Occurrence Of Nonsustained Ventricular Tachycardia Research Articles

Impact of SLGT2 inhibitors treatment initiation on the reduction of atrial and ventricular arrhythmias in patients with implanted cardiac defibrillator

Abstract Introduction Sodium-glucose cotransporter type 2 inhibitors (SGLT2i) have been associated with improved prognosis in patients with heart failure; however, their impact on atrial arrhythmic (AA) and ventricular arrhythmic (VA) events is not fully understood. Methods Retrospective multicentric study of heart failure patients with implantable cardiac defibrillator device (ICD) from 2015 to 2020 with or without cardiac resynchronization therapy (CRT) receiving SGLT2 inhibitors. Device-registered arrhythmic events were analyzed and compared in two time periods for each patient: one year before and one year after starting SGLT2i. Relevant VA were defined as the occurrence of any sustained VT (SVT) (>30 seconds), ventricular fibrillation (VF), or appropriate therapy (antitachycardia pacing or shock). All VA included all the relevant VA and the occurrence of non-sustained ventricular tachycardia (NSVT). AA included atrial fibrillation (AF) burden, and episodes of more than 24 hour of AF. Results A total of 195 patients (66.8 [61.3-73.1] years, 18.5% women) were included. A reduction was observed in the percentage of patients with any VA (pre: 52.3% vs post: 30.3%; P < 0.001) and clinically relevant VA (excluding NSVT) (pre: 21.5% vs post 8.7%; P < 0.001) in the post-SGLT2i period. There was also a reduction in the number of episodes per patient/year of NSVT (pre: 2 (1-5) vs post: 1 (0-2); P < .001), and SVT (pre: 1 (1-3) vs post: 0 (0-2); p = 0.046). This protective effect was also observed after controlling confusion factors (Any VA: OR 0.35 (0,24-0,50); p<0.001 and relevant VA: OR 0.30 (0,17-0,52); p<0.001). However, no differences were observed in the prevalence of AA (24.7% vs 18.8%; P = 0.117) or the burden of atrial fibrillation (pre: 0% (0-0.1) vs post 0% (0-0); p = 0.097). Conclusions Following the initiation of SGLT2i treatment, a reduction in the percentage of patients with relevant VA was observed. However, this effect was not observed for AA.Figure 1Figure 2

Premature ventricular contraction patterns associated with nonsustained ventricular tachycardia

BackgroundOccurrence of nonsustained ventricular tachycardia (NSVT) is associated with negative outcomes. It is not clear whether specific electrocardiographic characteristics of premature ventricular contractions (PVCs) are associated with the occurrence of NSVT. The aim of this study was to identify electrocardiographic patterns associated with the presence of NSVT during 24-h electrocardiographic monitoring in patients with >10 PVCs per hour. MethodsThis was a retrospective, observational, cross-sectional study. We reviewed consecutive patients who received 24-h ECG monitoring performed at a single outpatient cardiology center. Patients who received 24-h electrocardiographic monitoring, with a PVC burden ≥10 PVCs/h were included. Occurrence of NSVT during 24-h electrocardiographic monitoring was the main outcome. ResultsA total of 343 patients were analyzed (mean [SD] age, 69.7 [12.5] years; 177 men [51.6 %]). NSVT occurred in 72 patients who were compared with 271 patients without NSVT. The novel term “premature beat ratio”, which aims to correlate the coupling interval and compensatory pause, was introduced; a value >0.5 was independently associated with NSVT according to the multivariate model (OR = 3.73, 95 % CI = 1.57–8.82; P = 0.002). PVC burden (OR = 1.09, 95 % CI = 1.02–1.17; P = 0.006), and triplets (OR = 18.19, 95 % CI = 7.32–45.18 P = 0.0) were also associated with NSVT in the multivariate model. ConclusionThese findings suggest that patients with a high PVC burden, triplets, and a premature beat ratio greater than 0.5 have an increased probability of presenting with NSVT and may benefit from more rigorous follow-up.

Impact of sodium-glucose cotransporter-2 (SLGT2) inhibitors treatment initiation on the reduction of atrial and ventricular arrhythmias in patients with implanted cardiac devices

