The study sought to assess the impact of chronic kidney disease (CKD) on recurrences of ventricular tachyarrhythmias in implantable cardioverter defibrillator (ICD) recipients. Data regarding the ...outcome of patients with CKD in ICD recipients is limited. A large retrospective registry was used including consecutive ICD recipients surviving episodes of ventricular tachycardia (VT) or fibrillation (VF) from 2002 to 2016. CKD patients were compared to non-CKD patients. The primary endpoint was the first recurrence of ventricular tachyarrhythmias at 5 years. Secondary endpoints were ICD-related therapies, rehospitalization and all-cause mortality at 5 years. Kaplan–Meier, multivariable Cox regression and propensity score matching were applied. A total of 585 consecutive patients were included (non-CKD: 57%, CKD: 43%). CKD had higher rates of the primary endpoint of recurrent ventricular tachyarrhythmias compared to non-CKD patients (50% vs. 40%; log rank
p
= 0.008; HR = 1.398; 95% CI 1.087–1.770;
p
= 0.009), which was irrespective of a primary or secondary preventive ICD and mainly attributed to recurrent VF (11% vs. 5%;
p
= 0.007) and electrical storm (ES) (10% vs. 5%;
p
= 0.010). Accordingly, CKD patients had higher rates of the secondary endpoint of appropriate ICD therapies (41% vs. 30%; log rank
p
= 0.002; HR = 1.532; 95% CI 1.163–2.018;
p
= 0.002), mainly attributed to appropriate ICD shocks (19% vs. 11%;
p
= 0.005). After multivariable Cox regression CKD was associated with a 1.4-fold higher risk of appropriate device therapies (HR = 1.353; 95% CI 1.001–1.825;
p
= 0.049), but not with first recurrence of ventricular tachyarrhythmias (
p
= 0.177). Irrespective of propensity score matching, CKD was associated with increasing all-cause mortality at 5 years (
p
= 0.001). The presence of CKD is associated with increased rates of recurrent ventricular tachyarrhythmias, appropriate device therapies, mainly attributed to appropriate shock, and all-cause mortality in ICD recipients at 5 years.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Background: Sacubitril/valsartan decreased the risk of sudden cardiac death (SCD) in patients suffering from heart failure with reduced ejection fraction (HFrEF). However, long-term data are sparse. ...Objective: The aim of the present study was to compare the incidence of life-threatening arrhythmias consisting of ventricular tachycardia and/or ventricular fibrillation before and after initiation of sacubitril/valsartan treatment. Methods: Out of 12,000 patients with HFrEF from 2016–2018, 148 patients were newly prescribed sacubitril/valsartan, but the long-term data of only 127 patients were available and included in this study. Results: Patients with an average age of 66.8 ± 12.1 had a median left ventricular ejection fraction (LVEF) of 25% (interquartile range (IQR) 5.00–45.00) and 30% (IQR 10.00–55.00, p < 0.0005) before and after sacubitril/valsartan treatment, respectively. Systolic blood pressure decreased from 127.93 ± 22.01 to 118.36 ± 20.55 mmHg (p = 0.0035) at 6 months of follow-up. However, in 59 patients with a long-term outcome of 12 months, ventricular arrhythmias persistently increased (ventricular fibrillation from 27.6 to 29.3%, ventricular tachycardia (VT) from 12% to 13.8%, and nonsustained VT from 26.6 to 33.3%). Conclusions: Sacubitril/valsartan does not reduce the risk of ventricular tachyarrhythmias in chronic HFrEF patients over 12 months of follow-up.
Cardiac sodium channel β-subunit mutations have been associated with several inherited cardiac arrhythmia syndromes.
To identify and characterize variations in SCN1Bb associated with Brugada syndrome ...(BrS) and sudden infant death syndrome (SIDS).
All known exons and intron borders of the BrS-susceptibility genes were amplified and sequenced in both directions. Wild type (WT) and mutant genes were expressed in TSA201 cells and studied using co-immunoprecipitation and whole-cell patch-clamp techniques.
