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Author(s):  
Tusharkanti Patra ◽  
Prashant Kumar ◽  
Somnath Mukherjee ◽  
Anurag Passi ◽  
S. K. Saidul Islam

Background: Main objective of the study is details work up of the patients of ventricular tachy-arrhythmias and to find out its association with any structural heart disease.Methods: This institution based observational study was conducted in patients of documented sustained VT (ventricular tachycardia) with consecutive 102 patients.Results: The mean age of the VT patients was 56.7 years and the number of male patients were 70 (69%). In our study, among 102 patients 45 patients were diabetic, 64 patients were hypertensive, 30 patients were current smoker, family history of heart disease was present in 25 patients and family history of SCD (sudden cardiac death) was present in 5 patients. Among the patients who presented with symptoms of ventricular tachy arrhythmia, 25 patients had EF (ejection fraction) above 40%, 36 had EF between 31 to 40% and only 2 had EF below 30%. CAG (coronary angiography) done in 98 patients and 16 had normal coronaries. 20, 16 and 46 patients had single, double and triple vessel disease respectively. 80 patients had coronary heart disease (78%), 20 patients among them had acute ischemic events and 60 had chronic ischemic disease. 12 patients didn’t have any structural heart disease.Conclusions: Ischemic heart disease, acute or chronic, is the most common causes of ventricular tachyarrhythmia. male sex, diabetes mellitus, hypertension, smoking, family history of heart diseases or sudden cardiac death being the risk factors of coronary artery disease are also predisposing factors of ventricular tachyarrhythmia.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Masato Segawa ◽  
Koji Fukuda ◽  
Makoto Nakano ◽  
Masateru Kondo ◽  
Michinori Hirano ◽  
...  

Introduction: It is widely known that ventricular tachy-arrhythmias (VTs) are often observed in patients with cardiac sarcoidosis (CS) as one of the presentations of poor prognosis. However, the time-course and influencing factors of VTs after the introduction of corticosteroid therapy in CS patients remain to be elucidated. Methods and Results: We examined the influence of steroid therapy on VTs in 68 consecutive CS patients in Tohoku University Hospital from October 1998 until September 2014 (57±11 years-old, M/F 18/50). CS was diagnosed based on the original guidelines for diagnosis of CS from the Japanese Ministry of Health and Welfare. Corticosteroid therapy was performed in all CS patients. VTs were defined as sustained ventricular tachycardia/fibrillation or appropriate ICD therapy events. During a mean follow-up of 5.5 years, 20 out of 68 patients (29%) experienced VTs after the initiation of corticosteroid therapy, and 14 (70%) of them had VTs in the first 12 months (Figure A). Multivariable analysis showed that the positive gallium scintigraphy was an independent risk factor for VTs (odds ratio, 17.4; 95% CI, 1.03-294, P=0.047). Survival free from VTs events was significantly lower in the Ga-positive group than in the Ga-negative group (P<0.001), where most of the events were developed in the early phase in the Ga-positive group (Figure B). Furthermore, electrical storm (ES) of VTs was noted in 10 patients (14.7%), and most of them (8 out of the 10 patients) had ES in the first 12 months, whereas the recurrence of ES was relatively low (Figure C). Conclusions: VTs or ES in CS patients was frequently noted in the first 12 months after initiation of corticosteroid therapy, possibly representing inflammatory conditions, for which Ga scintigraphy is useful diagnostic strategy and Ga-positive is an independent prognostic factor in CS.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1967-1967
Author(s):  
Weston P Miller IV ◽  
Ryan Shanley ◽  
Parvin Dorostkar

