Articles

Atherosclerosis is an important promoter of cardiovascular disease potentiating myocardial infarction or stroke. Current demand in biomedical imaging necessitates noninvasive characterization of arterial changes responsible for transition of stable plaque into rupture-prone vulnerable plaque. in vivo contrast enhanced magnetic resonance (MR) imaging (MRI) allows quantitative and functional monitoring of pathomorphological changes through signal differences induced by the contrast agent uptake in the diseased vessel wall, therefore it is the ideal modality toward this goal. However, studies have so far focused on the cellular targets of persisting inflammation, leaving extracellular matrix (ECM) far behind. In this review, we portray ECM remodeling during atherosclerotic plaque progression by summarizing the state of the-art in MRI and current imaging targets. Finally, we aim to discuss glycosaminoglycans (GAGs) and their functional interactions, which might offer potential toward development of novel imaging probes for in vivo contrast-enhanced MRI of atherosclerosis.

Background: Pulmonary vein isolation (PVI) is the accepted standard nowadays for atrial fibrillation (AF) ablation. The most widespread ablation techniques are cryoballoon (CB) and point-by-point radiofrequency (RF) ablation. Comparative studies between both techniques have shown their equivalence for the first ablation procedure, but no trial has explored the potential incremental benefit of crossing over the ablation technique after AF recurrence. Objective: To explore the potential incremental benefit of a crossover ablation strategy for AF recurrences, comparatively with repeating the same ablation energy used for the first procedure. Methods: Retrospective analysis of patients undergoing a second AF ablation procedure after documented AF recurrence. Patients were excluded if all 4 PV were isolated at the beginning of the second procedure or extra-PVI ablation was used for the second procedure. Crossover group (n = 16) included patients in which two different techniques were used for the first and second procedure (CB-RF or RF-CB). Control group (n = 23) for those with same ablation procedure (RF-RF of CB-CB). Acute procedure end-point was PVI of all four pulmonary veins. Patients were followed-up at 3, 6, and 12 months with an electrocardiogram and a 24 h-holter. Arrhythmia-free survival at 1 year after the second ablation procedure was studied, comparing efficiency and safety of the two approaches (crossover vs. same energy). Success was defined as freedom from AF or atrial tachycardia lasting > 30 s off antiarrhythmic drugs (AADs) Results: A cohort of 39 paroxysmal and persistent AF patients was analyzed. PVI after the second procedure was 100% in all patients in both groups. There were no baseline relevant differences between the two groups. No deaths or hospitalizations occurred during follow up (data censored at 24h moths). At 1 year, arrhythmia free-survival was significantly higher in the crossover group compared to control group [93,3% vs. 47,8%; HR 0.19 (0.06-0.66);p = 0,009]. Conclusion: Crossing the ablation technique (point-by-point radiofrequency or cryoballoon PVI) after AF recurrence significantly improved arrhythmia free-survival at one year, despite no difference in acute success (PVI isolation). Randomized controlled trials with a higher amount of patients are needed to confirm the results and widespread this approach.

Implantable cardioverter defibrillators (ICDs) are electronic devices that can prevent sudden cardiac death (SCD) caused by arrhythmic events in patients. The latest ESC/EAS and ACC/AHA Guidelines deem the placement of an ICDs appropriate in patients with heart failure class NYHA II and III in the presence of an ejection fraction less than or equal to 35% [1,2]. ICDs are usually not indicated in either class I or IV patients. The Guidelines recommendations for primary prevention of SCD with ICD implantation do not take into account the age of the patients but only their life expectancy which must be at least 1 year. Our patients usually are over eighty years old with heart failure and severely reduced ejection fraction. We must consequently decide if it is right to implant these patients with an ICD. Is the use of ICD in the patients over 80, in particular over 90 years old, really make sense becomes particularly important considering demographic changes that await us in the coming decades.

Dual antiplatelet therapy (DAPT) combining aspirin and a P2Y12 receptor inhibitor has been consistently shown to reduce recurrent major adverse cardiovascular events (MACE) in patients with acute coronary syndrome (ACS) or undergoing percutaneous coronary intervention (PCI) for stable coronary artery disease (CAD) compared with aspirin monotherapy but at the expense of an increased risk of significant bleeding. Among patients with stable CAD undergoing PCI with drug-eluting stents (DES), shorter duration of DAPT (3–6 months) were shown non-inferior to 12 or 24 months duration concerning MACE but reduced the rates of major bleeding? Contrariwise, prolonged DAPT durations (18–48 months) reduced the incidence of myocardial infarction and stent thrombosis, but at the cost of an increased risk of majör bleeding and all-cause mortality. Until more evidence becomes available, the choice of optimal DAPT regimen and duration for patients with CAD requires a tailored approach based on the patient clinical presentation, baseline risk profile and management strategy. Patients with acute coronary syndromes (ACS) and a history of atrial fibrillation (AF) have indications for both dual antiplatelet therapy (DAPT) and oral anticoagulation (OAC). Triple therapy (TT), the combination of DAPT and OAC, is recommended in guidelines. This article provides a contemporary state-of-the-art review of the current evidence on DAPT for secondary prevention of patients with CAD and its future perspectives.

