference-based agents, uncovering an organized structure of behavioral choices where observed behavior can be reliably classified into one of six distinct regimes in the two respective parameter spaces. Second, to address the challenge that arises when animals use multiple strategies within single sessions, we developed a novel state-space method, block Hidden Markov Model (blockHMM), to infer switches in discrete latent states that govern the choice sequences across blocks of trials. Our results revealed a remarkable degree of mixing between different strategies even in expert animals, such that model-free and inference-based learning modes often co-existed within single sessions. Together, these results invite a re-evaluation of the stationarity of behavior during dynamic foraging, provide a comprehensive set of tools to characterize the evolution of learning strategies, and form the basis of understanding neural circuits involved in different modes of behavior within this domain.

Clustering of supernumerary centrosomes, potentially leading to cell survival and chromosomal instability, is frequently observed in cancers. However, the molecular mechanisms by which centrosome clustering is controlled in cancer cells remain largely unknown. A centrosomal kinesin, KIF24, was previously shown to restrain the assembly of primary cilia in mammalian cells. Here, we revealed that KIF24 depletion suppresses multipolar spindle formation by clustering centrosomes in pancreatic ductal adenocarcinoma (PDAC) cells harboring supernumerary centrosomes. KIF24 depletion also induced hyperproliferation and improved the mitotic progression in PDAC cells. On the other hand, disruption of primary cilia failed to affect the proliferation and spindle formation in KIF24-depleted cells. These results represent a novel role of KIF24 in suppressing centrosome clustering independent of primary ciliation in centrosome-amplified PDAC cells.

The electronic structure changes of SmS surfaces under potassium (K) doping are elucidated using synchrotron-based core-level photoelectron spectroscopy and angle-resolved photoelectron spectroscopy (ARPES). The Sm core-level and ARPES spectra indicate that the Sm mean valence of the surface increased from the nearly divalent to trivalent states, with increasing K deposition. Carrier-induced valence transition (CIVT) from Sm$^{2+}$ to Sm$^{3+}$ exhibits a behavior opposite to that under conventional electron doping. Excess electrons are trapped by isolated excitons, which is inconsistent with the phase transition from the black insulator with Sm$^{2+}$ to the gold metal with Sm$^{3+}$ under pressure. This CIVT helps to clarify the pressure-induced black-to-golden phase transition in this material, which originates from the Mott transition of excitons., Comment: 7 pages, 6 figures

Patient: Male, 78-year-old Final Diagnosis: Myocardial infarction Symptoms: Chest pain Medication: — Clinical Procedure: — Specialty: Cardiology Objective: Unusual clinical course Background: Thallium-201 has been widely used in clinical practice for the management of coronary heart disease, but little is known regarding its kinetics in the acute phase of myocardial infarction. Case Report: We report a 78-year-old man who developed acute inferior myocardial infarction during exercise thallium-201 scintigraphy. The patient underwent exercise testing with thallium-201 myocardial scintigraphy because of a single episode of chest pain. The workload was started with 25 watts and increased by 25 watts every 2 min on a bicycle ergometer with continuous monitoring of 12-lead electrocardiography. Thallium-201 was injected intravenously at 85% of the age-predicted maximal heart rate, and ST-segment elevations refractory to medication subsequently developed in the inferior leads, followed by chest pain. Scintigraphic image acquisition was deferred and he was transferred to the catheter laboratory in this hospital. Emergency coronary angiography showed occlusion in the right coronary artery, and stent implantation was successfully performed. The peak level of creatine kinase in the clinical course was 201 U/l. Scintigraphic images obtained 4 h after the onset of ST-segment elevation showed severely reduced activity in the left ventricular inferior wall, with partial redistribution 24 h later. Follow-up imaging performed 4 months later revealed increased accumulation of thallium-201 in the inferior wall. Conclusions: Our case highlights the kinetics of thallium-201 during acute myocardial infarction.

