Low dose CT detected interstitial lung abnormalities in a population with low asbestos exposure.

BACKGROUND: The use of low dose CT (LDCT) chest is becoming more widespread in occupationally exposed populations. There is a knowledge gap as to heterogeneity in severity and the natural course of asbestosis after low levels of exposure. This study reports the characteristics of LDCT-detected interstitial lung abnormalities (ILA). METHODS: The Asbestos Review Program offers annual LDCT, health assessments, and pulmonary function tests to an asbestos-exposed cohort. Asbestosis was defined using the Helsinki Consensus statement and the presence of ILA defined using a protocol for occupational CT reports. At least two of three pulmonary function tests: forced expiratory volume in 1 s (FEV1 );​ forced vital capacity (FVC); and diffusion capacity for carbon monoxide (DLco) were required for analysis of physiological decline. RESULTS: From 1513 cases, radiological ILA was present in 485 (32%). The cohort was 83.5% male with a median age of 68.3 years and a median (IQR) asbestos exposure of 0.7 (0.09-2.32) fiber/ml-year. A mixed occupation, mixed asbestos fiber cohort comprised the majority of the cohort (65.8%). Of those with ILA, 40 (8.2%) had an FVC decline of ≥10% and 30 (6.2%) had a DLco decline of ≥15% per year. Time since first exposure, increasing tobacco exposure and reported dyspnea were independently associated with the presence of ILA. CONCLUSIONS: In this population with relatively low asbestos exposure, LDCT-detected ILA that fits criteria for asbestosis is common, but physiological decline is not. This mild chronic stable phenotype of asbestos-associated ILA contrasts with the traditionally accepted views that asbestosis requires high exposures.

Lifestyle factors associated with cardiovascular risk among healthcare workers from the tertiary hospitals in Sarawak.

INTRODUCTION: A cross-sectional study is used to evaluate the lifestyle factors associated with cardiovascular disease (CVD) risk among healthcare workers in tertiary hospitals in Sarawak, Malaysia. METHODS: A questionnaire-based survey using the Simple Lifestyle Indicator Questionnaire (SLIQ) was administered to, and anthropometric measurements were collected from, 494 healthcare workers. RESULTS: The mean age of the subjects was 32.4±8.4, with a range of 19 to 59 years. The subjects were from the allied health (45.5%), management and professional (25.1%) and executive (29.4%) fields. Overall, 47.4% of the subjects were of normal weight, 30.2% were overweight, 17.2% were obese and 5.2% were underweight. The mean number of working hours per week for the subjects was 47.6±14.0 with the highest working hours found among the management and professional group, followed by the executive and allied health groups. Overall, 39.7% of the healthcare workers worked office hours, 36.6% worked within the shift system, 20.9% worked office hours and were on-call and the remaining 2.8% worked a mixture of office hours and shifts. Based on the SLIQ score, 58.1% were classified as at intermediate risk for CVD, 38.5% were in the healthy category and 3.4% were in the unhealthy category. Factors associated with a healthier lifestyle were being female (Odds Ratio [OR]= 12.1; CI=3.2-46.4), professional (mean score= 6.70), in the allied health group (mean score=7.33) and in the normal BMI group (OR= 9.3, CI= 1.8-47.0). CONCLUSION: In our study, healthcare workers had an intermediate risk of developing CVD in the future. Thus, there is a need to intervene in the lifestyle factors contributing to CVD.

Risk Factors for 3-Year-Mortality and a Tool to Screen Patient in Dialysis Population.

INTRODUCTION: Clinical parameters especially co-morbidities among end stage renal disease (ESRD) patients are associated with mortality. This study aims to determine the risk factors that are associated with mortality within three years among prevalent patients with ESRD. METHODS: This is a cohort study where prevalent ESRD patients' details were recorded between May 2012 and October 2012. Their records were matched with national death record at the end of year 2015 to identify the deceased patients within three years. Four models were formulated with two models were based on logistic regression models but with different number of predictors and two models were developed based on risk scoring technique. The preferred models were validated by using sensitivity and specificity analysis. RESULTS: A total of 1332 patients were included in the study. Majority succumbed due to cardiovascular disease (48.3%) and sepsis (41.3%). The identified risk factors were mode of dialysis (P < 0.001), diabetes mellitus (P < 0.001), chronic heart disease (P < 0.001) and leg amputation (P = 0.016). The accuracy of four models was almost similar with AUC between 0.680 and 0.711. The predictive models from logistic regression model and risk scoring model were selected as the preferred models based on both accuracy and simplicity. Besides the mode of dialysis, diabetes mellitus and its complications are the important predictors for early mortality among prevalent ESRD patients. CONCLUSIONS: The models either based on logistic regression or risk scoring model can be used to screen high risk prevalent ESRD patients.

