Rescue percutaneous repair of ischemic acute severe mitral regurgitation.

Acute severe mitral regurgitation (MR) because of secondary left ventricular impaired regional contractility can present with severe acute heart failure, associated with a high risk for rapid decompensation, pulmonary edema and cardiogenic shock. Frequently, in these highly unstable patients, surgical risk can be prohibitive. Evidence for percutaneous repair of acute MR is scarce, but a few case series show that this approach could be safe and effective for bailing out hemodynamically unstable patients. We report a case of an 84-year-old man with acute ischemic severe MR post-acute myocardial infarction (MI), who remained hemodynamically unstable despite coronary revascularization, positive pressure non-invasive ventilation, vasodilator therapy and intra-aortic balloon pump (IABP) support. In heart team discussions, he was considered a high risk surgical candidate. We decided on rescue off-label percutaneous mitral valve repair with a MitraClip device (Abbott Vascular, Santa Clara, California), with good clinical result, allowing weaning from the supports and discharge seven days after the procedure. At one-year follow-up, the patient maintained a MV repair results and had a good functional status. In unstable patients with acute ischemic MR, percutaneous MV repair could be a rescue therapeutic option to consider, allowing hemodynamic compensation with potential persistent MR improvement up to one-year follow-up.

Long-term outcomes after radiofrequency catheter ablation of the atrioventricular node: The experience of a Portuguese tertiary center.

INTRODUCTION: In patients with supraventricular arrhythmias and high ventricular rate, unresponsive to rate and rhythm control therapy or catheter ablation, atrioventricular (AV) node ablation may be performed. OBJECTIVES: To assess long-term outcomes after AV node ablation and to analyze predictors of adverse events. METHODS: We performed a detailed retrospective analysis of all patients who underwent AV node ablation between February 1997 and February 2019, in a single Portuguese tertiary center. RESULTS: A total of 123 patients, mean age 69±9 years and 52% male, underwent AV node ablation. Most of them presented atrial fibrillation at baseline (65%). During a median follow-up of 8.5 years (interquartile range 3.8-11.8), patients improved heart failure (HF) functional class (NYHA class III-IV 46% versus 13%, p=0.001), and there were reductions in hospitalizations due to HF (0.98±1.3 versus 0.28±0.8, p=0.001) and emergency department (ED) visits (1.1±1 versus 0.17±0.7, p=0.0001). There were no device-related complications. Despite permanent pacemaker stimulation, left ventricular ejection fraction did not worsen (47±13% vs. 47%±12, p=0.63). Twenty-eight patients died (23%). The number of ED visits due to HF before AV node ablation was an independent predictor of the composite adverse outcome (OR 1.8, 95% CI 1.24-2.61, p=0.002). CONCLUSIONS: Despite pacemaker dependency, the clinical benefit of AV node ablation persisted at long-term follow-up. The number of ED visits due to HF before AV node ablation was an independent predictor of the composite adverse outcome. AV node ablation should probably be considered earlier in the treatment of patients with supraventricular arrhythmias and HF, especially in cases that are unsuitable for selective ablation of the specific arrhythmia.

Late gadolinium enhancement location assessed by magnetic resonance and arrhythmogenic risk in hypertrophic cardiomyopathy.

INTRODUCTION AND OBJECTIVES: Late gadolinium enhancement (LGE) extent has emerged as a predictor of sudden cardiac death (SCD) in patients with hypertrophic cardiomyopathy (HCM), however little is known about the arrhythmogenic relevance of its specific location in the left ventricle. Our aim was to analyze the influence of LGE location on the occurrence of ventricular arrhythmias (VA) and SCD in patients with HCM. METHODS: We performed a retrospective analysis of clinical and Holter records of HCM patients who underwent cardiac magnetic resonance at our center. LGE extent and distribution were assessed using the American Heart Association 17-segment model. VA was defined as non-sustained or sustained ventricular tachycardia, ventricular fibrillation or SCD. RESULTS: Sixty-one patients (age 57.0±16.7 years) were included and VA occurred in 24.6% (n=15). Patients with VA showed greater LGE extent than those without (7.40±5.3 vs. 3.52±3.0 segments, p=0.007). Analyzing the distribution of LGE, a set of arrhythmogenic segments (apex/basal inferior/basal anterolateral/mid inferoseptal) was found. The extent of LGE involvement in these segments was also greater in patients with VA (2.07±1.03 vs. 0.65±0.71 segments, p<0.001; area under the curve 0.861 for VA) and this difference remained significant after adjustment for potentially confounding variables. CONCLUSIONS: The extent of LGE involvement of a set of segments with an apparent relation to cardiac areas of increased mechanical stress was significantly and independently associated with the occurrence of VA, suggesting that not only the extent but also the location of LGE is important for the assessment of SCD risk in HCM patients.

