Background Axillary vein access (AVA) using fluoroscopic landmarks is an effective and safe approach for cardiac implantable electronic devices (CIEDs) implantation. However, it may result in a higher radiation exposure. Ultrasound‐guided axillary access (USAA) is an effective alternative technique to conventional subclavian access for CIEDs implantation. Studies comparing USAA and AVA using fluoroscopic landmarks are lacking. The purpose of this study was to compare the safety, efficacy, and radiation exposure data of the USAA approach with the AVA using fluoroscopic landmarks. Methods The study population included 95 consecutive patients (61% male, median age 78 years [71‐85 years]) referred for CIEDs implantation using AVA with fluoroscopic landmark (n = 46) or USAA (n = 49). Baseline characteristics and radiation exposure data (Air‐Kerma [mGy], DAP [Gy‐cm2], fluoroscopy time [seconds], and X‐rays emission time [seconds]) were compared according to the technique used for the AVA. Results Axillary vein was successfully accessed in 45 of 49 (92%) patients using ultrasound and in 42 of 46 (91%) patients using fluoroscopic landmarks (P = 1.00). Air‐Kerma, DAP, fluoroscopy time, and X‐rays emission time were shorter for USAA group compared with AVA using fluoroscopic landmarks (11 mGy [8‐20] vs 37 mGy [24‐81], P < .00001; 3 Gy‐cm2 [2‐5] vs 10 Gy‐cm2 [6‐16], P < .00001; 97 seconds [62‐163] vs 271 seconds [185‐365], P < .00001; and 7 seconds [4‐10] vs 21 seconds [13‐39], P < .00001). There were no significant differences between the two groups in median implant procedure time (P = .55). We did not encounter any acute or long‐term complications in both groups. Conclusions Ultrasound‐guided axillary vein cannulation for CIEDs implantation is a feasible and safe alternative approach and offers a significant reduction in fluoroscopy times without increasing procedural time.

Introduction During the coronavirus disease-19 (COVID-19) outbreak in spring 2020, people may have been reluctant to seek medical care fearing infection. We aimed to assess the number, characteristics and in-hospital course of patients admitted for acute cardiovascular diseases during the COVID-19 outbreak. Methods We enrolled all consecutive patients admitted urgently for acute myocardial infarction, heart failure or arrhythmias from 1 March to 31 May 2020 (outbreak period) and 2019 (control period). We evaluated the time from symptoms onset to presentation, clinical conditions at admission, length of hospitalization, in-hospital medical procedures and outcome. The combined primary end point included in-hospital death for cardiovascular causes, urgent heart transplant or discharge with a ventricular assist device. Results A similar number of admissions were observed in 2020 (N = 210) compared with 2019 (N = 207). Baseline characteristics of patients were also similar. In 2020, a significantly higher number of patients presented more than 6 h after symptoms onset (57 versus 38%, P < 0.001) and with signs of heart failure (33 versus 20%, P = 0.018), required urgent surgery (13 versus 5%, P = 0.004) and ventilatory support (26 versus 13%, P < 0.001). Hospitalization duration was longer in 2020 (median 10 versus 8 days, P = 0.03). The primary end point was met by 19 (9.0%) patients in 2020 versus 10 (4.8%) in 2019 (P = 0.09). Conclusion Despite the similar number and types of unplanned admissions for acute cardiac conditions during the 2020 COVID-19 outbreak compared with the same period in 2019, we observed a higher number of patients presenting late after symptoms onset as well as longer and more complicated clinical courses.

The use of 2017 International criteria is associated with a substantial increase in specificity and a marginal decrease in sensitivity for differential diagnosis between HCM and athlete's heart.

Hypertrophic cardiomyopathy (HCM) and primary restrictive cardiomyopathy (RCM) have a similar genetic background as they are both caused mainly by variants in sarcomeric genes. These “sarcomeric cardiomyopathies” also share diastolic dysfunction as the prevalent pathophysiological mechanism. Starting from the observation that patients with HCM and primary RCM may coexist in the same family, a characteristic pathophysiological profile of HCM with restrictive physiology has been recently described and supports the hypothesis that familiar forms of primary RCM may represent a part of the phenotypic spectrum of HCM rather than a different genetic cardiomyopathy. To further complicate this scenario some infiltrative (amyloidosis) and storage diseases (Fabry disease and glycogen storage diseases) may show either a hypertrophic or restrictive phenotype according to left ventricular wall thickness and filling pattern. Establishing a correct etiological diagnosis among HCM, primary RCM, and hypertrophic or restrictive phenocopies is of paramount importance for cascade family screening and therapy.