Reduced cardiac function identified in severe COVID-19 patients in new study

By Bhavana KunkalikarReviewed by Aimee MolineuxOct 17 2022

In a recent study published in the Journal of Critical Care, researchers assessed the cardiac function in patients experiencing severe coronavirus disease 2019 (COVID-19).

Background

Cardiovascular changes have been linked to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections in infected patients. A sizable majority of COVID-19-infected patients have elevated troponin levels, which are linked to increased mortality. Additionally, case reports of fulminant myocarditis or cardiogenic shock have been published. Acute cor pulmonale (ACP), pulmonary embolism (PE), and right ventricular dilatation have also been documented.

There is insufficient information on how the heart functions concerning the lungs and the mechanics of breathing during artificial ventilation. These characteristics may also be important in severe COVID-19 because they have been linked to the cardiac dysfunction associated with adult respiratory distress syndrome (ARDS).

About the study

In the present study, researchers characterized cardiac function in critically ill patients diagnosed with severe COVID-19.

Patients with laboratory-confirmed COVID-19 hospitalized in the intensive care unit (ICU) between April and July 2020 in four university-affiliated hospitals in Chile were included in this prospective, multicenter study. All consecutive COVID-19 patients who required invasive mechanical ventilation (MV) were eligible for the study. The critical care echocardiography (CCE) examination was conducted concurrently with the collection of demographic information, the Sequential Organ Failure Assessment (SOFA), the Acute Physiology and Chronic Health Evaluation II (APACHE II), hemodynamic variables, respiratory system mechanics, biomarkers, and tissue perfusion parameters. An evaluation of the one-year follow-up was conducted via telephone interview or an online death registry.

A medical operator conducted the transthoracic echocardiography, overseen by the center's chief investigator. The team also performed echocardiographic estimations. Lung-protective ventilation techniques were used to manage patients throughout their treatment. The examination of the echocardiogram was conducted with adequate sedation. Measurements were obtained, and three successive cardiac cycles were averaged.

The left ventricular ejection fraction (LVEF), calculated using Simpson's modified formula, was used to evaluate the LV systolic function. The classification of patients into hyperkinetic having LVEF >60%, normokinetic with LVEF between 45% and 60%, and hypokinetic with LVEF less than 45%. The LV outflow tract (LVOT) was used to determine cardiac output (CO). The LVOT area and velocity time integral (VTI) were multiplied to determine the stroke volume (SV). The CO was determined as the sum of the heart rate and the SV. Tissue Doppler Imaging (TDI) was used to capture the peak mitral annular myocardial velocity wave (s').

Mitral inflow pulsed wave Doppler was used to determine the atrial velocity (A) and early peak velocity (E) of the left ventricular diastole. The left and right ventricular end-diastolic areas (LVEDA and RVEDA) were assessed, and the ratio of LVEDA and RVEDA was calculated. RV dilatancy connected to a paradoxical septal motion was referred to as ACP. Peak tricuspid annular myocardial velocity wave (s') and tricuspid annular plane systolic excursion (TAPSE) measurements were used to evaluate the RV's systolic function.

Results

The study group included a total of 140 individuals with an average age of 57±11 years, with 29% of the group being female. Obesity, hypertension, and diabetes mellitus were the three primary comorbidities. Almost 65 patients were in the prone position at the time of the echocardiographic measurement. The PaO2/FiO2 ratio was 155, and the MV settings closely followed lung protective ventilation techniques.

Cardiac output was 5.1 L/min, while 86% of the patients needed norepinephrine at a median dose of 0.05 g/kg/min to sustain their mean arterial pressure above 65 mmHg. Most patients had normal perfusion parameters, including 1.7 mmol/L lactate levels and a Pv-aCO2 gradient of 6. According to the parameters employed, 36 patients were fluid-responsive, and seven patients showed signs of elevated LV filling pressure.

In comparison to the patients having RV dilatation, patients with ACP displayed more severe lung illness as evidenced by reduced compliance, greater driving pressure, and the presence of respiratory acidosis linked with higher APACHE II and SOFA scores on admission. Compared to patients with TAPSE who had dilatation alone, individuals with ACP had significantly lower RV systolic function. ACP patients also required more norepinephrine and had a lower stroke volume and higher heart rate, a longer capillary refill time, higher troponin levels, and higher lactate levels linked to a higher prevalence of LV systolic dysfunction.

While 27 patients displayed LV or RV dysfunction, 82 patients displayed signs of diastolic dysfunction, including 66 patients with Grade I, 16 with Grade II, and zero with Grade III. LV systolic dysfunction and diastolic dysfunction showed no individual association with mortality. Forty-four patients succumbed, including 40 who died while in ICU. ICU mortality was higher in ACP patients. During the one-year follow-up, just one patient passed away. ACP and PaO2/FiO2 were independent predictors of death as per the multivariate analysis.

The study findings showed that mechanically ventilated patients diagnosed with COVID-19 ARDS commonly experienced right ventricular dilation. Only 40% of individuals with acute cor pulmonale had a concurrent pulmonary embolism, which was also related to decreased pulmonary function.