Abnormal serum carbohydrate antigen 19-9 levels in a patient with splenic retiform haemangioendothelioma concomitant with hepatic amyloidosis: A case report.

BACKGROUND: Carbohydrate antigen 19-9 (CA 19-9) is a glycoprotein that is used as a reliable tool for monitoring pancreatic cancer. Serum CA 19-9 levels are increased in patients suffering from liver, lung, and other non-malignant diseases. Haemangioendothelioma is a vascular neoplasm with a borderline biological behaviour. However, no case of haemangioendothelioma has yet been reported to be associated with CA 19-9. CASE SUMMARY: A 54-year-old Chinese man was referred to our hospital for discontinuous fatigue and unintentional weight loss for over one year. Laboratory investigations revealed an elevated serum CA 19-9 concentration of 39 IU/mL (reference interval, 0-37 IU/mL) over one year before admission. Afterwards, coagulopathy appeared, and the patient's serum CA 19-9 concentration increased continuously. At the time of admission, abdominal pain and haemorrhagic shock burst occurred, and emergency medical operation was performed. Laboratory investigations conducted upon admission showed a serum CA19-9 concentration of 392.56 IU/mL. Surgical resection of the spleen was undertaken, and pathological examination showed retiform haemangioendothelioma. The patient developed jaundice ten days after surgical excision of the spleen. Pathological examination of needle biopsy samples of the liver yielded a diagnosis of hepatic amyloidosis. CONCLUSION: We describe a rare case of splenic retiform haemangioenthelioma concomitant with hepatic amyloidosis. Physicians should note abnormal serum CA 19-9 levels with early symptoms of fatigue and unintentional weight loss.

Detection of sleep apnea-hypopnea syndrome with ECG derived respiration in Chinese population.

Evaluation of sleep apnea-hypopnea syndrome (SAHS) is mainly based on the polysomnogram (PSG), which is considered as the golden diagnostic criteria. As a novel noninvasive and low cost alternative method to detect SAHS patients, the diagnostic power of ECG-derived respiration (EDR) hasn't been well determined. In light of this, we tested whether EDR can be utilized as a feasible tool to diagnose SAHS in Chinese patients. Overnight sleep investigation was performed in 120 subjects using polysomnogram (PSG) and 24-hour ambulatory electrocardiogram (AECG). The apnea hypopnea index (AHI) was calculated from EDR and PSG respectively. With EDR assessments, 77 subjects were determined as SAHS (+), 43 were diagnosed as SAHS (-). The diagnostic accordance rate was 87.5% and the area under curve was 0.938. The coefficient correlation of AHI between EDR and PSG was 0.879 (P <0.001), while the correlation of maximum apnea and hypopnea time duration were 0.716 (P <0.001) and 0.281 (P <0.005), respectively. All correlations were statistically significant (P <0.01). EDR can be used as a practical tool for the diagnosis of SAHS.

Vagal effects on the occurrence of focal atrial fibrillation originating from the pulmonary veins.

BACKGROUND: There is evidence that the autonomic nervous system may be involved in the mechanism of focal atrial fibrillation (AF), so the present study investigated the effects of the parasympathetic nervous system on the occurrence of focal AF originating from the pulmonary veins (PVs). METHODS AND RESULTS: In 10 mongrel dogs, programmed stimulation and local burst stimulation (12.5 Hz, impulse duration 0.5 ms) were performed at each of the PVs. Pacing thresholds at different sites were determined and shown as a terraced distribution. The closer to the ostium of the PV, the lower was the pacing threshold (P<0.05-0.001). The local effective refractory period (ERP), AF induction and AF threshold were measured at baseline and during bilateral vagal nerve stimulation (VNS). VNS led to local ERP shortening at each of the PV sites (P<0.05-0.001), increased the inducibility of AF at all sites in the 4 PVs (P<0.05-0.001), and decreased the AF threshold at most sites, especially in the distal portions of the 4 PVs (P<0.05-0.01). CONCLUSIONS: VNS changes the electrophysiological characteristics of the PVs and facilitates the induction of AF. Interaction between the autonomic nervous system and local cardiac autonomic nerve system may be a potential mechanism.