Isolated septal myocardial infarction is an uncommon condition with diagnostic difficulty due to small infarction size and anatomical variations. We report a case of isolated septal myocardial infarction, in which the diagnosis was confirmed not by electrocardiographic, echocardiographic, or angiographic findings, but by nuclear imaging. A 46-year-old man with chest discomfort exhibited ST-segment elevations in leads V1 and V2, and borderline abnormalities of the septal wall motion on echocardiography. Emergency coronary angiography demonstrated delayed flow in the second septal branch of the left anterior descending coronary artery. Intravascular ultrasound showed plaque in the proximal portion of the septal branch without evidence of plaque rupture. No balloon angioplasty or stent implantation was required because the flow delay in the septal branch disappeared after the intravascular ultrasound procedure. Myocardial perfusion-metabolism mismatch, as assessed by resting thallium-201 and iodine-123-beta-methyl-p-iodophenyl-pentadecanoic acid, was seen in the mid-septal region.

The structure of brain regions is assumed to correlate with their function, but there are very few instances in which the relationship has been demonstrated in the live brain. This is due to the difficulty of simultaneously measuring functional and structural properties of brain areas, particularly at cellular resolution. Here, we performed label-free, third-harmonic generation (THG) microscopy to obtain a key structural signature of cortical areas, their effective attenuation lengths (EAL), in the vertical columns of functionally defined primary visual cortex and five adjacent visual areas in awake mice. EALs measured by THG microscopy in the cortex and white matter showed remarkable correspondence with the functional retinotopic sign map of each area. Structural features such as cytoarchitecture, myeloarchitecture and blood vessel architecture were correlated with areal EAL values, suggesting that EAL is a function of these structural features as an optical property of these areas. These results demonstrate for the first time a strong relationship between structural substrates of visual cortical areas and their functional representation maps in vivo. This study may also help in understanding the coupling between structure and function in other animal models as well as in humans.

Acute inferior myocardial damage can induce transient bradycardia and hypotension—the Bezold–Jarisch reflex, which is explained by the preferential distribution of vagal nerves in the inferior wall of the left ventricle. We report a 76‐year‐old man who showed a perfusion defect in the inferior wall with redistribution on exercise scintigraphy with thallium‐201. Of note, during exercise at an intensity of 100 watts, the patient's heart rate transiently decreased from 122 to 95 bpm in sinus rhythm, accompanied by ST‐segment depression. A diagnosis of coronary spastic angina was made since no stenotic lesions were observed on conventional coronary angiography.

Two-photon microscopy is used to image neuronal activity, but has severe limitations for studying deeper cortical layers. Here, we developed a custom three-photon microscope optimized to image a vertical column of the cerebral cortex > 1 mm in depth in awake mice with low (, Two-photon microscopy is a powerful tool for studying neuronal activity but cannot easily image deeper cortical layers. Here, the authors design a custom microscope for three-photon microscopy and use it to reveal response properties of layer 5, 6, and subplate visual cortical neurons.

In visual cortex, information is processed in multiple cortical layers. However, response features of neurons in deeper layers have remained unclear. Here, we design of a custom-made three-photon microscope to image a vertical column of the cerebral cortex >1 mm in depth in awake mice.

Prognostic prediction has been reported to affect the decision of doctors and non-physician health care providers such as nurses, social workers, pastors, and hospice volunteers on the selection of appropriate medical interventions. This was a case of a 65-year-old woman who presented with a poor oral intake. The patient had a history of sigmoid colon cancer with abdominal wall metastasis and peritoneal dissemination. On the day of admission, nausea, anorexia, and malaise were noted, requiring immediate intervention. The patient’s prognosis was predicted using the Palliative Prognostic Index. The pharmacist suggested the use of dexamethasone tablets in order to alleviate the patient’s symptoms. Indeed, the administration of dexamethasone alleviated the symptoms of nausea, loss of appetite, and malaise. To the best of our knowledge, this is the first case report to demonstrate that prognosis prediction is important not only for other medical staff but also for pharmacists when deciding the need to initiate a treatment and continue such treatment, and when providing pharmacist interventions.