An epigenome-wide DNA methylation study of PTSD and depression in World Trade Center responders.

Previous epigenome-wide association studies (EWAS) of posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) have been inconsistent. This may be due to small sample sizes, and measurement and tissue differences. The current two EWA analyses of 473 World Trade Center responders are the largest to date for both PTSD and MDD. These analyses investigated DNA methylation patterns and biological pathways influenced by differentially methylated genes associated with each disorder. Methylation was profiled on blood samples using Illumina 450 K Beadchip. Two EWA analyses compared current versus never PTSD, and current versus never MDD, adjusting for cell types and demographic confounders. Pathway and gene set enrichment analyses were performed to understand the complex biological systems of PTSD and MDD. No significant epigenome-wide associations were found for PTSD or MDD at an FDR P<0.05. The majority of genes with differential methylation at a suggestive threshold did not overlap between the two disorders. Pathways significant in PTSD included a regulator of synaptic plasticity, oxytocin signaling, cholinergic synapse and inflammatory disease pathways, while only phosphatidylinositol signaling and cell cycle pathways emerged in MDD. The failure of the current EWA analyses to detect significant epigenome-wide associations is in contrast with disparate findings from previous, smaller EWA and candidate gene studies of PTSD and MDD. Enriched gene sets involved in several biological pathways, including stress response, inflammation and physical health, were identified in PTSD, supporting the view that multiple genes play a role in this complex disorder.

Discrepancy in blood pressure between the left and right arms - importance of clinical diagnosis and role of radiological imaging.

INTRODUCTION: Differences in systolic blood pressure reading between arms are common but could signal trouble if the discrepancy is significant. Early detection of aortic dissection could invariably determine patient's survivability. Hence, a high index of suspicion with prompt diagnostic imaging is vital for accurate diagnosis. CASE PRESENTATION: A previously healthy 35-year-old lady was referred from district hospital for hypertensive cardiomyopathy complicated by acute pulmonary oedema. After being admitted to the Intensive Care Unit, the mean arterial pressure on the left arm was noted to be significant higher. On physical examination, both lower limbs were dusky in appearance because of poor perfusion. INVESTIGATIONS: Computed Tomography Angiography showed extensive arch and abdominal aorta dissection extending to the proximal common carotid artery. There was distal abdominal aorta thrombosis with partial left renal infarction. Echocardiogram showed global hypokinesia, presence of intimal flap, aortic regurgitation and mild pericardial effusion. Supine chest X-ray showed apparent cardiomegaly. TREATMENT: Repair of the ascending aortic dissection and suspension of the aortic valve by the cardiothoracic team on Day 2 of admission. The vascular team did bilateral high above knee amputation on Day 9 of admission. OUTCOME: Patient passed away on Day 10 of admission. DISCUSSION: With the absence of classical features of aortic dissection, establishing the diagnosis can be challenging and requires both good clinical judgment and prompt radiological imaging, such that early treatment can be initiated. CONCLUSION: A high index of suspicion and good clinical judgment is needed in cases of significant blood pressure discrepancy between arms.

Mutations in isocitrate dehydrogenase 1 and 2 occur frequently in intrahepatic cholangiocarcinomas and share hypermethylation targets with glioblastomas.