Abstract Introduction Sodium-glucose cotransporter-2 (SLGT2) inhibitors have demonstrated benefits on survival and hospital admissions in patients with heart failure and reduced ejection fraction. However, their impact on the burden of ventricular (VA) and atrial arrhythmias (AA) is unknown. Methods Retrospective multicentric study of heart failure patients with implantable cardiac defibrillator device (ICD) from 2015 to 2020 with or without cardiac resynchronization therapy (CRT) receiving SGLT2 inhibitors. Device-registered arrhythmic events were analyzed and compared during one year following SLGT2 inhibitor initiation and during one year before initiation. Relevant VA were defined as the occurrence of any sustained VT (SVT) (>30 seconds), ventricular fibrillation (VF), or appropriate therapy (antytachycardia pacing or shock). All VA included all the relevant VA and the occurrence of non-sustained ventricular tachycardia (NSVT). AA included atrial fibrillation (AF) burden, and episodes of more than 24 hour of AF. Results 147 patients (67 ± 10 years, 82.3% males, LVEF 30.3 ± 11%, CRT 39.3%), were included in the study. 77.6% had complete remote tele-monitoring during the entire follow up and there was no difference in the antiarrhythmic therapy between the two periods. Following SGLT2 inhibitor initiation, there was a significant reduction in the percentage of patients with relevant VA (19.7% pre vs 10.9% post; p=0.019) and all VA (47.6% pre vs 30.6% post; p<0.001) (Figure 1 and 2). There was a reduction in the prevalence of NSVT (40.1% pre vs. 27.2% post; p<0.001), of SVT (17.7% vs 8.8%; p<0.001), of VF (4.1% vs 2%; p=NS) and appropriate therapies (14.3% vs 9.5%; p=NS). Among patients with any VA, there was a significant reduction in the incidence of NSVT (p<0.001), but not in the incidence of SVT or appropriate therapies (p=NS). There was no impact on atrial fibrillation burden or in the number of AF episodes lasting more than 24 hours (p=NS). Conclusions In our study, initiation of a SGLT2 inhibitor in patients with heart failure, was associated with a reduction in the prevalence of relevant VA and any VA, with a significant reduction in the number of NSVT per patient. There was no impact on AF burden or the number of AF episodes lasting more than 24 hours. Prospective studies should be performed to sustain these conclusions.Relevant ventricular arrhythmiasAny ventricular arrhythmia

Cardiac magnetic resonance imaging predictors of ventricular arrhythmia in mid-cavity obstructive hypertrophic cardiomyopathy

Abstract Background/Introduction Left ventricular (LV) mid-cavity obstruction (LVMCO) in hypertrophic cardiomyopathy (HCM) is an uncommon phenotypic feature predisposed to the formation of myocardial fibrosis and apical aneurysms (LVAA). These features may be independently proarrhythmic, and LVAA is considered a class 2a indication for implantable cardioverter defibrillator (ICD) in current US, but not European guidelines for the primary prevention of sudden cardiac death (SCD). Cardiac magnetic resonance (CMR) imaging is the preferred modality for detecting these and other phenotypic features critical to SCD risk assessment. Purpose To assess the ability of CMR imaging parameters to predict occurrence of non-sustained ventricular tachycardia (NSVT) in HCM patients with Doppler-derived evidence of LVMCO. Methods Multi-modality imaging records were retrospectively assessed to identify HCM patients with Doppler-LVMCO and CMR scans. CMR images were assessed by an investigator blinded to clinical status. Late gadolinium enhancement (LGE) was quantified using the full-width, half-maximum technique. CMR imaging parameters were assessed for predictive ability using Cox proportional hazards during univariate and multivariate analyses, accounting for time to event (NSVT or censorship of follow-up). Results The study cohort included 58 patients (57±11 years, 74% male) with a median follow-up of 6.2 (IQR 4.3) years. Mean mid-cavity gradient was 33±23 mmHg. NSVT was detected in 27/58 (47%) patients, was 4 beats or longer in 23/27 (85%) and was monomorphic in 21/27 (77%). On univariate analysis, predictors of NSVT during follow-up include LV mass index (HR 1.02, 95% CI 1.00–1.04, p=0.03), LGE in grams (HR 1.04, 95% CI 1.01–1.06, p=0.005), and LVAA (HR 2.57, 95% CI 1.14–5.79, p=0.023). After multivariate adjustment (Table 2), none were significantly associated. Conclusions In LVMCO, magnitude of LV hypertrophy, extent of LGE and the presence of an apical aneurysm may not be independent predictors of ventricular arrhythmias. SCD algorithms based on qualitative assessments of these features may overestimate risk. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): National Institute of Health Research (NIHR)

Cellular determinants of arrhythmic risk in hypertrophic cardiomyopathy

The most devastating consequence of HCM is sudden cardiac death (SCD) due to ventricular fibrillation. The positive correlation between the extent of late gadolinium enhancement and the arrhythmic risk in HCM suggests that ventricular arrhythmias originate from the fibrotic regions. However, recent data suggest that enhanced cellular automaticity (early- or delayed-afterdepolarizations, EADs or DADs-) may be clinically more relevant in promoting ventricular arrhythmias in patients. Aiming to better understand the cellular and molecular mechanisms of arrhythmogenesis in HCM and to establish a reliable arrhythmic risk stratification in patients, we performed a translational study in HCM patients who underwent surgical myectomy, by combining a clinical follow-up study with in vitro assessments of cellular arrhythmogenicity. We retrospectively studied 61 HCM patients who underwent surgical myectomy. At the time of surgery, fresh ventricular tissue was collected and used to isolate single ventricular cardiomyocytes (CMs), which were used for patch-clamp and Ca 2+ imaging experiments to assess the occurrence of EADs and DADs. Patients were followed up for a median time of 8 years and the occurrence of non-sustained ventricular tachycardia (NSVT) or life-threateningarrhythmic events (LAE) was monitored. EADs occurred in CMs from 36% of patients and were associated with prolonged action potential duration. DADs occurred in 24% of patients and were associated with abnormalities of intracellular Ca 2+ handling. The occurrence of NSVT/ LAE in patients strongly correlated with the presence of DADs in cardiomyocytes. The presence of pro-arrhythmic changes appears to be necessary for arrhythmia generation in HCM and seems to be related with specific alterations at ECG level, that might be used as clinical arrhythmia predictors in HCM patients. Fibrosis per se is not a major predictor of arrhythmias in HCM but may contribute to generate sustained arrhythmias in the presence of substantial cellular triggers (DADs).