For the estimation of short-term prognosis in terminal cancer patients, it is important to establish a prognostic index that does not involve blood tests. We compared the prognostic ability of the Barthel Index (BI) with the Glasgow Prognostic Score (GPS). Ninety-seven inpatients with terminal cancer at Onomichi Municipal Hospital who died between 2018 and 2019 were retrospectively analyzed. The sensitivity, specificity, accuracy, and area under the receiver operating characteristic curve (AUROC) were compared between the BI and GPS. For predicting the 15 day prognosis, the BI showed higher specificity, accuracy, and AUROC than the GPS. For predicting the 30 day prognosis, the BI showed higher sensitivity, accuracy, and AUROC than the GPS. The BI can predict the 15 or 30 day prognosis in terminal cancer patients. As the BI does not require blood tests, it may be an option for prognostic prediction in terminal cancer patients.

Hypertrophic cardiomyopathy (HCM) patients sometimes develop subendocardial ischemia without coronary artery stenosis. We report a case of non-obstructive HCM, in which electrocardiographic changes were observed with improvement of subendocardial ischemia. A 76-year-old man presented with chest pain on exertion. The electrocardiogram revealed left ventricular (LV) hypertrophy with repolarization abnormalities. No coronary stenosis was found on computed tomography angiography, but thallium-201 exercise scintigraphy revealed transient LV cavity dilation after exercise, consistent with subendocardial ischemia. His chest symptoms disappeared after starting verapamil. Transient LV cavity dilation improved without a reduction in exercise tolerance, as did electrocardiographic abnormalities without any changes on echocardiography.

Cholinergic modulation of cortex powerfully influences information processing and brain states, causing robust desynchronization of local field potentials and strong decorrelation of responses between neurons. Here we show that intracortical cholinergic inputs to mouse visual cortex specifically and differentially drive a defined cortical microcircuit: they facilitate somatostatin-expressing (SOM) inhibitory neurons that in turn inhibit parvalbumin-expressing inhibitory neurons and pyramidal neurons. Selective optogenetic inhibition of SOM responses blocks desynchronization and decorrelation, demonstrating that direct cholinergic activation of SOM neurons is necessary for this phenomenon. Optogenetic inhibition of vasoactive intestinal peptide-expressing neurons does not block desynchronization, despite these neurons being activated at high levels of cholinergic drive. Direct optogenetic SOM activation, independent of cholinergic modulation, is sufficient to induce desynchronization. Together, these findings demonstrate a mechanistic basis for temporal structure in cortical populations, and the crucial role of neuromodulatory drive to specific inhibitory-excitatory circuits in actively shaping the dynamics of neuronal activity.

The emergence of oligoclonal bands (OB) has been reported in patients with multiple myeloma (MM) after stem cell transplantation (SCT) or successful chemotherapy. However, their clinical relevance remains unclear. We reviewed the clinical records of MM patients from January 2006 to May 2014. Treatment response was evaluated by International Working Group (IMWG) criteria. Serum immunofixation tests were performed at least every 3 months if the patient achieved more than very good partial response (VGPR). Free light chain (FLC) and minimal residual disease measurement by multicolor flow cytometry (MFC) were performed to evaluate the response to treatment. Among the 163 patients included in the study, 40 developed OB. Detection rates of OB in patients with complete response (CR), VGPR and partial response (PR) or less were 51.8, 36.3 and 0%, respectively. Patients with OB showed better progression-free survival (PFS) and overall survival (OS) rates than those without OB (P = 0.028 and P < 0.001, respectively). However, if the patients were limited to ≥VGPR or CR, development of OB did not affect PFS (P = 0.621 and P = 0.646, respectively) or OS (P = 0.189 and P = 0.766, respectively). OB was observed in 60% of patients after SCT, and in 36.6% of patients with more than VGPR without SCT (P < 0.001). Patients with OB tended to have less minimal residual disease than those without OB (P = 0.054) and its presence may affect the stringent CR criteria. In conclusion, the emergence of OB was seen exclusively in patients with favorable responses, but its emergence per se could not be translated to improved survival.

