Usefulness of P‐wave peak time as an electrocardiographic parameter in predicting left ventricular diastolic dysfunction in patients with mitral regurgitation

IntroductionConventional Doppler measurements have limitations in predicting left ventricular diastolic dysfunction (LVDD) in patients with mitral regurgitation (MR). Recently, electrocardiographic P‐wave peak time (PWPT) has been proposed as a parameter of detecting LVDD. This study aimed to evaluate the association between PWPT and left ventricular end‐diastolic pressure (LVEDP) in patients with MR.MethodsWe performed echocardiography and cardiac catheterization in 82 patients with moderate or severe MR. We classified patients into two groups: low LVEDP group (L‐LVEDP) (LVEDP <16 mmHg, n = 40) and high LVEDP group (H‐LVEDP) (LVEDP ≥16 mmHg, n = 42). We evaluated LVDD and PWPT based on echocardiographic and electrocardiographic findings in both groups.ResultsThe PWPT in lead II (PWPT_II) was significantly longer in patients in the H‐LVEDP group than in those in the L‐LVEDP group (67 vs. 47 ms, p < .001). Using correlation analysis, LVEDP was positively correlated with PWPT_II (r = .577, p < .001). Using multivariate analysis, PWPT_II was found to be an independent predictor of increased LVEDP (95% CI: 0.1030–0.110; p < .001). Using receiver operating characteristic (ROC) curve analysis, the optimal cutoff value of PWPT_II for predicting elevated LVEDP was 58.9 ms, with a sensitivity of 80.0% and a specificity of 73.8% (area under curve: 0.809, 95% CI: 0.713–0.905).ConclusionTo the best of our knowledge, this is the first study to assess the effect of a significant valvular disease on PWPT in lead II. These findings suggest that prolonged PWPT_II may be an independent predictor of increased LVEDP in patients with moderate or severe MR.     

Longitudinal MRI study of multiple system atrophy – when do the findings appear,and what is the course?

Several investigators have revealed features of multiple system atrophy (MSA) by magnetic resonance imaging (MRI). For use in clinical diagnosis, we determined the exact time when two main features of pontine and putaminal intensity changes appeared. Furthermore, in order to reveal the course from when the disorder first appeared and how it spread, we also investigated the course of MRI findings and differences between clinical subtypes. The cranial MRI of 42 patients with MSA were longitudinally studied including comments on the so called “cross sign” of pontine T2 high intensity, which was divided into 6 stages, and also on the linear T2 high intensity of the dorsolateral side of the putamen (“putaminal slit”) which was divided into 4 stages. Patients were classified as 16 MSA-C, 7 autonomic dominant type (MSA-A), and 19 MSA-P. The age at onset ranged from 41 to 74 years (mean, 55 ± 9). The duration of the disease in the MRI study ranged from 1 to 24 years. The pontine “cross sign” was completed (shows Cross, stage IV) earlier in MSA-C mainly before 5 years, later in MSA-P and even much later in MSA-A. Regarding the “putaminal slit”, MSA-P shows earlier bilateral changes (stage II), mostly before 3 years, compared with MSA-C, which requires 4 years to reveal even a unilateral change (stage I), or MSA-A which requires even more time. MRI findings showed a tendency to relate to clinical findings, since MSA-C exhibits “cross sign” completion earlier than bilateral “putaminal slit”; however, MSA-P shows bilateral “putaminal slit” earlier than “cross sign”, and MSA-A requires much more time to show both. Clinically, MSA-C, MSA-A, or MSA-P showed different MRI courses so that three subtypes could be defined also with MRI findings. Therefore these observations are useful not only for diagnosis of MSA itself, but also to distinguish clinical subtypes (MSA-C, MSA-A, or MSA-P) which have different rates of lesion progression. Received: 5 September 2001, Received in revised form: 10 December 2001, Accepted: 17 December 2001     

Detection, epitope-mapping and function of anti-Fas autoantibody in patients with silicosis

Dysregulation of apoptosis through the Fas-Fas ligand pathway is associated with the onset of autoimmune disease. Since autoantibodies directed against unknown antigens are present in the sera of these patients, sera samples were examined for the presence of autoantibodies directed against the Fas molecule. Using Western blotting and a ProteinChip analysis, autoantibodies against Fas were detected in patients with silicosis, systemic lupus erythematosus (SLE) and systemic sclerosis (SSc), and weakly detected in healthy individuals. Using epitope mapping employing 12-amino-acid polypeptides with the SPOTs system, a minimum of four epitopes and a maximum of 10 epitopes were found. Several amino acid residues involved in binding FasL, such as C66, R87, L90, E93 and H126, were presented within the epitopes. Serum containing a large amount of anti-Fas autoantibody from silicosis patients inhibited the growth of a Fas-expressing human cell line, but did not inhibit the growth of a low Fas-expresser nor a Fas-expresser in which the Fas gene had been silenced by small interference RNA. All epitopes in the intracellular region of Fas were located in the death domain. The possible roles of anti-Fas autoantibody detected in healthy volunteers and patients with silicosis or autoimmune diseases are discussed here.     

