[Cardiac compromise in patients recovered from COVID-19 without troponin elevation assessed by cardiac magnetic resonance imaging]. / Hallazgos en resonancia cardiaca post COVID-19 en pacientes sin elevación de troponinas.

Background: The disease caused by coronavirus (COVID-19) affects the cardiovascular system, whether by direct viral aggression or indirectly through systemic inflammation and multiple organ compromise. A widely used method to determine cardiac injury is troponin measurement. The aim of this study is to evaluate the prevalence of cardiac involvement (CINV) in a population recovered from COVID-19, referred to cardiac MRI (CMR), who did not present troponin elevation. Methods: There were 156 patients that recovered from COVID-19 and who did not present troponin elevation referred to CMR. CINV was considered to be the presence of: late gadolinium enhancement (LGE), edema, myocarditis, pericarditis, left ventricular systolic dysfunction (LVSD) and/or depressed right ventricular systolic dysfunction (RVSD). Results: Prevalence of CINV was 28.8%, being more frequent in men (p=0.002), in patients who required hospitalization (p=0.04) and in those who experienced non-mild cases of infection (p=0.007). RVSD (17.9%) and LVSD (13.4%) were the most frequent findings. The rate of myocarditis was 0.6%. LGE manifested in 7.1% of patients and its presence was related to less left ventricular ejection fraction (LVEF) (p=0.0001) and right ventricular ejection fraction (RVEF) (p=0.04). Conclusion: In patients who recovered from COVID-19, 28.8% of CINV was found. It was more frequent in men, in patients who required admission and in patients with cases of non-mild infection. The patients that presented LGE had less LVEF and RVSF.

Antecedentes: La enfermedad por coronavirus 2019 (COVID-19) afecta al sistema cardiovascular, ya sea mediante la agresión directa viral o indirectamente por medio de la inflamación sistémica y afectación multiorgánica. Las troponinas son ampliamente utilizadas para determinar lesión cardiaca. La finalidad de este estudio es evaluar la prevalencia de afectación cardiaca (ACARD) en una población recuperada de COVID-19, derivada a resonancia magnética cardiaca (RMC), sin elevación de troponinas al momento del estudio. Métodos: Ciento cincuenta y seis pacientes que se recuperaron de COVID-19 y que no presentaron elevación de troponinas fueron derivados a RMC. Se consideró ACARD a la presencia de: realce tardío de gadolinio (RTG), edema, miocarditis, pericarditis, deterioro de la función sistólica del ventrículo izquierdo (DFSVI) y/o depresión de la función sistólica del ventrículo derecho (DFSVD). Resultados: La prevalencia de ACARD fue del 28.8%, siendo más frecuente en hombres (p = 0.002), en pacientes que requirieron hospitalización (p = 0.04) y en aquellos que cursaron cuadro no leve de infección (p = 0.007). La DFSVD (17.9%) y la DFSVI (13.4%) fueron las hallazgos más frecuentes. La frecuencia de miocarditis fue del 0.6%. El RTG se manifestó en el 7.1% de los pacientes y se relacionó con menor fracción de eyección del ventrículo izquierdo (FEVI) (p = 0.0001) y derecho (FEVD) (p = 0.04). Conclusión: La prevalencia de ACARD fue del 28.8%. Esta es más frecuente en hombres, en pacientes que requirieron internación y que cursaron cuadros de infección no leve. La miocarditis presentó una prevalencia muy baja. Los pacientes que presentaron RTG tuvieron menor FEVI y FSVD.

Implications of myocardial injury in Mexican hospitalized patients with coronavirus disease 2019 (COVID-19).

