Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and augmented risk of sudden cardiac death. Little is known about ...the clinical presentation and prognosis of this disease in children.
Thirty children affected by Brugada syndrome who were <16 years of age (mean, 8+/-4 years) were included. All patients displayed a type I ECG pattern before or after drug provocation challenge. Diagnosis of Brugada syndrome was made under the following circumstances: aborted sudden death (n=1), syncope of unexplained origin (n=10), symptomatic supraventricular tachycardia (n=1), suspicious ECG (n=1), and family screening for Brugada syndrome (n=17). Syncope was precipitated by fever in 5 cases. Ten of 11 symptomatic patients displayed a spontaneous type I ECG. An implantable cardioverter-defibrillator was implanted in 5 children; 4 children were treated with hydroquinidine; and 1 child received a pacemaker because of symptomatic sick sinus syndrome. During a mean follow-up of 37+/-23 months, 1 child experienced sudden cardiac death, and 2 children received an appropriate implantable cardioverter-defibrillator shock; all of them were symptomatic and had manifested a type I ECG spontaneously. One child had a cardioverter-defibrillator infection that required explantation of the defibrillator.
In the largest population of children affected by Brugada syndrome described to date, fever represented the most important precipitating factor for arrhythmic events, and as in the adult population, the risk of arrhythmic events was higher in previously symptomatic patients and in those displaying a spontaneous type I ECG.
Among the distinctive features of coronavirus disease 2019 (COVID-19), numerous reports have stressed the importance of vascular damage associated with coagulopathy onset 1. Histological analysis of ...pulmonary vessels in patients with COVID-19 revealed severe endothelial injury associated with intracellular severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus and disrupted endothelial cell membranes together with widespread thrombosis and occlusion of alveolar capillaries. Microparticles (MPs) shed by apoptotic/stimulated cells of various cellular lineages, including platelets, leukocytes, macrophages or endothelial cells, are reliable markers of vascular damage 2 released upon pro-inflammatory conditions and behave as active participants in the early steps of clot formation 3. Circulating MPs promote procoagulant responses due to the exposure of tissue factor, the physiological activator of the coagulation cascade, and of negatively charged phospholipids, such as phosphatidylserine, required for the assembly of the tenase and prothrombinase coagulation complexes ultimately leading to thrombin generation, through which they can precisely be quantified 4. MPs carry angiotensin-converting enzyme (ACE)1 and upregulate ACE1 expression in neighbouring endothelial cells 5. By contrast, exosomes were recently reported to convey ACE2, the cell-entry receptor for SARS-CoV-2 4, in the vasculature 6. ACE2 converts angiotensin II (Ang II) into angiotensin 1–7 (Ang 1–7), which by virtue of its actions on the Mas receptor, limits the noxious effects of Ang II. Pioneering data have demonstrated that the renin–angiotensin system has a crucial role in severe acute injury and that ACE2 has a protective role in acute lung injury mediated by SARS-CoV 7. According to this paradigm, the loss of ACE2 function following binding by SARS-CoV-2 may contribute to unopposed Ang II accumulation that further exacerbates tissue injury and promotes inflammation, MPs release and thrombosis. During SARS-CoV-2 infection, we hypothesised that various factors including inflammatory burden, Ang II, altered shear stress and hypoxic vasoconstriction, could enhance MPs shedding by various cell lineages including the alveolar vascular endothelium and contribute to clot formation.
Procoagulant microparticles are associated with the extent of lung injuries in #COVID19 and pulmonary thrombosis
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Background Electrocardiographic strain pattern (ESP) has recently been associated with increased adverse outcome in aortic stenosis and after surgical aortic valve replacement. Our study sought to ...determine the impact and incremental value of ESP pattern in predicting adverse outcome after transcatheter aortic valve replacement. Methods and Results A total of 585 patients with severe aortic stenosis (mean age, 83±7 years; men, 39.8%) were enrolled for transcatheter aortic valve replacement from November 2012 to May 2018. ESP was defined as ≥1-mm concave down-sloping ST-segment depression and asymmetrical T-wave inversion in the lateral leads. The primary end points of the study were all-cause mortality, rehospitalization for heart failure, myocardial infarction, and stroke. A total of 178 (30.4%) patients were excluded because of left bundle-branch block (n=103) or right bundle-branch block (n=75). Among the 407 remaining patients, 106 had ESP (26.04%). At a median follow-up of 20.00 months (11.70-29.42 months), no impact of electric strain on overall and cardiac death could be established. By contrast, incidence of rehospitalization for heart failure was significantly higher (33/106 31.1% versus 33/301 11%;
<0.001) in patients with ESP. By multivariate analyses, ESP remained a strong predictor of rehospitalization for heart failure (hazard ratio, 2.75 95% CI, 1.61-4.67;
<0.001). Conclusions In patients with aortic stenosis who were eligible for transcatheter aortic valve replacement, ESP is frequent and associated with an increased risk of postinterventional heart failure regardless of preoperative left ventricular hypertrophy. ESP represents an easy, objective, reliable, and low-cost tool to identify patients who may benefit from intensified postinterventional follow-up.
