Heart Failure During the COVID-19 Pandemic: Clinical, Diagnostic, Management, and Organizational Dilemmas

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  Figure 1. Potential contributing factors and mechanisms of cardiac dysfunction in patients with COVID‐19. The first step in COVID‐19 pathogenesis is viral invasion via its target host cell receptors. SARS‐CoV‐2 infection induces cellular death and injury in various cellular types and determines overactivation of the host immune and neurohormonal responses. Viral‐mediated cell death causes release of damage‐associated molecules and cytokines, and maladaptive cytokine release is associated to further cellular destruction and multi‐organ dysfunction. The infection of endothelial cells could lead to severe endothelial dysfunction and microvascular thrombosis, factors that contribute to the ischaemic injuries observed in many tissues and organs. The maladaptive immune response can potentially destabilize atherosclerotic plaques and explain the development of Type I acute coronary syndrome. The direct myocyte's viral invasion and infiltration of the myocardium by activated T lymphocytes and macrophages lead to severe cardiac damage and in some instances to fulminant myocarditis. Ischaemic or non‐ischaemic myocardial damage, overactivation of the sympathetic nervous system, hypoxaemia, and…

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  Figure 2. Diagnostic process for differentiation between dyspnoea due to ARDS and cardiac dyspnoea: a detailed clinical laboratory and imaging algorithm could facilitate early diagnosis. ACEi, angiotensin‐converting enzyme inhibitors; AHF, acute heart failure; ARB, angiotensin receptor blockers; ARDS, acute respiratory distress syndrome; ARNI, angiotensin receptor neprilysin inhibitors; CT, chest tomography; CV, cardiovascular; GI, gastrointestinal; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; IABP, intra‐aortic balloon pump; MCS, mechanical circulatory support; MI, myocardial infarction; MV, mechanical ventilation; VA‐ECMO, venous arterial extracorporeal membrane oxygenation; VV‐ECMO, veno‐venous extracorporeal membrane oxygenation.

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  Figure 3. Remaining concerns and dilemmas in HF diagnosis, special population treatment, profile identifications, and research priorities. HF, heart failure; LVAD, left ventricular assist device.

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  Figure 4. Potential applications of telemedicine by a tailored programme by several wireless and interned application programmes addressed to identify common HF symptoms, blood test, ECG, and invasive and non‐invasive cardiac pressure. ECG, electrocardiogram; ICD, implantable cardioverter defibrillator.