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A major complication of blood donation is vasovagal reaction (VVR) with or without syncope. VVR occurs not only in the early phase, but also in the late phase after blood donation. We previously reported the hemodynamic characteristics of blood donors susceptible to early phase VVR. In the present study, we investigated the hemodynamic characteristics of those who developed late VVR. Ninety-six healthy volunteers donating 400 ml of whole blood were studied. After asking about their physical condition or routine questions for blood donation, blood pressure (BP) and heart rate (HR) were recorded while the donors were kept standing up for 3 min before and after blood collection. Questionnaires were distributed to all donors for reporting late VVR symptoms within 24 h. Those with younger age and lower diastolic blood pressure were more susceptible to late VVR (both p

Background Recent studies have reported the clinical usefulness of positive airway pressure ventilation therapy with various kinds of pressure support compared with simple continuous positive airway pressure (CPAP) for heart failure patients. However, the mechanism of the favorable effect of CPAP with pressure support can not be explained simply from the mechanical aspect and remains to be elucidated. Methods and Results In 18 stable chronic heart failure patients, we performed stepwise CPAP (4, 8, 12 cm H 2 O) while the cardiac output and intracardiac pressures were continuously monitored, and we compared the effects of 4 cm H 2 O CPAP with those of 4 cm H 2 O CPAP plus 5 cm H 2 O pressure support. Stepwise CPAP decreased cardiac index significantly in patients with pulmonary arterial wedge pressure (PAWP) −1 m −2 ( P = .001) compared with CPAP alone, regardless of basal filling condition or cardiac index. Conclusions Our results suggest that CPAP plus pressure support is more effective than simple CPAP in heart failure patients and that the enhancement might be induced by neural changes and not simply by alteration of the preload level.

To examine the effect of controlled-release nifedipine (nifedipine CR) given at bedtime on morning hypertension and to compare its effect with that of α-adrenergic blocker, doxazosin, given at bedtime, we performed a cross-over study in ten (5 males, 5 females) hypertensive patients with morning hypertension. After control measurements, the patients were assigned to either nifedipine CR (20-40 mg) first or doxazosin (1-2 mg) first. After 4 weeks of the treatment, measurements were repeated and medication was switched to another drug for another 4 weeks. Systolic and diastolic blood pressure (BP) and heart rate were measured using a 24-hour ambulatory BP monitoring system. While BP at evening and early nighttime (16 : 00-3 : 00) were the same in the three conditions (control, nifedipine CR, and doxazosin), nifedipine CR significantly suppressed BP at the latest nighttime (5 : 00-6 : 00) (systolic BP/diastolic BP : control 128.4±12.0/85.1±10.6 mmHg, doxazosin 124.5±11.6/81.4±10.7 mmHg, nifedipine CR 111.2±16.0/77.7±11.2 mmHg, p

A case of extensive inferior myocardial infarction complicated by a large ventricular aneurysm is presented. Magnetic resonance (MR) imaging 4 days after the onset showed a small protrusion from the necrotic inferior myocardium, which expanded 10 days after onset with a marked pericardial effusion. The follow-up examination by MR and CT imaging 6 months after the onset revealed a large ventricular aneurysm from the inferior cardiac wall. After the aneurysmectomy, the histological study revealed that the aneurysm wall was made up of 2 different types of walls; the peripheral part was a false-pseudo aneurysm and the central part was a pseudo aneurysm. From the serial MR imaging, it is considered that such an aneurysm is primarily formed from a small discontinuation of the LV wall followed by oozing type rupture. Finally, the ruptured central part of the LV wall, which was covered by the pericardium, formed a pseudo aneurysm and the stretched peripheral area, which contains myocardium, formed a false-pseudo aneurysm afterward and then they extended together. Thus, MR imaging provided the important information for the understanding of the formation process of the pseudo and false pseudo LV aneurysm.