Abstract Background To gain more insight into the involvement of inflammatory response and neurohumoral activation in Takotsubo cardiomyopathy (TTC), we investigated C-reactive protein (CRP), ...leukocytes, plasma catecholamines levels, iodine 123 meta-iodobenzylguanidine (123 I-mIBG) myocardial uptake, myocardial perfusion (thallium 201 201 Tl or technetium Tc 99m-tetrofosmin myocardial single photon emission computed tomography SPECT), and metabolism (fluorine 18-fluorodeoxyglucose positron emission tomography). Methods and Results Inflammatory status and brain natriuretic peptide (BNP) levels in 17 patients with TTC were compared with 14 age-matched patients. In TTC, elevated levels of CRP were evidenced on admission, reaching a peak in the following days ( P < .01). CRP levels were correlated to baseline left ventricular ejection fraction (LVEF) and BNP levels ( P < .05). Leukocytes were correlated to BNP and noradrenaline levels. Myocardial123 I-mIBG SPECT showed a reduced activity in the midventricle and apex corresponding to 35% ± 23% of the total myocardial mass, partially reversible at follow-up. An identical pattern was retrieved when assessing myocardial glucose metabolism. At rest, no relevant abnormalities of myocardial perfusion could be evidenced at the subacute phase. Conclusion Inflammatory status in TTC was related to LVEF impairment and to the extent of neurohormonal activation. The hypothesis of a catecholamine-induced myocardial “stunning” is emphasized by the evidence of a reduced123 I-mIBG myocardial activity, impairment of myocardial glucose metabolism, and wall motion kinetic after the same temporospatial distribution.
Four human induced pluripotent stem cell (hiPSC) lines have been generated from healthy control European donors, and validated. This resource represents a useful tool for stem cell-based research, as ...references for developmental studies and disease modeling linked to any type of human tissue and organ, in an ethnical-, sex- and age-matched context. They providea reliable in-vitro model for single cell- and tissue-based investigations, and are also a valuable tool for genome editing-based studies.
Background
Although less common, typical atrial flutter shares similar pathophysiological roots with atrial fibrillation. Following successful cavo‐tricuspid isthmus ablation using radiofrequency, ...many patients, however, develop atrial fibrillation in the mid‐to‐long‐term. This study sought to assess whether pulmonary vein isolation conducted at the same time as cavo‐tricuspid isthmus ablation would significantly modify the atrial fibrillation burden upon follow‐up in patients suffering from typical atrial flutter.
Methods
This was a multicenter randomized controlled study involving typical atrial flutter patients with history of non‐predominant atrial fibrillation (1 atrial fibrillation episode only, in 67% of population) who were scheduled for cavo‐tricuspid isthmus radiofrequency ablation. Patients were randomly assigned to either undergo cavo‐tricuspid isthmus ablation alone or cavo‐tricuspid isthmus plus pulmonary vein isolation (CTI+). Pulmonary vein isolation was performed using cryoballoon technology. An outpatient consultation with ECG and 1‐week Holter monitoring was performed at 3, 6 months, 1 year, and 2 years postprocedure. The primary endpoint was atrial fibrillation recurrences lasting more than 30 s at 2 years postablation.
Results
Of the patients enrolled, 36 were included in each group. At 2‐year follow‐up, the atrial fibrillation recurrence rate was significantly higher in the CTI vs CTI+group (25/36, 69% vs. 12/36, 33% respectively; P < .001), with similar typical atrial flutter recurrence rates. There were no differences in undesirable events, except for transient phrenic nerve palsy reported from three CTI+patients (8.3%).
Conclusion
Pulmonary vein isolation using cryoballoon technology was proven to significantly reduce the atrial fibrillation incidence at 2 years postcavo‐tricuspid isthmus ablation.
Atrial flutter (AFl) patients with prior occasionally recorded atrial fibrillation (AF) were randomly assigned to undergo cavo‐tricuspid isthmus (CTI) ablation or CTI plus pulmonary vein isolation (combined atrial flutter ablation). AF was neither the predominant (67% of the population with only one recorded AF episode) nor the targeted arrhythmia. At 2‐year FU, AF recurrences were significantly higher in atrial flutter ablation group vs combined atrial flutter group with similar AFL recurrences.
