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Aims The aim of our study is to assess the ability of left atrial (LA) strain values to improve left ventricular and diastolic pressure (LVEDP) non-invasive estimation as compared with traditional echocardiographic indexes in the acute phase of Takotsubo syndrome (TTS) and to predict adverse in-hospital outcomes in this population. Methods and results Consecutive TTS patients were prospectively enrolled. Left ventricular and diastolic pressure was measured at the time of catheterization. Transthoracic echocardiography was performed within 48 h from hospital admission. In-hospital complications (acute heart failure, death from any cause, and life-threatening arrhythmias) were collected. A total of 62 patients were analysed (72.2 ± 10.1 years, female 80%) and in-hospital complications occurred in 25 (40.3%). Left ventricular and diastolic pressure mean value was 24.53 ± 7.92 mmHg. Left atrial reservoir and pump strain values presented higher correlation with LVEDP (r −0.859, P < 0.001 and r −0.848, P < 0.001, respectively) in comparison with E/e ′ ratio, left atrial volume index (LAVi), and tricuspid regurgitation (TR) peak velocity. In addition, at receiver-operating characteristic curve analysis, LA reservoir and pump strain resulted to be better predictors of LVEDP above the mean of our population [0.909 (95% CI 0.818–0.999, P < 0.001) and 0.889 (95% CI 0.789–0.988, P < 0.001)], respectively] as compared with E/e′ ratio, LAVi, and TR peak velocity. Finally, LA reservoir strain resulted to be an independent predictor of worse in-hospital outcomes, together with LVEDP and left ventricular ejection fraction (all P < 0.001). Conclusion In our study, lower LA reservoir and pump strain values were better predictors of LVEDP as compared with traditional echocardiographic indexes in the acute phase of TTS syndrome. Moreover, LA reservoir strain was an independent predictor of adverse in-hospital outcomes.

Purpose of Review Ischemic cardiomyopathy refers to systolic left ventricular dysfunction in the setting of obstructive coronary artery disease and represents the most common cause of heart failure worldwide. It is often the combination of an irreversible loss of viable mass following an acute myocardial infarction (AMI) with a dysfunctional, but still viable, myocardium in the context of a chronically reduced myocardial blood flow and reduced coronary reserve. Medical treatments aiming at modulating neurohumoral response and restoring blood flow to the ischemic cardiomyocytes were shown to dramatically abate the occurrence of ventricular dysfunction and adverse remodeling in ischemic cardiomyopathy. Recent Findings Novel therapeutic approaches, such as mechanical unloading and modulation of the inflammatory response, appear to be promising. Furthermore, the understanding of the mechanisms by which, despite optimal treatment, heart failure ensues after AMI, with or without adverse remodeling and systolic dysfunction, is a critical step in the search for novel ways to tackle heart failure risk beyond preservation of left ventricular volumes and systolic function. Summary In this review article, we explore the principal pathophysiological mechanisms and pathways of heart failure in ischemic cardiomyopathy, therapeutic opportunities, and knowledge gaps in this area.

Insertion of venous access devices (VAD) is usually considered a procedure with low risk of bleeding. Nonetheless, insertion of some devices is invasive enough to be associated with bleeding, especially in patients with previous coagulopathy or in treatment with antithrombotic drugs for cardiovascular disease. The current practices of platelet/plasma transfusion in coagulopathic patients and of temporary suspension of the antithrombotic treatment before VAD insertion are based on local policies and are often inadequately supported by evidence, since many of the clinical studies on this topic are not recent and are not of high quality. Furthermore, the protocols of antithrombotic treatment have changed during the last decade, after the introduction of new oral anticoagulant drugs. Though some guidelines address some of these issues in relation with specific procedures (port insertion, etc.), no evidence-based document covering all the aspects of this clinical problem is currently available. Thus, the Italian Group of Venous Access Devices (GAVeCeLT) has decided to develop a consensus on the management of antithrombotic treatment and bleeding disorders in patients requiring VADs. After a systematic review of the available evidence, the panel of the consensus (which included vascular access specialists, surgeons, intensivists, anesthetists, cardiologists, vascular medicine experts, nephrologists, infective disease specialists, and thrombotic disease specialists) has structured the final recommendations as detailed answers to three sets of questions: (1) which is an appropriate classification of VAD-related procedures based on the specific bleeding risk? (2) Which is the appropriate management of the patient with bleeding disorders candidate to VAD insertion/removal? (3) Which is the appropriate management of the patient on antithrombotic treatment candidate to VAD insertion/removal? Only statements reaching a complete agreement were included in the final recommendations, and all recommendations were offered in a clear and synthetic list, so to be easily translated into clinical practice.