Abstract 12893: Early- and Delayed-Afterdepolarizations as Cellular Promoter of Ventricular Fibrillation in Hypertrophic Cardiomyopathy

Introduction: Hypertrophic cardiomyopathy (HCM) represents the main cause of sudden cardiac death (SCD) due to ventricular fibrillation in young adults. Recent data suggest that enhanced cellular automaticity as early- and delayed-afterdepolarizations (EADs and DADs) could represent a major trigger of arrhythmogenesis in HCM. Hypothesis: To deeper understand the cellular mechanisms of arrhythmogenesis and to establish an arrhythmic rysk stratification in HCM patients, we performed a translational and retrospective study in 61 HCM patients who underwent surgical interventricular-septum myectomy to relieve refractory obstruction-related symptoms, combining a clinical follow-up study with in vitro assessment of ventricular myocyte arrhythmogenicity. Methods: At the time of surgery, fresh ventricular tissue was collected and used to isolate single ventricular cardiomyocytes, which were then used to perform patch clamp experiments, to assess the occurrence of EADs and DADs. HCM patients were followed up for a median time of 8 years, monitoring the occurrence of non-sustained ventricular tachycardia (NSVT) or life-threatening arrhytmic events (LAE, including sustained VT and VF). Results: Our data show that EADs occurred in 36% of patients (22/61) and were correlated to a prolongation of action potential duration (due to larger I Nal and I CaL density), while DADs occurred in 27% of patients and were associated to an impairment of Ca 2+ handling. During follow up, NSVT events occurred in 19/62 patients, while LAE occurred in 4/62 patients (combined occurrence 37%). Moreover, patients with NSVT/LAE were more likely to show specific "pro-arrhythmic" ECG-patterns. The occurrence of NSVT/ LAE was strongly associated with the presence of DADs in cells but not with the presence of EADs. Interestingly, the occurrence of DADs in cells was also associated with the presence of "proarrhythmic" ECG-patterns. Conclusions: The presence of cellular triggers as DADs, related with changes of ion channels and intracellular calcium homeostasis, appear to be necessary for arrhythmia generation in HCM. Such pro-arrhythmic changes seem to be linked with specific alterations at ECG level, that might be used as clinical arrhythmia predictors in HCM patients.

Cellular determinants of arrhythmic rysk in hypertrophic cardiomyopathy

Abstract Background Hypertrophic cardiomyopathy (HCM) is the commonest inherited cardiac disease, with a prevalence of 1/500 in the general population. The most devastating consequence of HCM is sudden cardiac death (SCD) due to ventricular fibrillation, particularly common in children and young adults (age <30 years). The positive correlation between the extent of late gadolinium enhancement (LGE, reflecting myocardial fibrosis) and the arrhythmic risk in HCM suggests that ventricular arrhythmias are held to originate from the fibrotic regions, by a mechanism of electrical re-entry. However, recent data suggest that enhanced cellular automaticity (i.e. early- or delayed-afterdepolarizations, EADs or DADs-), rather than macro-reentry, may be clinically relevant in promoting ventricular arrhythmias in patients. Purpose Aiming to better understand the cellular and molecular mechanisms of arrhythmogenesis in HCM and to establish a reliable arrhythmic risk stratification in patients, we performed a translational study in HCM patients who underwent surgical myectomy, by combining a clinical follow-up study with in vitro assessments of cellular arrhythmogenicity in ventricular cardiomyocytes. Methods We retrospectively studied 61 HCM patients who underwent surgical interventricular-septum myectomy to relieve refractory obstruction-related symptoms. At the time of surgery, fresh ventricular tissue was collected and used to isolate single ventricular cardiomyocytes (CMs), which were used for patch-clamp measurements to assess the occurrence of EADs and DADs. Patients were followed up for a median time of 8 years and the occurrence of non-sustained ventricular tachycardia (NSVT) or life-threatening arrhythmic events (LAE) was monitored. Moreover, data from ECG and contract cardiac magnetic-resonance studies were collected. Results EADs occurred in CMs from 36% of patients and were associated with prolonged action potential duration. DADs occurred in 24% of patients and were associated with abnormalities of CM intracellular Ca2+ handling. The occurrence of NSVT/ LAE in patients was strongly associated with the presence of DADs in cardiomyocytes but not with the presence of EADs. Patients with NSVT/LAE were more likely to show specific “pro-arrhythmic” pathological ECG-patterns. Among patients with LGE, the presence of DADs in cells behaved as a necessary pre-requisite for NSVT/LAE, as none of the patients with evidence of fibrosis who were negative for DADs had arrhythmic events. Conclusions The presence of pro-arrhythmic changes appears to be necessary for arrhythmia generation in HCM and seems to be related with specific alterations at ECG level, that might be used as clinical arrhythmia predictors in HCM patients. Fibrosis per se is not a major predictor of arrhythmias in HCM but may contribute to generate sustained arrhythmias in the presence of substantial cellular triggers (DADs). Funding Acknowledgement Type of funding sources: Public grant(s) – EU funding. Main funding source(s): EU Horizon 2020. Grant number 777204 (silico FCM).