BACKGROUND: Respiratory illnesses is the most common manifestation of Coronavirus disease 2019 (COVID-19); however, myocardial injury has recently emerged as a frequent complication. METHODS: An observational, longitudinal, prospective, and multicenter study of hospitalized Mexican patients was made. We assessed the prevalence of myocardial injury and its relationship with complications and mortality. RESULTS: 254 COVID-19 patients were included. Their average age was 53.8 years old, 167 (65.7%) were male and 87 (34.3%) female. According to troponin levels, two populations were generated, those with and without myocardial injury. There was no difference in gender or age between both groups. However, there was a greater proportion of obesity and hypertension in myocardial injury group. Multivariate logistic regression analysis revealed that obesity (OR 2.029, 95% CI 1.039-3.961; p = 0.038), arterial oxygen saturation <90% (OR 2.250, 95% CI 1.216-3.560; p = 0.025), and systolic blood pressure <90 mmHg (OR 2.636, 95% CI 1.530-4.343; p = 0.042), were directly related to higher levels of troponins. Multivariate cox proportional hazards analysis showed that primary endpoint (mortality) was determined by overweight/obesity (OR 1.290, 95% CI 0.115-0.730; p = 0.009), ferritin levels (OR 1.001, 95% CI 1.000-1.001; p < 0.001), myocardial injury (OR 3.764, 95% CI 1.307-10.838; p = 0.014), septic shock (OR 4.104, 95% CI 1.142-14.132; p = 0.024), acute respiratory distress syndrome (OR 3.001, 95% CI 1.008-10.165; p = 0.040), and treatment with Hydroxychloroquine/Azithromycin (OR 0.357, 95% IC 0.133-0.955; p = 0.040). Secondary endpoint (Mechanical ventilation risk) was associated to the same factors. CONCLUSIONS: Myocardial injury represents an increased risk of complications and death in Mexican hospitalized patients with COVID-19.

EVALUATION OF PERIOPERATIVE HIGH-SENSITIVE CARDIAC TROPONIN I AS A PREDICTIVE BIOMARKER OF MAJOR ADVERSE CARDIOVASCULAR EVENTS AFTER NONCARDIAC SURGERY.

BACKGROUND: Various studies suggest that perioperative concentrations of high-sensitivity troponins are incremental and predictive factors of a major adverse cardiac event (MACE) and all-cause mortality. OBJECTIVE: The objective of the study was to evaluate the predictive value of high-sensitivity cardiac troponin I (hs-cTnI) in the development of MACE and all-cause mortality, within 30-days and 1-year follow-up after noncardiac surgery. METHODS: In this prospective cohort study, we included men ≥ 45 years and women ≥ 55 years with ≥ 2 cardiovascular risk factors and undergoing intermediate or high-risk noncardiac surgery. Demographic and clinical information was collected from clinical charts. We measured baseline hs-cTnI 24 h before surgery, and its post-operative concentration 24 h after surgery. RESULTS: In the entire sample, 8 patients (8.6%) developed MACE at 30-days follow-up (4 deaths), 12 (12.9%) within the 1st year (7 deaths), and 17 (18.2%) after complete post-surgical follow-up (10 deaths). We observed higher baseline and post-operative concentrations in patients who presented MACE (12 pg/ml vs. 3.5 pg/ml; p = 0.001 and 18.3 pg/ml vs. 5.45 pg/ml; p = 0.009, respectively). The hazard ratios (HRs) calculated by Cox regression analysis between the hs-cTnI baseline concentration and the post-operative development of MACE at 30-days and 1-year were 5.70 (95% confidence interval [CI], 1.10-29.40) with hs-cTnI > 6.2 pg/ml and 12.86 (95% CI, 1.42-116.34) with hs-cTnI > 3.3 pg/ml, respectively. The estimated post-operative HR death risk at 1-year was 14.43 (95% CI, 1.37-151.61) with hs-cTnI > 4.5 pg/ml. CONCLUSIONS: Pre-operative hs-cTnI was an independent predictive risk factor for MACE at 30-days and 1-year after noncardiac surgery and for all-cause mortality at 1-year after noncardiac surgery.

