Persistent Primitive Hypoglossal Artery with Ipsilateral Symptomatic Carotid Artery Stenosis and Cerebral Aneurysm.

OBJECTIVE: Persistent primitive hypoglossal artery (PPHA) is a rare type of persistent carotid-basilar anastomosis sometimes associated with other vascular lesions. We treated an extremely rare case of PPHA with concomitant ipsilateral symptomatic cervical internal carotid artery (ICA) stenosis and unruptured aneurysm. CASE PRESENTATION: A 67-year-old woman visited our institution with acute onset of diplopia. Magnetic resonance imaging revealed multiple acute infarctions in the right anterior and posterior circulations. Digital subtraction angiography demonstrated the right PPHA concomitant with ipsilateral cervical ICA stenosis and an unruptured ICA aneurysm with maximum diameter of 8 mm. The multiple infarctions were considered to result from artery-to-artery embolism due to microthrombi from the ICA plaque passed along the PPHA, so carotid endarterectomy was performed as the first step with preoperative modified Rankin Scale (mRS) grade 1. During the operation, the patient had impaired ICA perfusion due to internal shunt catheter migration into the PPHA followed by acute infarction in the right hemisphere causing mild left hemiparesis. The patient was transferred to the rehabilitation hospital with mRS grade 3. After 3 months of rehabilitation, the patient recovered to mRS grade 1 and clipping surgery for the unruptured right ICA aneurysm was performed as the second step with uneventful postoperative course. CONCLUSION: The treatment strategy should be carefully considered depending on the specific blood circulation for such cases of PPHA with unique vasculature.

Topological Boundary Modes from Translational Deformations.

Localized states universally appear when a periodic potential is perturbed by defects or terminated at its surface. In this Letter, we theoretically and experimentally demonstrate a mechanism that generates localized states through continuous translational deformations of periodic potentials. We provide a rigorous proof of the emergence of the localized states under the deformations. The mechanism is experimentally verified in microwave photonic crystals. We also demonstrate topological phase windings of reflected waves for translated photonic crystals.

Cerebrospinal fluid leak presented with the C1-C2 sign caused by spinal canal stenosis: a case report.

BACKGROUND: Intracranial hypotension is a disorder characterized by low cerebrospinal fluid (CSF) pressure typically caused by loss of CSF. Although some mechanisms account for the CSF leakage have been elucidated, spinal canal stenosis has never been reported as a pathological cause of intracranial hypotension. C1-C2 sign is a characteristic imaging feature, which indicates CSF collection between the spinous processes of C1 and C2, occasionally observed on magnetic resonance imaging (MRI) in patients with intracranial hypotension. CASE PRESENTATION: A 58-year-old man was presented to our institute with complaints of posterior cervical pain persisting for 3 months, along with numbness and muscle weakness of extremities. A fat suppression T2-weighted image of MRI illustrated fluid collection in the retrospinal region at C1-C2 level, and an 111In-DTPA cisternoscintigram clearly revealed the presence of CSF leakage into the same region. The MRI also showed stenosis in spinal canal at C3/4 level, and a computed tomography (CT) myelogram suggested a blockage at the same level. We gave a diagnosis as intracranial hypotension due to the CSF leakage, which might be caused by the spinal canal stenosis at C3/4 level. Despite 72 h of conservative therapy, a brain CT showed the development of bilateral subdural hematomas. We, therefore, performed burr-hole drainage of the subdural hematoma, blood-patch therapy at C1/2 level, and laminoplasty at C3-4 at the same time. Improvement of symptoms and imaging features which suggested the CSF leak and subdural hematoma were obtained post-operatively. CONCLUSION: The present case suggested the mechanism where the CSF leakage was revealed as fluid collection in the retrospinal region at C1-C2 level. Increased intradural pressure due to the spinal canal stenosis resulted in dural tear. CSF leaked into the epidural space and subsequently to the retrospinal region at C1-C2 level, due to the presence of spinal canal stenosis caudally as well as the vulnerability of the tissue structure in the retrospinal region at C1-C2 level. Thus, our theory supports the mechanisms of previously reported CSF dynamics associated to C1-C2 sign, and also, we suggest spinal canal stenosis as a novel etiology of intracranial hypotension.