Relation of Mitral Leaflet Elongation to Nonsustained Ventricular Tachycardia in Patients with Obstructive Hypertrophic Cardiomyopathy

The impact of mitral valve abnormality on the occurrence of non-sustained ventricular tachycardia (NSVT) in patients with hypertrophic cardiomyopathy (HC) has not been well determined. We sought to demonstrate the relation of mitral valve abnormalities with NSVT in patients with obstructive HC. Three hundred and sixteen adult patients with obstructive HC with at least 1 Holter electrocardiographic monitoring and cardiac magnetic resonance (CMR) from 2014 to 2018 were enrolled. CMR images and Holter electrocardiography were analyzed in all patients. NSVT occurred in 50 patients (16%). Compared with those without NSVT, anterior mitral leaflet and posterior mitral leaflet lengths was significantly increased in patients with NSVT (AML 32.0 ± 5.0mm vs. 26.1±4.8mm, p<0.001; PML 17.7±3.7mm vs. 15.2±2.7mm, p<0.001, respectively). Multivariate logistic regression analysis indicated that elongated AML and PML were significantly independent predictors of NSVT (AML: OR 1.261, 95%CI 1.156-1.375, p<0.001; PML: OR 1.126, 95%CI 1.001-1.265, p=0.047). Furthermore, the area under the receiver operating characteristic curve for AML was 0.812. At a cutoff valve of 27.5mm, AML length had a sensitivity of 86% and specificity of 65%. Elongated mitral leaflets independently correlated with NSVT in patients with obstructive HC. Furthermore, the morphological abnormalities of mitral valve could serve as a useful marker for improving risk stratification of SCD and may play a role in optimizing surgical strategy for patients with obstructive HC.

The Role of the Cardioversion Defibrillator in Post Myocardial Infarction Sudden Cardiac Death: A Systematic Review of Clinical Trials and Observational Studies.

Sudden cardiac death (SCD) accounts for approximately half of all the deaths attributed to cardiovascular disease in the United States. Survivors of an acute myocardial infarction (AMI) are at high risk of SCD, largely due to cardiac arrhythmias and severe left ventricular (LV) systolic dysfunction. The implantable cardioverter defibrillator (ICD) or automated implantable cardioverter defibrillator (AICD) is a device that is implantable inside the body, able to perform cardioversion, defibrillation, and (in modern versions) pacing of the heart. According to a study included in our review, patients who received an ICD contributed to an adjusted 44% reduction (hazard ratio [HR] 0.56, 95% CI: 0.32-1.01; P = 0.053) of all-cause mortality compared to those with a comparable baseline. Patients with an ICD implant three months after a myocardial infarction (MI) demonstrated a non-significantly higher mortality than patients who did not receive an ICD. The factors favoring ICD implantation were multiple MIs, increased resting heart rate, occurrence of non-sustained ventricular tachycardia, QRS duration = 120 ms, syncope events, anti-arrhythmic drug treatment (mostly Class III), and an index MI of more than one year. The likelihood of receiving an ICD diminished with the patient’s age. Increased periodic repolarization dynamics were a significant predictor of mortality. It can be concluded that cardioverter defibrillators help reduce not only all-cause mortality but also sudden cardiac death. It is important to note that ICDs are only significant if implanted after a sufficient time-gap post-MI.

Left ventricular twist in hypertrophic cardiomyopathy : Predictor of nonsustained ventricular tachycardia.