Peguero-Lo Presti criteria for diagnosis of left ventricular hypertrophy: a cardiac magnetic resonance validation study.

AIMS: The diagnostic performance of the new Peguero-Lo Presti ECG criteria for left ventricular hypertrophy (LVH) has not been validated by cardiac magnetic resonance (CMR). The aim of this study was to evaluate and compare the diagnostic performance of Peguero-Lo Presti, Cornell and Sokolow--Lyon voltage criteria for LVH as defined by CMR in an all-comers European population. METHODS: A total of 240 consecutive patients referred for CMR who had a concomitant electrocardiogram for review were evaluated. LVH group patients were defined according to the reference values for sex and age of left ventricular mass index (LVMi). A control group, adjusted by sex, was randomly selected from a population without LVH. We applied the ECG voltage criteria to both groups and evaluated their diagnostic accuracy. Diagnostic sensitivity and specificity were compared. RESULTS: Two hundred and forty patients (mean age 63 years; 65% men) were divided into two groups (LVH n = 149; control n = 91). The main causes of LVH were hypertension (24.8%) and hypertrophic cardiomyopathy (21.5%). The remaining patients of this group had a diagnosis of dilated cardiomyopathy (14.8%), valvular heart disease (7.4%) and infiltrative cardiomyopathy (2.0%). Overall, the sensitivity for LVH diagnosis of the Peguero-Lo Presti criteria outperformed both the Cornell (47 vs. 29%, P < 0.001) and Sokolow--Lyon voltage criteria (vs. 25%, P < 0.001). The specificities of all the criteria were above 94%, without significant differences between them. CONCLUSION: In an all-comers European population with LVH defined by CMR, the criteria of Peguero-Lo Presti showed increased sensitivity for this diagnosis, when compared with the Sokolow--Lyon and Cornell voltage criteria. As such, they could become the preferred ECG diagnostic tool when evaluating patients at risk for LVH.

Sequential Percutaneous Approach for Severe Mitral and Aortic Regurgitation.

Percutaneous approach for valvular heart disease is accepted as a safe and feasible strategy to treat patients considered at high surgical risk with aortic stenosis and mitral regurgitation. Additionally, the growing experience led to the increasing use of transcatheter aortic valve implantation in several indications, such as in pure aortic regurgitation. The authors present the case of a 72-year-old woman with prohibitive surgical risk due to several comorbidities, including a chronic arterial dissection from the right carotid artery to the femoral arteries bilaterally that presented with signs and symptoms of heart failure, having a transthoracic echocardiography that showed severe functional mitral and aortic regurgitation. Combined percutaneous intervention for multivalvular disease in this clinical scenario is challenging, and the reported experience is still scarce and limited to inoperable patients.

Anti-cardiac troponin antibodies in clinical human disease: a systematic review.

Anti-cardiac troponin antibodies have been studied in different types of clinical diseases and in healthy populations. A systematic review of published data on anti-troponin antibodies was carried out (search performed on PubMed, ISI Web of Knowledge and Scopus databases). From title and abstract analysis, thirty-three articles were included that met the pre-specified criteria; after full-text analysis, nine articles were excluded. Most studies assessed anti-troponin I antibodies. The prevalence of anti-cardiac troponin antibodies in healthy individuals ranged from 0.0% to 20.0%. The prevalence of anti-troponin I autoantibodies in dilated cardiomyopathy (DCM) ranged from 7.0% to 22.2%. Other conditions under study were myocardial infarction, ischemic cardiomyopathy (ICM), peripartum cardiomyopathy (PPCM), Chagas disease, Emery-Dreifuss muscular dystrophy (EDMD) and renal transplantation. In the different patient populations studied, anti-cardiac troponin antibodies have been shown to be either positively or negatively associated with prognostic and clinical features. In what concerns a possible value as biomarkers, these assays have not emerged up to the present moment as important aids for practical clinical decisions in cardiac or other types of patients. In what concerns pathophysiology, anti-cardiac troponin autoantibodies may play a role in different diseases. It can be speculated that these antibodies could be involved in perpetuating some degree of cardiac injury after an event, such as myocardial infarction or PPCM.

Association between implantation depth assessed by computed tomography and new-onset conduction disturbances after transcatheter aortic valve implantation.