Summary We report a 30-year-old man with severe obesity hypoventilation syndrome (OHVS) complicated by right-sided heart failure. Polysomnography revealed severe obstructive sleep apnea with apnea–hypopnea index (AHI) 70.4/h and gradual decrease in minimum oxygen saturation (SpO 2 ) from 86% before sleep to 36% during sleep. Cardiac output (CO) was suppressed from 3.9L/min before sleep to 2.5L/min during sleep. Noninvasive positive pressure ventilation (NPPV) treatment drastically restored CO to the level before sleep, and improved AHI to 9.4/h and minimum SpO 2 to 87%. NPPV may provide rapid and powerful symptom relief in patients with OHVS complicated with right sided heart failure.

Though complex sleep apnea syndrome (compSAS) has recently been recognized as a new category of sleep apnea syndrome, its prevalence has not been determined, especially in Japan. Hence, we surveyed the prevalence of compSAS in Japan from the data of 4582 patients at eight sleep institutes who were diagnosed with obstructive SAS (apnea-hypopnea index [AHI] > 20). Using Morgenthaler’s criteria we diagnosed as compSAS in 194 patients with a larger proportion of cardiac patients than in all titrated patients. Thus, the prevalence of compSAS in Japan was estimated to be 4.2%. We concluded that compSAS is an interesting condition but is not frequently found in Japan.

Adhesion molecules are key molecules for inflammatory cardiovascular diseases and are known to be up-regulated by inflammatory cytokines. However, the role of adhesion molecules in the cytokine-induced myocardial dysfunction in vivo remains unclear. This role was examined in our novel canine model, in which chronic treatment of the heart with IL-1 beta-bound microspheres (MS), but not control MS, causes sustained myocardial dysfunction in vivo. The expression of P-selectin (mRNA and immunoreactivity) was more prominent in the IL-1 beta group than in the control group (treated with control MS alone) after MS injection. The extent of neutrophil infiltration and myocardial myeloperoxidase (MPO) activity were significantly increased in the IL-1 beta group (P0.01). Pre-treatment with SLeX-OS (a novel oligosaccharide analog of sialyl LewisX) or PB1.3 (a monoclonal antibody to P-selectin) prevented the myocardial dysfunction and significantly suppressed the neutrophil infiltration and the increase in myocardial MPO activity induced by IL-1 beta (P0.01 each). These results indicate that adhesion molecules play an important role in the pathogenesis of the cytokine-induced sustained myocardial dysfunction in dogs in vivo.

Studies in vitro suggested that inflammatory cytokines could cause myocardial dysfunction. However, the detailed mechanism for the cytokine-induced myocardial dysfunction in vivo remains to be examined. We thus examined this point in our new canine model in vivo, in which microspheres with and without IL-1beta were injected into the left main coronary artery. Left ventricular ejection fraction (LVEF) was evaluated by echocardiography for 1 wk. Immediately after the microsphere injection, LVEF decreased to approximately 30% in both groups. While LVEF rapidly normalized in 2 d in the control group, it was markedly impaired in the IL-1beta group even at day 7. Pretreatment with dexamethasone or with aminoguanidine, an inhibitor of inducible nitric oxide synthase, prevented the IL-1beta-induced myocardial dysfunction. Nitrotyrosine concentration, an in vivo marker of the peroxynitrite production by nitric oxide and superoxide anion, was significantly higher in the myocardium of the IL-1beta group than in that of the control group or the group cotreated with dexamethasone or aminoguanidine. There was an inverse linear relationship between myocardial nitrotyrosine concentrations and LVEF. These results indicate that IL-1beta induces sustained myocardial dysfunction in vivo and that nitric oxide produced by inducible nitric oxide synthase and the resultant formation of peroxynitrite are substantially involved in the pathogenesis of the cytokine-induced sustained myocardial dysfunction in vivo.

