Incidence and cumulative recurrence rates of venous thromboembolism in the Taiwanese population.

SUMMARY BACKGROUND: Little information is available on the epidemiology of venous thromboembolism (VTE) in Asian populations. OBJECTIVES: To investigate VTE incidence, VTE cumulative recurrence rates and risk factors for VTE recurrence among the adult Taiwanese population. METHODS: This population-based cohort study used the Taiwanese National Health Insurance claims databases to identify 5347 adult patients (2463 men, 46.1%) with VTE diagnosed in 2001 and 2002. We calculated the crude incidence of VTE and its recurrence. We also conducted a nested case-control study (n = 3576) among this population to estimate the association between VTE recurrence and exposure to potential VTE risk factors by conditional logistic regression. RESULTS: The crude incidence of VTE was 15.9 per 100,000 person-years, and its recurrence rate was 5.1% per person-year. During 11 566 person-years of follow-up, the cumulative rates of VTE recurrence at 6, 12, 24, 36 and 47 months were 6.7%, 9.4%, 12.4%, 13.9%, and 14.4%, respectively. By conditional logistic regression, histories of VTE [adjusted odds ratio (OR) 1.71, 95% confidence interval (CI) 1.32-2.16] or malignant neoplasm (adjusted OR 1.64, 95% CI 1.26-1.99), major extremity trauma (adjusted OR 2.76, 95% CI 1.82-4.52), serious neurologic diseases (adjusted OR 1.43, 95% CI 1.12-1.84) or undergoing major surgery (adjusted OR 4.57, 95% CI 1.72-12.50) were associated with higher risks of VTE recurrence. CONCLUSIONS: The incidence of VTE is lower in the Taiwanese population than in Caucasians. Most VTE recurrences occur within 12 months, but they continue to occur beyond 1 year. The VTE recurrences are associated with malignancy, history of VTE, and major surgery after a previous VTE.

Evidence for microRNA-mediated regulation in rheumatic diseases.

MicroRNA (miRNA), a group of short non-coding RNA of approximately 20-22 nucleotides modulating the stability and translational efficiency of target messenger RNA, present an important new layer controlling gene expression. Hundreds to a thousand miRNA have been identified and are predicted to regulate at least one-third of protein-coding transcripts in the mammalian genome. This study reviews the recent advances reinforcing the awareness that miRNA are key players in rheumatic diseases by regulating major pathogenic molecules, such as tumour necrosis factor, central signal pathways, such as type I interferon pathway and critical immunoregulatory cells, such as regulatory T cells. In animals, blockade of miRNA maturation by the deletion of Dicer or Drasha, interference with miRNA function by the mutation of Roquin and the altered expression of individual miRNA (miR-146a) or miRNA cluster (miR-17-92) all lead to the development of autoimmune diseases. Growing evidence also reveals the differential expression of certain immunity-regulating miRNA in rheumatoid patients. The features of miRNA-mediated regulation, the direction of future miRNA study in rheumatic diseases and the application of miRNA in diagnosis, therapy and prognosis will also be briefly discussed.

The sodium-dependent glucose cotransporter SLC5A11 as an autoimmune modifier gene in SLE.

Genetic studies in several human autoimmune diseases suggest that the pericentromeric region of chromosome 16 might harbor an autoimmune modifier gene. We hypothesized that the sodium-dependent glucose cotransporter gene SLC5A11 is such a gene, and so might interact with immune-related genes. Herein, this hypothesis was tested in a genetic evaluation of the multiple gene effect in systemic lupus erythematosus (SLE). We used the case-control candidate gene association approach. Eight immune-related genes involved in inflammation and autoantibody generation and clear-up [interleukin 1 receptor antagonist (IL1RN), interleukin 1-beta (IL1-beta), tumor necrosis factor-alpha (TNF-alpha), lymphotoxin-alpha (LTA), tumor necrosis factor ligand superfamily, member 6 (TNFSF6), programmed cell death 1 (PDCD1), C2, and complement component 4 (C4)] were selected for study. Frequency of each candidate's genotype and allele between case and control were compared. Results were stratified by reanalyzing genotype data with relevant symptoms. Finally, improved computational data mining was used to analyze the phenotypes in a large data set. In the frequency analysis, only IL1-beta was significantly associated with SLE. Stratification analysis showed a significant association with SLE symptoms between SLC5A11 and the other immune-related genes, with the exceptions of TNFSF6 and C4. SLC5A11 was significantly associated with low C4 (as was TNF-alpha), anti-Smith antibody (anti-Sm) (as was C2), serositis, and alopecia. Finally, SLC5A11 interacted with PDCD1, TNF-alpha, LTA, and C4. After our study, we concluded that SLC5A11 is involved with some immune effects and interacts with immune-related gene(s), consistent with its function as an autoimmune modifier gene. Furthermore, SLC5A11 might induce apoptosis through the TNF-alpha, PDCD1 pathway. The present genotype-phenotype mapping approach should be applicable to genetic study of other complex diseases.