Focal atrial tachycardia originating from the left atrial appendage: electrocardiographic and electrophysiologic characterization and long-term outcomes of radiofrequency ablation.

INTRODUCTION: This study sought to investigate electrophysiologic characteristics and radiofrequency ablation (RFA) in patients with focal atrial tachycardia (AT) arising from the left atrial appendage (LAA). METHODS: This study included seven patients undergoing RFA with focal AT. Activation mapping was performed during tachycardia to identify an earlier activation in the left atria and the LAA. The atrial appendage angiography was performed to identify the origin in the LAA before and after RFA. RESULTS: AT occurred spontaneously or was induced by isoproterenol infusion rather than programmed extrastimulation and burst atrial pacing in any patient. The tachycardia demonstrated a characteristic P-wave morphology and endocardial activation pattern. The P wave was highly positive in inferior leads in all patients. Lead V1 showed upright or biphasic (+/-) component in all patients. Lead V2-V6 showed an isoelectric component in five patients or an upright component with low amplitude (<0.1 mV) in two patients. Earliest endocardial activity occurred at the distal coronary sinus (CS) ahead of P wave in all seven patients. Mean tachycardia cycle length was 381 +/- 34 msec and the earliest endocardial activation at the successful RFA site occurred 42.3 +/- 9.6 msec before the onset of P wave. RFA was acutely successful in all seven patients. Long-term success was achieved in seven of the seven over a mean follow-up of 24 +/- 5 months. CONCLUSIONS: The LAA is an uncommon site of origin for focal AT (3%). There were consistent P-wave morphology and endocardial activation associated with this type of AT. The LAA focal ablation is safe and effective. Long-term success was achieved with focal ablation in all patients.

Inositol-1,4,5-trisphosphate and ryanodine-dependent Ca2+ signaling in a chronic dog model of atrial fibrillation.

Ca2+ signaling regulation plays an important role in triggering and/or maintaining atrial fibrillation (AF). Little is known about the relationship of the inositol-1,4,5-triphosphate receptors (InsP3Rs) and ryanodine receptors (RyRs) in left atrium to chronic AF. In this study, we investigated the expression and function of InsP3R1, InsP3R2 and RyR2 in a chronic dog model of AF. AF was induced in 6 dogs by rapid right atrial pacing for 24 weeks, and a sham procedure was performed in 5 dogs (control group). The intact left atrial myocytes were used to examine the expression and function of InsP3Rs, RyRs by BODIPY(O,R) TR-X ryanodine, heparin-fluorescein conjugate, and were stimulated by caffeine, ATP to release Ca2+ through RyRs, InsP3Rs separately. We also assessed the molecular components of left atrial tissue underlying the amount of RyR2, InsP3R1 and InsP3R2 determined by RT-PCR, immunohistochemistry and Western blot analysis. In the chronic AF group, the Ca2+ released through RyRs is not altered, but the Ca2+ released through InsP3Rs increased significantly. RyR2 distributed in cytosol of myocytes, cellular membrane; its expression significantly decreased in AF group compared to controls. InsP3R1 distributed in cytosol, InsP3R2 distributed not only in cytosol, cellular membrane, but also in nuclear envelope and intercalated discs. The InsP3R1 and InsP3R2 expression significantly increased in chronic AF group compared to controls. These results indicated that in a chronic dog model of AF, the expression and function of RyR2 down-regulated; on the contrary, the expression and function of InsP3R1, InsP3R2 up-regulated, and InsP3R2 may be the major InsP3Rs, which regulate intracellular or even intercellular Ca2+ signal transmission.

[The relationship of paroxysmal atrial fibrillation and regional sympathetic innervations in the atria and pulmonary veins: experiment with dogs].

