Isolated trochlea osteochondral fracture of the distal humerus in a 6-year-old patient surgically fixed using biodegradable pins: A case study with over 3 years of follow-up.

Isolated humeral trochlea fracture, particularly in skeletally immature children, is extremely rare. The exact mechanism of this injury remains unknown because the humeral trochlea is embraced within the olecranon fossa without any muscular or ligamentous attachment. We report the treatment of a 6-year-old boy who sustained an isolated trochlea osteochondral fracture when he fell with his elbow in a flexed position while skateboarding. The patient had a history of lateral condyle fracture of the ipsilateral humerus one year previously. At the diagnosis, computed tomography (CT) revealed a small bony fragment displaced anteromedially from the superior border of the trochlea with lifting of its lateral border. Ultrasonography confirmed instability of the fractured segment. At the time of surgery, the anterior trochlea surface fracture formed a hinged fracture line on its proximal and medial border. The fracture was anatomically reduced and fixed using biodegradable pins. Postoperatively, the involved elbow showed a sufficient functional recovery to a normal level without complications during 3 years of observation, although the biodegradable pins remained radiographically in place with partial degradation. The laterally opened avulsed fragment on primary CT clearly depicted the mechanism of injury: the impact entered from the lateral side of the elbow and progressed from the longitudinal ridge of the coronoid process onto the sulcus of the trochlea to shear off the anteromedial portion of the trochlea in a medial direction. The use of biodegradable pins for fixing a trochlea fracture in a skeletally immature patient provided favorable fracture healing; however, close observation is necessary until the completion of skeletal growth because of the lack of sufficient information on the long-term prognosis of trochlea fracture, especially when treated using biodegradable implants.

Grading of Left Ventricular Diastolic Dysfunction with Preserved Systolic Function by the 2016 American Society of Echocardiography/European Association of Cardiovascular Imaging Recommendations Contributes to Predicting Cardiovascular Events in Hemodialysis Patients.

BACKGROUND: Left ventricular diastolic dysfunction (LVDD) causes heart failure with a preserved left ventricular ejection fraction (LVEF) in the general population. OBJECTIVE: To examine the relationships between the LVDD grades of the 2016 American Society of Echocardiography/European Association of Cardiovascular Imaging (ASE/EACVI) recommendations and several arteriosclerotic parameters and major cardiovascular events (MACE) in hemodialysis patients with preserved LVEF. METHOD: Sixty-three prevalent hemodialysis patients (median age [interquartile range], 69 [64-75] years, 31.7% female) with normal systolic function (LVEF > 50%) were enrolled. LVDD evaluated by echocardiography at baseline was divided into three groups according to ASE/EACVI recommendations (normal diastolic function [ND], n = 24; intermediate, n = 19; diastolic dysfunction [DD], n = 20). All patients underwent analyses of several arteriosclerotic parameters (carotid intima-media thickness [CIMT], plaque score [PS], ankle brachial index [ABI], and brachial-ankle pulse wave velocity [baPWV]). The presence or absence of postdialysis orthostatic hypotension was assessed in each dialysis session. MACE during the 1-year follow-up period was obtained from medical records. Kaplan-Meier and Cox's regression analyses were used to investigate the relationship between LVDD grades and MACE. RESULTS: Postdialysis orthostatic hypotension and PS, but not CIMT, ABI, or baPWV, increased proportionally with LVDD grades. Eleven patients developed MACE, including 2 cardiovascular deaths. The Kaplan-Meier analysis showed that MACE frequently occurred in the DD grade (p = 0.002 by the log-rank test). Cox's regression analysis adjusted for potential confounders (age, sex, diabetes, systolic blood pressure, and body mass index) revealed that the DD grade was associated with MACE when the ND grade was set as a reference. CONCLUSIONS: In maintenance hemodialysis patients with normal ventricular systolic function, a classification of LVDD by the 2016 ASE/EACVI recommendations may be a useful tool for predicting cardiovascular events.

Risk Factor Analysis for C5 Palsy after Double-Door Laminoplasty for Cervical Spondylotic Myelopathy.