We investigated the efficacy of clinical and classic echocardiographic parameters in predicting the occurrence of nonsustained ventricular tachycardia (NsVT) in patients with hypertrophic cardiomyopathy (HCM). The study comprised 59patients with HCM (47male, [80%]; mean age, 48.48± 14.16years). Clinical, electrocardiographic, as well as classic two-dimensional and speckle-tracking echocardiography (STE) data were collected. All patients had Holter monitoring within 24-72 h of the echocardiographic examination. NsVT was defined as three or more consecutive premature wide QRS complexes with aheart rate of> 100bpm. The patient population was categorized into groups based on the occurrence or absence of NsVT on the 24-h Holter recordings. NsVT was observed in 17patients (29%). In these patients, higher twist (14.4± 3.8 vs.18± 7.9; p= 0.02), higher apical rotation (8.7± 4.2 vs. 12.2± 7; p= 0.02), higher sudden cardiac death risk score (4.4± 2.2 vs. 7± 3.3; p= 0.007), and decreased global longitudinal peak strain (GLPS; -12.8± 3.1 vs. -10.6± 2.8; p= 0.014) were observed. In the multivariate logistic regression analysis, including GLPS and twist, GLPS (Odds Ratio [OR]: 1.406; 95%CI: 1.087-1.818; p= 0.009) and twist (OR: 1.236; 95%CI: 1.056-1.446; p= 0.008) were found to be independent predictors of NsVT. In the receiver operating characteristic curve analysis, GLPS< -11.9% predicted NsVT with 82% sensitivity and 60% specificity (area under the curve [AUC]: 0.70; p= 0.014) and twist> 15.2° predicted NsVT with 70% sensitivity and 58% specificity (AUC: 0.69; p= 0.027). Decreased GLPS and increased twist were predictive of NsVT in HCM patients. Parameters that can easily be measured with STE can help detect patients who may develop arrhythmia.

Primary prevention of sudden cardiac death with an entirely subcutaneous defibrillator in a patient with a large right atrial thrombus

The entirely subcutaneous implantable cardioverter defibrillator represents an innovative new technique for protecting patients from sudden cardiac death. The presented case refers to the implantation of such a system in a 75-yearold male with coronary artery disease, impaired left ventricular function (ejection fraction 31 %) and permanent atrial fibrillation, who presented for primary preventive placement of an implantable cardioverter defibrillator (ICD) after the occurrence of non-sustained ventricular tachycardia of up to 15 beats. Routine transthoracic echocardiography disclosed a large (29 9 28 9 30 mm) right atrial mass which in the subsequent transoesophageal echocardiography appeared highly suggestive of a thrombus (Fig. 1a). Contrast enhanced cardiac magnetic resonance imaging confirmed the etiology of a thrombus and gave no hint to the presence of a tumor. Uncommonly, the thrombus had developed under a therapy of phenprocoumon (INR documented between 2.0 and 3.0) and ASS and did not show signs of regression after 2 months of intensified anticoagulation (INR 3.0–3.5). The patient was supplied with an entirely subcutaneous ICD system (SQ RX 1010, Cameron Health, San Clemente, CA, USA) (Fig. 1b). During a follow-up of 6 months neither device complications nor arrhythmias have been encountered and the patient is doing fine. Although rare, intra-cardiac thrombi can develop despite adequate anticoagulation and negative thrombophilia screening [1]. Transvenous lead passage around the right ventricular thrombus might have been challenging but feasible. This was not attempted because it was feared that the added foreign body would have increased the risk of further thrombus creation. Due to the lack of thrombus regression during intensified anticoagulation, a wearable cardioverterdefibrillator was not deemed as a suitable solution in terms of ‘‘bridge-to-thrombus-regression’’. Instead, an entirely subcutaneous defibrillator was implanted. Our case represents an unusual indication for the entirely subcutaneous defibrillator, which has previously been proposed for niche indications such as difficult venous access, inability to reach the right ventricle transvenously, primary electrical disease, congenital heart disease [2–4] or even broader use [5].

Risk factors of self-terminating and perpetuating ventricular tachyarrhythmias in post-infarction patients with moderately depressed left ventricular function, a CARISMA sub-analysis

The present study aimed to assess whether there are differences in risk indicators for perpetuating ventricular tachyarrhythmias (pVT) and self-terminating ventricular tachyarrhythmias (stVT). Patients with acute myocardial infarction (AMI) and baseline left ventricular ejection fraction ≤ 40% (n = 292) received an implantable electrocardiogram loop recorder from 5 to 21 days after AMI and were followed up for 24 months to document arrhythmic events in the Cardiac Arrhythmias and Risk Stratification after Acute Myocardial Infarction (CARISMA) study. Several risk markers, such as the inducibility to sustained ventricular tachycardia during programmed electrical stimulation (PES), the signal-averaged ECG QRS duration (SAECG-QRS), heart rate variability (HRV) and turbulence (HRT), T-wave alternans, and non-sustained ventricular tachycardia on Holter were analysed at 6 weeks after the AMI. During the follow-up, 26 patients (9%) experienced an stVT (≥ 16 beats and < 30 s), and 21 patients (7%) a pVT. The occurrence of non-sustained ventricular tachycardia on Holter significantly predicted stVT [hazard ratio (HR) = 2.90, 1.26-6.67, 95% confidence interval (CI), P = 0.01], but not pVT during the follow-up. The inducibility during PES (HR = 5.02, 1.85-13.60, 95% CI, P = 0.001), SAECG-QRS ≥ 130 ms (HR = 8.73, 3.38-22.56, 95% CI, P < 0.001), the short-term scaling exponent HRV parameter ≤ 0.77 (HR = 5.65, 2.12-15.10, 95% CI, P = 0.001), and HRT slope ≤ 1.75 ms/NN (HR = 4.57, 1.80-11.59, 95% CI, P = 0.001) were significant predictors of pVT, even after adjustments with relevant clinical parameters (P from < 0.01 to < 0.001), but did not significantly predict the occurrence of stVT (P from 0.35 to 0.75). Self-terminating ventricular tachyarrhythmia and pVT have differences in electrophysiological substrate and arrhythmia modifiers in post-AMI patients with moderate left ventricular dysfunction.