Mutations in the genes encoding isocitrate dehydrogenase, IDH1 and IDH2, have been reported in gliomas, myeloid leukemias, chondrosarcomas and thyroid cancer. We discovered IDH1 and IDH2 mutations in 34 of 326 (10%) intrahepatic cholangiocarcinomas. Tumor with mutations in IDH1 or IDH2 had lower 5-hydroxymethylcytosine and higher 5-methylcytosine levels, as well as increased dimethylation of histone H3 lysine 79 (H3K79). Mutations in IDH1 or IDH2 were associated with longer overall survival (P=0.028) and were independently associated with a longer time to tumor recurrence after intrahepatic cholangiocarcinoma resection in multivariate analysis (P=0.021). IDH1 and IDH2 mutations were significantly associated with increased levels of p53 in intrahepatic cholangiocarcinomas, but no mutations in the p53 gene were found, suggesting that mutations in IDH1 and IDH2 may cause a stress that leads to p53 activation. We identified 2309 genes that were significantly hypermethylated in 19 cholangiocarcinomas with mutations in IDH1 or IDH2, compared with cholangiocarcinomas without these mutations. Hypermethylated CpG sites were significantly enriched in CpG shores and upstream of transcription start sites, suggesting a global regulation of transcriptional potential. Half of the hypermethylated genes overlapped with DNA hypermethylation in IDH1-mutant gliobastomas, suggesting the existence of a common set of genes whose expression may be affected by mutations in IDH1 or IDH2 in different types of tumors.

Gender differences in body mass index, body weight perception and weight loss strategies among undergraduates in Universiti Malaysia Sarawak.

INTRODUCTION: This study was carried out among undergraduate students in Universiti Malaysia Sarawak with the objective of examining gender differences in body mass index (BMI), body weight perception, eating attitudes and weightloss strategies. METHODS: Subjects consisted of 600 undergraduates (300 males and 300 females) recruited from the various faculties between September 2008 until mid-November 2008. The Original Figure Rating Scale: Body Weight Perception, Body Shape Questionnaire (BSQ) and Eating Attitudes Test-26 (EAT-26) were used as assessment tools. RESULTS: Overall, 52.8% of students had normal BMI, with approximately an equal number of both sexes. More males than females were overweight (33.7%), while more females were underweight (25.3%). Males were more likely to perceive themselves as overweight, and fail to see themselves as underweight. More than half of the females preferred their ideal figure to be underweight, whereas about 30% males chose an overweight figure as their ideal model. Females were generally more concerned about body weight, body shape and eating than males. They diet more frequently, had self-induced vomiting, and used laxatives and exercise as their weight-loss strategies. CONCLUSION: Issues pertaining to body weight perception, eating attitudes and weight-loss strategies exist with differences among male and female undergraduates. Thus, in order to correct misperceptions among young adults, a more tailored intervention programme and more in-depth studies into the various factors involved are required.

Prospective study of warfarin dosage requirements based on CYP2C9 and VKORC1 genotypes.

Polymorphisms in CYP2C9 and VKORC1 have been shown to be associated with warfarin dose requirements and could be used to predict warfarin dose. We conducted a prospective study in which warfarin dose was prescribed based on CYP2C9 and VKORC1 polymorphisms in 108 Han-Chinese patients without prior warfarin treatments. Using the genotype-based dosing, 83% of patients reached stable, therapeutic international normalized ratio (INR) within 2 weeks of treatment initiation and none of the patients developed clinical bleeding or thromboembolic event. Ten percent (11) of patients with INR > 4 and no clinical bleeding were detected during this study. At 12 weeks, 69% of the patients' maintenance doses matched the prediction. Dosing algorithms incorporating genetic factors, age, and body surface area were developed, which could explain up to 62% of the total variation (R(2) of 0.62). This study demonstrated that pharmacogenetics-based dosing could improve time to stable, therapeutic INR, reduce adverse events, and achieve high sensitivity.

Three dimensional optic disc visualisation from stereo images via dual registration and ocular media optical correction.

BACKGROUND/AIMS: The three dimensional (3-D) visualisation of the optic disc in true colour will give essential meaning in clinical application. It is not only useful for clinicians in the evaluation of the condition of the optic disc, but it also simplifies the pathological diagnosis and disease progression monitoring. This paper describes a complete 3-D optic disc reconstruction method from a pair of stereo images by a series of robust procedures including camera calibration, image registration, depth recovery, and ocular media optical inclusion. METHODS: Two registration techniques (correlation and feature based methods) are combined together to prune the uncertain matching points in order to improve the overall accuracy of registration. The ocular media within the eyeball are lump modelled as a single lens and integrated into the reconstruction process to obtain an accurate 3-D optic disc image. CONCLUSION: The recovered 3-D optic disc images show good consistency and compatibility when compared with the results from Heidelberg retina tomography (HRT) under clinical validation, with an additional advantage of implementing a more economical and conventional mode of retinal image acquisition.