STUDY DESIGN: A retrospective comparative study. PURPOSE: To clarify the risk factors related to the development of postoperative C5 palsy through radiological studies after cervical double-door laminoplasty (DDL). OVERVIEW OF LITERATURE: Although postoperative C5 palsy is generally considered to be the result of damage to the nerve root or segmental spinal cord, the associated pathology remains controversial. METHODS: A consecutive case series of 47 patients with cervical spondylotic myelopathy treated by DDL at our institution between April 2008 and April 2015 were reviewed. Postoperative C5 palsy occurred in 5 of 47 cases after DDL. We investigated 9 radiologic factors that have been reported to be risk factors for C5 palsy in various studies, and statistically examined these between the two groups of palsy and the non-palsy patients. RESULTS: We found a significant difference between patients with and without postoperative C5 palsy with regards to the posterior shift of spinal cord at C4/5 (p=0.008). The logistic regression analyses revealed posterior shift of the spinal cord at C4/5 (odds ratio, 12.066; p=0.029; 95% confidence interval, 1.295-112.378). For the other radiologic factors, there were no statistically significant differences between the two groups. CONCLUSIONS: In the present study, we showed a significant difference in the posterior shift of the spinal cord at C4/5 between the palsy and the non-palsy groups, indicating that the "tethering phenomenon" was likely a greater risk factor for postoperative C5 palsy.

Cervical myelopathy caused by disc herniation at the segment of existing osteochondroma in a patient with hereditary multiple exostoses.

Hereditary multiple exostoses (HME) is a benign hereditary disorder characterized by multiple osteochondromas. Osteochondroma appears occasionally in the spinal column as a part of HME. A 37-year-old man presented with a history of HME and cervical compressive myelopathy caused by intraspinal osteochondroma arising from the lamina of the C5 and disc herniation at the C5-6. He was treated by open-door laminoplasty at the C5 and C6 with excision of the tumor. The neurological symptoms were immediately relieved after surgery. Magnetic resonance images demonstrated a sufficient decompression of the spinal cord with a spontaneous regression of the herniated disc at one year after surgery. There was no recurrence of the tumor and no appearance of kyphosis and segmental instability of the cervical spine on postoperative imaging studies for three years after surgery. The patient could be successfully treated by laminoplasty with excision of the tumor and without removal of the herniated disc.

Long-term follow-up of a case of aneurysmal bone cyst in the lumbar spine.

BACKGROUND CONTEXT: Aneurysmal bone cyst (ABC) in the spine is relatively rare, so little is known about the natural history of the disease. PURPOSE: The purpose of this study was to describe a spinal ABC that was followed for an extended period from lesion enlargement to spontaneous regression. STUDY DESIGN: Case report. METHODS: A 63-year-old woman had a 1-year-long history of mild low back and bilateral leg pain without any significant neurologic deficits caused by lumbar spinal stenosis. At her first visit to our hospital, magnetic resonance imaging (MRI) showed a small cystic lesion on the left side of the L5 vertebral body. The patient's clinical symptom progression and MRI and computed tomography evaluations were reported for >13 years. RESULTS: After 6 years, the cystic lesion enlarged significantly and extended into the left pedicle and transverse process of the L5 vertebra. The lesion was diagnosed as an ABC based on multilocular cysts with fluid-fluid levels on MRI and bony septations on computed tomography. Thirteen years after the first visit, the lesion regressed spontaneously without a clear reason, such as biopsy or fracture, and most of the lesion was replaced by fatty marrow. The patient's symptoms stabilized without neurologic deterioration during the follow-up period. CONCLUSIONS: Although spinal ABC is an expandable cystic lesion, we should consider that such a lesion in an elderly patient could spontaneously regress.

Translaminar microendoscopic herniotomy for cranially migrated lumbar disc herniations encroaching on the exiting nerve root in the preforaminal and foraminal zones.