The Relation Between Early Ventricular Tachycardia and QT Dispersion in Patients with Acute Myocardial Infarction Treated with Thrombolytic Therapy.

In this study, we investigated the influence of increased QT dispersion (defined as maximal QT interval minus minimal QT interval) on the occurrence of early nonsustained ventricular tachycardia (NSVT) in patients with acute myocardial infarction (AMI) who received thrombolytic therapy. In the retrospective analysis of 96 patients with clinical reperfusion criteria, 36 had NSVT within the first 12 hours after the onset of thrombolytic therapy (group A), and 60 patients did not have NSVT during the same period (group B). On admission ECG, QT and QT(c) dispersion and the amount of jeopardized myocardial area (Aldrich score) were calculated. In group A, Aldrich score was significantly higher (21.4 +/- 7.2% vs 14.2 +/- 4.9%; p < 0.005). There were significantly higher QT dispersion values on admission (83.3 +/- 23.4 vs 67.5 +/- 23.7 msec; p < 0.005), at 24th hour (87.1 +/- 12.6 vs 72.1 +/- 27.4 msec; p < 0.005) and on the 10th day (63.5 +/- 31.2 vs 49.5 +/- 14.3 msec; p < 0.005) in group A. In subgroup analysis of group A, patients with NSVT between 6-12 hours (group A2) had significantly higher Aldrich score and QT dispersion values at all above time points compared to patients with NSVT between 0-6 hours (group A1) after AMI. In conclusion, in this study we found a strong relation between the occurrence of NSVT within 12 hours and increased QT dispersion on admission ECG in patients with AMI who received thrombolytic therapy. This relation was even stronger for the subgroup of patients with NSVT within 6-12 hours. Thus, these results may indicate that NSVT is related to increased QT dispersion which is secondary to larger jeopardized myocardial area in patients with AMI. </hea

Evaluation of Ventricular Arrythmia with Vasospastic Angina by T-Wave Alternans Based on Holter Recording

Background: T-wave alternans (TWA) has been known to be useful for evaluations of repolarization abnormalities and a predictor of ventricular arrhythmia. Ventricular arrhythmia in vasospastic angina (VSA) was reported to be associated with repolarization abnormalities. Therefore, we investigated the association between TWA and ventricular arrhythmia in VSA. Method: We investigated max MMA-TWA and occurrence of non-sustained ventricular tachycardia (NSVT) in Holter recording for 45 consecutive VSA patients (21 males, 60.3±13.1 years-old). TWA ≥65 µV was considered positive. Result: NSVT were recorded in 6 patients. Max MMA-TWA in 6 patients with NSVT was significantly higher than those in 39 patients without NSVT (83±12 vs. 65±21 µV; p<0.02). Coronary vasospasm in Right coronary artery (RCA) was induced in 5 of 6 patients. Moreover, incidence of positive TWA was significantly higher in patients with RCA spasm (21/31 patients; 68%) than patients without RCA spasm (4/14 patients; 28% p<0.01). Max MMA-TWA in 31 patients with RCA spasm was higher than those in 14 patients with vasospasm in other vessels excluding RCA. Conclusion: There was a significant relationship between TWA and RCA spasm. Moreover, most of VSA patients with NSVT had not only RCA spasm but also repolarization abnormalities associated with high risk of ventricular arrhythmia.

206 Ventricular arythmias in cardiac pacing patients: monocentric study

The new pacemaker (PM) generations featuring extended memory functions (MF) document the occurrence of arrhythmias over periods of several months. Recordings of all atrial episodes and their characteristics contribute to the efficacious treatment of these patients. However, ventricular arrhythmia (VA) characteristics and occurrences are less well-known in this population. The goal of this study was to evaluate the pertinence of MF at the ventricular level and to describe the MF-documented VAs. the study involved a continuous series of 93 pts (M 66%, aged 75 ± 10 yrs) implanted with SC or DC Kappa and EnPulse PMs (Medtronic, MN, USA) for AVB 41%, SD 55%. 497 visits were analyzed (follow-up at 7 months avg.) over a period from 2 to 81 months after implantation, and occurrences of VA validated by EGMs, defined by at least 5 QRS complexes >175/mn. The number of episodes and the duration and heart rate during the longest arrhythmia episodes were recorded. 24 pts (26%) average ages 74 ± 13 yrs of whom 78% males, showed ventricular arrhythmias in 88 visits (18%). The average number of episodes was 9 per follow-up (1–140), average duration was 4 ± 4 seconds (1–27 sec), and average rate was 214 ± 33 bpm. (174–307). The totality of the episodes were classified as non-sustained ventricular tachycardia (NSVT). The ejection fraction was 51 ± 11%. 84% showed cardiopathy: CAD (12), HCM(4) and DCM (4). Statistical analysis showed that age, pacing indication, pacing mode and cumulated percentage of pacing are not relevant factors in NSVT. VAs are observed in π of pts implanted for standard pacing indications. A major determining factor in the occurrence of NSVT is the presence of an associated cardiopathy. FMs featuring EGM recordings are a tool for reliable diagnostic and monitoring of these events. Further studies are required to evaluate the prognostic significance of these VAs.