Background and ObjectivesProlonged poststroke cardiac rhythm monitoring (PCM) reveals a substantial proportion of patients with ischemic stroke (IS) with atrial fibrillation (AF) not detected by conventional rhythm monitoring strategies. We evaluated the association between PCM and the institution of stroke preventive strategies and stroke recurrence.MethodsWe searched MEDLINE and SCOPUS databases to identify studies reporting stroke recurrence rates in patients with history of recent IS or TIA receiving PCM compared with patients receiving conventional cardiac rhythm monitoring. Pairwise meta-analyses were performed under the random effects model. To explore for differences between the monitoring strategies, we combined direct and indirect evidence for any given pair of monitoring devices assessed within a randomized controlled trial (RCT).ResultsWe included 8 studies (5 RCTs, 3 observational; 2,994 patients). Patients receiving PCM after their index event had a higher rate of AF detection and anticoagulant initiation in RCTs (risk ratio [RR] 3.91, 95% CI 2.54–6.03; RR 2.16, 95% CI 1.66–2.80, respectively) and observational studies (RR 2.06, 95% CI 1.57–2.70; RR 2.01, 95% CI 1.43–2.83, respectively). PCM was associated with a lower risk of recurrent stroke during follow-up in observational studies (RR 0.29, 95% CI 0.15–0.59), but not in RCTs (RR 0.72, 95% CI 0.49–1.07). In indirect analyses of RCTs, the likelihood of AF detection and anticoagulation initiation was higher for implantable loop recorders compared with Holter monitors and external loop recorders.DiscussionPCM after an IS or TIA can lead to higher rates of AF detection and anticoagulant initiation. There is no solid RCT evidence supporting that PCM may be associated with lower stroke recurrence risk.

An increasing number of detection tools are available and several detection strategies have been described to pursue the diagnosis of atrial fibrillation to prevent ischemic stroke. Monitoring tools include standard electrocardiography, snapshot single-lead recordings with professional or personal devices (e.g. smartphone-based), Holter monitor, external devices with long-term recording capabilities, and cardiac implantable electronic devices, including pacemakers, implantable cardioverter defibrillators and insertable cardiac monitors. Insertable cardiac monitors have shown high sensitivity and specificity for the detection of atrial fibrillation, allow up to three years of continuous monitoring, do not require cooperation of the patient, are well tolerated, have a short device-related time delay between detection of atrial fibrillation and notification to the physician, provide information on atrial fibrillation burden and are minimally invasive. On the other hand, insertable cardiac monitors require a considerable use of resources to process the recordings and have a significant initial cost. Studies conducted with insertable cardiac monitors on patients with prior stroke and on patients with risk factors for stroke but no prior cerebrovascular events or atrial fibrillation have consistently shown a measurable incidence of atrial fibrillation at follow-up. However, the effectiveness of oral anticoagulations in reducing the incidence of ischemic stroke in patients with atrial fibrillation lasting less than 24 h, though reasonable, is currently unproven. The future of atrial fibrillation detection tools and atrial fibrillation detection strategies will be influenced by ongoing studies exploring whether oral anticoagulations reduce the incidence of stroke in patients with atrial fibrillation burden lower than 24 h.

