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3.
Eur Heart J ; 43(11): 1141-1153, 2022 03 14.
Article in English | MEDLINE | ID: covidwho-1462320

ABSTRACT

AIMS: The severity of myocardial tissue damage following ST-elevation myocardial infarction (STEMI) strongly determines short- and long-term prognosis. This study explored the impact of the coronavirus disease 2019 (COVID-19) pandemic and associated public health restrictions on infarct severity. METHODS AND RESULTS: STEMI patients treated with primary percutaneous coronary intervention (PCI) and included in the prospective Magnetic Resonance Imaging in Acute ST-Elevation Myocardial Infarction (MARINA-STEMI) cohort study from 2015- 2020 (n = 474) were categorized according to (i) timeframes with and without major public health restrictions in 2020, and (ii) timeframes of major public health restrictions during 2020 and during the corresponding timeframes between 2015-2019. Myocardial damage was evaluated by cardiac magnetic resonance imaging. During major public health restrictions in 2020 (n = 48), there was an increase in infarct size (22 [IQR 12-29] vs. 14 [IQR 6-23]%, P < 0.01), a higher frequency (77% vs. 52%, P < 0.01) and larger extent of microvascular obstruction (1.5 [IQR 0.1-11.4] vs. 0.2 [IQR 0.0-2.6]%, P < 0.01) and a higher rate of intramyocardial haemorrhage (56% vs. 34%, P = 0.02) as compared to the phases without major restrictions in 2020 (n = 101). These findings were confirmed in adjusted analysis and were consistent when comparing patients admitted in 2020 versus patients admitted in the "pre-pandemic" era (2015-2019). Patient characteristics were comparable between groups, except for a significantly longer total ischemia time (P < 0.01) and higher frequency of pre-PCI Thrombolysis in Myocardial Infarction (TIMI) flow 0 during times of major restrictions (P = 0.03). CONCLUSION: This study provides novel mechanistic insights demonstrating a significant increase in myocardial damage in STEMI patients admitted during the COVID-19 pandemic with a temporal relation to major public health restrictions.


Subject(s)
COVID-19 , Myocardial Infarction , Percutaneous Coronary Intervention , ST Elevation Myocardial Infarction , COVID-19/epidemiology , Cohort Studies , Humans , Magnetic Resonance Imaging , Myocardial Infarction/therapy , Pandemics , Percutaneous Coronary Intervention/methods , Prospective Studies , ST Elevation Myocardial Infarction/epidemiology
4.
Lancet Respir Med ; 9(8): 863-872, 2021 08.
Article in English | MEDLINE | ID: covidwho-1340915

ABSTRACT

BACKGROUND: SARS-CoV-2 entry in human cells depends on angiotensin-converting enzyme 2, which can be upregulated by inhibitors of the renin-angiotensin system (RAS). We aimed to test our hypothesis that discontinuation of chronic treatment with ACE-inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) mitigates the course o\f recent-onset COVID-19. METHODS: ACEI-COVID was a parallel group, randomised, controlled, open-label trial done at 35 centres in Austria and Germany. Patients aged 18 years and older were enrolled if they presented with recent symptomatic SARS-CoV-2 infection and were chronically treated with ACEIs or ARBs. Patients were randomly assigned 1:1 to discontinuation or continuation of RAS inhibition for 30 days. Primary outcome was the maximum sequential organ failure assessment (SOFA) score within 30 days, where death was scored with the maximum achievable SOFA score. Secondary endpoints were area under the death-adjusted SOFA score (AUCSOFA), mean SOFA score, admission to the intensive care unit, mechanical ventilation, and death. Analyses were done on a modified intention-to-treat basis. This trial is registered with ClinicalTrials.gov, NCT04353596. FINDINGS: Between April 20, 2020, and Jan 20, 2021, 204 patients (median age 75 years [IQR 66-80], 37% females) were randomly assigned to discontinue (n=104) or continue (n=100) RAS inhibition. Within 30 days, eight (8%) of 104 died in the discontinuation group and 12 (12%) of 100 patients died in the continuation group (p=0·42). There was no significant difference in the primary endpoint between the discontinuation and continuation group (median [IQR] maximum SOFA score 0·00 (0·00-2·00) vs 1·00 (0·00-3·00); p=0·12). Discontinuation was associated with a significantly lower AUCSOFA (0·00 [0·00-9·25] vs 3·50 [0·00-23·50]; p=0·040), mean SOFA score (0·00 [0·00-0·31] vs 0·12 [0·00-0·78]; p=0·040), and 30-day SOFA score (0·00 [10-90th percentile, 0·00-1·20] vs 0·00 [0·00-24·00]; p=0·023). At 30 days, 11 (11%) in the discontinuation group and 23 (23%) in the continuation group had signs of organ dysfunction (SOFA score ≥1) or were dead (p=0·017). There were no significant differences for mechanical ventilation (10 (10%) vs 8 (8%), p=0·87) and admission to intensive care unit (20 [19%] vs 18 [18%], p=0·96) between the discontinuation and continuation group. INTERPRETATION: Discontinuation of RAS-inhibition in COVID-19 had no significant effect on the maximum severity of COVID-19 but may lead to a faster and better recovery. The decision to continue or discontinue should be made on an individual basis, considering the risk profile, the indication for RAS inhibition, and the availability of alternative therapies and outpatient monitoring options. FUNDING: Austrian Science Fund and German Center for Cardiovascular Research.