Middle Cerebral Artery Occlusion Presenting as Upper Limb Monochorea.

BACKGROUND: Hemichorea is usually caused by a structural lesion in the contralateral basal ganglia or subthalamic nuclei or it develops as a form of a neurologic complication including hyperglycemia. We report a rare case of a patient who developed choreic movement in the right upper extremity associated with a contralateral middle cerebral artery (MCA) occlusion. METHODS: A 76-year-old man presented with chorea in the right upper limb, known as monochorea, which occurred after recovery from losing consciousness while standing. He was found to have idiopathic orthostatic hypotension. His diffusion-weighted magnetic resonance imaging did not show signal changes indicative of acute ischemic lesions. A left carotid artery angiogram showed occlusion of the left MCA. (123)I-N-isopropyl-4-iodoamphetamine single-photon emission computed tomography of the brain showed marked hypoperfusion in the left MCA territory. His cerebrovascular reserve capacity determined using acetazolamide was relatively decreased in this territory. This decrease in cerebrovascular reserve capacity, however, did not require surgical treatment, such as extracranial-intracranial bypass surgery. RESULTS: The recurrence of chorea was not observed after antiplatelet therapy and instruction on how to cope with orthostatic hypotension. CONCLUSIONS: It is considered that transient hemodynamic ischemia in the right basal ganglia-thalamocortical circuits because of the combination of MCA occlusion and hypotension was the underlying cause of the monochorea in this patient.Vascular imaging studies for early identification of occlusion or severe stenosis of cerebral major arteries should be carried out in patients acutely presenting with chorea, even in the absence of other clinical signs.

Emergency care of acute myocardial infarction and the great East Japan earthquake disaster.

BACKGROUND: Although emergency care of acute myocardial infarction (AMI) could theoretically be improved through improved patient delay, this notion remains to be confirmed. Additionally, the influence of large earthquakes on the emergency care of AMI cases remains to be elucidated. The Great East Japan Earthquake (March 11, 2011) has enabled us to address these issues. METHODS AND RESULTS: We analyzed the data from 2008 to 2011 (n=3,937) in the Miyagi AMI Registry Study. In-hospital mortality was significantly lower in 2011 as compared with the previous 3 years (7.3% vs. 10.5%, P<0.05). This improvement was noted especially during the first 2 months after the Earthquake, associated with shorter elapsing time from onset to admission (120 vs. 240min, P<0.001) and higher performance rate of primary percutaneous coronary intervention (PCI) (86.8% vs. 76.2%, P<0.01). Importantly, after the Earthquake, patients with early admission (≤3h from onset) was significantly increased (59.1% vs. 47.0%, P<0.05) and their prognosis became better (7.9% vs. 11.4%, P=0.02), associated with a lower prevalence of heart failure on admission (6.9% vs. 16.2%, P=0.02) and higher performance rate of primary PCI (89.1% vs. 76.4%, P<0.01). CONCLUSIONS: Emergency care of AMI improved soon after the Great East Japan Earthquake compared with ordinary times by the contribution of earlier admission from onset and higher performance rate of primary PCI. (Circ J 2014; 78: 634-643).

Circadian variation of Rho-kinase activity in circulating leukocytes of patients with vasospastic angina.

BACKGROUND: Vasospastic angina (VSA) is known to exhibit circadian variation with an early morning peak. We examined whether Rho-kinase activity in circulating leukocytes, which is a useful biomarker for disease activity assessment of VSA, exhibits circadian variation in patients with VSA. METHODS AND RESULTS: In consecutive 31 VSA patients (M/F 23/8, 57±13 [SD] years) and 18 non-VSA patients (M/F 8/10, 57±14 years), we measured Rho-kinase activity in circulating leukocytes at 6:00, 12:00 and 21:00. We also examined the relationship between the Rho-kinase activity and coronary vasomotor responses during provocation test. Rho-kinase activity was significantly higher in VSA patients than in non-VSA patients at 6:00 (1.17±0.17 vs. 0.92±0.22, P<0.001), and showed a significant circadian variation with a peak at 6:00 (1.00±0.15 at 21:00, 1.17±0.17 at 6:00 and 1.12±0.22 at 12:00, P<0.001) in VSA patients, whereas no such variation was noted in non-VSA patients. Importantly, Rho-kinase activity at spasm provocation test was significantly correlated with basal coronary tone defined by vasodilating responses to intracoronary nitrate (r=0.40, P<0.05) and coronary vasoconstricting responses to acetylcholine (r=0.44, P<0.05) in VSA patients. Furthermore, their Rho-kinase activity at 6:00 was positively correlated with nocturnal parasympathetic activity as evaluated by heart rate variability in Holter monitoring (r=0.48, P<0.05). CONCLUSIONS: Rho-kinase activity exhibits distinct circadian variation associated with alterations in coronary vasomotor responses and autonomic activity in VSA patients.

