Bioimpedance Spectroscopy Offers An Objective Measure Of Heart Failure Stability During A Viral Pandemic
HFSA ePoster Library. Accardi A. 09/10/21; 343642; 83
Andrew Accardi
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Abstract
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Background: Patients with serious COVID infections frequently develop shock. Cardiac involvement has been demonstrated, but the relationship between LV function, hemodynamics, and troponin release has not been well characterized.
Methods: Of 1275 patients hospitalized with COVID pneumonia, 215 had shock requiring vasopressors. 162 had echocardiography to assess ventricular function and stroke volume. Ejection fraction (EF) was measured using Simpson’s rule and stroke volume (SV) by Doppler. Patients were divided into groups with low or preserved EF (EFL or EFP, cutoff <e 5%), and low or normal cardiac index, CI (CIL or CIN, cutoff <e2.2 L/min/m2).
Results: Mean age was 66.7, EF 58.7+/-13.9; CI 2.41+/-0.89, troponin 1.00+/-0.9. 5 patients had obstructive shock from pulmonary embolism (normal LVEF, low SV, RV dysfunction) and were excluded. The other 157 patients were divided into groups based on EF and CI (Figure). Overall hospital mortality in the cohort was 77%. Troponin was measured in 131/157 patients within 7 days of the first echo, and was increased in patients with low compared to preserved EF (3.18+/-1.7 vs 0.56+/-0.21, p=<0.01), but did not differ by CI within those groups. (Figure)
Conclusion: COVID-induced shock had a cardiogenic profile (EFLCIL) in 10% of patients, and another 5% had low EF but normal CI. Troponin was more elevated in patients with low EF, suggesting that effects of COVID on the myocardium impact cardiac function. Lack of difference by CI suggests contribution of other factors, such as fluid status, ventricular filling, and vascular function, to cardiac output in COVID patients with shock.
Methods: Of 1275 patients hospitalized with COVID pneumonia, 215 had shock requiring vasopressors. 162 had echocardiography to assess ventricular function and stroke volume. Ejection fraction (EF) was measured using Simpson’s rule and stroke volume (SV) by Doppler. Patients were divided into groups with low or preserved EF (EFL or EFP, cutoff <e 5%), and low or normal cardiac index, CI (CIL or CIN, cutoff <e2.2 L/min/m2).
Results: Mean age was 66.7, EF 58.7+/-13.9; CI 2.41+/-0.89, troponin 1.00+/-0.9. 5 patients had obstructive shock from pulmonary embolism (normal LVEF, low SV, RV dysfunction) and were excluded. The other 157 patients were divided into groups based on EF and CI (Figure). Overall hospital mortality in the cohort was 77%. Troponin was measured in 131/157 patients within 7 days of the first echo, and was increased in patients with low compared to preserved EF (3.18+/-1.7 vs 0.56+/-0.21, p=<0.01), but did not differ by CI within those groups. (Figure)
Conclusion: COVID-induced shock had a cardiogenic profile (EFLCIL) in 10% of patients, and another 5% had low EF but normal CI. Troponin was more elevated in patients with low EF, suggesting that effects of COVID on the myocardium impact cardiac function. Lack of difference by CI suggests contribution of other factors, such as fluid status, ventricular filling, and vascular function, to cardiac output in COVID patients with shock.
Background: Patients with serious COVID infections frequently develop shock. Cardiac involvement has been demonstrated, but the relationship between LV function, hemodynamics, and troponin release has not been well characterized.
Methods: Of 1275 patients hospitalized with COVID pneumonia, 215 had shock requiring vasopressors. 162 had echocardiography to assess ventricular function and stroke volume. Ejection fraction (EF) was measured using Simpson’s rule and stroke volume (SV) by Doppler. Patients were divided into groups with low or preserved EF (EFL or EFP, cutoff <e 5%), and low or normal cardiac index, CI (CIL or CIN, cutoff <e2.2 L/min/m2).
Results: Mean age was 66.7, EF 58.7+/-13.9; CI 2.41+/-0.89, troponin 1.00+/-0.9. 5 patients had obstructive shock from pulmonary embolism (normal LVEF, low SV, RV dysfunction) and were excluded. The other 157 patients were divided into groups based on EF and CI (Figure). Overall hospital mortality in the cohort was 77%. Troponin was measured in 131/157 patients within 7 days of the first echo, and was increased in patients with low compared to preserved EF (3.18+/-1.7 vs 0.56+/-0.21, p=<0.01), but did not differ by CI within those groups. (Figure)
Conclusion: COVID-induced shock had a cardiogenic profile (EFLCIL) in 10% of patients, and another 5% had low EF but normal CI. Troponin was more elevated in patients with low EF, suggesting that effects of COVID on the myocardium impact cardiac function. Lack of difference by CI suggests contribution of other factors, such as fluid status, ventricular filling, and vascular function, to cardiac output in COVID patients with shock.
Methods: Of 1275 patients hospitalized with COVID pneumonia, 215 had shock requiring vasopressors. 162 had echocardiography to assess ventricular function and stroke volume. Ejection fraction (EF) was measured using Simpson’s rule and stroke volume (SV) by Doppler. Patients were divided into groups with low or preserved EF (EFL or EFP, cutoff <e 5%), and low or normal cardiac index, CI (CIL or CIN, cutoff <e2.2 L/min/m2).
Results: Mean age was 66.7, EF 58.7+/-13.9; CI 2.41+/-0.89, troponin 1.00+/-0.9. 5 patients had obstructive shock from pulmonary embolism (normal LVEF, low SV, RV dysfunction) and were excluded. The other 157 patients were divided into groups based on EF and CI (Figure). Overall hospital mortality in the cohort was 77%. Troponin was measured in 131/157 patients within 7 days of the first echo, and was increased in patients with low compared to preserved EF (3.18+/-1.7 vs 0.56+/-0.21, p=<0.01), but did not differ by CI within those groups. (Figure)
Conclusion: COVID-induced shock had a cardiogenic profile (EFLCIL) in 10% of patients, and another 5% had low EF but normal CI. Troponin was more elevated in patients with low EF, suggesting that effects of COVID on the myocardium impact cardiac function. Lack of difference by CI suggests contribution of other factors, such as fluid status, ventricular filling, and vascular function, to cardiac output in COVID patients with shock.
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