STUDY DESIGN: Case series. PURPOSE: The aim of this study was to describe translaminar microendoscopic herniotomy (TL-MEH) for cranially migrated lumbar disc herniations encroaching on the exiting nerve root in the preforaminal and foraminal zones and to report preliminary results of the procedure. OVERVIEW OF LITERATURE: Conventional interlaminar approaches for preforaminal and foraminal lumbar disc herniations result in extensive removal of the lamina and facet joint to remove disc fragments safely. More destructive approaches increase the risk of postoperative segmental instability. METHODS: TL-MEH is a minimally invasive procedure for herniotomy via the translaminar approach using a microendoscopic technique. TL-MEH was performed in seven patients with a cranially migrated lumbar disc herniation encroaching on the exiting nerve root. The disc fragments were located in the preforaminal zone in four patients, and in the preforaminal and foraminal zones in three. RESULTS: All patients experienced immediate relief from symptoms after surgery and satisfactory results at the final follow-up. Surgical complications, such as a dural tear, nerve injury, and surgical site infection, were not investigated. CONCLUSIONS: TL-MEH seemed to be an effective and safe alternative minimally invasive surgical option for patients with a cranially migrated lumbar disc herniation encroaching the exiting nerve root in the preforaminal and foraminal zones.

Cardiogenic shock due to left ventricular outflow obstruction and complete atrioventricular block in a patient with hypertrophic cardiomyopathy with acute myocarditis.

A 67-year-old woman was referred to our hospital with a sudden syncopal attack. She suffered from cardiogenic shock due to left ventricular (LV) outflow stenosis with simultaneous complete atrioventricular (AV) block. An endomyocardial biopsy of the left ventricle demonstrated myocardial disarray and myocardial fibrous and edematous tissue with infiltration of mononuclear cells. Cardiac magnetic resonance imaging (cMRI) detected a damaged septal area that was likely associated with the conduction disturbance. The diagnosis was hypertrophic cardiomyopathy accompanied by acute myocarditis. Although the LV outflow stenosis was transient, the complete AV block was persistent, thus requiring permanent pacemaker implantation.

Protective human leucocyte antigen haplotype, HLA-DRB1*01-B*14, against chronic Chagas disease in Bolivia.

BACKGROUND: Chagas disease, caused by the flagellate parasite Trypanosoma cruzi affects 8-10 million people in Latin America. The mechanisms that underlie the development of complications of chronic Chagas disease, characterized primarily by pathology of the heart and digestive system, are not currently understood. To identify possible host genetic factors that may influence the clinical course of Chagas disease, Human Leucocyte Antigen (HLA) regional gene polymorphism was analyzed in patients presenting with differing clinical symptoms. METHODOLOGY: Two hundred and twenty nine chronic Chagas disease patients in Santa Cruz, Bolivia, were examined by serological tests, electrocardiogram (ECG), and Barium enema colon X-ray. 31.4% of the examinees showed ECG alterations, 15.7% megacolon and 58.1% showed neither of them. A further 62 seropositive megacolon patients who had undergone colonectomy due to acute abdomen were recruited. We analyzed their HLA genetic polymorphisms (HLA-A, HLA-B, MICA, MICB, DRB1 and TNF-alpha promoter region) mainly through Sequence based and LABType SSO typing test using LUMINEX Technology. PRINCIPAL FINDINGS: The frequencies of HLA-DRB1*01 and HLA-B*14:02 were significantly lower in patients suffering from megacolon as well as in those with ECG alteration and/or megacolon compared with a group of patients with indeterminate symptoms. The DRB1*0102, B*1402 and MICA*011 alleles were in strong Linkage Disequilibrium (LD), and the HLA-DRB1*01-B*14-MICA*011 haplotype was associated with resistance against chronic Chagas disease. CONCLUSIONS: This is the first report of HLA haplotype association with resistance to chronic Chagas disease.

Lineage analysis of circulating Trypanosoma cruzi parasites and their association with clinical forms of Chagas disease in Bolivia.