The different expression patterns of interleukin-1 receptor antagonist in systemic lupus erythematosus.

The interleukin-1 receptor antagonist (IL1RN or IL-1Ra) is a natural antagonist of IL-1-beta. Using IL1RN as a possible marker in patients with systemic lupus erythematosus (SLE), we evaluated whether uIL1RN single nucleotide polymorphisms (SNPs) were associated with the pathogenesis of SLE in Taiwanese, and specifically whether IL1RN (rs315952) was significantly associated with end-stage renal disease. We examined IL1RN isoform expression patterns in patients with SLE to determine whether the expressions play a role in the pathogenesis of SLE. Both case-control and family-based association studies were used. For the case-control study, 104 patients with SLE and 97 normal controls were recruited, and for the family-based study, 11 families with SLE without renal disorder were recruited from the 104 patients with SLE. Eight IL1RN SNPs (rs2234678, rs2234679, rs315951, rs315952, rs419598, rs432014, rs447713, and rs451578) were selected for the family-based study. Reverse-transcriptase-polymerase chain reaction (RT-PCR) was used to determine the expression pattern of each isoform. Our results showed that IL1RN (rs315952) was significantly associated with SLE in patients without renal disorder in the family-based study, after disease stratification, but was not significantly associated with SLE in the case-control study. In the family-based study, the haplotype of IL1RN (AGCCTTAG) was significantly associated with SLE (chi2 = 11.714, P < 0.001). Using RT-PCR to determine the expression pattern of the IL1RN isoforms, we found different expression patterns between normal controls and patients with SLE, with an addition of IL1RN isoform4 or the low expression of IL1RN isoform1. We concluded that IL1RN and its isoforms were involved in the pathogenesis of SLE.

Platelet-activating factor-acetylhydrolase A379V (exon 11) gene polymorphism is an independent and functional risk factor for premature myocardial infarction.

BACKGROUND: Oxidation of low density lipoproteins is an initial step of atherogenesis that generates pro-inflammatory phospholipids, including platelet-activating factor (PAF). PAF is degraded by PAF-acetylhydrolase (PAF-AH), which has been postulated to be a risk factor for myocardial infarction (MI). The role of PAF-AH for the onset of premature MI is unclear. METHODS: Polymorphisms located in putatively functional regions were investigated in a cohort of patients having premature MI onset prior to 46 years of age (n = 200) and a sex-age-matched control group (n = 200). The activity of PAF-AH and coronary angiograms were evaluated for the severity of coronary atherosclerosis. RESULTS: The V allele of A379V (exon 11) polymorphism on PAF-AH gene was more frequent in patients with premature MI (P = 0.001). This V allele polymorphism was also associated with a lower activity of plasma PAF-AH and a more complex coronary atherosclerosis (p Trends <0.05). Multiple logistic regression analysis showed that this polymorphism was an independent risk factor (Odds Ratio [OR] 1.66, 95% CI 1.14.1 to 5.80, P = 0.008) as well as smoking (OR 3.72, 95% CI 1.77 to 9.28, P = 0.001), diabetes mellitus (OR 2.25, 95% CI 1.40 to 5.32, P = 0.007) and hypertension (OR 1.88, 95% CI 1.25 to 5.36, P = 0.003) for the onset of premature MI. CONCLUSION: We conclude that a functional and significant association between the A379V polymorphism on exon 11 of PAF-AH gene and premature MI exists in this Taiwanese population. This polymorphism is significantly associated with the PAF-AH activity and the severity of coronary atherosclerosis.