Abstract Abstract 1967 Introduction: The cardiac QT interval (QT) has gained deserved scrutiny among electrophysiologists. Reflecting the duration of the ventricular myocardial depolarization/repolarization cycle, the QT depends upon ion exchange across cardiomyocyte membranes. Ion flux perturbations (due to abnormalities of membrane-bound ion channel number, structure or function) can predispose to QT prolongation that, in turn, is associated with linearly increasing risks of ventricular tachy-arrhythmias and sudden death. As both polypharmacy and dys-electrolytemia have been reported to affect QT, we studied the interval's behavior in the potentially at-risk population of children and adults undergoing hematopoietic cell transplantation (HCT). Methods: We retrospectively reviewed over 2600 cardiologist-evaluated electrocardiograms (ECG) and transplant-related data for 995 consecutive children and adults undergoing HCT between 2006 and 2010, inclusive. Patients underwent routine pre-HCT ECG screening; repeat studies were obtained for various clinical indications. Corrected QT intervals (QTc) were noted; any study demonstrating non-sinus rhythm was disregarded. Multivariate regression models tested the association between QTc and other patient or transplant-related covariates (including age, gender, primary diagnosis, intensity of conditioning, and donor relatedness/graft-versus host disease prophylaxis for allograft recipients); reference groups representing fixed covariate characteristics were defined among the cohort for comparison. Student's t-test was used to determine the significance of aggregate intra-patient change in QTc from pre- to post-HCT. Results: Pre-HCT: 952 patients had an evaluable pre-HCT maximum QTc observed at a median Day −22. Median QTc was 428 ms (range, 330 to 569; interquartile range [IQR], 409 to 447). Statistically significant QTc variability with age was observed and reflected widely accepted age-dependent phenomena in the population-at-large. Factors predicting shorter QTc included male gender (-11 ms compared to reference group [CRG], p < 0.01) and inherited metabolic disorder (IMD) as HCT indication (-10 ms CRG, p = 0.03). Factors predicting longer QTc were myeloproliferative disorder (+22 ms CRG, p = 0.01) and acute myeloid leukemia (+7 ms CRG, p = 0.02) as HCT indications. Post-HCT: 578 patients had an evaluable post-HCT maximum QTc observed at a median Day +69. Median QTc was 454 ms (range, 367 to 619; IQR, 433 to 476). Age was not significantly predictive of maximum QTc post-HCT. Factors predicting shorter QTc were male gender (-7 ms CRG, p = 0.05) and no exposure to mycophenolate mofetil (MMF) for graft-versus-host disease (GvHD) prophylaxis (-11 ms CRG; p = 0.05). Patients diagnosed with acute lymphoblastic leukemia (ALL) demonstrated longer QTc (+17 ms CRG, p = 0.03). δQTc: 559 patients had at least one evaluable pre- and one evaluable post-HCT ECG. The median δQTc (defined per patient as [mean post-HCT QTc] - [mean pre-HCT QTc]) was 15.7 ms (range, −72 to 142; IQR, −2 to 32). A highly significant difference between post-HCT and pre-HCT QTc per patient was observed in this cohort (p < 0.01). Very Long QTc: 92 (15%) males demonstrated QTc ≥ 480 ms and 39 (10%) females demonstrated QTc ≥ 500 ms on any ECG. Of patients with ≥ 2 evaluable ECGs, 306 (50%) demonstrated prolongation ≥ 40 ms. Factors significantly predicting extreme prolongation included age < 1 year (+39 ms CRG, p < 0.01) and diagnosis of ALL (+15 ms CRG, p = 0.04); a trend toward more extreme prolongation was seen in patients with myelodysplastic syndrome (+14 ms CRG, p = 0.05). The factor protecting from extreme QTc prolongation was treatment with a related allograft (-9 ms CRG, p = 0.03); trends toward less extreme prolongation were also seen in autologous HCT and those not receiving MMF for GvHD prophylaxis. Conclusion: Prolonged QTc is associated with life-threatening ventricular tachy-arrhythmias. This retrospective analysis of a large, diverse HCT cohort shows statistically significant prolongation during transplantation. Too, we identify sub-populations demonstrating very-long QTc and/or experiencing marked QT prolongation during HCT. Further analysis regarding pharmacologic, electrolytic and HCT-related predictors as well as outcomes for the cohort is underway. Disclosures: No relevant conflicts of interest to declare.


1988 ◽  
Vol 9 (5) ◽  
pp. 484-488 ◽  
Author(s):  
A. BIAGINI ◽  
M. EMDIN ◽  
C. MICHELASSI ◽  
M. G. MAZZEI ◽  
C. CARPREGGIANI ◽  
...  

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