BACKGROUND: The causative agent of Chagas disease, Trypanosoma cruzi, is divided into 6 Discrete Typing Units (DTU): Tc I, IIa, IIb, IIc, IId and IIe. In order to assess the relative pathogenicities of different DTUs, blood samples from three different clinical groups of chronic Chagas disease patients (indeterminate, cardiac, megacolon) from Bolivia were analyzed for their circulating parasites lineages using minicircle kinetoplast DNA polymorphism. METHODS AND FINDINGS: Between 2000 and 2007, patients sent to the Centro Nacional de Enfermedades Tropicales for diagnosis of Chagas from clinics and hospitals in Santa Cruz, Bolivia, were assessed by serology, cardiology and gastro-intestinal examinations. Additionally, patients who underwent colonectomies due to Chagasic magacolon at the Hospital Universitario Japonés were also included. A total of 306 chronic Chagas patients were defined by their clinical types (81 with cardiopathy, 150 without cardiopathy, 100 with megacolon, 144 without megacolon, 164 with cardiopathy or megacolon, 73 indeterminate and 17 cases with both cardiopathy and megacolon). DNA was extracted from 10 ml of peripheral venous blood for PCR analysis. The kinetoplast minicircle DNA (kDNA) was amplified from 196 out of 306 samples (64.1%), of which 104 (53.3%) were Tc IId, 4 (2.0%) Tc I, 7 (3.6%) Tc IIb, 1 (0.5%) Tc IIe, 26 (13.3%) Tc I/IId, 1 (0.5%) Tc I/IIb/IId, 2 (1.0%) Tc IIb/d and 51 (25.9%) were unidentified. Of the 133 Tc IId samples, three different kDNA hypervariable region patterns were detected; Mn (49.6%), TPK like (48.9%) and Bug-like (1.5%). There was no significant association between Tc types and clinical manifestations of disease. CONCLUSIONS: None of the identified lineages or sublineages was significantly associated with any particular clinical manifestations in the chronic Chagas patients in Bolivia.

Ventricular fibrillation in a patient with prominent j wave in the inferior and lateral electrocardiographic leads after gastrostomy.

We describe the case of a 39-year-old man who experienced a ventricular fibrillation storm related to a prominent J wave in the inferior and lateral electrocardiographic leads on the day after gastrostomy. The J wave slowly decreased after amiodarone therapy (400 mg/day) was started, and ventricular fibrillation disappeared.

The influence of beta-adrenergic agonists and antagonists on T-wave alternans in patients with and without ventricular tachyarrhythmia.

BACKGROUND: T-wave alternans (TWA) is an important noninvasive measurement of ventricular tachyarrhythmia (VT) and is known to be influenced by the sympathetic nervous system. We examined the correlation between TWA measurement and the sympathetic nervous system in patients with and without VT. METHODS AND RESULTS: Thirty-five patients (28 men, 7 women; mean age, 59 +/- 15 years) with tachyarrhythmia were assigned to two groups: VT group (n = 15) and supraventricular tachyarrhythmia (SVT) group (n = 20). Alternans voltage in lead vector magnitude (eVM) was measured during atrial pacing (90, 110 beats/min (bpm)). After eVM was measured at baseline, propranolol was administered, and eVM was measured again. In a subset of 18 patients (10 with VT and 8 with SVT), isoproterenol was administered prior to propranolol infusion. After propranolol infusion, eVM of both the VT and the SVT groups decreased significantly compared to baseline. The changes in absolute value of eVM at 110 bpm after propranolol infusion were greater in the VT group than in the SVT group (-1.3 +/- 0.8 microV vs -0.5 +/- 0.8 microV, P < 0.05). The eVM values of both the VT and the SVT groups increased after administration of isoproterenol compared to the baseline value. The changes in absolute value and percentile of eVM after isoproterenol infusion were smaller in the VT group than in the SVT group (2.0 +/- 1.8 microV vs 3.9 +/- 3.5 microV, P < 0.05; 21 +/- 18% vs 48 +/- 36%, P < 0.05). CONCLUSIONS: The sympathetic nervous system has an influence over microvolt-level TWA. Administration of a beta-adrenergic antagonist caused a significant decrease in TWA, particularly in the VT group. This may partially explain the mechanism by which adrenergic antagonists inhibit VTs.