Mitral annular disjunction in myxomatous mitral valve disease: a relevant abnormality recognizable by transthoracic echocardiography

BackgroundMitral annular disjunction (MAD) consists of an altered spatial relation between the left atrial wall, the attachment of the mitral leaflets, and the top of the left ventricular (LV) free wall, manifested as a wide separation between the atrial wall-mitral valve junction and the top of the LV free wall. Originally described in association with myxomatous mitral valve disease, this abnormality was recently revisited by a surgical group that pointed its relevance for mitral valve reparability. The aims of this study were to investigate the echocardiographic prevalence of mitral annular disjunction in patients with myxomatous mitral valve disease, and to characterize the clinical profile and echocardiographic features of these patients.MethodsWe evaluated 38 patients with myxomatous mitral valve disease (mean age 57 ± 15 years; 18 females) and used standard transthoracic echocardiography for measuring the MAD. Mitral annular function, assessed by end-diastolic and end-systolic annular diameters, was compared between patients with and without MAD. We compared the incidence of arrhythmias in a subset of 21 patients studied with 24-hour Holter monitoring.ResultsMAD was present in 21 (55%) patients (mean length: 7.4 ± 8.7 mm), and was more common in women (61% vs 38% in men; p = 0.047). MAD patients more frequently presented chest pain (43% vs 12% in the absence of MAD; p = 0.07). Mitral annular function was significantly impaired in patients with MAD in whom the mitral annular diameter was paradoxically larger in systole than in diastole: the diastolic-to-systolic mitral annular diameter difference was -4,6 ± 4,7 mm in these patients vs 3,4 ± 1,1 mm in those without MAD (p < 0.001). The severity of MAD significantly correlated with the occurrence of non-sustained ventricular tachycardia (NSVT) on Holter monitoring: MAD›8.5 mm was a strong predictor for (NSVT), (area under ROC curve = 0.74 (95% CI, 0.5-0.9); sensitivity 67%, specificity 83%). There were no differences between groups regarding functional class, severity of mitral regurgitation, LV volumes, and LV systolic function.ConclusionsMAD is a common finding in myxomatous mitral valve disease patients, easily recognizable by transthoracic echocardiography. It is more prevalent in women and often associated with chest pain. MAD significantly disturbs mitral annular function and when severe predicts the occurrence of NSVT.

The risk of non-sustained ventricular tachycardia after percutaneous alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy

Percutaneous alcohol septal ablation (ASA) becomes an alternative option of treatment for symptomatic patients with hypertrophic obstructive cardiomyopathy (HOCM). The procedure relieves left ventricular outflow tract obstruction, but produces a myocardial scar in patients who already have a substrate for life-threatening ventricular arrhythmia. To examine the effect of ASA on the occurrence of non-sustained ventricular tachycardia (nsVT) on 24 h ambulatory Holter monitoring in HOCM patients. Sixty-one consecutive patients (34 males, mean age 48 years), who underwent ASA between 1997 and 2003 were analyzed. Holter recordings were performed in each patient before and after ablation. Follow-up ranged from 60 to 125 months (median 116 months). The mean number of Holter recordings per patient was 2.7 (range 1-11) before and 8.3 (range 2-23) after ASA (p < 0.001). Non-sustained ventricular tachycardia occurred in 14 patients before and 27 patients after ASA (23 vs. 44%, p = 0.01). The percentage of Holter recordings with nsVT before and after ablation was similar (14.5 vs. 15.7%, p = 0.56, respectively). No difference was observed between the number of nsVT per Holter recording before and after ablation (0.21 vs. 0.24%, p = 0.65, respectively). The percentage of patients with nsVT after ASA was comparable to the proportion of patients with nsVT in a control group consisting of 705 patients with hypertrophic cardiomyopathy under follow-up at our institution (44.3 vs. 43.2%, p = 0.91). There was no significant difference in percentage of Holter recordings with nsVT with respect to sex, amount of alcohol used during ASA, peak creatine phosphokinase level, and gradient reduction at rest. Alcohol septal ablation affected neither the percentage of Holter recordings with nsVT nor the number of nsVT episodes per Holter recording among HOCM patients.

