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Introduction: Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) exhibits 25-30% mortality in hospitalized patients with heart failure (HF). Cardiovascular disease is the most significant comorbidity associated with increased mortality in COVID-19 patients with data suggesting local and systemic inflammation play a critical role in cardiac functional abnormalities. SARS-CoV-2 vaccination reportedly reduces severity of infection. We sought to characterize if vaccination had any protective effect on patients with HF hospitalized for acute COVID-19. Hypothesis: Baseline cardiac biomarkers including CRP, ferritin, high sensitivity cardiac troponin I (hs-cTnI), and pro-brain natriuretic peptide (pBNP) may be lower in vaccinated COVID-19 HF patients revealing the impact of vaccination on reducing inflammation by SARS-CoV-2 infection. Method(s): Electronic health records underwent IRB exempted extraction of demographics, anthropometrics, vital signs, laboratory tests, and ICD-10-CM-based Elixhauser comorbidity categories. Continuous data summarized with median [IQR] were compared using Kruskal-Wallis test and discrete data with chi-squared test. Result(s): Among HF patients with a recorded vaccine status admitted between July 3, 2021 and March 17, 2022, 206 underwent acute COVID-19 hospitalization. Vaccinated (n=91, 44%) and unvaccinated (115, 56%) patients exhibited statistically similar distribution of males (56%), aged 78[69-86] years with comorbidities 5[4-7] distributed across Whites (88%), Blacks (8%), and other races (4%). There were no intergroup differences with most prevalent comorbidities at admission including hypertension (99%), diabetes (41%), chronic pulmonary disease (37%), obesity (36%), deficiency anemia (31%), and renal failure (25%). There were no intergroup differences in initiation of COVID-19 directed treatments. Baseline biomarkers in vaccinated versus unvaccinated were CRP 6.0[1.3-9.5] vs. 6.9[2.7-11.3] mg/dL (p=.25), ferritin 171[76-552] vs. 432[79-876] ng/mL (p=.13), LDH 245[192-317] vs. 338[260-439] U/L (p=.003), D-dimer 0.89[0.53-1.73] vs. 1.36[0.95-2.80] mg/L FEU (p=.06), hs-cTnI 27[14-67] vs. 28[16-81] ng/L (p=.39), and pro-BNP 3487[1516-7162] vs. 3278[1549 vs. 9001] pg/mL (p=.90). Clinical visit criteria respectively were hospital LOS 4.9[2.9-10.3] vs. 5.4[3.4-10.3] days (p=.27), ICU admission 10% vs. 17% (p=.15), and discharge disposition expired or Hospice 15% vs. 16% (p=.48). Rehospitalization occurred similarly between groups and was not significant. Conclusion(s): Acute and chronic inflammation are pathogenic drivers of HF. Inflammatory biomarkers lower among vaccinated patients with HF included CRP, ferritin, D-dimer, and hs-cTnI, although not significant. LDH, however, was significantly lower suggesting improved host widespread tissue perfusion as one mechanism of reduced severity in patients with HF undergoing SARS-CoV-2 vaccine breakthrough infection. One study caveat is that despite inclusion of all patients, these preliminary findings are likely not sufficiently powered to validate our hypothesis.Copyright © 2022
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Background: The impact of SARS-CoV-2 infection on intrinsic myocardial conduction continues to be an area of focus amongst the medical community. Our objective was to investigate if specific myocardial conduction abnormalities were independently associated with mortality in patients hospitalized with COVID 19. Method(s): Under IRB exemption, the electronic medical records of COVID-19 patients (N=3840) undergoing index hospitalization were reviewed to extract presentation ECG conduction data, demographics, and laboratory results (within 8h). This patient cohort was then separated into two groups based on mortality vs. no mortality (N=520). Logistical regression was used to test association of ECG conduction intervals with mortality. A subgroup analysis of 651 patients who underwent at least 1 ECG in the 12 months prior to their COVID hospitalization were analyzed to detect statistically significant differences in conduction intervals pre and post SARS-CoV-2 infection. Result(s): According to our nominal logistic fit for hospital mortality, Heart Rate (HR) >100 (p=0.0007;LW 4.14), QRS duration > 120 ms (p=0.0053;LW 2.27), and QTc prolongation (defined as QTc > 450ms in males;QTc > 460ms in females) (p=0.0089;LW 2.04) were independently associated with higher risk of mortality. LogWorth (LW) calculations were included in an effort to estimate the proportional effect each variable has on overall mortality. LW > 2 were shown to be statistically significant with p< 0.05 with HR > 100 (LW 4.14) having the highest proportional effect on mortality followed by QRSd (LW 2.27) then QTc prolongation (LW 2.04). PR interval> 200ms (p=0.30) and QRS axis (p=0.15) were not associated with higher risk of mortality. Our subgroup analysis of the 651 patients mentioned above yielded no statistically significant differences in conduction intervals pre & post SARS-CoV-2 infection. Conclusion(s): : Amongst our patient cohort, HR > 100, QRSd > 120ms, and QTc prolongation (QTc > 450 in males;QTc > 460 in females) were each independently associated with higher risk of mortality in patients hospitalized with COVID 19. Subgroup analysis of 651 patients showed no statistically significant differences in conduction intervals pre and post SARS-CoV-2 infection. These findings support the use of objective ECG data in risk stratifying patients hospitalized with COVID 19.Copyright © 2022