Evaluation of perioperative high-sensitive cardiac troponin i as a predictive biomarker of major adverse cardiovascular events after noncardiac surgery

ABSTRACT Background: Various studies suggest that perioperative concentrations of high-sensitivity troponins are incremental and predictive factors of a major adverse cardiac event (MACE) and all-cause mortality. Objective: The objective of the study was to evaluate the predictive value of high-sensitivity cardiac troponin I (hs-cTnI) in the development of MACE and all-cause mortality, within 30-days and 1-year follow-up after noncardiac surgery. Methods: In this prospective cohort study, we included men ≥ 45 years and women ≥ 55 years with ≥ 2 cardiovascular risk factors and undergoing intermediate or high-risk noncardiac surgery. Demographic and clinical information was collected from clinical charts. We measured baseline hs-cTnI 24 h before surgery, and its post-operative concentration 24 h after surgery. Results: In the entire sample, 8 patients (8.6%) developed MACE at 30-days follow-up (4 deaths), 12 (12.9%) within the 1st year (7 deaths), and 17 (18.2%) after complete post-surgical follow-up (10 deaths). We observed higher baseline and post-operative concentrations in patients who presented MACE (12 pg/ml vs. 3.5 pg/ml; p = 0.001 and 18.3 pg/ml vs. 5.45 pg/ml; p = 0.009, respectively). The hazard ratios (HRs) calculated by Cox regression analysis between the hs-cTnI baseline concentration and the post-operative development of MACE at 30-days and 1-year were 5.70 (95% confidence interval [CI], 1.10-29.40) with hs-cTnI > 6.2 pg/ml and 12.86 (95% CI, 1.42-116.34) with hs-cTnI > 3.3 pg/ml, respectively. The estimated post-operative HR death risk at 1-year was 14.43 (95% CI, 1.37-151.61) with hs-cTnI > 4.5 pg/ml. Conclusions: Pre-operative hs-cTnI was an independent predictive risk factor for MACE at 30-days and 1-year after noncardiac surgery and for all-cause mortality at 1-year after noncardiac surgery.

High-sensitivity troponin is associated with high risk clinical profile and outcome in acute heart failure.

BACKGROUND: The aim of the study was to evaluate the value of high-sensitivity cardiac troponin (hs-cTn) for identifying high-risk patients. METHODS AND RESULTS: One hundred and eighty-seven patients admitted with acute heart failure (HF) (without myocardial infarction) were consecutively included; hs-cTn was measured at admission; the relation between elevated hs-cTn and the clinical outcome during hospitalization and at 90 days was analyzed; 93% (n = 174) had hs-cTn above the maximal normal value (14 ng/L); median hs-cTn was 42 ng/L (IQR 24-81). Patients with ejection fraction (EF) ≤ 45% had higher hs-cTn values (p = 0.0004). Patients with low cardiac output syndrome (LCOS) or shock had higher troponin levels compared with those with less severe clinical presentations (p = 0.004). Patients who required inotropic presented higher troponin values (p = 0.002), troponin values were also higher in those requiring complex therapies (intra-aortic balloon pump, mechanical ventilation or hemodialysis, p = 0.002). At 90-day follow-up, 28 (15.5%) patients died and 27 rehospitalizations occurred (55 events). The risk of events was greater in patients with hs-cTn > 42 ng/L (0.021), low blood pressure at admission (p = 0.002), LCOS or shock (p < 0.0001), EF ≤ 45% (p = 0.005) and inotropic use (p < 0.0001). In multivariate analysis, only inotropic agents requirements was associated independently with a high risk of death or rehospitalizations at 90 days (p = 0.007). CONCLUSIONS: Elevation of hs-cTn is a finding almost constant in patients with decompensated HF. In subjects with higher troponin levels ventricular dysfunction is frequent. The use of hs-cTn for risk stratification at admission helps to identify populations with poor outcome during hospitalization and increased risk of death or rehospitalizations during follow-up who will require rapid implementation of aggressive treatment.