Background In detecting coronary artery disease (CAD), fusion images obtained by combining myocardial perfusion imaging (MPI) and computed tomography coronary angiography (CTCA) have shown a higher accuracy and clinical usefulness than these modalities used separately or a simple comparison of individual images. However, the clinical use of fusion images has been restricted by the necessity of obtaining images with an integral type device or with devices made by the same manufacturer. Thus, we evaluated the detection of hemodynamically significant CAD by fusion images created with a newly developed general-purpose application that can be used with any type of device. Methods and results In 49 patients, MPI during exercise and at rest and CTCA were obtained separately and combined into fusion images using the new application. As the reference standard, a comparative interpretation of MPI and the conventional coronary arteriography (CAG) was adopted. Hemodynamically significant CAD were diagnosed when MPI showed a reversible perfusion defect in a region with greater than 50% luminal stenosis on CAG. The capability of fusion images to detect CAD was compared with that of CTCA images alone. Fusion images showed a higher ability to detect CAD (sensitivity 80%, specificity 94%, positive predictive value 77%, and negative predictive value 95%) than CTCA alone (77, 77, 46, and 93%, respectively; fusion vs. CTCA: specificity P=0.0002, positive predictive value P=0.0001). Conclusion Fusion images obtained with a general-purpose application were superior to CTCA images alone for detecting hemodynamically significant CAD.

Initiating and weaning procedure of noninvasive positive pressure ventilation (NIPPV) on acute cardiogenic pulmonary edema (ACPE) has been determined empirically, and the total time of its use has been sometimes prolonged unnecessarily. A simple protocol for its use may facilitate initiation and avoids prolongation of the NIPPV treatment. We designed a step-wise protocol for NIPPV use and retrospectively examined the clinical outcome of our protocol for initiation and weaning of NIPPV in 45 patients with ACPE. Almost all patients recovered from respiratory distress successfully. There was no intubation nor complication related to NIPPV. In most of the cases, maximal-end expiratory pressure was less than 7-cm H2O. The mean duration of NIPPV was 19.5±28.0 h and the median duration was 8.0 h (interquartile range=14.0 h). This simple step-wise NIPPV protocol for ACPE can facilitate quick and safe initiation and termination of the treatment.

Several studies have examined the ability of electrocardiography to differentiate between takotsubo cardiomyopathy (TC) and anterior wall acute ST-segment elevation myocardial infarction (AA-STEMI). In those studies, the magnitude of ST-segment elevation was not measured at the J point. The American Heart Association, American College of Cardiology Foundation, and Heart Rhythm Society guidelines recommend that the magnitude of ST-segment elevation should be measured at the J point. Accordingly, the aim of this study was to retrospectively examine whether electrocardiography, using the magnitude of ST-segment elevation measured at the J point, could differentiate 62 patients with TC from 280 with AA-STEMI. Patients with AA-STEMI were divided into following subgroups: 140 with left anterior descending coronary artery occlusions proximal to the first diagonal branch (AA-STEMI-P), 120 with left anterior descending occlusions distal to the first diagonal branch and proximal to the second diagonal branch (AA-STEMI-M), and 20 with left anterior descending occlusions distal to the second diagonal branch (AA-STEMI-D). TC had a much lower prevalence of ST-segment elevation ≥1 mm in lead V(1) (19.4%) compared to AA-STEMI (80.4%, p

The L/N-type calcium channel blocker cilnidipine has unique effects including sympathetic nerve suppression and the balanced vasodilatation of arteries and veins that may alleviate morning hypertension (MHT) or peripheral edema caused by calcium channel antagonists. We used ambulatory blood pressure monitoring (ABPM) and a unique peripheral edema measurement to evaluate the effect of morning and bedtime cilnidipine in patients with MHT. Forty-three patients with MHT (60 ± 12 years) were randomly assigned to a morning or bedtime cilnidipine (10-20 mg/day). MHT was defined as a mean systolic blood pressure (SBP) ≥ 135 mm Hg by ABPM within 2 hours after awaking. After 3 months, greater SBP reductions were observed in the bedtime administration group (versus the morning administration group) at 3:30-6:00 AM (-24 ± 20 mm Hg vs. -10 ± 4 mm Hg; P.05) and at 6:30-9:00 AM (-26 ± 15 mm Hg vs. -14 ± 17 mm Hg; P.05). Although physical examinations showed leg edema in 16% of the patients, quantitative evaluations did not reveal significant volume gains. Cilnidipine had a greater effect on MHT, without causing significant leg edema, when administered at bedtime.