Hypertrophic cardiomyopathy (HCM) patients often develop subendocardial ischemia in the left ventricle without atherosclerotic coronary stenosis. Myocardial ischemia plays an important role in the pathophysiology of HCM, but diagnostic techniques for the detection of subendocardial ischemia have not been widely available. We developed specific techniques to quantify subendocardial ischemia on stress scintigraphy, and have compared the results with various clinical features in patients with HCM. This article reviews our understanding of subendocardial ischemia in HCM based on more than 20 years of experience.

An abnormal blood pressure response to exercise has been reported to be associated with left ventricular subendocardial ischemia in patients with hypertrophic cardiomyopathy (HCM), but the underlying mechanism remains unclear. We report a case of HCM with an abnormal blood pressure response and subendocardial ischemia, in which the analysis of heart rate variability revealed exercise-induced vagal enhancement. The present case highlights the possible mechanism linking abnormal blood pressure response and left ventricular subendocardial ischemia in patients with HCM.

Acetylcholine (ACh) modulates diverse vital brain functions. Cholinergic neurons from the basal forebrain innervate a wide range of cortical areas, including the primary visual cortex (V1), and multiple cortical cell types have been found to be responsive to ACh. Here we review how different cell types contribute to different cortical functions modulated by ACh. We specifically focus on two major cortical functions: plasticity and cortical state. In layer II/III of V1, ACh acting on astrocytes and somatostatin-expressing inhibitory neurons plays critical roles in these functions. Cell type specificity of cholinergic modulation points towards the growing understanding that even diffuse neurotransmitter systems can mediate specific functions through specific cell classes and receptors., National Institutes of Health (U.S.) (U01NS090473), National Institutes of Health (U.S.) (R01EY007023), National Science Foundation (U.S.) (EF1451125)

Multiple hypothalamic neuronal populations that regulate energy balance have been identified. Although hypothalamic glia exist in abundance and form intimate structural connections with neurons, their roles in energy homeostasis are less known. Here we show that selective Ca[superscript 2+] activation of glia in the mouse arcuate nucleus (ARC) reversibly induces increased food intake while disruption of Ca[superscript 2+] signaling pathway in ARC glia reduces food intake. The specific activation of ARC glia enhances the activity of agouti-related protein/neuropeptide Y (AgRP/NPY)-expressing neurons but induces no net response in pro-opiomelanocortin (POMC)-expressing neurons. ARC glial activation non-specifically depolarizes both AgRP/NPY and POMC neurons but a strong inhibitory input to POMC neurons balances the excitation. When AgRP/NPY neurons are inactivated, ARC glial activation fails to evoke any significant changes in food intake. Collectively, these results reveal an important role of ARC glia in the regulation of energy homeostasis through its interaction with distinct neuronal subtype-specific pathways., Massachusetts Institute of Technology. Poitras Center for Affective Disorders Research, Singapore. Agency for Science, Technology and Research, National Institutes of Health (U.S.) (R01EY007023), National Institutes of Health (U.S.) (R01EY018648), National Institutes of Health (U.S.) (U01NS090473), National Science Foundation (U.S.) (EF1451125), Simons Foundation, Massachusetts Institute of Technology. Simons Center for the Social Brain, Autism Science Foundation

Background: Brain natriuretic peptide (BNP) is a useful biomarker for managing patients with heart failure. Left ventricular morphology is an important determinant of left ventricular wall stress or BNP secretion, but little data is available regarding the long-term prognostic value of BNP in relation to left ventricular morphology in patients with heart failure. Methods: Plasma BNP levels and left ventricular morphology including end-diastolic/end-systolic volume and mass index on echocardiography were assessed before discharge in 89 consecutive patients hospitalized with acute decompensated heart failure. All patients were prospectively followed for cardiac events defined as cardiac death or rehospitalization due to heart failure. Results: During a follow-up period of up to 10 years, 28 patients died and 24 survived with cardiac events. Levels of BNP in nonsurvivors, survivors with cardiac events, and survivors without cardiac events were as follows: 240 ± 107 pg/ml, 357 ± 71 pg/ml, and 177 ± 23 pg/ml at 1 year after discharge (P = 0.01); 300 ± 63 pg/ml, 307 ± 66 pg/ml, and 157 ± 24 pg/ml at 5 years (P = 0.03); and 357 ± 65 pg/ml, 222 ± 43 pg/ml, and 145 ± 25 pg/ml at 10 years (P