Landiolol for junctional ectopic tachycardia refractory to amiodarone after pediatric cardiac surgery

Postoperative junctional ectopic tachycardia (JET) in children undergoing cardiac surgery is a serious arrhythmia that is associated with considerable morbidity and mortality. We present here a case of successful landiolol therapy for postoperative JET in a 3-month-old infant who underwent ventricular septal defect closure and right pulmonary artery plasty. His left ventricular function was poor postoperatively. The JET was refractory to amiodarone and caused severe hypotension, which was required cardiac massage. Continuous intravenous infusion of low-dose landiolol reduced the persistent JET rate immediately, and restored to sinus rhythm with stable hemodynamics.     

Common cytological and cytogenetic features of Epstein-Barr virus (EBV)-positive natural killer (NK) cells and cell lines derived from patients with nasal T/NK-cell lymphomas,chronic active EBV infection and hydroa vacciniforme-like eruptions

In this study, we describe the cytological and cytogenetic features of six Epstein-Barr virus (EBV)-infected natural killer (NK) cell clones. Three cell clones, SNK-1, -3 and -6, were derived from patients with nasal T/NK-cell lymphomas; two cell clones, SNK-5 and -10, were isolated from patients with chronic active EBV infection (CAEBV); and the other cell clone, SNK-11, was from a patient with hydroa vacciniforme (HV)-like eruptions. An analysis of the number of EBV-terminal repeats showed that the SNK cell clones had monoclonal EBV genomes identical to the original EBV-infected cells of the respective patients, and SNK cells had the type II latency of EBV infection, suggesting that not only the cell clones isolated from nasal T/NK-cell lymphomas but also those isolated from CAEBV and HV-like eruptions had been transformed by EBV to a certain degree. Cytogenetic analysis detected deletions in chromosome 6q in five out of the six SNK cell clones, while 6q was not deleted in four control cell lines of T-cell lineage. This suggested that a 6q deletion is a characteristic feature of EBV-positive NK cells, which proliferated in the diseased individuals. The results showed that EBV-positive NK cells in malignant and non-malignant lymphoproliferative diseases shared common cytological and cytogenetic features.     

Improved cognitive function, mood and brain blood flow in single photon emission computed tomography following individual reminiscence therapy in an elderly patient with Alzheimer's disease

An 88-year-old man who was suffering from chronic renal failure and hypertension visited our memory clinic because of recent cognitive decline and a gradual decrease in his vitality and volition. His Mini-Mental State Examination (MMSE) score was 22, his 15-item Geriatric Depression Scale (GDS-15) score was 10, and his Vitality Index (VI; full score, 10) was 6. We diagnosed Alzheimer's disease with depressive mood, and this was supported by findings of global brain atrophy by magnetic resonance imaging and decrease in brain blood flow in the posterior cingulated gyrus and frontal association area by single photon emission computed tomography (SPECT). After completion of a life review of the patient, individual reminiscence therapy was performed once a week for 2 months. After the therapy, a comprehensive geriatric assessment showed that cognitive function, depressive mood and decreased vitality had all markedly improved (MMSE, 29; GDS, 7; VI, 9). Moreover, SPECT showed improved brain blood flow, especially in the frontal lobe. We believe that this is the first case in which reminiscence therapy alone not only improved cognitive function and mood but also reduced neuroimaging abnormalities.     

Thrombopoietin maintains cell numbers of hematopoietic stem and progenitor cells with megakaryopoietic potential

Thrombopoietin has long been known to influence megakaryopoiesis and hematopoietic stem and progenitor cells, although the exact mechanisms through which it acts are unknown. Here we show that MPL expression correlates with megakaryopoietic potential of hematopoietic stem and progenitor cells and identify a population of quiescent hematopoietic stem and progenitor cells that show limited dependence on thrombopoietin signaling. We show that thrombopoietin is primarily responsible for maintenance of hematopoietic cells with megakaryocytic differentiation potential and their subsequent megakaryocyte differentiation and maturation. The loss of megakaryocytes in thrombopoietin knockout mouse models results in a reduction of megakaryocyte-derived chemokine platelet factor 4 (CXCL4/PF4) in the bone marrow and administration of recombinant CXCL4/PF4 rescues the loss of quiescence observed in these mice. CXCL4/PF4 treatment does not rescue reduced hematopoietic stem and progenitor cell numbers, suggesting that thrombopoietin maintains hematopoietic stem and progenitor cell numbers directly.