Plasma cyclophilin A is a novel biomarker for coronary artery disease.

BACKGROUND: Oxidative stress induces secretion of cyclophilin A (CyPA) from vascular smooth muscle cells and it plays a crucial role in the pathogenesis of atherosclerosis in mice. Therefore, we tested our hypothesis that plasma CyPA levels are increased in patients with coronary artery diseases (CAD). METHODS AND RESULTS: In 320 consecutive patients undergoing coronary angiography, we examined the relationship between plasma CyPA levels and the severity of CAD. We measured plasma CyPA by an immunoassay based on the sandwich technique. Plasma CyPA levels were significantly higher in patients with significant coronary stenosis compared to those without it (P<0.001). A positive correlation was noted between plasma CyPA levels and significant coronary stenosis. The average number of stenotic coronary arteries and the need for coronary intervention were significantly increased in the quartiles of higher CyPA levels (both P<0.001). Indeed, the plasma CyPA level significantly correlated with the presence of CAD (adjusted odds ratio for CAD, 6.20; 95% confidence interval, 3.14-12.27; P<0.001). Interestingly, plasma levels of CyPA increased according to the number of atherosclerotic risk factors, all of which induce oxidative stress. Furthermore, plasma levels of CyPA significantly reduced after medical treatment of risk factors. Finally, CyPA was strongly expressed in coronary atherosclerotic plaque in patients with myocardial infarction. CONCLUSIONS: Plasma CyPA level is a novel biomarker for oxidative stress and CAD in humans.

Long-term treatment with nifedipine suppresses coronary hyperconstricting responses and inflammatory changes induced by paclitaxel-eluting stent in pigs in vivo: possible involvement of Rho-kinase pathway.

AIMS: Accumulating evidence indicates that coronary vasoconstricting responses are enhanced at the edges of coronary segment implanted with a drug-eluting stent (DES) compared with a bare-metal stent (BMS) in humans. We have recently demonstrated that Rho-kinase pathway plays an important role in DES-induced coronary hyperconstricting responses associated with inflammatory changes in pigs in vivo. This study examined whether long-term treatment with calcium channel blocker suppresses DES-induced coronary hyperconstricting responses in pigs in vivo. METHODS AND RESULTS: Paclitaxel-eluting stent (PES) and a BMS were randomly implanted in the left coronary arteries in male domestic pigs with and without long-acting nifedipine (NIF, 4 mg/kg/day) for 4 weeks (n = 7 each). Coronary vasomotion was evaluated by quantitative coronary angiography at least 24 h after withdrawal of NIF to avoid its direct effects on coronary vasomotion. In the control group (without NIF), coronary vasoconstricting responses to serotonin (10 and 100 µg/kg, i.c.) were significantly enhanced at the PES site compared with the BMS site (P = 0.009), which were abolished by hydroxyfasudil (90 and 300 µg/kg, i.c.), a selective Rho-kinase inhibitor. The PES-induced vasoconstricting responses were significantly inhibited in the NIF group (P = 0.019). Histological examination showed that inflammatory cell accumulation and microthrombus formation were enhanced at the PES site compared with the BMS site (P < 0.05), both of which were significantly suppressed by NIF associated with reduced Rho-kinase expression and activity (P < 0.05). CONCLUSION: These results indicate that long-term treatment with NIF suppresses PES-induced coronary abnormalities partly through Rho-kinase pathway inhibition in vivo.