Stromelysin-1 promoter 5A/6A polymorphism is an independent genetic prognostic risk factor and interacts with smoking cessation after index premature myocardial infarction.

OBJECTIVE: To evaluate the prognostic roles of multiple polymorphisms and smoking cessation for premature myocardial infarction (MI). METHODS: We studied 170 patients with MI onset before the age of 45 years (range 27-45 years, 84% men) and analyzed the traditional risk factors and several candidate genes' associations with their subsequent coronary events. RESULTS: Follow-up data were available for a total of 162 individuals (95.3%) with the other 38 individuals (4.7%) being lost-to-follow-up premature MI patients. During a mean period of 4.43 years' follow-up, diabetes mellitus (DM), hypertension, hypercholesterolemia and Killip's status > or =II were more frequent among patients with subsequent cardiac events (all P-values <0.05). The frequency of 5A allele of stromelysin-1 gene was significantly higher among event group (P = 0.01). Smoking cessation after MI, use of beta-blocker or angiotensin-converting enzyme inhibitor (ACEI) could improve outcome (all P-values <0.05). After multivariate analysis, we found that DM was an independent risk factor for survival [Hazard ratio (HR) 2.45, P = 0.01]. Successful smoking cessation and therapy with ACEI could have a protective effect (HR 0.33 and 0.09, P = 0.01 and <0.01, respectively). The stromelysin-1 5A gene polymorphism was also an independent survival predictor (HR 2.51, P = 0.03). In addition, smoking cessation could significantly modify the risk, especially among patients with 5A allele polymorphism (HR 6.75 vs. 1.50). CONCLUSION: We thus conclude that the stromelysin-1 gene polymorphism alone or in combination with smoking cessation can influence the prognosis after index premature MI.

Antihypertensive action and blockade of alpha1-adrenoceptors by DL-017, a quinazoline derivative.

3-[[4-(2-Methoxyphenyl)piperazin-1-yl]methyl]-5-(methylthio)-2,3-dihydroimidazo[1,2-c]quinazoline (DL-017), a quinazoline derivative, exhibits alpha 1 -adrenoceptor antagonistic and type I antiarrhythmic effects on mammalian cardiac tissues. In the current study, the effects of DL-017 on the hemodynamic profile in anesthetized, spontaneously hypertensive rats were evaluated. Intravenous administration of DL-017 induced dose-dependent reductions of heart rate and blood pressure, which persisted over 2 h. DL-017 exerted a maximal antihypertensive effect at 0.1 mg/kg, which was similar to that of 0.1 mg/kg of prazosin. DL-017 was able to block the pressor response to phenylephrine but not to angiotensin II. Regional cerebral blood flow of the right parietal cortex decreased by 14 +/- 4% 10 min after bolus injection and then rapidly returned to control levels while the arterial pressure was still low. These results indicate that blockade of the alpha 1 -adrenoceptor by DL-017 contributes to reduction of arterial pressure. The antihypertensive effect without reflex tachycardia and loss of autoregulation of cerebral blood flow makes DL-017 suitable for chronic long-term treatment of hypertension.

Emergency medical technicians' disaster training by tabletop exercise.

The objective of this study was to assess the attitudes of emergency medical technicians (EMTs) toward tabletop drills to determine the effect of tabletop simulation on the EMT student perception of disaster preparedness and management. In November 1998 and April 1999, 59 firefighters underwent 260 hours of EMT intermediate level training at the National Cheng Kung University Hospital in Tainan, Taiwan. All participants had experience in field disaster exercise training before they attended this EMT training course. The EMT courses included a disaster and mass-casuality incident program. A 9-item questionnaire was completed by the 59 EMTs before (for field exercise) and after undergoing the tabletop drills. The results of the survey revealed that the field operation exercise could not provide adequate provisions to link the results of disaster exercises to appropriate changes in terms of training, equipment, supplies, and plans. Field operation failed to show the ability of others to fill in during the absence of key officials. Tabletop drilling provided better performance for these 2 issues. Tabletop exercise also provided a better chance than field exercise to evaluate the response without the use of telephones, which are not always reliable in real emergency situation. For disaster exercises, limitations of field operation drills such as communications, coordination, assignment of responsibilities, and postevent mitigation priorities were noted, and tabletop drills provided additional benefits for these settings. Large-scale effect evaluation of different drills may be necessary to design future disaster preparedness programs.