OBJECTIVE: To test the hypothesis that regional sympathetic innervation in the atria and pulmonary veins are correlated with atrial fibrillation (AF). METHODS: Sixteen adult mongrel dogs underwent thoracotomy under general anesthesia. Bilateral cervical vagal trunks were decentralized. Multipolar catheters were placed into right atrial appendage (RAA), left atrial appendage (LAA), left atrium (LA), left superior pulmonary vein (LSPV), left inferior pulmonary vein (LIPV), right superior pulmonary vein (RSPV), and left inferior pulmonary vein (LIPV). The bilateral sympathovagal trunks were stimulated, S1S1 burst stimulation and S1S2 stimulation procedure were performed on different points of RAA, LAA, LA, LSPV, LIPV, RSPV, and LIPV. The TF thus induced was monitored. After that, the dogs were killed with their hearts and lungs were taken out. Immunocytochemical staining of cardiac nerves was performed using anti-tyrosine hydroxylase (TH) antibodies. The nerve fiber density was counted manually for each case and expressed as the mean number per slice. RESULTS: Two dogs died during the experiment and the whole procedure was completed on 14 dogs. There was no significant difference in the AF induction rate among the most points, however, the AF induction rate of the RIPV was significantly lower than those of the other points (all P < 0.05). The levels of density of TH-positive nerves in the atria and atrial appendages were significantly higher than those in the pulmonary veins (P = 0.02). The density of TH-positive nerves in the dogs with AF was significantly higher than that in the dog without AF (P < 0.05). The innervation of sympathetic nerves in atria and pulmonary veins was highly correlated to the induction of atrial fibrillation (r = 0.83). CONCLUSION: Regional sympathetic hyperinnervation plays an important role in atrial fibrillation induction.

[Screening of sleep apnea syndrome by ECG derived respiration of ambulatory electrocardiogram].

OBJECTIVE: To evaluate the feasibility of screening sleep apnea-hypopnea syndrome (SAHS) by from electrocardiogram derived respiration (EDR) of ambulatory electrocardiogram (AECG) monitoring. METHODS: The overnight sleep investigation was administered to 80 subjects by polysomnogram (PSG) and 24 hours AECG monitoring simultaneously during February through November, 2004. The electrocardiogram analyzers did not know the PSG results at all, They were both asked to give the apnea hypopnea index (AHI) by EDR and PSG respectively. The PSG result was considered as the gold standard so as to evaluate the feasibility of screening SAHS by EDR of AECG monitoring. RESULTS: The average age, male gender, body mass index, history of hypertension were higher in the SAHS(+) patients than those of the SAHS(-) patients. Automatic analysis was performed with software in a sensitivity of 75%, 87.5% and 100% respectively. When software sensitivity adjusted to 75%, the sensitivity of screening SAHS with EDR was 26.7%, with the specificity of 80%, the positive predictive value of 80%, the negative predictive value of 26.7%, the diagnose accordance rate of 40%. When software sensitivity was adjusted to 87.5%, the sensitivity of screening SAHS with EDR was 55%, with the specificity of 45%, the positive predictive value of 75%, the negative predictive value of 25%, and the diagnose accordance rate of 52.5%. When software sensitivity was adjusted to 100%, the sensitivity of screening SAHS with EDR was 88.3%, with the specificity of 35%, the positive predictive value of 84.1%, the negative predictive value of 50%, and the diagnose accordance rate of 75%. CONCLUSION: EDR technique of AECG was useful to screen the suspicious SAHS patients, sensitivity and the diagnosis coincidence rate was higher when the sensitivity of automatic analysis software was adjusted to 100%.

[Vagal effects on inducibility of atrial fibrillation at different sites of pulmonary veins after autonomic denervation].