Urbanization, life style changes and the incidence/in-hospital mortality of acute myocardial infarction in Japan: report from the MIYAGI-AMI Registry Study.

BACKGROUND: It remains to be examined whether urbanization and lifestyle changes are associated with the incidence and mortality from acute myocardial infarction (AMI) in Japan. METHODS AND RESULTS: A total of 19,921 AMI patients (male/female 14,290/5,631) registered by the MIYAGI-AMI Registry Study from 1988 to 2009 were divided into 2 groups according to their residences; inside (urban area, n=7,316) and outside (rural area, n=11,402) of Sendai City. From 1988 to 2009, the incidence of AMI (/100,000 persons/year) increased more rapidly in the rural area (24.2 to 51.4) than in the urban area (31.3 to 40.8) (P<0.001), with rapid aging in both areas. Moreover, from 1998 to 2009, the age-adjusted incidence of AMI in young (<44 years) and middle-aged (45-64 years) male patients (both P<0.05) in the rural area increased significantly, along with a markedly increased prevalence of dyslipidemia (P<0.001). Although in-hospital mortality from AMI decreased in both areas over the last 20 years (both P<0.001), it remained relatively higher in female than in male patients and was associated with higher age of the onset, longer elapsing time for admission and lower prevalence of primary coronary intervention in female patients in both areas. CONCLUSIONS: These results demonstrate that urbanization and lifestyle changes have been associated with the incidence and mortality from AMI, although sex differences still remain to be improved.

Involvement of rho-kinase activation in the pathogenesis of coronary hyperconstricting responses induced by drug-eluting stents in patients with coronary artery disease.

BACKGROUND: Activation of Rho-kinase plays a central role in the pathogenesis of drug-eluting stents (DES)-induced coronary hyperconstricting responses in pigs in vivo has been previously demonstrated. In the present study, Rho-kinase activation involved in those responses in patients with coronary artery disease (CAD) is examined. METHODS AND RESULTS: In 24 patients with CAD who underwent coronary intervention with either DES or bare-metal stents (BMS), coronary vasomotor responses to intracoronary acetylcholine (ACh) before and after intracoronary pre-treatment with a Rho-kinase inhibitor, fasudil was examined. Coronary vasomotor responses by quantitative coronary angiography (QCA) and coronary vascular structure by optical coherence tomography (OCT) was evaluated. QCA showed that the coronary vasoconstricting responses to ACh were significantly enhanced in the DES group compared with the BMS group both at the proximal and the distal segments adjacent to the stents (proximal: BMS -13.0±10.7% vs. DES -25.4±14.3%, P=0.036; distal: BMS -24.4±12.2% vs. DES -43.8±14.7%, P=0.003). Importantly, fasudil markedly attenuated the enhanced vasoconstricting responses to ACh in the DES group (proximal 10.2±11.7%, distal 14.4±10.5% vs. before fasudil, both P<0.01). In the OCT imaging analysis, there was no significant correlation between intimal thickness and coronary vasoconstriction to ACh. CONCLUSIONS: These results indicate that Rho-kinase activation is substantially involved in the pathogenesis of the DES-induced coronary hyperconstricting responses in patients with CAD, suggesting the therapeutic importance of Rho-kinase pathway.

Enhanced Rho-kinase activity in patients with vasospastic angina after the Great East Japan Earthquake.

BACKGROUND: It remains unclear whether disease activity of vasospastic angina (VSA) is altered during a disaster. METHODS AND RESULTS: Before and after the Great East Japan Earthquake, we examined Rho-kinase activity in circulating neutrophils of 11 VSA patients and their mental stress with the post-traumatic stress disorder (PTSD) questionnaire. Rho-kinase activity was significantly increased at 6 months after the Earthquake, and was returned to baseline level at 12 months. Importantly, percent change in Rho-kinase activity was significantly correlated with the PTSD score. CONCLUSIONS: These results indicate that the Rho-kinase activity of VSA patients was transiently enhanced associated with disaster-related mental stress.

Eicosapentaenoic acid reduces ischemic ventricular fibrillation via altering monophasic action potential in pigs.