We retrospectively analyzed the outcomes of 175 consecutive patients admitted to our hospital between April 2004 and June 2014, and identified 42 (24%), 80 (46%), and 53 (30%) patients ≥ 80, 66-79, and ≤ 65 years old, respectively. The median progression-free survival (PFS) and overall survival (OS) of the ≥ 80, 66-79, and ≤ 65 years old groups were 19.1, 26.3, and 54.3 months, and 31.9, 54.8, and 83.8 months, respectively. Patients ≥ 80 but not ≤ 79 years old with ECOG performance score (PS) ≥ 3 and/or Charlson comorbidity index (CCI) ≥ 5 showed significantly shorter survival. ECOG PS and CCI predicted the treatment outcome of patients ≥ 80 but did not predict ≤ 79 years old.

Intramyocardial calcification is a very rare condition. We report a case of a 72-year-old man with apical hypertrophic cardiomyopathy, who was initially suspected of having a thrombus in the left ventricular apex on echocardiography, but was finally diagnosed as having apical intramyocardial calcification on multidetector computed tomography. The mechanism of developing intramyocardial calcification remains to be elucidated, but the patient has been stable for more than 2 years.

Aims A necropsy study of patients with hypertrophic cardiomyopathy (HCM) who died at a young age exhibited marked disarray and fibrosis in the mid-wall layer of the left ventricular (LV) myocardium. We assessed ultrasonic tissue characteristics in the three layers of the ventricular septum (VS), and correlated the result with long-term prognosis in HCM. Methods and results The magnitude of cyclic variation of integrated backscatter (CV-IB) was calculated in the three layers of the VS and the whole aspect of the LV posterior wall in 58 non-obstructive HCM patients and 20 healthy controls. All HCM patients were prospectively followed for an average period of 7.1 years for the occurrence of cardiac death or hospitalization due to heart failure. Each CV-IB of four regions was lower in HCM patients than in controls (all P < 0.01). CV-IB of the VS mid-wall layer was lower in 14 HCM patients with cardiac events than in patients without (5.4 ± 0.6 vs. 7.4 ± 0.5 dB, P = 0.033) although CV-IB of three other regions did not differ between the two groups. The optical cut-off point of %CV-IB

Aims An attenuated heart rate response to exercise, termed chronotropic incompetence (CI), has been reported to be an independent predictor of cardiovascular mortality. We examined the change in autonomic function during exercise testing and correlated the results with CI. Methods and results Exercise testing using a bicycle ergometer was performed in 172 patients who had no evidence of cardiac disease. Chronotropic incompetence was defined as the failure to achieve 85% of the age-predicted maximum heart rate, heart rate reserve

Background: Acute inferior myocardial infarction (MI) often induces transient sinus bradycardia through vagal enhancement, known as Bezold-Jarisch reflex, which is explained by preferential distribution of vagal nerve in the inferior wall. We examined vagal activity in relation to the occurrence of residual ischemia in patients with old inferior MI and assessed its diagnostic usefulness. Methods: Exercise myocardial scintigraphy was performed in 15 patients with old inferior MI, 19 angina pectoris (AP) patients with inferior ischemia but no MI, and 32 control subjects who had no evidence of cardiac disease. We analyzed the connection of residual ischemia in old MI with ST-segment response to exercise and with vagal activity as determined by coefficient of component variance of high frequency (CCVHF). Results: Exercise-induced percentage change in CCVHF was higher in patients with old MI and residual ischemia (18.8 ± 13.5%) and AP (5.5 ± 9.7%) than old MI but no residual ischemia (–24.1 ± 4.9%) or control (–22.8 ± 4.5%, P = 0.006). Percentage change in CCVHF > –5% had a good diagnostic value for the detection of residual ischemia in patients with old inferior MI with sensitivity of 83%, specificity of 89%, accuracy of 87%, and positive likelihood ratio of 7.50, which was higher than that of ST-segment depression (67%, 50%, 56%, and 1.33). Conclusions: Vagal enhancement was associated with residual ischemia in old inferior MI as well as inferior AP. Measurement of CCVHF is useful in improving the diagnostic reliability of exercise electrocardiography in patients with old inferior MI.