Combined cord blood stem cells and gene therapy enhances angiogenesis and improves cardiac performance in mouse after acute myocardial infarction.

BACKGROUND: Gene and stem cell therapies hold promise for the treatment of ischaemic cardiovascular disease. However, combined stem cell and angiogenic growth factor gene therapy for acute ischaemic myocardium has not been previously reported. This study hypothesized that combined stem cell and gene therapy would not only augment new vessels formation but also improve myocardial function in acute ischaemic myocardium. METHODS: Human angiopoietin-1 (Ang1) cDNA and VEGF(165) cDNA were ligated into AAV vector. The purified CD34(+) cells were obtained from human umbilical cord blood samples. Cord blood CD34(+) cells were transduced with AAV vector encoding either the human Ang1 (AAV-Ang1) or VEGF(165) (AAV-VEGF) cDNA alone, or both (AAV-Ang1 plus VEGF). Immediately after ligation of the left anterior descending coronary artery in male SCID mice, culture-expanded CD34(+) cells transduced with AAV-Ang1, AAV-VEGF or AAV-Ang1 plus VEGF were injected intramyocardially at the left anterior free wall. RESULTS: Western blot showed that Ang1 and VEGF protein expressions were enhanced in the CD34(+)cells transduced with AAV-Ang1 and AAV-VEGF, respectively. Infarct size significantly decreased and capillary density significantly increased after treatment with CD34(+)/AAV-Ang1 plus VEGF when compared with treatment by CD34(+) only. Combined therapy with CD34(+) and AAV-Ang1, CD34(+) and AAV-VEGF, CD34(+) and AAV-Ang1 plus VEGF, all showed significantly higher cardiac performance in echocardiography than the therapy with CD34(+) alone 4 weeks after myocardial infarction. CONCLUSIONS: Combined therapy with human umbilical cord blood CD34(+) cells and both Ang1 and VEGF genes reduced infarct size, attenuated the progression of cardiac dysfunction and increased capillary density in acute myocardial infarction in mice.

Anatomical evidence for transsynaptic influences of estrogen on brain-derived neurotrophic factor expression.

Several studies have demonstrated that estrogen modulates brain-derived neurotrophic factor (BDNF) mRNA and protein within the adult hippocampus and cortex. However, mechanisms underlying this regulation are unknown. Although an estrogen response element (ERE)-like sequence has been identified within the BDNF gene, such a classical mechanism of estrogen-induced transcriptional activation requires the colocalized expression of estrogen receptors within cells that produce BDNF. Developmental studies have demonstrated such a relationship, but to date no studies have examined colocalization of estrogen receptors and BDNF within the adult brain. By utilizing double-label immunohistochemistry for BDNF, estrogen receptor-alpha (ER-alpha), and estrogen receptor-beta (ER-beta), we found only sparse colocalization between ER-alpha and BDNF in the hypothalamus, amygdala, prelimbic cortex, and ventral hippocampus. Furthermore, ER-beta and BDNF do not colocalize in any brain region. Given the recent finding that cortical ER-beta is almost exclusively localized to parvalbumin-immunoreactive GABAergic neurons, we performed BDNF/parvalbumin double labeling and discovered that axons from cortical ER-beta-expressing inhibitory neurons terminate on BDNF-immunoreactive pyramidal cells. Collectively, these findings support a potential transsynaptic relationship between estrogen state and cortical BDNF: By directly modulating GABAergic interneurons, estrogen may indirectly influence the activity and expression of BDNF-producing cortical neurons.

Immediate and long-term outcomes of stent implantation for unprotected left main coronary artery disease.

Left main coronary artery (LMCA) disease is now uniformly treated with coronary artery bypass grafting (CABG). However, some patients with LMCA disease do not receive CABG because of high operative risks. The advent of stent implantation has permitted a non-operative improvement in myocardial blood flow in many patients with single- and multi-vessel coronary artery disease. However, the outcomes of stent implantation for unprotected LMCA disease are still unclear. Stent implantation was performed for unprotected LMCA disease in 13 patients; eight patients had high operative risk and five patients had refused CABG. The primary success rate was 100% (13/13 patients). One patient (8%) developed a non-Q-wave myocardial infarction after LMCA stenting. Repeat angiography was obtained in five patients (38%) with recurrent angina, and three patients (23%) received repeated percutaneous transluminal coronary angioplasty (PTCA) for LMCA restenosis. In the follow-up period of 18+/-3 months, 12 patients (92%) remained in satisfactory condition with no further need for surgical intervention. One patient (8%) ultimately required CABG, and she died after CABG at 3 months after LMCA stenting. In conclusion, although CABG remains the standard treatment for LMCA disease, the present study demonstrates that stent implantation is a safe and clinically beneficial revascularization procedure for unprotected LMCA disease in patients who have high operative risk as well as those who refuse CABG.