Subject(s)
Angiotensin Receptor Antagonists , Angiotensin-Converting Enzyme Inhibitors , COVID-19 , Hypertension , Renin-Angiotensin System , SARS-CoV-2 , Angiotensin Receptor Antagonists/administration & dosage , Angiotensin Receptor Antagonists/adverse effects , Angiotensin-Converting Enzyme 2/metabolism , Angiotensin-Converting Enzyme Inhibitors/administration & dosage , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Area Under Curve , COVID-19/epidemiology , COVID-19/metabolism , COVID-19/therapy , Female , Humans , Hypertension/drug therapy , Hypertension/epidemiology , Male , Middle Aged , Organ Dysfunction Scores , Outcome and Process Assessment, Health Care , Renin-Angiotensin System/drug effects , Renin-Angiotensin System/physiology , Risk Adjustment/methods , SARS-CoV-2/drug effects , SARS-CoV-2/physiology , Severity of Illness Index , Withholding Treatment/statistics & numerical data
5.
J Clin Med ; 9(7)2020 Jul 10.
Article in English | MEDLINE | ID: covidwho-646862

ABSTRACT

Coronavirus disease 19 (COVID-19) and its associated restrictions could affect ischemic times in patients with ST-segment elevation myocardial infarction (STEMI). The objective of this study was to investigate the influence of the COVID-19 outbreak on ischemic times in consecutive all-comer STEMI patients. We included consecutive STEMI patients (n = 163, median age: 61 years, 27% women) who were referred to seven tertiary care hospitals across Austria for primary percutaneous coronary intervention between 24 February 2020 (calendar week 9) and 5 April 2020 (calendar week 14). The number of patients, total ischemic times and door-to-balloon times in temporal relation to COVID-19-related restrictions and infection rates were analyzed. While rates of STEMI admissions decreased (calendar week 9/10 (n = 69, 42%); calendar week 11/12 (n = 51, 31%); calendar week 13/14 (n = 43, 26%)), total ischemic times increased from 164 (interquartile range (IQR): 107-281) min (calendar week 9/10) to 237 (IQR: 141-560) min (calendar week 11/12) and to 275 (IQR: 170-590) min (calendar week 13/14) (p = 0.006). Door-to-balloon times were constant (p = 0.60). There was a significant difference in post-interventional Thrombolysis in myocardial infarction (TIMI) flow grade 3 in patients treated during calendar week 9/10 (97%), 11/12 (84%) and 13/14 (81%; p = 0.02). Rates of in-hospital death and re-infarction were similar between groups (p = 0.48). Results were comparable when dichotomizing data on 10 March and 16 March 2020, when official restrictions were executed. In this cohort of all-comer STEMI patients, we observed a 1.7-fold increase in ischemic time during the outbreak of COVID-19 in Austria. Patient-related factors likely explain most of this increase. Counteractive steps are needed to prevent further cardiac collateral damage during the ongoing COVID-19 pandemic.

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