Patients with hypertrophic cardiomyopathy (HCM) often develop myocardial ischemia in association with abnormal blood pressure response to exercise. Vagal nerves mediate cardioinhibitory stimuli, with little knowledge regarding vagal response to myocardial ischemia in patients with HCM.Exercise Tc-99m-tetrofosmin myocardial scintigraphy was performed in 59 HCM patients and 39 controls who had no evidence of cardiac disease. We examined how reversible regional perfusion abnormality and transient left ventricular cavity dilation, a parameter of subendocardial ischemia, are related to vagal modulation as assessed by coefficient of high frequency component variance (CCV(HF)) on heart rate variability. We then correlated the results with abnormal blood pressure response to exercise, defined as failed increaseor=25 mm Hg during exercise.Regional perfusion abnormality and left ventricular cavity dilation were observed in 26 and 21 HCM patients, respectively. The percentage change of CCV(HF) from before to after exercise was higher in HCM patients with left ventricular cavity dilation than without or controls (5.2+/-9.8%, -23.5+/-5.7%, -14.5+/-5.5%, P=0.004). By contrast, the change of CCV(HF) was similar in HCM patients with regional perfusion abnormality, those without, and controls. The change of CCV(HF) was correlated with exercise-induced increase in systolic blood pressure (rho=-0.64, P0.001); HCM patients with abnormal blood pressure response were characterized by a higher percentage change in CCV(HF) (50.0+/-18.3%).Subendocardial ischemia provoked vagal enhancement in patients with HCM, which may be related to the development of abnormal blood pressure response to exercise.

Background Small Q waves in the left lateral leads are termed septal q waves, and their response to exercise has been reported to be a marker of septal ischemia in coronary artery disease. Patients with hypertrophic cardiomyopathy (HCM) sometimes develop septal ischemia in the absence of coronary stenosis, but little data are available concerning the association of the septal q wave response with septal ischemia. Methods and Results Exercise electrocardiography and Tc-99m-tetrofosmin myocardial scintigraphy were recorded to detect myocardial ischemia in 29 HCM patients with asymmetric septal hypertrophy. The septal q wave amplitude was summed up in V5 and V6 during exercise testing, and the results were correlated with septal ischemia defined as a regional septal ischemia or a part of diffuse subendocardial ischemia. A decrease in the sum of the septal q wave amplitude during exercise testing yielded a sensitivity of 100% and specificity 33% for regional septal ischemia, and a sensitivity of 100% and specificity of 43% for diffuse subendocardial ischemia, although an absent septal q wave at rest provided a low sensitivity for the detection of regional septal ischemia (43%) and diffuse subendocardial ischemia (33%). Conclusions The septal q wave response to exercise is a useful marker of septal ischemia in HCM with asymmetric septal hypertrophy. (Circ J 2008; 72: 953 - 957)

Patients with apical hypertrophic cardiomyopathy (APH) associated with paradoxic jet flow (ie, diastolic flow away from the apex) may gradually develop an apical aneurysm, which often leads to arrhythmia and mural thrombus formation. We observed systolic outward motion of the left ventricular apical myocardium in patients with APH using a magnetic resonance tagging procedure and examined the relationship of the outward motion to echocardiographic and scintigraphic findings and to cardiac events. Systolic displacement of the myocardial tags of the apical region perpendicular to the long axis in the 4-chamber view was recorded in 31 patients with APH. Of these patients, 14 showed no outward movement of tags (group A), and 17 showed outward movement (group B). In group B, apical hypertrophy was more severe (35 +/- 7 mm vs. 29 +/- 6 mm, p < 0.05), paradoxic jet flow was more frequent (64% vs. 14%, p < 0.05) and the defect score in I-123-beta-methyliodophenylpentadecanoic acid scintigraphy was higher (2.1 +/- 0.7 vs. 1.3 +/- 0.7, p < 0.01). During a mean follow-up period of 55 months, only 1 patient experienced paroxysmal atrial fibrillation in group A. In group B, 1 patient died suddenly, 1 was admitted to hospital because of congestive heart failure, 2 developed angina pectoris, 2 exhibited non-sustained ventricular tachycardia, and 1 showed multifocal premature ventricular contraction; in these 7 patients the outward movement was greater than in the 10 patients in Group B who had no cardiac events (1.00 +/- 0.59 vs. 0.52 +/- 0.40, p < 0.05). Hence, our results show that outward tag displacement is frequently associated with severe apical hypertrophy, paradoxic jet flow, apical ischemia, and cardiac events. The tagging method may be useful in assessing the severity of APH and predicting the occurrence of cardiac events at an early stage.