To systematically review the accuracy of early (≤7 days) predictors of poor outcome defined as death or vegetative state (Cerebral Performance Categories [CPC] 4-5) or death, vegetative state or severe disability (CPC 3-5) in comatose survivors from cardiac arrest not treated using therapeutic hypothermia (TH). PubMed, Scopus and the Cochrane Database of Systematic reviews were searched for eligible studies. Sensitivity, specificity, false positive rates (FPR) for each predictor were calculated and results of predictors with similar time points and outcome definitions were pooled. Quality of evidence (QOE) was evaluated according to the GRADE guidelines.50 studies (2828 patients) were included in final analysis. Presence of myoclonus at 24-48h, bilateral absence of short-latency somatosensory evoked potential (SSEP) N20 wave at 24-72h, absence of electroencephalographic activity20-21μV ≤72h and absence of pupillary reflex at 72h predicted CPC 4-5 with 0% FPR and narrow (10%) 95% confidence intervals. Absence of SSEP N20 wave at 24h predicted CPC 3-5 with 0% [0-8] FPR. Serum thresholds for 0% FPR of biomarkers neuron specific enolase (NSE) and S-100B were highly inconsistent among studies. Most of the studies had a low or very low QOE and did not report blinding of the treating team from the results of the investigated predictor.In comatose resuscitated patients not treated with TH presence of myoclonus, absence of pupillary reflex, bilateral absence of N20 SSEP wave and low EEG voltage each predicted poor outcome early and accurately, but with a relevant risk of bias.

Radiofrequency catheter ablation (RFCA) of supraventricular tachyarrhythmias carries a small but non-negligible radiation risk. Studies in children already showed the feasibility of using three-dimensional mapping systems as the primary guide for catheter visualization and positioning in these RFCAs. We aim to demonstrate the feasibility and safety of such an approach in young and middle-aged patients.Fifty patients (age 34 ± 12) with supraventricular tachyarrhythmias underwent electrophysiological study; of these, 47 patients proceeded to RFCA guided by the EnSite NavX(TM) system (23 with atrioventricular nodal reentry tachycardia, 16 with an accessory pathway, six with typical atrial flutter, and two with right atrial tachycardia).In 38/50 cases (76%), electroanatomical mapping avoided fluoroscopy entirely, including four cases requiring access to the left heart chambers by a retrograde approach. In the remaining 12/50 cases (24%), fluoroscopy use was limited to 122 ± 80 s, with a correspondingly low radiation exposure (dose area product 1.3 ± 1.1 mGy × m(2)). All procedures were acutely successful, with a procedural time of 113 ± 37 minutes, and without incurring in any major complication. Over a mean follow-up of 12 ± 3 months, we observed one recurrence of pre-excitation and one relapse of atrial flutter.Our study shows that non-fluoroscopic RFCA of supraventricular tachyarrhythmias using the EnSite NavX(TM) system is feasible, safe, and effective in a population of relatively young adults. Our experience of a non-fluoroscopic approach in these procedures deserves consideration, particularly in the young or in other patients at higher radiation risk.

The Andersen-Tawil syndrome (ATS) is characterized by hypo-normokaliemic muscle periodic paralysis, dysmorphic features and ventricular arrhythmias. Most cases are caused by mutations in KCNJ2, encoding for the potassium inwardly rectifying channel, Kir2.1 (ATS1). Although KCNJ2 mutations show no obvious genotype-phenotype correlations and incomplete penetrance, signs of cardiac involvement are usually present in most ATS1 cases. In contrast, here we describe an Italian ATS1 patient, carrying a c.574A→G mutation in KCNJ2, who had both facial dysmorphisms and muscle periodic paralysis but who did not manifest any cardiac involvement, although the same mutation was originally described in a Japanese kindred, in which all affected individuals manifested a severe cardiac phenotype.