Although high intake of n-3 fatty acids is associated with reduced mortality of patients with ischemic heart disease, especially reduction in sudden cardiac death (SCD), the detailed mechanisms remain to be elucidated. Thus, the present study was designed to examine whether long-term treatment with eicosapentaenoic acid (EPA), a major component of n-3 fatty acids, reduces ischemia-induced ventricular fibrillation (VF) in pigs in vivo, and if so, what molecular mechanisms are involved. Male pigs were treated with either a control chow (control group) or a control chow plus EPA (600 mg/kg/day, PO, EPA group) for 3 weeks and were subjected to myocardial ischemia for 90 min (n=8 each) with measurement of the monophasic action potential (MAP), as a marker of ventricular electrophysiological activities. The EPA treatment significantly attenuated the occurrence of VF (control 5.1±1.7 vs. EPA 1.5±0.8 times/animal, P<0.05) and markedly reduced the mortality (control 50% vs. EPA 0%, P<0.05), with the attenuation of MAP duration shortening during ischemia (control -28.1±3.0% vs. EPA -18.2±1.4%, P<0.05). These beneficial effects of EPA were abolished by pre-treatment with cromakalim, a K(ATP) channel opener (0.3 µg/kg/min, IC). Furthermore, EPA significantly inhibited the mRNA and protein expression of Kir6.2, a major component of sarcolemmal K(ATP) channels, in both the ischemic region and non-ischemic regions. These results indicate that long-term treatment with EPA reduces ischemia-induced VF and SCD in pigs in vivo, for which attenuation of MAP duration shortening may be involved.

Long-term treatment with eicosapentaenoic acid ameliorates myocardial ischemia-reperfusion injury in pigs in vivo. -Involvement of Rho-kinase pathway inhibition-.

BACKGROUND: Eicosapentaenoic acid (EPA), the major n-3 fatty acid in fish oil, exerts cardioprotective effects against ischemic heart disease; however, the detailed mechanisms remain to be elucidated. Rho-kinase plays an important role in the pathogenesis of cardiovascular diseases including ischemia-reperfusion (I/R) injury. Thus, the hypothesis that long-term EPA treatment ameliorates myocardial I/R injury through Rho-kinase pathway inhibition in pigs in vivo was investigated. METHODS AND RESULTS: Male pigs were treated with either a control chow or EPA (600·mg·kg⁻¹·day⁻¹) for 3 weeks (n=8 each) and were subjected to myocardial ischemia by 90-min occlusion of the left circumflex coronary artery and subsequent 60-min reperfusion. The EPA group had an increased EPA level in red blood cells (4.4 ± 0.3mol%). The EPA treatment significantly ameliorated myocardial I/R injury, including regional wall motion abnormality (EPA 5.3 ± 3.6 vs. control 35.1 ± 3.8 unit, P<0.0001), left ventricular ejection fraction (EPA 43 ± 9% vs. control 32 ± 7%, P<0.05), occurrence of ventricular arrhythmias (EPA 181 ± 73 vs. control 389 ± 51 events, P<0.0001) and histological accumulation of inflammatory cells (P<0.01). Importantly, the EPA treatment significantly inhibited myocardial Rho-kinase activity (assessed by the extent of the myosin-binding subunit phosphorylation) (EPA 0.47 ± 0.11 vs. control 0.77 ± 0.14, P<0.05) and preserved myocardial eNOS activity (EPA 0.56 ± 0.13 vs. control 0.23 ± 0.07, P<0.01) with a significant correlation noted between them. CONCLUSIONS: Long-term treatment with EPA ameliorates I/R injury partly through Rho-kinase pathway inhibition in vivo.

Pulmonary Tumor Thrombotic Microangiopathy with Administration of Pulmonary Vasodilator Resulting in Clinical Improvement Prior to Final Diagnosis.

