• Cardiovascular Manifestations of COVID-19 Infection

      Center for Translational Medicine (Temple University) (2020-11-19)
      SARS-CoV-2 induced the novel coronavirus disease (COVID-19) outbreak, the most significant medical challenge in the last century. COVID-19 is associated with notable increases in morbidity and death worldwide. Preexisting conditions, like cardiovascular disease (CVD), diabetes, hypertension, and obesity, are correlated with higher severity and a significant increase in the fatality rate of COVID-19. COVID-19 induces multiple cardiovascular complexities, such as cardiac arrest, myocarditis, acute myocardial injury, stress-induced cardiomyopathy, cardiogenic shock, arrhythmias and, subsequently, heart failure (HF). The precise mechanisms of how SARS-CoV-2 may cause myocardial complications are not clearly understood. The proposed mechanisms of myocardial injury based on current knowledge are the direct viral entry of the virus and damage to the myocardium, systemic inflammation, hypoxia, cytokine storm, interferon-mediated immune response, and plaque destabilization. The virus enters the cell through the angiotensin-converting enzyme-2 (ACE2) receptor and plays a central function in the virus’s pathogenesis. A systematic understanding of cardiovascular effects of SARS-CoV2 is needed to develop novel therapeutic tools to target the virus-induced cardiac damage as a potential strategy to minimize permanent damage to the cardiovascular system and reduce the morbidity. In this review, we discuss our current understanding of COVID-19 mediated damage to the cardiovascular system.
    • Cardiovascular Manifestations of COVID-19 Infection

      Center for Translational Medicine (Temple University) (2020-11-19)
      SARS-CoV-2 induced the novel coronavirus disease (COVID-19) outbreak, the most significant medical challenge in the last century. COVID-19 is associated with notable increases in morbidity and death worldwide. Preexisting conditions, like cardiovascular disease (CVD), diabetes, hypertension, and obesity, are correlated with higher severity and a significant increase in the fatality rate of COVID-19. COVID-19 induces multiple cardiovascular complexities, such as cardiac arrest, myocarditis, acute myocardial injury, stress-induced cardiomyopathy, cardiogenic shock, arrhythmias and, subsequently, heart failure (HF). The precise mechanisms of how SARS-CoV-2 may cause myocardial complications are not clearly understood. The proposed mechanisms of myocardial injury based on current knowledge are the direct viral entry of the virus and damage to the myocardium, systemic inflammation, hypoxia, cytokine storm, interferon-mediated immune response, and plaque destabilization. The virus enters the cell through the angiotensin-converting enzyme-2 (ACE2) receptor and plays a central function in the virus’s pathogenesis. A systematic understanding of cardiovascular effects of SARS-CoV2 is needed to develop novel therapeutic tools to target the virus-induced cardiac damage as a potential strategy to minimize permanent damage to the cardiovascular system and reduce the morbidity. In this review, we discuss our current understanding of COVID-19 mediated damage to the cardiovascular system.
    • Heart failure in COVID‐19: the multicentre, multinational PCHF‐COVICAV registry

      Sokolski, Mateusz; Trenson, Sander; Sokolska, Justyna M.; D'Amario, Domenico; Meyer, Philippe; Poku, Nana K.; Biering-Sørensen, Tor; Højbjerg Lassen, Mats C.; Skaarup, Kristoffer G.; Barge-Caballero, Eduardo; Pouleur, Anne-Catherine; Stolfo, Davide; Sinagra, Gianfranco; Ablasser, Klemens; Muster, Viktoria; Rainer, Peter P.; Wallner, Markus; Chiodini, Alessandra; Heiniger, Pascal S.; Mikulicic, Fran; Schwaiger, Judith; Winnik, Stephan; Cakmak, Huseyin A.; Gaudenzi, Margherita; Mapelli, Massimo; Mattavelli, Irene; Paul, Matthias; Cabac-Pogorevici, Irina; Bouleti, Claire; Lilliu, Marzia; Minoia, Chiara; Dauw, Jeroen; Costa, Jérôme; Celik, Ahmet; Mewton, Nathan; Montenegro, Carlos E.L.; Matsue, Yuya; Loncar, Goran; Marchel, Michal; Bechlioulis, Aris; Michalis, Lampros; Dörr, Marcus; Prihadi, Edgard; Schoenrath, Felix; Messroghli, Daniel R.; Mullens, Wilfried; Lund, Lars H.; M.C. Rosano, Giuseppe; Ponikowski, Piotr; Ruschitzka, Frank; Flammer, Andreas J.; Wallner|0000-0001-7692-892X (2021-09-17)
      Aims: We assessed the outcome of hospitalized coronavirus disease 2019 (COVID-19) patients with heart failure (HF) compared with patients with other cardiovascular disease and/or risk factors (arterial hypertension, diabetes, or dyslipidaemia). We further wanted to determine the incidence of HF events and its consequences in these patient populations. Methods and results: International retrospective Postgraduate Course in Heart Failure registry for patients hospitalized with COVID-19 and CArdioVascular disease and/or risk factors (arterial hypertension, diabetes, or dyslipidaemia) was performed in 28 centres from 15 countries (PCHF-COVICAV). The primary endpoint was in-hospital mortality. Of 1974 patients hospitalized with COVID-19, 1282 had cardiovascular disease and/or risk factors (median age: 72 [interquartile range: 62–81] years, 58% male), with HF being present in 256 [20%] patients. Overall in-hospital mortality was 25% (n = 323/1282 deaths). In-hospital mortality was higher in patients with a history of HF (36%, n = 92) compared with non-HF patients (23%, n = 231, odds ratio [OR] 1.93 [95% confidence interval: 1.44–2.59], P < 0.001). After adjusting, HF remained associated with in-hospital mortality (OR 1.45 [95% confidence interval: 1.01–2.06], P = 0.041). Importantly, 186 of 1282 [15%] patients had an acute HF event during hospitalization (76 [40%] with de novo HF), which was associated with higher in-hospital mortality (89 [48%] vs. 220 [23%]) than in patients without HF event (OR 3.10 [2.24–4.29], P < 0.001). Conclusions: Hospitalized COVID-19 patients with HF are at increased risk for in-hospital death. In-hospital worsening of HF or acute HF de novo are common and associated with a further increase in in-hospital mortality.