Contact point-to-point electroanatomic mapping (Pt-Map) is a validated tool to evaluate right ventricular (RV) substrate. When using the EnSite NavX system (St. Jude Medical, St Paul, Minnesota), geometry reconstruction by dragging the mapping catheter (Geo-Map) allows for quicker acquisition of a large number of points and better definition of anatomy, but it is not validated for substrate mapping.This study evaluates the feasibility and accuracy of Geo-Map.Thirteen patients (mean age 38 +/- 12 years) with RV arrhythmias and an apparently normal heart underwent cardiac magnetic resonance imaging (MRI), Pt-Map, and Geo-Map. The 2 maps were compared in terms of mapping procedural time, radiation time, and total number of points acquired. We finally compared the number and characteristics of low-potential areas on each patient's Pt-Map, Geo-Map, and cardiac MRI.Geo-Map required significantly shorter mapping and radiation times in comparison to Pt-Map (12.4 +/- 4.6 vs. 31.9 +/- 10.1 and 5.8 +/- 2.1 vs. 12.1 +/- 3.9, P.001). Furthermore, Geo-Map was based on a significantly higher density of points in comparison to Pt-Map (802 +/- 205 vs. 194 +/- 38, P.001). Taking into consideration the total number of RV regions analyzed, the Pt-Map and Geo-Map disagreed in 2 of 65 (3%) regions (P = NS), which only Geo-Map identified as low-potential areas and indeed corresponded to wall motion abnormalities on MRI.Voltage maps obtained through RV geometry acquisition have accuracy comparable to that of conventional point-by-point mapping in detecting low-voltage areas, have a good correlation with MRI wall motion abnormalities, and allow a significant reduction in procedural time and x-ray exposure.

Biventricular implantation procedures require contrast venography of the coronary sinus. The aim of our study was to evaluate the efficacy and safety of contrast venography obtained by direct manual contrast injection into the guiding catheter, compared with venography obtained after occlusion of the coronary sinus by a Swan-Ganz catheter.Eighty-three patients were randomly assigned to direct or occlusive venography technique. The primary endpoint was complication rate. The secondary endpoints were rate of and time required for an adequate venography, total dose of contrast medium and total procedure time.Four dissections of the coronary sinus were observed with the occlusive venography technique group while no complications were observed with the direct venography technique group (p=0.04). Rate of adequate venography was similar in the two groups (p=NS). The time needed for coronary sinus venography and the total dose of contrast medium was significantly lower in the direct venography technique group compared with the alternative (p0.0001 and p=0.003, respectively); the total procedure time was not significantly different between the two groups (p=NS).The direct venography technique shows a significantly lower incidence of complications and should be considered to be the first line approach to coronary sinus venography during biventricular pacemaker implantation.

Biventricular pacing system implantation is a time-consuming and challenging procedure. A critical step in biventricular pacemaker implantation is coronary sinus (CS) cannulation. CS cannulation can be achieved either using dedicated guiding catheters (guiding catheter alone positioning strategy, GCA) or with the aid of an electrophysiology catheter advanced inside the guiding catheter (electrophysiology catheter aided positioning strategy, EPA).To evaluate whether the EPA technique is useful for reducing CS cannulation time compared to a conventional GCA technique.Thirty-four consecutive patients were randomly assigned to the GCA (18 patients) or EPA (16 patients) CS cannulation strategy.Time to successful catheterization of CS was 5.0 +/- 2.4 min in the EPA group versus 10.1 +/- 5.4 min in the GCA group p = 0.004. Fluoroscopy time was 4.6 +/- 2.3 min in the EPA group versus 9.2 +/- 4.9 min in the GCA group p = 0.004. Total contrast dye volume to search and engage the CS ostium was 0.0 ml in the EPA group versus 14.3 +/- 3.4 ml in the GCA group p0.001.Cannulation of CS with the adjunct of an electrophysiology catheter to dedicated delivery systems significantly reduces procedural time, fluoroscopy time and contrast dye volume compared to a conventional strategy.