Angiotensin II receptor antagonist blocks the expression of connexin43 induced by cyclical mechanical stretch in cultured neonatal rat cardiac myocytes.

Mechanical forces have profound effects on cardiomyocytes. To test whether angiotensin II is a potential mediator of stretch-induced effects on gap junctions, we used the angiotensin II (AT1) receptor antagonist, losartan, to investigate the cyclical stretch-induced expression of connexin43 (Cx43), the major cardiac muscle gap junction channel protein. Cultured neonatal rat cardiomyocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation, at 60 cycles/min. The levels of Cx43 protein began to increase as early as 2 h after stretch was applied, reached a maximum of six-fold over the control by 24 h and remained at this level another 24 h (i.e. up to 48 h after stretch was applied). These increases of Cx43 protein at 24 h were largely (73%) and completely (100%) attenuated (P<0.001) by the addition (30 min before stretch) of 10 n M and 100 n M losartan, respectively. Similarly, the Cx43 mRNA levels in stretched cardiomyocytes rose 89% (P<0.01) above control (non-stretched cells) mRNA levels. This increase also was blocked by losartan. Cyclical stretch increased (and losartan decreased) the immunohistochemical labeling of Cx43 and significantly increased release of angiotensin II into the culture media from 7.5+/-0.6 ng/ml to 23.8+/-1.0 ng/ml (P<0.01) after a 1 h stretch. These findings indicate that cyclical mechanical stretch augments angiotensin II production and Cx43 gene expression in cultured cardiomyocytes, partially through mediation of the AT1 receptors, and suggests interaction between the cardiomyocyte local rennin-angiotensin system and Cx43 in response to stretch.

Cyclical mechanical stretching increases the expression of vascular endothelial growth factor in rat vascular smooth muscle cells.

BACKGROUND AND PURPOSE: Mechanical forces have profound effects on vascular smooth muscle cells (VSMCs). The mechanism by which mechanical stimuli regulate vascular endothelial growth factor (VEGF) expression and regulation has yet to be elucidated. We investigated the effect of cyclical mechanical stretching on regulation of the VEGF gene in VSMCs. MATERIALS AND METHODS: Cultured rat VSMCs grown on a flexible membrane base were stretched by applying a vacuum at 60 cycles/minute. VEGF concentration in the cultured media was determined by enzyme-linked immunoassay. VEGF gene expression was determined by Western blot and Northern blot. The location of VEGF in the VSMC was studied immunohistochemically. Chimeric constructs of the VEGF promoter were deleted and the promoter activity was determined by luciferase activity. RESULTS: VEGF concentration increased by 21 to 32% as early as 10 minutes after stretching and remained at this level for up to 12 hours. The concentration of VEGF reached a maximum of 2.8-fold over that in control cells by 2 hours after stretching and declined slightly thereafter. The amount of VEGF mRNA in stretched cells increased as early as 1 hour after stretching, reached a maximum of 3.2-fold over the amount in control cells by 2 hours, and remained at this level for up to 6 hours after stretching. Immunohistochemical study confirmed increased VEGF expression in VSMCs after stretching. Stretched cells transfected with a Sac-Nhe fragment showed only 46% of the luciferase activity of unstretched control cells. However, stretched cells transfected with chimeric plasmids containing a Spe-Nhe fragment showed 2.8-fold luciferase activity over that in control cells. CONCLUSIONS: Cyclical mechanical stretching upregulates expression of the VEGF gene in VSMCs at the transcription level. The VEGF 5'-flanking region contains a negative stretch-response element located in the 0.4-kb Sac-Pst fragment and a positive stretch-response element located in the 0.6-kb Spe-Sac fragment.

Effects of norepinephrine on apoptosis in rat neonatal cardiomyocytes.