Transcatheter aortic valve implantation (TAVI) has become an alternative to surgical aortic valve replacement for patients with symptomatic severe aortic stenosis in elderly and comorbid population. ...Significant improvement in heart function has been observed in patients undergoing TAVI, but numerous patients are readmitted to hospital for heart failure (HF). Moreover, repeat HF hospitalization is strongly associated with an adverse prognosis and increases the financial burden of health care. Although studies have identified pre‐existing and post‐procedural factors that contribute to HF hospitalization after TAVI, there is a paucity of data regarding optimal post‐procedural pharmacological treatments. This review aims to provide an overview of the current understanding of mechanisms, determinants, and potential treatments of HF following TAVI. We first review the pathophysiology of left ventricular (LV) remodelling, coronary microcirculation disorder, and endothelial dysfunction in patients with aortic stenosis and then examine the impact of TAVI on these conditions. We then present evidence of various factors and complications that may interplay with LV remodelling and contribute to HF events after TAVI. Next, we describe the triggers and predictors of early and late HF rehospitalizations following TAVI. Lastly, we discuss the potential of conventional pharmacological treatments, including renin–angiotensin blockers, beta‐blockers, and diuretics in TAVI patients. The paper explores the potential of newer drugs, including sodium–glucose co‐transporter 2 inhibitors, anti‐inflammatory drugs, and ion supplementation. Comprehensive knowledge in this field may aid in recognizing successful existing therapies, developing effective new treatments, and establishing dedicated patient care strategies during follow‐up after TAVI.
Experimental data suggest that use of cryoablation in pulmonary vein isolation (PVI) is associated with less cell damage and less thrombus formation compared to radiofrequency (RF) energy.
The ...purpose of this study was to test the hypothesis that cryoablation significantly reduces markers of cell damage, platelet activation, and inflammation in patients undergoing PVI for treatment of atrial fibrillation (AF).
Sixty patients with symptomatic drug-resistant AF (age 56 ± 9 years, 48 males, 38 with paroxysmal AF) were randomly assigned to undergo PVI using either an open irrigated-tip RF catheter or a cryoballoon. Markers of cell damage (high-sensitive troponin T hs-TnT, microparticles), platelet activation (platelet reactivity by aggregometry, expression of platelet surface proteins P-selectin and activated glycoprotein GP IIb/IIIa), and inflammatory response (high-sensitive C-reactive protein hs-CRP) were determined before and up to 48 hours after the procedure.
PVI resulted in a significant rise in hs-TnT, microparticles, markers of platelet activation, and hs-CRP over time, with distinct temporal patterns for each parameter. However, after Bonferroni correction for repeated measurements, no significant differences were noted in these parameters between patients treated with cryoablation or RF energy. Procedural time was significantly shorter in patients treated with cryoballoon (177 ± 30 minutes vs 200 ± 46 minutes, P = .03), with no differences in fluoroscopic time, periprocedural complications, or success rate.
Cryoablation and RF energy result in a comparable rise of markers of cell damage, platelet activation and inflammatory response. The data do not support the concept of an improved safety profile for cryoablation in PVI.
Introduction. Acute pulmonary embolism (APE) is a frequent condition in patients with COVID-19 and is associated with worse outcomes. Previous studies suggested an immunothrombosis instead of a ...thrombus embolism, but the precise mechanisms remain unknown. Objective. To assess the determinants and prognosis of APE during COVID-19. Methods. We retrospectively included all consecutive patients with APE confirmed by computed tomography pulmonary angiography hospitalized at Strasbourg University Hospital from 1 March to 31 May 2019 and 1 March to 31 May 2020. A comprehensive set of clinical, biological, and imaging data during hospitalization was collected. The primary outcome was transfer to the intensive care unit (ICU). Results. APE was diagnosed in 140 patients: 59 (42.1%) with COVID-19, and 81 (57.9%) without COVID-19. A 812% reduction of non-COVID-19 related APE was registered during the 2020 period. COVID-19 patients showed a higher simplified pulmonary embolism severity index (sPESI) score (1.15 ± 0.76 vs. 0.83 ± 0.83, p = 0.019) and were more frequently transferred to the ICU (45.8% vs. 6.2%, p < 0.001). No difference regarding the most proximal thrombus localization, Qanadli score (8.1 ± 6.9 vs. 9.0 ± 7.4, p = 0.45), the proportion of subsegmental (10.2% vs. 11.1%, p = 0.86), and segmental pulmonary embolism (35.6% vs. 24.7%, p = 0.16) was evidenced between COVID-19 and non-COVID-19 APE. In COVID-19 patients with subsegmental or segmental APE, thrombus was, in all cases (27/27 patients), localized in areas with COVID-19-related lung injuries. Marked inflammatory and prothrombotic biological markers were associated with COVID-19 APE. Conclusions. APE patients with COVID-19 have a particular clinico–radiological and biological profile and a dismal prognosis. Our results emphasize the preeminent role of inflammation and a prothrombotic state in these patients.
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