Usefulness of Delayed Enhancement by Magnetic Resonance Imaging in Hypertrophic Cardiomyopathy as a Marker of Disease and Its Severity

The aim of the present study was to evaluate, in patients with hypertrophic cardiomyopathy (HC), the association between late gadolinium enhancement and clinical end points, such as nonsustained ventricular tachycardia, arrhythmic risk factors, New York Heart Association class, symptoms, and left ventricular functional parameters. A total of 20 normal subjects (mean age 38 years, 16 men) and 100 patients with HC (mean age 46 years, 70 men) were enrolled in the present study. In the late gadolinium enhancement images, the extent of unenhanced, mildly enhanced, and higher enhanced myocardium was measured. Higher enhancement was present in 80% of the HC population and was significantly greater in patients with a New York Heart Association class >1. Mild enhancement was present in all the patients with HC. Receiver operating characteristic analysis revealed that a cutoff of >4.9% of mild enhancement had 100% sensitivity and 86% specificity to predict the occurrence of nonsustained ventricular tachycardia, and a cutoff of >2.4% of hyperenhancement had 77% sensitivity and 96% specificity. In conclusion, late gadolinium enhancement was associated with nonsustained ventricular tachycardia, arrhythmic risk factors, and worse New York Heart Association class.

The hemodynamic and pharmacokinetic interactions between chronic use of oral levosimendan and digoxin in patients with NYHA Classes II

Levosimendan is a calcium-sensitizing drug for the treatment of heart failure. The aim of this exploratory study was to assess the hemodynamic and pharmacokinetic interactions between digoxin and oral levosimendan as well as the proarrhythmic potential of this combination in patients with chronic heart failure. Male or female patients (n = 24) with chronic heart failure of NYHA Classes II-III. A randomized, placebo-controlled, double-blind, parallel-group trial. After a 1-week digoxin-free washout period, the patients were randomized to receive either digoxin and levosimendan (digoxin + levosimendan), or digoxin and placebo (digoxin) orally for 14 +/- 2 days. The levosimendan dose was 1 mg 3 times daily, and the digoxin dose was 0.125-0.25 mg once daily. Systolic time intervals, electrocardiography (ECG), magneto-cardiography (MCG) and 24-h ambulatory ECG were performed at baseline and at the end of each treatment period. Pharmacokinetic variables of levosimendan and digoxin were calculated in both treatment periods. Steady-state concentrations of the active metabolites OR-1855 and OR-1896 were determined at baseline at Visit 2. There tended to be a greater shortening of QS2i (suggesting trend to positive inotropy) in the digoxin + levosimendan group (-14ms) compared with the digoxin group (-5ms), although the difference was not statistically significant (p=0.359). However, the change from baseline in QS2i after digoxin + levosimendan was of statistically borderline significance (p=0.05). The change from baseline in the digoxin group was not statistically significant. ECG and MCG repolarization measures and occurrence of nonsustained ventricular tachycardia showed no substantial differences. After 2 weeks of digoxin + levosimendan treatment, mean area under the curve (AUC) of levosimendan increased approximately by 49% (p<0.01). The maximum plasma concentration (Cmax) of levosimendan increased from 17 to 23 ng/ml. The mean concentrations of the metabolites OR-1855 and OR-1896 in plasma were 4.3 and 8.3 ng/ml, respectively. The addition of oral levosimendan to digoxin therapy produced only a modest statistically nonsignificant additive inotropic effect. In contrast to the earlier data with intravenous levosimendan, the results indicate a pharmacokinetic interaction between levosimendan and digoxin. Data obtained from repolarization analyses and ambulatory ECG did not indicate any possible proarrhythmic effects of the combination.

Do statins influence the prognostic impact of non-sustained ventricular tachycardia after ST-elevation myocardial infarction?

The study evaluates the effect of statin therapy on the prognostic impact of non-sustained ventricular tachycardia (NSVT) occurring after acute ST-elevation myocardial infarction (STEMI). From the German Acute Coronary Syndrome Registry (ACOS), 3137 patients with STEMI and in-hospital Holter monitoring were analysed. Three hundred and forty-six (11.0%) patients had NSVT. When compared with patients with no documented NSVT, patients with NSVT were older, more often had myocardial infarction in their history, diabetes mellitus, and an ejection fraction <40%. Regarding frequency of drug application, medication at discharge did not (beta-blockers, ACE-inhibitors, amiodarone) or only slightly (acetylsalicylic acid, statins, and sotalol) differ between both groups. Multivariable analysis of 1 year mortality, adjusted for age, gender, diabetes, reperfusion therapy, ejection fraction <40%, and beta-blocker therapy showed the following results: In patients without statin treatment and no NSVT, 1 year mortality after STEMI was 9.2%, but increased to 25.0% [odds ratio (OR) 3.02; 95% confidence interval (CI) 1.47-6.20], if NSVT were present. In patients on statin treatment and no NSVT, 1 year mortality was only 3.2%, and in the presence of NSVT 1 year mortality was not significantly increased anymore (5.3%; OR 1.03; 95% CI 0.55-1.92). After STEMI, only in patients not on statin treatment, the occurrence of NSVT is associated with a significant and marked increase in 1 year mortality.