OBJECTIVE: To investigate the vagal effects on the inducibility of atrial fibrillation (AF) at different sites of pulmonary vein after autonomic denervation. METHODS: The bilateral cervical vagal trunks of 10 male mongrel dogs were isolated and decentralized. The ansae subclaviae were exposed, ligated, and cut. Needle electrodes were inserted into the subcutaneous tissue of the 4 extremities to record the myocardiogram. Right ventricle electrode was introduced via femoral vein and an electrode with 4 poles was sutured with the right appendage (RAA), left appendage (LAA), left atrium (LA), left superior pulmonary vein (LSPV), right superior pulmonary vein (RSPV), left inferior pulmonary vein (LIPV), and right inferior pulmonary vein (RIPV) respectively. Local burst stimulation (S1S1 = 80 ms, impulse duration = 0.5 ms) was performed on these sites to record the baseline AF inducibility. When sinus cardiac arrest for 2 s or complete atrio-ventricular block occurred programmed bilateral vagal nerves stimulation (VNS) was performed with the frequency of 12.5 Hz, impulse duration of 0.5 ms, and voltage of 5-8 V. Atropine 0.04 mg/kg was dripped intravenously. The changes of AV inducibility were observed. RESULTS: In the baseline state, S1S1 programmed stimulation on all the sites evoked single or multiple atrial premature beats and short runs of atrial tachycardia, only a few sites induced AF. However, S1S1 programmed stimulation combined with VNS significantly increased the frequencies of induced AV at the sites of 4 PVs (P < 0.05, P < 0.01). When atropine was dripped the AV induction rates at all sites did not changed significantly (all P > 0.05). CONCLUSION: Vagal nerve may play an important role in the initiation of AF originating from pulmonary veins.

[Immediate cardioversion of atrial fibrillation and atrial flutter lasting less than 90 days by ibutilide versus propafenone: a multicenter study].

OBJECTIVE: To compare the efficacy and safety of ibutilide versus propafenone in immediate cardioversion of atrial fibrillation (AF) and atrial flutter (AFL) lasted less than 90 days. METHODS: 212 consecutive patients suffering from AF or AFL all lasting less than 90 days that were diagnosed and treated in 5 medical centers were randomly assigned into two groups: ibutilide group (n = 107, including 75 AF cases and 32 AFL cases, receiving intravenous injection of ibutilide 1mg over 10 minutes) and propafenone group as control group (n = 105, including 76 AF cases and 29 AFL cases, receiving intravenous injection of propafenone 70 mg over 10 minutes). If AF/AFL still persisted 10 minutes after treatment, the above dose was repeated. The conversion rate within 1.5 hours and adverse effects within 4 hours were observed. RESULTS: (1) The conversion rate on AFL of the ibutilide group was 78.1%, significantly higher than that of the propafenone group (48.3%, P < 0.01), while no significant difference was observed in the conversion rate on AF (54.7% vs. 39.5%, P > 0.05) and the mean conversion time (P > 0.05). However the overall conversion rate on AFL and AF of the ibutilide group was 61.7%, significantly higher than that of the propafenone group (41.9%, P < 0.05). (2) The conversion rate on AF/AFL lasting less than 48 h was 65.9% in the ibutilide group, not significantly different from that of the propafenone group (55.7%), the conversion rate on AF/AFL lasting 3 approximately 30 d in the ibutilide group was 66.7%, significantly higher than that of the propafenone group (26.3%, P < 0.05), and the conversion rate on AF/AFL lasting 31 - 88 d was 50%, significantly higher than that of the propafenone group (0, P < 0.01). (3) There was no difference in the times needed for conversion between these 2 groups. (4) The most severe adverse effect in the ibutilide group was short run of ventricular tachycardia occurring in 5 cases among which 4 cases recovered simultaneously and one case recovered after accepting a bolus dose of 100 mg lidocaine. The most severe adverse effects in propafenone group were RR interval longer than 1.5 s (4 cases) and transient hypotension. An acute coronary event was also seen in propafenone group, however, unrelated to the experimental drug. CONCLUSION: Intravenous administration of ibutilide in cardioversion of AF and AFL is safe and effective.