BACKGROUND: Transcatheter aortic valve replacement (TAVR) is often associated with intraventricular conduction disturbances. We aimed to determine the association between implantation depth assessed by multidetector computed tomography (MDCT) and new-onset conduction abnormalities after TAVR. METHODS: Retrospective single-center study including patients consecutively submitted to TAVR, between August/2007 and October/2016, who underwent routine MDCT 3 months after the procedure. The endpoint of conduction disturbances included permanent pacemaker implantation and/or new-onset left bundle-branch block. Implantation depth was determined as the distance between the ventricular end of the prothesis and the native ring, at the level of the non-coronary cusp. RESULTS: 138 patients were included (female gender 52.2%, mean age 78.7 ± 6.9 years). The EuroSCORE II was 4.0 ± 3.9% and 57.2% were treated with self-expanding prosthesis. The endpoint of conduction abnormalities was found in 45.7% (n = 63). The implantation depth was greater in the group with conduction disturbances (7.7 vs 6.4 mm, p = 0.006). Chronic obstructive pulmonary disease, oversizing and implantation depth were independent predictors of conduction abnormalities. Implantation depth had an AUC of 0.64 (p = 0.004) for the prediction of conduction abnormalities and a cut-off value of 7.1 mm predicted the composed endpoint with a sensitivity and specificity of 65% and 70%, respectively. CONCLUSIONS: Implantation depth assessed by MDCT is associated with new-onset conduction disturbances after TAVR. In patients with conduction abnormalities, which do not qualify for the immediate implantation of pacemaker, the assessment of implantation depth by MDCT may be an additional marker of risk to aid decision-making.

Combination effects of anticholinesterasics in acetylcholinesterase of a fish species: effects of a metallic compound, an organophosphate pesticide, and a pharmaceutical drug.

The simultaneous presence of distinct compounds in the aquatic environment can be causative of various toxicological interactions. This scenario challenges ecotoxicologists, since the assessment of toxicological effects caused by the simultaneous presence of multiple substances is by far more complicated. An illustrative example can be given by mentioning the anticholinesterasic compounds: by studying the level of cholinesterase impairment of an exposed organism, it is possible to ascertain the level of exposure to all anticholinesterasics (despite their chemical classes and natures) that the organism was subjected to. In this work, we describe the effects of three chemically different, albeit mechanistically, and toxicologically similar compounds (copper, chlorfenvinphos, and pyridostigmine) on cholinesterases of the fish Gambusia holbrooki. The results showed that the combinatorial effects may be of considerable extent, even for levels of exposure that are close to the ones already reported in the wild, for each isolated compound.

Polymorphism in ftsI gene and {beta}-lactam susceptibility in Portuguese Haemophilus influenzae strains: clonal dissemination of beta-lactamase-positive isolates with decreased susceptibility to amoxicillin/clavulanic acid.

OBJECTIVES: The aim of this study was to characterize ampicillin resistance mechanisms in clinical isolates of Haemophilus influenzae from Portugal. Association between specific patterns of amino acid substitutions in penicillin-binding protein 3 (PBP3) (with or without ß-lactamase production) and ß-lactam susceptibility as well as genetic relatedness among isolates were investigated. METHODS: Two-hundred and forty non-consecutive H. influenzae isolates chosen according to their different ampicillin MICs [101 ß-lactamase-non-producing ampicillin-resistant (BLNAR) isolates, 80 ß-lactamase-producing ampicillin-resistant (BLPAR) isolates and 59 ß-lactamase-non-producing ampicillin-susceptible (BLNAS) isolates] were analysed. The ß-lactamase-encoding bla(TEM-1) gene was detected by PCR. The ftsI gene encoding PBP3 was sequenced. Genetic relatedness among isolates was examined by PFGE. RESULTS: Of the 240 H. influenzae isolates, 141 had mutations in the transpeptidase domain of the ftsI gene, including most BLNAR strains (94/101, 93.1%) and a high percentage of BLPAR strains (47/80, 58.8%). As previously reported, the latter have been described as ß-lactamase-positive amoxicillin/clavulanic acid resistant (BLPACR). The most common amino acid substitutions were identified near the KTG motif: N526K (136/141, 96.5%), V547I (124/141, 87.9%) and N569S (121/141, 85.8%). The 141 strains were divided into 31 ftsI mutation patterns and included six groups (I, IIa, IIb, IIc, IId and III-like). BLNAR strains were genetically diverse but close genetic relationships were demonstrated among BLPACR strains. CONCLUSIONS: This study shows that the non-enzymatic mechanism of resistance to ß-lactams is widespread among H. influenzae isolates in Portugal. Clonal dissemination of BLPACR strains showing high resistance to ampicillin and reduced susceptibility to amoxicillin/clavulanic acid was documented.