As of January 2020, a new pandemic has spread from Wuhan and caused thousands of deaths worldwide. Several studies have observed a relationship between coronavirus disease (COVID-19) infection and the cardiovascular system with the appearance of myocardial damage, myocarditis, pericarditis, heart failure and various arrhythmic manifestations, as well as an increase in thromboembolic risk. Cardiovascular manifestations have been highlighted especially in older and more fragile patients and in those with multiple cardiovascular risk factors such as cancer, diabetes, obesity and hypertension. In this review, we will examine the cardiac involvement associated with SARS-CoV-2 infection, focusing on the pathophysiological mechanism underlying manifestations and their clinical implication, taking into account the main scientific papers published to date.

Heart involvement in Cardiac Amyloidosis (CA) results in a worsening of the prognosis in almost all patients with both light-chain (AL) and transthyretin amyloidosis (ATTR). The mainstream CA is a restrictive cardiomyopathy with hypertrophic phenotype at cardiac imaging that clinically leads to heart failure with preserved ejection fraction (HFpEF). An early diagnosis is essential to reduce cardiac damage and to improve the prognosis. Many therapies are available, but most of them have late benefits to cardiac function; for this reason, novel therapies are going to come soon.

Background: Pulmonary arterial elastance (Ea) is a helpful parameter to predict the risk of acute postoperative right ventricular failure (RVF) after left ventricular assist device (LVAD) implantation. A new method for calculating Ea, obtained by the ratio between transpulmonary gradient and stroke volume (Ea^B), has been proposed as a more accurate measure than the Ea obtained as the ratio between pulmonary artery systolic pressure and stroke volume (Ea^C). However, the role of Ea^B in predicting acute RVF post-LVAD implantation remains unclear. Methods and Results: A total of 35 patients who underwent LVAD implantation from 2018 to 2021 were reviewed in this retrospective analysis. Acute RVF after LVAD implantation occurred in 12 patients (34%): 5 patients with moderate RVF (14% of total) and 7 patients with severe RVF. The Ea^B was not significantly different between the “severe RVF” vs. “not-severe RVF” groups (0.27 ± 0.04 vs 0.23 ± 0.1, p < 0.403). However, the combination of arterial elastance and central venous pressure was significantly different between the “not-severe RVF” group (central venous pressure < 14 mmHg and Ea^C < 0.88 mmHg/mL or Ea^B < 0.24 mmHg/mL; p < 0.005) and the “severe RVF” group (central venous pressure > 14 mmHg and Ea^C > 0.88 mmHg/mL or Ea^B > 0.24 mmHg/mL; p < 0.005). Conclusions: Ea is a reliable parameter of right ventricular afterload and helps discriminate the risk of acute RVF after LVAD implantation. The combined analysis of Ea and central venous pressure can also risk stratify patients undergoing LVAD implantation for the development of RVF.

Amyloidosis is a group of diseases in which amyloid fibrils build up in tissues, leading to organ dysfunction. Cardiac involvement is observed in immunoglobulin light chain amyloidosis (AL) and transthyretin amyloidosis (ATTR) and, when it occurs, the prognosis worsens. Cardiac tissue infiltration can lead to restrictive cardiomyopathy with clinical signs of diastolic heart failure, without reduction of ejection fraction (HFpEF). The aim of multiple and less invasive diagnostic tests is to discern peculiar characteristics and reach the diagnosis without performing an invasive endomyocardial biopsy. These diagnostic tools allow early diagnosis, and they are crucial to best benefit from target therapy. In this review article, we describe the mechanism behind amyloid fibril formation, infiltration of tissues, and consequent clinical signs, focusing on the diagnostic tools and the red flags to obtain a diagnosis.