Characteristics of repeated ambulance use in an urban emergency medical service system.

BACKGROUND AND PURPOSE: Although many studies have examined the reasons for repeated use of emergency medical service (EMS), little information is available concerning repeated ambulance use in Taiwan. This study evaluated the characteristics of repeated EMS ambulance use in an urban EMS system in Taiwan. METHODS: Data from a local EMS computerized database for the period from January 1996 through December 1998 were collected for analysis. All calls to the dispatch center that resulted in EMS transports were included. Repeat users were identified by matching the user name, sex, age, and home address. Transports were categorized according to how many times the patient was transported by ambulance during the 3-year period: single use, one time; repeated use, two or three times; or frequent use, more than three times. RESULTS: During the 36-month study period, there were 41,792 calls, with 13,076 non-transports (a non-transport rate of 31.3%). Of the 28,716 transports during the study period, 2,101 represented repeated or frequent use (7.3%); the rate of frequent use was 1.4% (406/28,716). The frequency of repeated use reached a daily first peak at 8:00 AM, with the second and third peaks at 1:00 PM and 7:00 PM. The mean age increased with increasing repeated use of transport (37.25 +/- 0.24 vs 41.55 +/- 1.03 vs 46.23 +/- 1.57 years, respectively; p < 0.001). The percentage of non-trauma missions increased with increasing repeated use of transport (26.3% vs 55.6% vs 73.2%; p < 0.001). Response time significantly increased for repeated use (analysis of variance [ANOVA], p < 0.001). The on-scene interval (time from arrival until departure) in the single-use group was shorter than in the repeated and frequent use groups (ANOVA, p < 0.005). CONCLUSIONS: The results of this study indicate that the characteristics of repeat users of EMS transport differ from those of single users. Characteristics of service time, reason for transport, and interval to each subsequent call varied among different groups of users. Studies of repeat use under a wider range of conditions such as in rural EMS systems and after implementation of a priority-dispatch system are needed to determine the implications of repeated ambulance use.

Blockade of alpha1-adrenoceptors and cardiac depressant effect by a newly synthetic antihypertensive drug, DL-017 of quinazoline derivative.

The electromechanical effects of 3-[[4-(2-methoxy phenyl)piperazin-1-yl]methyl]-5-(methylthio)-2,3-dihydroimidazo[1,2-c]quinazoline (DL-017), a newly synthesized quinazoline-derived antihypertensive agent, on mammalian cardiac tissues were evaluated. In driven canine Purkinje fibers, DL-017 decreased twitch tension, the maximal rate of upstroke of the action potential (Vmax), and intracellular Na+ activity (a(i)Na) in a concentration-dependent manner. The action potential duration was decreased in canine Purkinje fibers but increased in guinea pig papillary muscles. In guinea pig ventricular papillary muscles, phenylephrine in the presence of 1 microM propranolol increased the twitch tension in a concentration-dependent manner. At 10 microM, phenylephrine significantly decreased a(i)Na and shortened the action potential duration. DL-017 at 0.01 microM inhibited these phenylephrine-induced effects and shifted the concentration-dependent curve to the right. In sinoatrial nodes, DL-017 inhibited pacemaker activity, involving decreases in the slope of diastolic depolarization and Vmax and an increase in a delay of repolarization. These results suggest that, in addition to blockade of alpha1-adrenoceptors and Na+ channels, DL-017 reduces cardiac excitability and contractility in association with inhibition of slow inward Ca2+ and outward K+ channels. Since two order higher concentrations are required, the contribution of DL-017 to cardiac depressant from blockade of ionic channels seems to be less important when this compound is clinically used as an antihypertensive drug.

Sodium nitroprusside increases pacemaker rhythm of sinoatrial nodes via nitric oxide-cGMP pathway.