Patient 1 was a 44-year-old man with an ajmaline-induced type 1 ST-segment elevation in V1 and V2 supporting the diagnosis of BrS. Patient 2 was a 62-year-old woman displaying a coved-type BrS electrocardiogram who developed cardiac arrest during fever. Patient 3 was a 4-month-old female SIDS case. A R214Q variant was detected in exon 3A of SCN1Bb (Na(v)1B) in all three probands, but not in any other gene previously associated with BrS or SIDS. R214Q was identified in 4 of 807 ethnically-matched healthy controls (0.50%). Co-expression of SCN5A/WT + SCN1Bb/R214Q resulted in peak sodium channel current (I(Na)) 56.5% smaller compared to SCN5A/WT + SCN1Bb/WT (n = 11-12, P<0.05). Co-expression of KCND3/WT + SCN1Bb/R214Q induced a Kv4.3 current (transient outward potassium current, I(to)) 70.6% greater compared with KCND3/WT + SCN1Bb/WT (n = 10-11, P<0.01). Co-immunoprecipitation indicated structural association between Na(v)β1B and Na(v)1.5 and K(v)4.3.
Our results suggest that R214Q variation in SCN1Bb is a functional polymorphism that may serve as a modifier of the substrate responsible for BrS or SIDS phenotypes via a combined loss of function of sodium channel current and gain of function of transient outward potassium current.
Background The study sought to assess the prognostic impact of acute myocardial infarction ( AMI ) with and without ST -segment-elevation myocardial infarction ( STEMI and NSTEMI ) in patients with ...ventricular tachyarrhythmias and sudden cardiac arrest ( SCA ) on admission. Methods and Results A large retrospective registry was used including all consecutive patients presenting with ventricular tachycardia ( VT ), fibrillation ( VF ), and sudden cardiac arrest ( SCA ) on admission from 2002 to 2016. AMI versus non- AMI and STEMI versus NSTEMI were compared applying multivariable Cox regression models and propensity-score matching for evaluation of the primary prognostic end point defined as long-term all-cause mortality at 2.5 years. Secondary end points were 30 days all-cause mortality, cardiac death at 24 hours, in hospital death, and recurrent percutaneous coronary intervention (re- PCI ) at 2.5 years. In 2813 unmatched high-risk patients with ventricular tachyarrhythmias and SCA , AMI was present in 29% (10% STEMI , 19% NSTEMI ) with higher rates of VF (54% versus 31%) and SCA (35% versus 26%), whereas VT rates were higher in non- AMI (56% versus 30%) ( P < 0.05). AMI -related VT ≥48 hours was associated with higher mortality (log rank P = 0.001). Multivariable Cox regression models revealed non- AMI (hazard ratio = 1.458; P = 0.001) and NSTEMI (hazard ratio = 1.460; P = 0.036) associated with increasing long-term all-cause mortality at 2.5 years, which was also proven after propensity-score matching (non- AMI versus AMI : 55% versus 43%, log rank P = 0.001, hazard ratio = 1.349; NSTEMI versus STEMI : 45% versus 34%, log rank P = 0.047, hazard ratio = 1.372). Secondary end points including 30 days and in-hospital mortality, as well as re- PCI were higher in non- AMI patients. Conclusions In high-risk patients presenting with ventricular tachyarrhythmias and SCA , non- AMI revealed higher mortality than AMI , respectively NSTEMI than STEMI , alongside AMI -related VT ≥48 hours.
Objectives. Diagnostic guidelines for chronic obstructive pulmonary disease (COPD) are based on spirometry and clinical criteria. However, this does not address the pathophysiological complexity of ...the disease sufficiently. Until now, inspiratory chest computed tomography (CT) has been considered as the preferred imaging method in these patients. We hypothesized that expiratory CT may be superior to demonstrate pathophysiological changes. The aim of this prospective study was to systematically compare lung function tests with quantified CT parameters in inspiration and expiration. Materials and Methods. Forty-six patients with diagnosed COPD underwent spirometry, body plethysmography, and dose-optimized CT in maximal inspiration and expiration. Four quantified CT parameters were acquired in inspiration, expiration, and their calculated delta values. These parameters were correlated with seven established lung function parameters. Results. For inspiratory scans, a weak-to-moderate correlation with the lung function parameters was found. These correlations significantly improved when adding the expiratory scan (p<0.05). Moreover, some parameters showed a significant correlation only in expiratory datasets. Calculated delta values showed even stronger correlation with lung function testing. Conclusions. Expiratory quantified CT and calculated delta values significantly improve the correlation with lung function parameters. Thus, an additional expiratory CT may improve image-based phenotyping of patients with COPD.
