Francesco Adamo

EKG ABNORMALITIES DISTRIBUTION BETWEEN COMPETITIVE ATHLETES, NON COMPETITIVE ATHLETES AND NON ATHLETES IN A POPULATION OF 12,000 YOUNG ITALIAN STUDENTS

Introduction: The European Society of Cardiology recommends cardiovascular screening to competitive athletes. In young population the execution of 12-lead ECG screening is still controversial. Hypothesis: The aim of our study is to evaluate the distribution of ECG abnormalities between competitive athletes, non competitive athletes and non athletes. Methods: From October 2010 to October 2015, we evaluated prospectively 11916 high school students (age 17.2 ± 2.4 years old; 45.9% male): 4533 (38.04 %) non athletes (G-A), 4936 (41.42 %) non competitive athletes (G-B) and 2447 (20.54%) competitive athletes (G-C). They were screened using 12-lead ECG. The statistical difference was considered significant only for p-value l this suggest that an ECG screening is recommended also in non athletes.

Heart Failure With Preserved, Mid-Range, and Reduced Ejection Fraction: The Misleading Definition of the New Guidelines

The European Society of Cardiology (ESC) recently published new guidelines for the diagnosis and treatment of acute and chronic heart failure (HF).1 The new nomenclature includes separating patients with HF into 3 distinct groups depending on the left ventricular ejection fraction (LVEF): preserved LVEF (≥50%), mid-range LVEF (40–49%), and reduced LVEF (≤40%). Although there have been several studies that argue for and against stratifying HF patients by LVEF, the latest guidelines continue to focus mainly on the LVEF as the central determinant of prognosis in HF. However, further characterization of HF phenotype using etiology, comorbidities, and nonresponse to therapy among the 3 proposed groups are not incorporated into the definition. It is important to identify pathophysiological mechanisms and specific etiologies that underlie the clinical status, beyond the simplistic definition of preserved, mid-range, and reduced LVEF. Moreover, the term “preserved” could be misleading and confusing: quite comforting and mistakenly reassuring. As observed in the literature and in clinical practice, patients with preserved LVEF may have worse prognosis in terms of rehospitalization and mortality. Furthermore, it is necessary to highlight that the determination of LVEF from 2D echocardiographic images with Simpson’s biplane technique is relatively unreliable, with intra and interobserver variability of up to 13% and 15%, respectively, because of foreshortened views and geometric assumptions.2 Moreover, LVEF calculation is sensitive to changes in hemodynamic loading conditions. This is what occurs in patients with mitral regurgitation who have preserved LVEF despite severe ventricular dysfunction.3,4 The consequence of such variability in measurement and sensitivity to loading conditions may lead to a significant overlap among the 3 proposed categories that are separated by only a few percentage points. Moreover, calculating LVEF is considered a simple method to estimate ventricular function, but in fact it may be too simplistic. In the management of HF patients, it is more important to focus on ventricular function estimated by chamber volumes and pressures, as well as by Doppler flows and tissue Doppler imaging (TDI). In fact, in our opinion, the key means by which to determine the prognosis of HF patients involves establishing the presence or absence of ventricular dysfunction, that could be (1) systolic, ie, with increased ventricular volumes; (2) diastolic, ie, with abnormalities in transmitral and pulmonary veins flows, in TDI mitral annular velocities, and in left atrium volume; or (3) systo-diastolic, ie, including features of both systolic and diastolic dysfunction. The presence of systolic, diastolic, or systo-diastolic ventricular dysfunction determines low cardiac output, which is the crucial pathophysiological element of HF.

A-V block as presentation of cardiac amyloid: prominent infiltration of conduction tissue revealed by endomyocardial biopsy

Cardiac infiltration by amyloid generates a progressive restrictive cardiomyopathy culminating in diastolic heart failure. Conduction tissue can be affected as well by amyloidosis particularly in the advanced stage of the disease. Endomyocardial biopsy documentation of prominent infiltration of conduction tissue by cardiac amyloid causing A-V block and syncope, has never been provided before. A 68-year-old man with an untreated carpal tunnel syndrome was admitted because of recurrent syncopal episodes. The patient had normal blood pressure (130/80mmHg) and no peripheral oedema. ECG (Figure 1 panel A) documented a sinus rhythm with preserved QRS voltages and diffuse compromise of impulse conduction manifested by right bundle branch block, left anterior hemiblock, 1 and 2 degree A-V block with ventricular rate of 38 beats/min. At 2D-echo (Figure 1 panel B) a moderate diffuse thickening of left and right ventricular wall (maximal wall thickness 16 and 10mm, respectively) was recognized with left ventricular diastolic dysfunction and preserved systolic function (left ventricular ejection fraction 60%). The patient denied previous inflammations/infections and no monoclonal gammopathy was recognized at immunoelectrophoresis of serum and urines. He underwent a coronary angiography that showed a normal network and then a left ventricular endomyocardial biopsy. Histology of endomyocardial samples showed hypotrophic and degenerated cardiomyocytes surrounded by extensive areas of pale pink material at H&E (Figure 1, panel C) showing green birefringence at polarized light after Congo red staining (Figure 1, panel D) and suggesting cardiac amyloid. Electron microscopy confirmed the infiltrating material to consist of 100 Å wide amyloid fibrils (insert in Figure 1, panel D). In the tissue, samples were included sections of conduction tissue (CT) (Figure 1, panel E–F), appearing as small, loosely arranged myocytes positive to potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) immunostaining (Figure 1, panel G), supplied by a centrally placed arteriole and circumscribed by a fibrous membrane in a fascicle configuration (Monckeberg and Aschoff criteria). CT was nearly completely replaced by amyloid deposits positive to immunostaining for transthyretin (TTR) (insert in Figure 1, panel H). A genetic test revealed a mutation of TTR gene (TTRThr59Lys, p.Thr79Lys) in the affected patient and in some (a 30-year-old son and 9-yearold nephew) carrier family members still not manifesting the disease. The patient had a pacemaker implantation with functional recovery to NYHA class I. Substitution of Lys for the wild-type Thr residue at 59 position of TTR is known to be associated with autosomal dominant cardiac amyloidosis [1]. Early recognition of this entity may benefit from use of new drugs like tafamidis able to stabilize the mutant TTR, preventing the generation of amyloidogenic and toxic intermediates [2].