Effects of sodium nitroprusside (SNP), a nitric oxide donor, on the action potential in isolated guinea-pig sinoatrial nodes and ventricular papillary muscles were investigated. In the driven ventricular papillary muscle, SNP (10(-10)-10(-3) M) decreased the twitch tension in a concentration-dependent manner without significantly changing the configuration of action potential and the maximal velocity of depolarizing upstroke. In isolated sinoatrial nodes, SNP (10(-8)-10(-3) M) increased the pacemaker rhythm in a concentration-dependent manner. At 10(-5) M SNP, the pacemaker activity increased from 197.2+/-6.1 to 221.4+/-9.7 bpm. Changes of configuration of the action potential included a decrease of the duration of repolarization, i.e., from peak to the maximal diastolic potential (MDP), from 141.4+/-6.4 to 130.0+/-7.0 ms and an increase of the slope of the diastolic membrane potential from 101.6+/-5.3 to 116.5+/-7.3 mV/s (n=6, p<0.05). However, MDP and threshold potential were not significantly changed. Methylene blue (MB, 10(-5) M), a guanylate cyclase inhibitor, significantly decreased the pacemaker activity of the sinoatrial node by increasing the durations of repolarization and diastolic depolarization. After pretreatment with 10(-5) M MB, the effect of SNP was inhibited. The results indicate that nitric oxide, released from SNP, increases the pacemaker activity by enhancing the rates of repolarization and diastolic depolarization. These effects are possibly due to increases in delayed-rectifier K+ and diastolic slow inward currents, which are involved in a mechanism associated with the NO-cGMP pathway.

Sick sinus syndrome in a patient with single coronary artery anomaly.

Single coronary artery anomaly is very rare. The reported manifestations include angina pectoris and congestive heart failure. Here we describe a case of single coronary artery anomaly presenting as sick sinus syndrome, which has no literature precedence. A 47-year-old woman had complained of intermittent dizziness for years. A Holter electrocardiogram showed sinus bradycardia and junctional or ventricular rhythm with a maximal ventricular pause of up to 3.2 seconds. Electrophysiologic study revealed prolonged corrected sinus nodal recovery time. Coronary angiography showed that the left anterior descending artery had a long course with a side branch originating from the proximal part and coursing anteriorly to the territory of the proximal portion of the right coronary artery. The sinus node is usually supplied by the sinoatrial branch via the right coronary artery. Aortography showed that the right coronary artery ostium was absent. A permanent pacemaker was implanted and the patient was discharged in good condition. The present case suggests that coronary artery anomaly may lead to compromised blood supply to the sinus node, and hence sick sinus syndrome.

G-33A mutation in the promoter region of thrombomodulin gene and its association with coronary artery disease and plasma soluble thrombomodulin levels.

Thrombomodulin is an endothelial glycoprotein that decreases thrombin activity and activates protein C. A recent study has shown that G-33A promoter mutation of the thrombomodulin gene occurs particularly in Asians. In this study, we analyzed the distribution of G-33A mutation in the promoter region of the thrombomodulin gene in the Chinese population and determined whether the mutation might be a risk for coronary artery disease (CAD). In addition, the influence of this mutation on plasma soluble thrombomodulin levels in patients with CAD was also examined. We studied 320 consecutive patients (mean age 63 years; 73% men) with CAD and 200 age- and sex-matched control subjects. Screening for thrombomodulin G-33A promoter mutation was conducted using polymerase chain reaction, single-strand conformation polymorphism, and direct deoxyribonucleic acid sequencing. The frequency of the G-33A mutation (GA+AA genotypes) was significantly higher in the CAD group (23.8% vs 15.5%, odds ratio [OR] 1.70, p = 0.031). Multiple logistic regression analysis showed that the mutation was an independent risk factor (OR 1.81, p = 0.016) for CAD, as was hypertension (OR 1.44, p = 0.040), diabetes mellitus (OR 2.50, p <0.001), and smoking (OR 2.15, p <0.001). In CAD patients with GG genotype, the soluble thrombomodulin level increased with the extent of CAD (36 +/- 15 vs 47 +/- 18 vs 55 +/- 36 ng/ml in 1-, 2-, or 3-vessel CAD, p <0.001). However, in CAD patients with G-33A mutation, there was no difference between the levels of soluble thrombomodulin (39 +/- 17 vs 37 +/- 15 vs 42 +/- 18 ng/ml, p = NS) in 1-, 2-, or 3-vessel CAD. Our observations suggest that there is a significant association of the G-33A mutation in thrombomodulin gene with CAD, and this mutation may influence the soluble thrombomodulin levels in patients with CAD.