BACKGROUND The pathophysiology of pulmonary tumor thrombotic microangiopathy (PTTM) was recently revealed by autopsy. Considered rare, we suggest that this fatal disease is not rare, but has not been diagnosed pre-mortem. Some patients with pulmonary thromboembolism with unknown thrombus source or with sudden death have been treated for malignant carcinoma. We report a patient with PTTM who was successfully rescued acutely by treatment with soluble guanylate cyclase (sGC), resulting in appropriate palliative care. CASE REPORT An 80-year-old Japanese woman was transferred to our emergency room for severe dyspnea owing to type I respiratory failure. Her clinical findings indicated pulmonary thromboembolism, but we found no thrombus in either the pulmonary artery or inferior vena cava. However, we incidentally found gallbladder cancer with peritoneal metastases. These findings raised the suspicion of PTTM. We began concurrent sGC and direct oral anticoagulant (DOAC) on the assumption that PTTM had occurred, while performing peripheral pulmonary artery sampling for cytology, and pulmonary perfusion scintigraphy. Cytology revealed several aplastic cells; consequently, we finally diagnosed PTTM. Because she did not wish to undergo examination and active treatment for carcinoma, we initiated palliative care while continuing sGC. She was able to spend time with her family for more than 100 days, without dyspnea. CONCLUSIONS We must recognize PTTM, which is a lesser-known disease, and introduce diagnostic therapy with a pulmonary vasodilator, such as sGC, immediately, when we suspect PTTM, leading to appropriate clinical care.

Double-blind and placebo-controlled study of the effectiveness and safety of extracorporeal cardiac shock wave therapy for severe angina pectoris.

BACKGROUND: Low-energy shock wave (SW) therapy has improved myocardial ischemia in both a porcine model and in patients with severe angina pectoris. METHODS AND RESULTS: To further confirm the effectiveness and safety of SW therapy, 8 patients with severe angina pectoris were treated with SW therapy in a double-blind, placebo-controlled and cross-over manner. SW therapy, but not placebo, significantly improved chest pain symptoms and cardiac function without any complications or adverse effects. CONCLUSIONS: Extracorporeal cardiac SW therapy is an effective, safe and non-invasive therapeutic option for severe angina pectoris.

[Surgery for the chest wall tuberculous abscess; report of a case].

The patient was a 70-year-old woman who visited our hospital due to right chest pain. Chest computed tomography (CT) and magnetic resonance imaging (MRI) revealed an abscess in the chest wall which was diagnosed as tuberculous abscess by a bacterial examination of needle aspiration. In spite of anti-tuberculosis chemotherapy, the abscess was ruptured on day 15 after starting treatment, and a radical resection of the abscess was performed after 10-days conservative treatment. Skin over the abscess and a part of right 7th and 8th rib were also resected. Postoperative anti-tuberculosis chemotherapy was added and no relapse was seen for 40 months postsurgery.

Important role of erythropoietin receptor to promote VEGF expression and angiogenesis in peripheral ischemia in mice.

We have recently demonstrated that endogenous erythropoietin (Epo)/Epo receptor (EpoR) system plays an important protective role in hypoxia-induced pulmonary hypertension. However, it remains to be examined whether vascular EpoR system contributes to angiogenesis in response to ischemia. We examined angiogenesis in EpoR(-/-)-rescued mice that lack EpoR in most organs including cardiovascular system except erythroid-lineage cells. Two weeks after femoral artery ligation, blood flow recovery, activation of VEGF/VEGF receptor system, and mobilization of endothelial progenitor cells were all impaired in EpoR(-/-)-rescued mice as compared with wild-type (WT) mice. Bone marrow (BM) transplantation with WT-BM cells in EpoR(-/-)-rescued mice partially but significantly improved blood flow recovery after hindlimb ischemia. The extent of VEGF upregulation and the number of BM-derived cells in ischemic tissue were significantly less in EpoR(-/-)-rescued mice compared with WT mice even after BM reconstitution with WT-BM cells. Similarly, the recovery of blood flow was significantly impaired in recipient EpoR(-/-)-rescued mice that had been transplanted with WT-BM or EpoR(-/-)-rescued-BM as compared with recipient WT mice. Furthermore, the Matrigel implantation assay and aortic ring assay showed that microvessel growth in vitro was significantly reduced in EpoR(-/-)-rescued mice as compared with WT mice. These results indicate that vascular EpoR system also plays an important role in angiogenesis in response to hindlimb ischemia through upregulation of VEGF/VEGF receptor system, both directly by enhancing neovascularization and indirectly by recruiting endothelial progenitor cells and BM-derived proangiogenic cells.