Background Patients with hypertrophic cardiomyopathy (HCM) sometimes display characteristic electrocardiographic (ECG) findings at rest and develop subendocardial ischemia during exercise in the absence of coronary lesions. However, their relationship has not yet been fully clarified. Methods Exercise Tc-99m-tetrofosmin myocardial scintigraphy was performed in 48 patients with non-obstructive HCM. We quantified transient left ventricular cavity dilation (LVCD) on exercise scintigrams, a parameter of subendocardial ischemia, and correlated the results with the ECG findings at rest and during exercise. Results Transient LVCD occurred during exercise in 17 (35%) patients with HCM. Hemodynamic parameters during exercise did not differ between HCM patients with and without transient LVCD. Multiple logistic regression analysis showed that transient LVCD was significantly associated with ST-segment depression at rest ( χ 2 =5.00, odds ratio=5.70, 95% confidence intervals 1.24–26.18, P =0.025) and a greater total number of leads with resting ST-segment depression ( χ 2 =6.38, odds ratio=1.60, 95% confidence intervals 1.12–2.42, P =0.012). The degree of LVCD was correlated with the total number of leads with ST-segment depression at rest ( P =0.002); the optimal cutoff for the diagnosis of transient LVCD was 3 with a sensitivity of 65%, a specificity of 90%, and an accuracy of 81%. Conclusions In patients with HCM, ST-segment depression at rest was accompanied by exercise-induced subendocardial perfusion abnormality as detected by myocardial scintigraphy. ST-segment depression at rest suggests that the subendocardium is predisposed to exertional ischemia.

To determine whether the Bezold-Jarisch reflex or enhancement of vagal nerves, which are preferentially distributed in the inferoposterior myocardium, results from exercise induced ischaemia in this region.On the basis of exercise myocardial scintigraphy and coronary angiography, 145 patients were classified as follows: group I, 34 patients with inferoposterior ischaemia; group A, 32 with anterior ischaemia; and control, 79 without ischaemia. The relation between ischaemic areas and ECG leads with ST segment changes and vagal modulation assessed by heart rate variability (HRV) (high frequency (HF) component (0.15-0.40 Hz) and coefficient of HF component variance (CCVHF), which is the square root of HF divided by mean RR interval) were assessed.The rate of ST segment depression in any lead did not differ between group I and group A. HF and CCV(HF) were similar before exercise but higher in group I than in group A and the control group after exercise (mean (SEM) HF: 94 (17) ms2, 41 (7) ms2, and 45 (6) ms2, respectively, p = 0.021; CCV(HF): 1.18 (0.09)%, 0.81 (0.07)%, and 0.89 (0.05)%, p = 0.0053). Furthermore, the percentage change in CCV(HF) before and after exercise was higher in group I than in group A or controls (mean (SEM) 22 (10)%, -24 (4)%, and -21 (3)%, p0.0001). The optimal cut off for diagnosis of inferoposterior ischaemia was -5% with a sensitivity of 74%, specificity 75%, and accuracy 75%.Vagal modulation as assessed by HRV analysis was enhanced in association with exercise induced inferoposterior ischaemia. Exercise ECG testing combined with HRV analysis would increase accuracy in the diagnosis of ischaemic areas in selected patients with angina pectoris.