Correlation of homocytsteine levels with the extent of coronary atherosclerosis in patients with low cardiovascular risk profiles.

Elevation of homocysteine is now known as an independent risk factor for vascular diseases. However, influences of homocysteine to the extent of coronary atherosclerosis in patients with different coronary risk profiles have not been studied. In this study, we used angiographic "diffuse score" and "clinical vessel score" to evaluate the extent of coronary atherosclerosis, and examined the correlation between levels of serum total homocysteine and angiographic scores among patients with high- and low-risk profiles. Seventy consecutive patients (58 men and 12 women, mean age 50 years) undergoing selective coronary angiography for the first time were recruited for this study. Patients were divided into high-risk (risk factor > or =3, n = 35) and low-risk (risk factor <3, n = 35) groups. Linear regression analysis revealed that levels of serum homocysteine were only significantly correlated with diffuse (r = 0.217, p = 0.007) and clinical vessel (r = 0.078, p = 0.037) scores in low-risk patients. These correlations could not be observed in diffuse (r = 0.070, p = 0.319) and clinical vessel (r = -0.001, p = 0.970) scores in the high-risk group. In conclusion, levels of homocysteine correlated with the extent of coronary atherosclerosis only among patients with low cardiovascular risk profiles.

Clinical presentations and prognostic factors of a glyphosate-surfactant herbicide intoxication: a review of 131 cases.

OBJECTIVE: Suicide attempts with agricultural chemicals are common in southern Taiwan. Among them, glyphosate-surfactant herbicide (GlySH) intoxication has been encountered with increasing frequency. Although a number of reports have described the clinical course and outcomes following ingestion, predictors of serious complications and mortality have not been elucidated. The purpose of this study was to define predictors of serious complications and probable mortality. METHODS: This was a retrospective study of 131 GlySH-intoxicated patients treated at the National Cheng Kung University Hospital from 1988 to 1995. Medical charts were reviewed and clinical and laboratory variables were abstracted, looking for predictors of mortality. RESULTS: The most common symptoms included sore throat (79.5%), and nausea with or without vomiting (73.8%). The most common laboratory findings were leukocytosis (68.0%), low serum bicarbonate (48.1%), and acidosis (35.8%). Overall, 11 of 131 patients (8.4%) died; the mean +/- SEM time to death was 2.8 +/- 0.8 days after presentation. When comparing the clinical and laboratory characteristics among the survivor and fatality groups, significant differences were identified. Respiratory distress, pulmonary edema, respiratory distress necessitating intubation, shock (systolic blood pressure less than 90 mm Hg), altered consciousness, abnormal chest x-ray, renal failure necessitating hemodialysis, larger amount of ingestion (>200 mL), and hyperkalemia were predictors highly associated with poor outcomes and mortality. Using multiple logistic regression, three predictors were identified, which may predict mortality in severely intoxicated patients. CONCLUSIONS: In managing patients who have larger amount of GlySH ingestion, airway protection, early detection of pulmonary edema, and prevention of further pulmonary damage and renal damage appear to be of critical importance.

Effect of atrial fibrillation on pulmonary venous flow patterns assessed by Doppler transesophageal echocardiography.