Introduction: Bland, White and Garland syndrome is a coronary anomaly with high mortality without treatment. Its clinical presentation is varied which makes epidemiological documentation difficult. Echocardiography is a useful non-invasive tool for diagnosis. Objective: To determine the echocardiographic variables that lead to the diagnosis of Bland, White and Garland syndrome and their clinical relevance. Material: Observational, prospective and cross-sectional study in 31 patients of the “William Soler” Pediatric Cardiocenter, from 2005 to 2018. To check the association of echocardiographic variables with the diagnosis of Bland, White and Garland syndrome, an effectiveness study was carried out that included the analysis of the incidence of echocardiographic variables that lead to the diagnosis of this entity. The clinical relevance was estimated according to the minimum importance limit. The statistical validation of the research results adopted a significance level of less than 5% (p < 0.05). Results: The variables that facilitate the echocardiographic diagnosis of Bland, White and Garland syndrome were the echocardiographic visualization of the anomalous connection and the reversed flow in the anomalous left coronary artery. These echocardiographic measures have clinical relevance according to the quantification of risk estimators (incidence) the echocardiographic visualization of the anomalous connection, RR 39.00 and the reversed flow in the anomalous coronary artery, RR 26.31. LIM´s calculation value amounted to 6.31 and coincided with the risk estimators (incidence). Conclusion: The echocardiographic visualization of the anomalous origin of the left coronary artery from the pulmonary arterial trunk and the detection of the local intracoronary reversed flow instituted as factors to be considered for the effective diagnosis of the disease. The documentation of the diagnostic aspects of the syndrome through echocardiography contains high statistical value and clinical relevance.

Background: Infants of diabetic mothers (IDMs) are at increased risk of developing congenital anomalies including cardiac defects. Pathological left ventricular hypertrophy, asymmetrical septal hypertrophy and outflow tract obstruction is a rare but known cardiac comorbidity in infants of diabetic mothers. The severity of this condition in IDMs can vary from an incidental finding on echocardiography to an infant with severe symptoms of congestive heart failure and specific management of the condition varies. Aim: The aim of this article is to report this clinical entity in a Nigerian infant born to a mother with poor glycaemic control in pregnancy and highlight management. Case report: We report a term neonate who was diagnosed as a case of pathological left ventricular hypertrophy, asymmetrical septal hypertrophy and outflow tract obstruction delivered to a mother with gestational diabetics with poor glycaemic control in pregnancy. Child was treated successfully with β-adrenergic blocker and showed resolution of hypertrophy in follow-up echocardiography. Conclusion: Infants of diabetic mothers are very high risk infants. Pathological left ventricular hypertrophy in IDM have good prognosis. Early recognition and prompt intervention is advocated.

Biventricular (BiV) pacing revolutionized the heart failure management in patients with sinus rhythm and left bundle branch block; however, left ventricular-lead placement is not always technically possible. Also, BiV pacing does not fully normalize ventricular activation and, therefore, the ventricular resynchronization is imperfect. On the other hand, right ventricular pacing for bradycardia may cause or worsen heart failure in some patients by causing dyssynchronous ventricular activation. His bundle pacing comes as an alternative to current approaches as it activates the ventricles via the native His-Purkinje system, resulting in true physiological pacing, and, therefore, is a promising site for pacing in bradycardia and traditional CRT indications in cases where it can overcome left bundle branch block. Furthermore, it has the potential to open up new indications for pacing therapy in heart failure, such as targeting patients with PR prolongation, but a narrow QRS duration. In this article we explore the history, clinical evidence, proposed mechanisms, procedural characteristics, and the role in current therapy of His bundle pacing in the prevention and treatment of heart failure.

This is demonstration of selected ECGs for learning or for exams; guided by lessons from great teachers as Prof. Hein Wellens MD. Here we provide advanced examples with comment and analysis.

This is a review of features in ECG to diagnose the culprit artery responsible for the infarction. Localization of the occluded vessel in acute myocardial infarction is important for many reasons: to know which artery is to dilate and stent; to assess the severity of the lesion; to compare with the echocardiographic area with hypokinesia or akinesia and to differentiate the recent from the old occluded vessel. The ST-segment changes in 12-lead ECG form the basis of diagnosis, management, and prognosis.

The involvement of the angiotensin II type 1 receptor in the Frank-Starling Law of the Heart, where the various activations are very limited, allows simple analysis of the kinase systems involved and thence extrapolation of the mechanism to that of angiotensin control of activation of cardiac and skeletal muscle contraction. The involvement of phosphorylation of the myosin light chain in the control of contraction is accepted but not fully understood. The involvement of troponin-I phosphorylation is also indicated but of unknown mechanism. There is no known signal for activation of myosin light chain kinase or Protein Kinase C-βII other than Ca2+/calmodulin but the former is constitutively active and thus has to be under control of a regulated inhibitor, the latter kinase may also be the same. Ca2+/calmodulin is not activated in Frank-Starling, i.e. there are no diastolic or systolic [Ca2+] changes. I suggest here that the regulated inhibition is by myosin light chain phosphatase and/or β-arrestin. Angiotensin activation, not involving G proteins. is by translocation of the β-arrestin from the sarcoplasm to the plasma membrane thus reducing its kinase inhibition action in the sarcoplasm. This reduced inhibition has been wrongly attributed to a mythical downstream agonist property of β-arrestin.