Clinical comparison of ibutilide and propafenone for converting atrial flutter.

OBJECTIVE: To evaluate the efficacy and safety of intravenous ibutilide and propafenone for immediate treatment of atrial flutter. METHODS: Forty patients with atrial flutter with an arrhythmia duration of three hours to 90 days were randomized to receive up to two 10-minute infusions of ibutilide (1 and 1 mg) or propafenone (70 and 70 mg) with a 10-minute interval. RESULTS: Ibutilide was superior to propafenone for treating atrial flutter (90% vs. 30%, p < 0.01). The median conversion time in the ibutilide group was 11 min (the 25th and 75th percentile was 10 and 45 min), and the median conversion time in the propafenone group was 35 min (range 20-55 min). In all patients, the duration of arrhythmia before treatment was a predictor of arrhythmia termination, although this was more obvious in the group that received ibutilide. Conversion of atrial flutter by ibutilide was characterized mainly by increased cycle length variability. Bradycardia (2/20) and hypotension (4/20) were more common side effects with propafenone. Of 20 patients given ibutilide, 8 (40%) who developed monomorphic ventricular extrasystoles or repetitive atrial flutter with aberrant conduction tachycardia, no one required any specific treatment except for the interruption of ibutilide infusion. CONCLUSION: Ibutilide is highly effective for rapidly terminating atrial flutter. This new class III drug, under monitored conditions, is a potential alternative to currently available cardioversion options.

[Expression and function changes of ryanodine receptors and inositol 1,4,5-triphosphate receptors of atrial myocytes during atrial fibrillation].

OBJECTIVE: To investigate the expression and function changes of inositol 1,4,5-triphosphate receptor (IP3R) and ryanodine receptor (RyR) in the atrial myocytes during atrial fibrillation. METHODS: Ten adult mongrel dogs were randomly divided into 2 groups: 5 dogs underwent continuous rapid atrial pacing (500 beats/min) for twenty-four weeks to create persistent atrial fibrillation, and the other 5 size-matched dogs without pacemaker implantation were used as controls. Twenty-four weeks after the dogs' hearts were taken out and the canine atrial myocytes were isolated by enzymatic dissociation: fluorescent indicator Fluo-3/AM was added into the buffer to load the myocytes and then the Ca(2+) concentration was determined by confocal microscopy. BODIPY TR-X ryanodine was added into the buffer to stain the myocytes. Caffeine and ATP were added separately to stimulate the release of Ca(2+) from RyR. RESULTS: (1) The expression of RyR in the sarcoplasmic reticulum of the atrial myocytes of the control group was (2.70 +/- 0.23), significantly higher than that of the atrial fibrillation group (0.25 +/- 0.14, P < 0.05). RyR was expressed mostly around the nucleus and only expressed in a small amount in the nucleus in the atrial fibrillation group. However, it was not expressed in the nucleus of the control group. The expression of IP3R in the atrial fibrillation group was significantly higher than that of the control group (P < 0.05). (2) After caffeine stimulation, the concentration in the atrial myocytes of the control group was (1.74 +/- 0.16), significantly higher than that of the fibrillation group (1.26 +/- 0.06, P < 0.05). (3) After ATP stimulation the Ca(2+) concentration in the atrial myocytes of the control group was (1.23 +/- 0.23), not significantly increased in comparison with that before ATP stimulation; however, the Ca(2+) concentration in the atrial myocytes of the fibrillation group after ATP stimulation was (2.29 +/- 0.65), significantly increased in comparison with that before ATP stimulation (P < 0.05). CONCLUSIONS: (1) The expression of RyR is down-regulated, the function of RyR is decreased, and it is expressed in the nucleus during atrial fibrillation which shows that RyR is possibly translocated into the nucleus. (2) The expression of IP3R is up-regulated and the function of IP3R is increased during atrial fibrillation, which may be one of the major mechanisms of intracellular Ca(2+)-overload during atrial fibrillation.