Efectos del envejecimiento sobre los períodos refractarios y la conducción auricular en pacientes con fibrilación auricular paroxística idiopática obtenidos mediante estimulación auricular programada / The effects of aging on the refractoriness and conduction of the atrium in patients with lone paroxysmal atrial fibrllation revealed with programmed atrial stimulation

El propósito de este estudio es determinar si el envejecimiento influye sobre la vulnerabilidad auricular inducida por la estimulación auricular programada en pacientes con fibrilación auricular paroxística idiopática. La investigación incluyó a 148 pacientes, de los cuales 78 tenían fibrilación auricular paroxística idiopática y 70 eran pacientes control. Para determinar los efectos de la edad sobre la vulnerabilidad auricular, dividimos a los pacientes con fibrilación auricular en dos grupos: el grupo mayor tuvo 38 pacientes ®g60 años de edad y el grupo más joven tuvo 40 pacientes <60 años de edad. Los siguientes parámetros de vulnerabilidad auricular fueron estudiados y medidos cuantitativamente: 1) el período refractario efectivo auricular, 2) la zona del retardo de la conducción auricular, y 3) el máximo retardo en la conducción auricular. El período refractario efectivo auricular promedio del grupo más joven (201±28 msec) fue significativamente más corto que el del grupo mayor de edad (215±27 msec, p<0.05) y que el del grupo control (215± 29 msec. p<0.02). La zona del retardo en la conducción auricular promedio del grupo mayor (50±25 msec) y la del grupo más joven (50±31 msec) fueron significativamente más amplias que la del grupo control (34±22 msec) (p<0.01). El máximo retardo en la conducción auricular del grupo mayor (65±31 msec) y el del grupo más joven (58±27 msec) fueron significativamente más amplios que el del grupo control (43±20 msec) (p<0.01). Por lo tanto, si bien el retardo en la conducción auricular se observa tanto en los pacientes más jóvenes como en los mayores de edad, el período refractario efectivo auricular es más corto en los pacientes más jóvenes con fibrilación auricular paroxística idiopática. Estos resultados sugieren diferencias dependientes de la edad en la fisiopatología de la fibrilación auricular

Sotalol-induced coronary spasm in a patient with dilated cardiomyopathy associated with sustained ventricular tachycardia.

A 54-year-old man with severe left ventricular dysfunction due to dilated cardiomyopathy was referred to our hospital for symptomatic incessant sustained ventricular tachycardia (VT). After the administration of nifekalant hydrochloride, sustained VT was terminated. An alternate class III agent, sotalol, was also effective for the prevention of VT. However, one month after switching over nifekalant to sotalol, a short duration of ST elevation was documented in ECG monitoring at almost the same time for three consecutive days. ST elevation with chest discomfort disappeared since he began taking long-acting diltiazem. Coronary vasospasm may be induced by the non-selective beta-blocking properties of sotalol.

Relation between history of paroxysmal atrial fibrillation and electrophysiological abnormalities of atrial muscle.

Although electrophysiological abnormalities of atrial muscle have been evaluated in patients with paroxysmal atrial fibrillation (PAF), no prior study has determined the contribution of the patient's history of PAF to electrophysiological abnormalities. The study population consisted of 108 patients (71 men; mean age, 57 +/- 14 years) with symptomatic and idiopathic PAF who underwent electrophysiological study. Before electrophysiological study, histories of frequency, number of PAF episodes per month, and duration, a time interval from the first episode of PAF to electrophysiological study, were examined. At electrophysiological study, endocardial electrograms from 12 right atrial sites were recorded during sinus rhythm, and the right atrial effective refractory period was determined. Longest duration of atrial electrograms, maximal number of fragmented deflections, and number of abnormal atrial electrograms recorded at the right atrial sites were significantly greater in the frequent group (> 1 PAF episode per month, n = 57) than in the infrequent group (< 1 PAF episode per month, n = 51) (98 +/- 18 ms vs 88 +/- 16 ms, P < 0.005; 8.7 +/- 2.6 vs 7.5 +/- 2.6, P < 0.05; and 2.2 +/- 2.2 vs 1.4 +/- 1.6, P < 0.05, respectively). Indices of atrial vulnerability were also greater in the frequent group. Duration of PAF history was significantly correlated with longest duration r = 0.52, P < 0.0001), maximal number of fragmented deflections r = 0.51, P < 0.0001), and number of abnormal atrial electrograms r = 0.58, P < 0.0001). More frequent episodes and longer history of PAF significantly increased the electrophysiological abnormalities of the atrial muscle, suggesting that PAF results in gradual electrical remodeling of the atrial muscle.