Reduced perioperative immune response in video-assisted versus open surgery in a rat model.

PURPOSE: To establish the best technique for thoracoscopic pneumonectomy in the rat and to analyze the differences in perioperative immune response between open and video-assisted thoracoscopic surgery (VATS) in a rat model. METHODS: The four experimental groups studied were as follows: VATS pneumonectomy, open pneumonectomy, thoracoscopic observation, and open observation. We measured the immunocyte counts and serum cytokine levels postoperatively in each group. RESULTS: The CD3+, CD4+, and CD8+ lymphocyte counts were decreased significantly 12-24 h postoperatively in all groups. Immunosuppression peaked later in the open approach groups than in the VATS groups. The interleukin-6 level was significantly higher in the open approach groups than in the VATS groups. CONCLUSIONS: From the viewpoint of immunity, in this rat model VATS was less invasive than open surgery, and open surgery caused greater immunosuppression than VATS, irrespective of organ resection.

Influence of atrial fibrillation on cardiac prognosis in chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD), a known risk factor for the development of congestive heart failure (CHF), was recently shown to predict the prevalence of atrial fibrillation (AF). Here, we explore the influence of AF on cardiac prognosis in COPD patients. METHODS: A total of 339 consecutive patients who underwent spirometry from 2010 to 2013 for various reasons were retrospectively examined. Based on the diagnostic criteria, patients were stratified into COPD and non-COPD groups, which were both further divided into those with AF (chronic AF or paroxysmal AF) or sinus rhythm (SR) based on previous electrocardiography results. Significances of differences in cardiac events were assessed by the chi-square test. Multivariate logistic regression analyses and Cox proportional hazard models were applied to evaluate the influence of AF on cardiac events. RESULTS: Of the 339 patients, 190 were diagnosed with COPD, with 42 of these were having AF. During the mean follow-up period of 7.4 ± 0.8 years, CHF developed more frequently in COPD patients with AF than in COPD patients without AF [50% vs 7%; odds ratio (OR) 12.4, 95% confidence interval (CI): 5.25-29.49, p < 0.05]. AF was an independent predictor of CHF development (OR 20.4, 95% CI: 6.55-79.80, p < 0.05) and cardiac mortality (OR 2.8, 95% CI: 1.79-4.72, p < 0.05). Moreover, positive correlations were found between the severity of pulmonary obstruction with AF and CHF development (R = 0.69, p < 0.05), as well as cardiac mortality (R = 0.78.p < 0.05). CONCLUSIONS: These results suggest that AF may be strongly associated with cardiac mortality and CHF in COPD patients.

Influence of cognitive impairment on cardiac mortality after percutaneous coronary intervention in very elderly patients: a retrospective observational study.

BACKGROUND: Cognitive impairment (CI) increases cardiac mortality among very elderly patients. Percutaneous coronary intervention (PCI) for ischemic heart disease (IHD) patients is considered a favorable strategy for decreasing cardiac mortality. Here, we investigated the influence of CI on cardiac mortality after PCI in very elderly patients. METHODS: We performed a retrospective observational analysis of patients who received PCI between 2012 and 2014 at the South Miyagi Medical Center, Japan. IHD patients over 80 years old who underwent the Mini-Mental State Examination for CI screening during hospitalization and/or who had been diagnosed with CI were included. Participants were divided into CI and non-CI groups, and cardiac mortality and incidence of adverse cardiac events in a 3-year follow-up period were compared between groups. Statistical analyses were performed using the t-test, χ2 test, and multivariable Cox regression analysis, with major comorbid illness and conventional cardiac risk factors as confounders. RESULTS: Of 565 patients, 95 were included (41 CI, 54 non-CI). Cardiac mortality during the follow-up period was significantly higher in the CI group (36%) compared with the non-CI group (13%) (OR = 4.3, 95% CI: 1.56-11.82, P < 0.05). CI was an independent cardiac prognostic factor after PCI and, for CI patients, living only with a CI partner was an independent predictor of cardiac death within three years. CONCLUSIONS: CI significantly affected cardiac prognosis after PCI in very elderly patients, particularly those living with a CI partner. To improve patients' prognoses, social background should be considered alongside conventional medical measures.