STUDY OBJECTIVES: To investigate the effect of atrial fibrillation (AF) on pulmonary venous flow (PVF) patterns in a cohort with nonrheumatic AF. DESIGN AND SETTINGS: A prospective and controlled study undertaken at a tertiary referral medical center. PATIENTS AND MEASUREMENTS: The echocardiographic parameters of left superior PVF as assessed by Doppler transesophageal echocardiography in 40 patients with chronic AF (group 1) were compared to those of 33 volunteers with sinus rhythm (group 2) and well-matched baseline characteristics. RESULTS: : All group 1 patients presented with single systolic forward flow (SFF) patterns. In contrast, single and double SFF patterns were found equally in group 2. With regard to reverse flow (RF), most group 1 patients (33 of 40) had an early systolic RF and none had atrial RF; however, most group 2 subjects (29 of 33) had an atrial RF. Some of the group 1 patients (17%) had a late systolic RF in the absence of significant mitral regurgitation. In group 1, the SFF appeared later and disappeared earlier than in group 2. The mean systolic peak velocity and time-velocity integral (TVI) of the SFF were significantly lower in group 1 compared to group 2. The diastolic peak velocity and TVI were not significantly different between groups. CONCLUSIONS: : Our data indicate that AF independently and significantly affects the PVF and leads to characteristic flow patterns different from sinus rhythm. The presence of AF reduces SFF in addition to the absence of atrial RF. These changes in the flow patterns should be taken into account while interpreting the implications of PVF in the presence of AF.

Association of follow-up change of left atrial appendage blood flow velocity with spontaneous echo contrast in nonrheumatic atrial fibrillation.

STUDY OBJECTIVES: To evaluate the time-related change of left atrial (LA) appendage flow velocity in chronic atrial fibrillation (AF) by follow-up transesophageal echocardiography (TEE) and to investigate its association with the occurrence of LA spontaneous echo contrast. DESIGN: Prospective follow-up study. SETTING: University-based, tertiary referral medical center. PATIENTS: Forty-seven patients with chronic nonrheumatic AF. INTERVENTIONS: All studied patients underwent both a baseline and follow-up TEE during a mean period of 13 +/- 7 months. MEASUREMENTS AND RESULTS: Baseline TEE revealed that LA spontaneous echo contrast was present in 28 patients (group 1) and was absent in 19 patients (group 2). The LA appendage flow velocity profiles at baseline were significantly lower in group 1 than in group 2; on follow-up, the appendage flow velocities decreased significantly in group 2, but were not significantly changed in group 1. Follow-up TEE revealed that spontaneous echo contrast was persistent in all group 1 patients. In group 2, LA spontaneous echo contrast was newly observed in 9 patients (group 2A) but was persistently absent in 10 patients (group 2B). In group 2A, all of the LA appendage flow velocity profiles decreased significantly at the follow-up study. In group 2B, however, only LA appendage inflow velocity integral showed significant decrease on follow-up; there were no significant changes in LA appendage outflow velocity indexes and peak inflow velocity. CONCLUSIONS: LA appendage flow velocity may decrease with time in some patients with AF, and this change is associated with a new occurrence of LA spontaneous echo contrast. For patients without LA spontaneous echo contrast, serial follow-up of the LA appendage flow velocity profiles may be useful for predicting future development of spontaneous echo contrast. Once LA spontaneous echo contrast occurs in AF patients, it tends to persist with time and the LA appendage is usually under a persistently low flow state.

Pulmonary artery leiomyosarcoma.

Pulmonary artery leiomyosarcoma is a rare but highly lethal disease, and can be mistaken for pulmonary thromboembolism. We report a case of pulmonary artery leiomyosarcoma managed with surgical resection, chemotherapy, and radiotherapy. A 57-year-old woman was admitted with complaints of aggravated dyspnea. She was initially treated with oxygen therapy and heparinization for a suspected pulmonary embolism. Echocardiography revealed a dilated right atrium and ventricle and severe tricuspid regurgitation, with an estimated systolic right ventricular pressure of 95 mm Hg; a shadow of a mass in the main pulmonary artery was also noted. Right ventriculography revealed a filling defect, and to-and-fro motion of the mass in the main pulmonary artery. The left pulmonary artery was almost totally occluded by the mass. The patient's condition improved dramatically after palliative excision of the mass and patch reconstruction of the outflow tract of the right ventricle with a bicuspid xenograft. Pathologic examination of the mass revealed leiomyosarcoma. Chemotherapy and radiotherapy were subsequently administered and follow-up imaging studies 3 months postoperatively revealed no recurrence of the tumor. The patient remains well, more than 1 year after treatment. This report emphasises that pulmonary artery sarcoma should be considered in the differential diagnosis in cases of suspected pulmonary thromboembolism.