Abnormal right atrial electrograms predict the transition to chronic atrial fibrillation in paced patients with sick sinus syndrome.

Although pacing therapy for sick sinus syndrome (SSS) is established, the risk of developing chronic atrial fibrillation (CAF) makes pacing therapy infeasible in some patients. We evaluated whether electrophysiological characteristics of atrial muscle can serve as predictors of the transition to CAF after pacemaker implantation in patients with SSS. Eighty-nine patients with SSS underwent electrophysiological study before pacing therapy. Catheter mapping of 12 right atrial sites was performed during sinus rhythm during electrophysiological. An abnormal atrial electrogram was defined as having a duration of 100 ms or longer, or eight or more fragmented deflections, or both. Right atrial extrastimulation was also performed for atrial vulnerability. After electrophysiological study, all patients underwent pacemaker implantation and were followed up. During the follow-up period of 85 +/- 50 months, development of CAF was observed in 12 patients (group A). The remaining 77 patients remained in sinus rhythm (group B). There were significantly more abnormal atrial electrograms in group A than group B (2.7 +/- 2.3 vs 0.8 +/- 1.2; P < 0.001). The distribution of abnormal atrial electrograms was also greater in group A; patients in group A had more abnormal atrial electrograms than patients in group B in both the high and middle right atrium (P < 0.005 and P < 0.01, respectively). Kaplan-Meier analysis showed that almost 50% of the paced patients with abnormal atrial electrograms (n = 42) developed CAF (P < 0.005). Our data suggest that the existence of abnormal atrial electrograms is predictive of the transition to CAF in paced patients with SSS.

Effects of intravenous nifekalant, a class III antiarrhythmic drug, on atrial vulnerability parameters in patients with paroxysmal atrial fibrillation.

Nifekalant, a class III antiarrhythmic drug, has been shown to suppress ventricular tachyarrhythmias, but its effects on AF are unclear. The aim of this study was to clarify the effects of nifekalant on the atrial vulnerability parameters in patients with paroxysmal AF. The study included 18 patients with paroxysmal AF who underwent electrophysiological study before and after intravenous infusion of nifekalant. The atrial electrophysiological parameters including the atrial effective refractory period (AERP), maximum intraatrial conduction delay, and wavelength index, calculated as the ratio of AERP to the maximum conduction delay, were quantitatively measured at baseline and during nifekalant infusion. The mean AERP was significantly prolonged from 214 +/- 27 ms at baseline to 242 +/- 39 ms after nifekalant (P < 0.001). Although earlier studies have shown that nifekalant does not affect the atrial conduction time, the mean maximum conduction delay of the study patients was significantly prolonged from 59 +/- 19 ms at baseline to 72 +/- 28 ms after nifekalant (P = 0.015). There was no significant difference in the wavelength index at baseline (4.1 +/- 1.7) and after nifekalant (4.1 +/- 2.5). However, when the differences of AERP and wavelength index were defined as each parameter during nifekalant infusion minus that at baseline, the difference of AERP showed a direct positive correlation with that of the wavelength index (P = 0.013). In conclusion, nifekalant may be effective in the prevention of AF due to prolongation of the AERP. However, in those patients who have a lesser degree of prolongation of the AERP by nifekalant, the wavelength index tended to be decreased, suggesting that the drug might augment the propensity for AF.

A patient with LQTS in whom verapamil administration and permanent pacemaker implantation were useful for preventing torsade de pointes.

A 21-year-old woman with long QT syndrome and missense mutation in HERG (T613M), suffered from repeated attacks of pause dependent torsade de pointes, even though she was given beta-blockers and underwent stellate ganglion block twice at the age of eight. After she received permanent pacemaker implantation and administration of verapamil, no premature beats or pause dependent torsade de pointes was observed.