Myotonic dystrophy (dystrophia myotonica, DM) is the most frequently inherited neuromuscular disease of adult life. DM is a multisystem disease with major cardiac involvement. Core features of myotonic dystrophy are myotonia, muscle weakness, cataract, and cardiac conduction abnormalities. Classical DM (first described by Steinert and called Steinert’s disease or DM1) has been identified as an autosomal dominant disorder associated with the presence of an abnormal expansion of a CTG trinucleotide repeat on chromosome 19q13.3 (the DM 1 locus). A similar but less common disorder was later described as proximal myotonic myopathy, caused by alterations on a different gene on chromosome 3q21 (the DM2 locus). This article will mainly focus on DM1. It will provide an insight into the epidemiology and genetic alterations of the disease and provide up-to-date information on postmortem and clinical findings and on diagnostic and therapeutic options in patients presenting cardiac involvement. The incidence of DM1 is estimated to be 1 in 8000 births and its worldwide prevalence ranges from 2.1 to 14.3/100 000 inhabitants.1 Based on the age of onset and on its clinical features, DM1 can be divided into three forms: congenital, classical, and minimal, which may occur in the same kindred. Congenital DM1 presents at birth or during the first year of life in a severe form. It is characterised by neonatal hypotonia, facial diplegia, joint contractures, frequent and often fatal respiratory failure, feeding difficulties, and developmental delay. The risk of dying from congenital DM1 in the neonatal period is high.1 Patients who survive exhibit non-progressive psychomotor retardation and may subsequently exhibit the features of the adult-type, classical form of DM1. In the classical form, which is the most common, symptoms become evident between the second and the fourth decade of life, showing a slow progression over time (table 1). The key …

The Andersen-Tawil syndrome (ATS) is characterized by hypo-normokaliemic muscle periodic paralysis, dysmorphic features and ventricular arrhythmias. Most cases are caused by mutations in KCNJ2, encoding for the potassium inwardly rectifying channel, Kir2.1 (ATS1). Although KCNJ2 mutations show no obvious genotype-phenotype correlations and incomplete penetrance, signs of cardiac involvement are usually present in most ATS1 cases. In contrast, here we describe an Italian ATS1 patient, carrying a c.574A→G mutation in KCNJ2, who had both facial dysmorphisms and muscle periodic paralysis but who did not manifest any cardiac involvement, although the same mutation was originally described in a Japanese kindred, in which all affected individuals manifested a severe cardiac phenotype.

Autoimmune autonomic neuropathy refers to a group of autoimmune disorders characterized by the failure of both sympathetic and parasympathetic systems,1 related to the presence of autoantibodies against neuronal ganglionic acetylcholine (AChR) receptors.2 These antibodies are detectable in the serum of about 30% of patients with paraneoplastic-acquired autoimmune autonomic neuropathy and in 50% of patients with idiopathic subacute autoimmune autonomic neuropathy.3 We describe a 59-year-old woman who presented 6 months after the gradual development of severe dysautonomia, characterized by recurrent orthostatic syncope, dry mouth, early satiety, constipation, and urinary retention. Family history was negative and she denied any viral illness preceding the onset of the above symptoms. The results of physical examination showed her blood pressure to be 115/70 mm Hg in a supine position, but fell to 80/50 mm Hg in a sitting position; the patient was unable to stand upright for more than a few seconds because of a fainting sensation. Pupillary responses to light were torpid; however, the remaining neurologic examination was normal. Routine blood tests, including glucose determination, were normal. X-ray gastrointestinal transit evaluation after barium ingestion documented markedly delayed gut motility …

The follow-up of 1440 consecutive post-MI patients (68.9±10.9 years) with an LVEF≤40% was analyzed in 19 Italian hospitals to evaluate how many patients with clinical nonsustained VT and inducible sustained VT or VF underwent post-discharge risk assessment (RA). During 38 (range, 4–76) months follow-up, 611 patients (42.4%) qualified for and 294 (20.4%) effectively underwent RA combining LVEF assessment and Holter monitoring, 29 (2.0%) subsequently underwent programmed electrical stimulation and 19 (1.3%) received an ICD.