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FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
The left atrial appendage (LAA) represents both a predisposing source of thrombus formation and of neuro-humoral haemostasis. This study aims to evaluate changes of biomarker expression before and ...after successful percutaneous closure of the LAA. Patients with atrial fibrillation and contraindication for oral anticoagulant therapy were enrolled. Blood samples were taken within 24 hours before (T1) and at least 6 months (mid-term) (T2) after successful implantation of LAA occlusion devices. Blood levels of high sensitivity troponin I and T (hsTnI, hsTnT), aminoterminal pro-brain natriuretic peptide (NT-proBNP) and mid-regional pro-atrial natriuretic peptide (MR-proANP) were evaluated at both time points. A total of 42 patients with successful percutaneous LAA closure were included. Median mid-term follow-up was of 183 days. HsTnT, hsTnI and NT-proBNP did not show any significant differences over time. Serum levels of MR-proANP increased significantly between immediate pre-intervention (T1: median = 245.7 pmol/l, IQR 155.8-361.3 pmol/l) and at mid-term follow-up (T2: median = 254 pmol/l, IQR 183.4-396.4 pmol/l) (p = 0.037). These results indicate, that percutaneous LAA closure affects neuro-humoral haemostasis by increasing MR-proANP serum levels at mid-term follow-up.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Short QT syndrome (SQTS) is a rare syndrome and affects different types of genes. However, data on differences of clinical profile and outcome of different SQTS types are sparse.
We conducted a ...pooled analysis of 110 SQTS patients. Patients have been diagnosed between 2000 and 2017 at our institution (n = 12) and revealed using a literature review (n = 98). 29 studies were identified by analysing systematic data bases (PubMed, Web of Science, Cochrane Libary, Cinahl).
67 patients with genotype positive SQTS origin and 43 patients with genotype negative origin were found. A significant difference is documented between the sex with a higher predominance of male in genotype negative SQTS patients and predominance of females in genotype positive SQTS patients (male 52% versus 84%, female 45% versus 14%; p = 0.0016). No relevant difference of their median age (genotype positive 27 ± 19 versus genotype negative 29 ± 15; p = 0.48) was found. Asymptomatic patients and patients reporting symptoms such as syncope, sudden cardiac death, atrial flutter and ventricular fibrillation documented in both groups were similar except atrial fibrillation (genotype positive 19% versus genotype negative 0%; p = 0.0055). The QTc interval was not significantly different in both groups (genotype positive 315 ± 32 versus genotype negative 320 ± 19; p = 0.30). The treatments (medical treatment and ICD implantation) in both groups were comparable. Electrophysiology studies were not significantly higher documented in patients with genotype positive and negative origin (24% versus 9%; p = 0.075). Events at follow up such as VT, VF, and SCD were not higher presented in patients with genotype positive (13% versus 9%) (p = 0.25). 54% of genotype positive SQTS patients showed SQTS 1 followed by STQS 2 (21%) and SQTS 3 (10%).
The long-term risk of a malignant arrhythmic event is not higher in patients with genotype positive. However, patients with genotype positive present themselves more often with AF with a female predominance. Also, other events at follow up such as syncope, atrial flutter and palpitation were not significantly higher (9% versus 0%; p = 0.079).
Short QT syndrome (SQTS) is an inherited cardiac channelopathy characterised by an abnormally short QT interval and increased risk for atrial and ventricular arrhythmias. Diagnosis is based on the ...evaluation of symptoms (syncope or cardiac arrest), family history and electrocardiogram (ECG) findings. Mutations of cardiac ion channels responsible for the repolarisation orchestrate electrical heterogeneity during the action potential and provide substrate for triggering and maintaining of tachyarrhythmias. Due to the malignant natural history of SQTS, implantable cardioverter defibrillator (ICD) is the first-line therapy in affected patients. This review summarises current data and addresses the genetic basis and clinical features of SQTS.
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