Isolated left venticular noncompaction (IVNC) is a rare congenital heart disease charactrized by a pattern of an excessively prominent trabecular meshwork with deep intertrabecular recesses. Heart rate variability (HRV) has been reported to be impaired in various heart diseases, though little is known regarding HRV in adult patients with IVNC.We measured spectral components of HRV using fast Fourier transformation of 24-h Holter recordings in 10 adult patients with IVNC, 40 patients with myocardial infarction (MI), 40 patients with hypertrophic cardiomyopathy (HCM) and 40 healthy controls.The low frequency component and the high frequency component of HRV were lower in IVNC patients tahn those in controls (265 +/- 213 ms(2) vs. 469 +/- 195 ms(2), p0.01; 80 +/- 51 ms(2) vs. 185 +/- 126 ms(2), p0.01). Furthermore, 3 IVNC patients with a previous history of heart failure exhibited more decreased HRV (low frequency, 75 +/- 56 ms(2); high frequency, 39 +/- 18 ms(2)). Contrary, the ratio of low frequency to high frequency component was higher in patients with IVNC than controls (3.5+/-0.5 vs. 3.2 +/- 0.3, p0.05). The degree of impaired HRV was severest in MI patients, intermediate in IVNC patients and mildest in HCM patients compared with controls.HRV is impaired in adult patients with IVCN, especially in patients with a previous history of heart failure, suggesting vagal withdrawal or sympathetic enhancement. HRV in IVNC adults is less impaired than in MI patients, and more impaired than in HCM patients of our cohort.

【目的】心拍数には性差が存在し, 一般に女性は男性より高値である.一方, 心拍数を規定する洞結節は, 自律神経活動の修飾を受ける.そこで今回, 心拍数の性差に対する自律神経活動の関与を検討した.【方法】明らかな心疾患を有さない287例 (平均年齢45.4歳, 4～85歳) に, 24時間ボルター心電図検査を施行した.連続する洞調律QRS波よりなるRR間隔 (NN間隔) の一日平均値と心拍変動解析から算出した6指標 (時間領域のSDNN, SDANN, RMSSD; 周波数領域のHF, LF, LF/HF) の性差を, 10歳ごとに層別化した各群で検討した.【結果】全対象における平均NN間隔は女性で低値であった (791±119msecvs820±111msec, p=0.047) .年齢ごとの比較では, 30～59歳の女性で男性より平均NN間隔が低値であった.RMSSDとHFは両性で加齢とともに減少したが (男性Spearmanr=-0.52, 女性Spearmanr=-0.51; 男性Spearmanr=-0.60, 女性Spearmanr=-0.62; ともにp

Hypercholesterolemia is a risk factor for development of coronary artery disease (CAD), however, several reports have suggested that low serum cholesterol is associated with a worse prognosis in patients with congestive heart failure (CHF). The objective of this study was to determine the prognostic value of cholesterol for CHF. The study subjects consisted of 133 consecutive patients hospitalized in our institution for progressive heart failure from April 2000 to March 2003. Thirty-two percent of the patients had CAD. After improvement of congestive heart failure and discharge from the hospital, lipid profiles, including serum total cholesterol (TC), triglycerides, and high and low density lipoprotein cholesterol (HDL, LDL, respectively), were obtained. During the follow-up period (2.3 +/- 0.9 years), 21 patients died. There was a significant difference between survivors and nonsurvivors in HDL (53 +/- 15, 43 +/- 15 mg/dL, P = 0.01), but no differences were observed in other variables. In patients with CAD, survivors had significantly lower TC concentrations (179 +/- 30 versus 246 +/- 55 mg/dL, P = 0.004), although in patients without CAD, survivors had significantly higher TC concentrations (203 +/- 37 versus 170 +/- 40 mg/dL, P = 0.02). Multivariate analysis showed high TC predicted a worse outcome in patients with CAD (odds ratio (OR) = 1.052, 95% confidence interval (CI) 1.002-1.104, P = 0.04), but a better outcome in patients without CAD (OR = 0.972, 95% CI 0.948-0.997, P = 0.03), independent of age, gender, medication, and complications. Thus, low serum cholesterol is associated with an improved outcome in patients with CAD, while it predicts a worse outcome in patients without CAD.