BACKGROUND AND PURPOSE: Norepinephrine (NE) is elevated in heart failure and can induce apoptosis in adult cardiac myocytes. However, it is not known whether NE can induce apoptosis in neonatal cardiac myocytes. This study examined the ability of NE to stimulate apoptosis in rat neonatal cardiac myocytes in vitro. METHODS: Neonatal rat cardiac myocytes were exposed to NE alone, NE + propranolol, or NE + prazosin for 24 hours. Apoptosis was assayed by DNA laddering with agarose gel electrophoresis and immunofluorescent terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Reverse transcription polymerase chain reaction was used to evaluate the expression of Mcl-1. Creatine kinase activity in the cultured medium was used as a measure of the toxicity of NE on myocytes. RESULTS: NE increased DNA laddering on agarose gel electrophoresis and increased the number of apoptotic cells in a dose-dependent manner. No increase in apoptosis was found in response to NE doses between 1 and 50 mumol/L. NE at concentrations of 100 to 400 mumol/L increased apoptosis from 10% to 31% of cells. The ability of NE to stimulate apoptosis in rat neonatal cardiac myocytes was completely blocked by propranolol, but not prazosin. NE treatment at high concentrations sharply reduced the level of Mcl-1 mRNA, coincident with the increase in the number of apoptotic cells. Creatine kinase activity in the cultured medium was similar among the controls and NE-treated myocytes. CONCLUSIONS: Our results showed that NE at high concentrations stimulated apoptosis in rat neonatal cardiac myocytes in vitro. Apoptosis induced by NE was associated with down-regulation of Mcl-1. However, NE at the same concentration was not toxic to rat neonatal cardiac myocytes.

The role of P wave in prediction of atrial fibrillation after coronary artery surgery.

Atrial fibrillation (AF) is a common arrhythmia after coronary artery bypass surgery (CABG). The purpose of this study was to determine the role of P wave duration, amplitude and dispersion in the prediction of AF after CABG. This study included 120 patients undergoing elective CABG. Clinical characteristics, 12-lead electrocardiogram (ECG), echocardiogram and coronary angiogram were obtained in all patients. We measured P wave duration, amplitude and dispersion from 12-lead ECG in each patient. After CABG, all patients were continuously monitored for AF attacks in the intensive care unit and ordinary ward. Our results showed that age greater than 60 years was the strongest predictor of postoperative AF (p<0.01), with a 3.7-fold greater likelihood of developing postoperative AF compared to ages less than 60 years. Gender was another independent predictor of postoperative AF, with men being 3.0 times more likely to develop postoperative AF compared to women (p = 0.03). The presence of prolonged P wave duration (> or =100 ms in lead II) was also an independent predictor (p = 0.04), with 2.9-fold greater risk of developing postoperative AF compared to a P wave duration of less than 100 ms. The P wave dispersion was similar between patients with and without postoperative AF (29+/-15 vs. 33+/-15 mm, p = NS). In conclusion, old age, male gender and prolonged P wave duration were independent predictors of AF after CABG. However, P wave dispersion and amplitude did not provide significant information in the prediction of postoperative AF.

Circadian variation of paroxysmal supraventricular tachycardia.

BACKGROUND: Various clinical manifestations of cardiovascular diseases have a pattern of circadian variation. In this study, we investigated whether the onset and duration of paroxysmal supraventricular tachycardia (PSVT) has a circadian variation. METHODS AND RESULTS: In our analysis, we included 105 patients with 498 PSVT episodes. In this study, the onset of PSVT did not have a uniform distribution throughout the 24-h period. There were nearly equal peaks in the time periods from 8:00 to 9:00 AM, 12:00 to 1:00 PM, and 5:00 to 6:00 PM, with a trough at night. The duration of PSVT also did not show a uniform distribution throughout the 24-h period; it increased significantly during the daytime, with a peak between 1:00 and 2:00 PM, another peak between 6:00 and 7:00 PM, and a significant reduction at night. CONCLUSIONS: The onset and duration of PSVT showed a circadian variation. However, the time-oriented antiarrhythmic therapy for preventing PSVT needs further study.

Regional differences in the recovery course of tachycardia-induced changes of atrial electrophysiological properties.