RESUMEN
BACKGROUND: The impact of SARS-CoV-2 infection on intrinsic myocardial conduction continues to be an area of focus amongst the medical community. Our objective was to investigate if specific myocardial conduction abnormalities were independently associated with mortality in patients hospitalized with COVID 19. METHODS: Under IRB exemption, the electronic medical records of COVID-19 patients (N=3840) undergoing index hospitalization were reviewed to extract presentation ECG conduction data, demographics, and laboratory results (within 8h). This patient cohort was then separated into two groups based on mortality vs. not (N=520). Logistical regression was used to test association of ECG conduction intervals with mortality. RESULTS: According to our nominal logistic fit for hospital mortality, Heart Rate (HR) >100 (p=0.0007;LW 4.14), QRS duration > 120 ms (p=0.0053;LW 2.27), and QTc prolongation (defined as QTc > 450ms in males;QTc > 460ms in females) (p=0.0089;LW 2.04) were independently associated with higher risk of mortality. LogWorth (LW) calculations were included in an effort to estimate the proportional effect each variable has on overall mortality. LW > 2 were shown to be statistically significant with p< 0.05 with HR > 100 (LW 4.14) having the highest proportional effect on mortality followed by QRSd (LW 2.27) then QTc prolongation (LW 2.04). PR interval> 200ms (p=0.30) and QRS axis (p=0.15) were not associated with higher risk of mortality. CONCLUSIONS: Amongst our patient cohort, HR > 100, QRSd > 120ms, and QTc prolongation (QTc > 450 in males;QTc > 460 in females) were each independently associated with higher risk of mortality in patients hospitalized with COVID 19. These findings support the use of objective ECG data in risk stratifying patients hospitalized with COVID 19.
RESUMEN
BACKGROUND: Severe acute respiratory syndrome-coronavirus-2 (SARSCoV- 2) has substantial morbidity and mortality in patients with heart failure (HF). Hospital mortality exceeds 30% in the American Heart Association's COVID-19 Cardiovascular Disease registry. We characterized clinical traits associated with progression to critical illness (PCI, ICU admission or hospital death) during index and subsequent hospitalizations in SARS-CoV-2 infected patients with extant HF. METHODS: Electronic health records underwent extraction of demographics, anthropometrics, vital signs, laboratory tests, and ICD-10-CM-based Elixhauser comorbidity categories. Univariate logistic regression was used to identify features associated with PCI. Continuous data summarized with median [IQR] were compared using Kruskal-Wallis test and discrete data with chi-squared test. Confounders statistically balanced included age, sex, race, COVID-19 directed treatment, and 4-waves of pandemic. RESULTS: Among HF patients admitted between March 14, 2020 and September 30, 2021, 530 underwent index COVID-19 hospitalization. Among those, 111 were readmitted once, and 43 readmitted at least twice. Index admission median age was 75 [65-84] years, body mass index (BMI) 29.5 [24.9-35.3], and time to readmission 247.7 [44.7-784.1] days. Subsequent time to readmission was 34.7 [5.7-92] days. Most common admission comorbidities were hypertension (81%), diabetes (43%), renal failure (42%), obesity (38%), chronic pulmonary disease (36%), and deficiency anemia (32%). The most common comorbidities at second readmission were renal failure (60%), deficiency anemia (53%), diabetes (40%), and chronic pulmonary disease (40%). PCI occurred in 32% of index admissions, 21% of first readmissions, and 14% of second readmissions. Hospital death or discharge to hospice occurred in 28%, 18%, and 23% of readmissions respectively. CONCLUSIONS: Days to readmission declined revealing impact of inflammation and immunomodulation caused by SARS-CoV-2. Although hypertension was the most common comorbidity at index admission it was the least common at subsequent readmissions. This may represent improved control or death of those poorly controlled. Renal failure being the most common comorbidity at second readmission may represent worsening function due to SARS-CoV-2 infection and injury or worsening HF syndrome. Progressively worsening pBNP and hsTnI likely reflect direct myocyte injury by heightened entry of SARS-CoV-2 viral particle due to expression of angiotensinconverting enzyme 2. HF patients should be urged to undergo SARS-CoV-2 vaccination with apropos boost.