Although studies in vitro have implicated oxygen-derived free radicals as possible mediators of inflammatory cytokine-induced cell injury, the role of the radicals in the cytokine-induced myocardial dysfunction in vivo remains unclear. The present study was designed to address this point in our novel canine model of cytokine-induced myocardial dysfunction in vivo.Studies were performed in mongrel dogs, in which microspheres (MS, 15 microns in diameter) with and without interleukin-1 beta (IL-1 beta) were injected into the left main coronary artery (control and IL-1 beta group). Left ventricular ejection fraction (LVEF) was evaluated by echocardiography for 1 week.Immediately after the intracoronary injection of MS (10(6)/kg), LVEF equally decreased to approximately 30% in both the control and IL-1 beta group. While LVEF rapidly recovered within 2 days in the control group, it remained depressed in the IL-1 beta group until day 7 (p0.0001 vs. control group). Pretreatment with OPC-6535 (an inhibitor of superoxide production) before (2 mg/kg i.v.) and 1 and 2 days after IL-1 beta MS application (1 mg/kg i.v.) prevented the IL-1 beta-induced myocardial dysfunction. Superoxide production in the myocardium was significantly higher in the IL-1 beta group than in the control group at day 2 (p0.01), and OPC-6535 significantly suppressed the IL-1 beta-induced superoxide production (p0.01). An HPLC assay showed that nitrotyrosine, a marker of the formation of peroxynitrite by superoxide anion and nitric oxide, was present in the myocardium treated with IL-1 beta but not in that with control MS. OPC-6535 abolished the IL-1 beta-induced formation of myocardial nitrotyrosine.These results indicate that superoxide anion and the resultant formation of peroxynitrite may substantially be involved in the pathogenesis of the cytokine-induced myocardial dysfunction in dogs in vivo.

Non-invasive positive pressure ventilation (NIPPV) has long been used in the treatment of acute respiratory failure in patients with acute cardiogenic pulmonary edema (ACPE) and it has became a first line therapy for this kind of patients. Continuous positive airway pressure (CPAP) and bi-level positive airway pressure (bi-level PAP) are the two main NIPPV modalities. Though the results of meta-analysis of the difference in the effectiveness of these two modalities showed almost the same efficacy for ACPE patients, we have felt that bi-level PAP produces greater improvement in oxygenation parameters in some of the most severe type of ACPE patients. As the technique of using bi-level PAP is somewhat complex and requires more experience compared with CPAP, we designed a simple step-wise protocol for initiation and weaning of bi-level PAP. We have examined the clinical outcome of 45 patients with ACPE with whom this protocol was used and found that almost all patients successfully recovered from respiratory distress. There was no intubation nor complication related to their bi-level PAP treatment. In most of the cases, maximal end expiratory pressure was less than 7-cm H2O. The median duration was 8.0 hours. This simple step-wise bi-level PAP protocol for ACPE could be used even by co-medical staff safely and could facilitate quick and safe initiation and termination of the treatment.

We report the case of an otherwise healthy 64-year-old female who developed cardiopulmonary arrest after the administration of pilsicainide for treatment of paroxysmal atrial fibrillation. She had had an episode of paroxysmal atrial fibrillation, but no liver dysfunction, renal dysfunction, or echocardiographic abnormality before her admission. On the day of admission and the following day, 50mg of pilsicainide was administered intravenously over 10min (total 100mg). Shortly after the second injection, she developed marked bradycardia and hypotension and eventually fell into a state of pulseless electrical activity. Immediate cardiopulmonary resuscitation was started. Although application of a temporary pacemaker restored her heart rate, echocardiography revealed no left ventricular contraction. We started percutaneous cardiopulmonary support (PCPS) and intra-aortic balloon pumping (IABP). Her cardiac contraction gradually recovered and returned to completely normality 3 days after the onset. The patient was discharged in an ambulatory condition.