BACKGROUND: Regional differences in recovery of tachycardia-induced changes of atrial electrophysiological properties have not been well studied. METHODS AND RESULTS: In the control group (5 dogs), atrial effective refractory period (AERP) and inducibility of atrial fibrillation (AF) were assessed before and every 4 hours for 48 hours after complete atrioventricular junction (AVJ) ablation with 8-week VVI pacing. In experimental group 1 (15 dogs), AERP and inducibility of AF were assessed before and after complete AVJ ablation with 8-week rapid right atrial (RA) pacing (780 bpm) and VVI pacing. In experimental group 2 (7 dogs), AERP and inducibility of AF were assessed before and after 8-week rapid left atrial (LA) pacing and VVI pacing. AERP and inducibility and duration of AF were obtained from 7 epicardial sites. In the control group, atrial electrophysiological properties obtained immediately and during 48-hour measurements after pacing did not show any change. In the 2 experimental groups, recovery of atrial electrophysiological properties included a progressive recovery of AERP shortening, recovery of AERP maladaptation, and decrease of duration and episodes of reinduced AF. However, recovery of shortening and maladaptation of AERP and inducibility of AF was slower at the LA than at the RA and Bachmann's bundle. CONCLUSIONS: The LA had a slower recovery of tachycardia-induced changes of atrial electrophysiological properties, and this might play a critical role in initiation of AF.

Cardiac troponin T, creatine kinase, and its isoform release after successful percutaneous transluminal coronary angioplasty with or without stenting.

BACKGROUND: Cardiac troponin T is a sensitive and specific marker for the detection of minor myocardial injury. However, it has been rarely used to monitor myocardial injury after coronary stenting. The purpose of the study was to measure troponin T after apparently successful percutaneous transluminal coronary angioplasty (PTCA) with or without coronary stenting and to compare its result with serum creatine kinase and its isoform, CKMB. METHODS: The incidence of cardiac troponin T elevation was compared with that of creatine kinase or CKMB in 120 consecutive patients with symptomatic ischemia undergoing visually successful PTCA with (n = 59) or without stenting (n = 61). Troponin T, creatine kinase, and CKMB were measured before, immediately after, and 18 to 24 hours after the procedures were performed. RESULTS: No patient had abnormal troponin T, creatine kinase, or CKMB levels before and immediately after the procedures. Moreover, no patient showed electrocardiographic evidence of myocardial infarction. Troponin T was elevated in 17 patients at 18 to 24 hours after coronary stenting and in eight patients after PTCA. Both creatine kinase and CKMB were elevated in five patients after coronary stenting and in three patients after PTCA. The frequency of abnormal troponin T levels was significantly higher than that of creatine kinase or CKMB after coronary interventions (21% vs 6.7%; p < 0.01), and it was significantly higher after stenting when compared with angioplasty alone (29% vs 13%; p < 0.05). Patients with abnormal troponin T levels were more likely to undergo repeat revascularization than those without (24% vs 6%; p < 0.01). CONCLUSION: Cardiac troponin T is more sensitive than creatine kinase and CKMB in detecting minor myocardial injury after coronary interventions. The incidence of troponin T release is higher in the patients undergoing stent implantation than in patients treated with angioplasty alone.

Radiofrequency catheter modification of sinus node for inappropriate sinus tachycardia: a case report.

We present here, the case of a 22-year-old male suffering from persistent tachycardia for the past 3 years. His resting pulse rate was rarely below 100 beats/min, and it frequently increased to as high as 150 beats/min even after a minimal of activity. Associated symptoms included palpitation, chest tightness, dyspnea and presyncope, either during rest or with exercise. Propranolol and verapamil could not control the tachycardia. The application of radiofrequency energy to an area in the superior right atrium that demonstrated a discrete electrogram with earliest endocardial activation during tachycardia resulted in a decrease in sinus rate from 120 beats/min to 70 beats/min. Follow-up on Holter monitor, performed one month later, demonstrated an average heart rate of 84 beats/min (range 60-125). In exercise tolerance test, the patient exercised for 9 minutes, achieving a maximum heart rate of 140 beats/min. This patient remained asymptomatic without any antiarrhythmic drug during the 3-month follow-up period. Medical management in case of patients showing disabling inappropriate sinus tachycardia refractory, sinus node modification could be considered as an suitable alternative to complete atrioventricular junctional ablation.