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1.
Curr Probl Cardiol ; 47(9): 101268, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1867027

ABSTRACT

Coronavirus Disease 2019 (COVID-19) has been a significant cause of global mortality and morbidity since it was first reported in December 2019 in Wuhan, China. COVID19 like previous coronaviruses primarily affects the lungs causing pneumonia, interstitial pneumonitis, and severe acute respiratory distress syndrome (ARDS). However, there is increasing evidence linking COVID-19 to cardiovascular complications such as arrhythmias, heart failure, cardiogenic shock, fulminant myocarditis, and cardiac death. Given the novelty of this virus, there is paucity of data on some cardiovascular complications of COVID-19, specifically myocarditis. Myocarditis is an inflammatory disease of the heart muscle with a heterogenous clinical presentation and progression. It is mostly caused by viral infections and is the result of interaction of the virus and the host's immune system. There have been several case reports linking COVID-19 with myocarditis, however the true mechanism of cardiac injury remains under investigation. In this paper we review the clinical presentation, proposed pathophysiology, differential diagnoses and management of myocarditis in COVID-19 patients.


Subject(s)
COVID-19 , Myocarditis , Arrhythmias, Cardiac , COVID-19/complications , Humans , Myocarditis/diagnosis , Myocarditis/etiology , Myocarditis/therapy , SARS-CoV-2 , Shock, Cardiogenic/diagnosis , Shock, Cardiogenic/etiology , Shock, Cardiogenic/therapy
2.
Ochsner J ; 21(3): 238-239, 2021.
Article in English | MEDLINE | ID: covidwho-1436549
3.
Lancet ; 398(10304): 991-1001, 2021 09 11.
Article in English | MEDLINE | ID: covidwho-1373313

ABSTRACT

BACKGROUND: Previous studies have suggested that haemodynamic-guided management using an implantable pulmonary artery pressure monitor reduces heart failure hospitalisations in patients with moderately symptomatic (New York Heart Association [NYHA] functional class III) chronic heart failure and a hospitalisation in the past year, irrespective of ejection fraction. It is unclear if these benefits extend to patients with mild (NYHA functional class II) or severe (NYHA functional class IV) symptoms of heart failure or to patients with elevated natriuretic peptides without a recent heart failure hospitalisation. This trial was designed to evaluate whether haemodynamic-guided management using remote pulmonary artery pressure monitoring could reduce heart failure events and mortality in patients with heart failure across the spectrum of symptom severity (NYHA funational class II-IV), including those with elevated natriuretic peptides but without a recent heart failure hospitalisation. METHODS: The randomised arm of the haemodynamic-GUIDEed management of Heart Failure (GUIDE-HF) trial was a multicentre, single-blind study at 118 centres in the USA and Canada. Following successful implantation of a pulmonary artery pressure monitor, patients with all ejection fractions, NYHA functional class II-IV chronic heart failure, and either a recent heart failure hospitalisation or elevated natriuretic peptides (based on a-priori thresholds) were randomly assigned (1:1) to either haemodynamic-guided heart failure management based on pulmonary artery pressure or a usual care control group. Patients were masked to their study group assignment. Investigators were aware of treatment assignment but did not have access to pulmonary artery pressure data for control patients. The primary endpoint was a composite of all-cause mortality and total heart failure events (heart failure hospitalisations and urgent heart failure hospital visits) at 12 months assessed in all randomly assigned patients. Safety was assessed in all patients. A pre-COVID-19 impact analysis for the primary and secondary outcomes was prespecified. This study is registered with ClinicalTrials.gov, NCT03387813. FINDINGS: Between March 15, 2018, and Dec 20, 2019, 1022 patients were enrolled, with 1000 patients implanted successfully, and follow-up was completed on Jan 8, 2021. There were 253 primary endpoint events (0·563 per patient-year) among 497 patients in the haemodynamic-guided management group (treatment group) and 289 (0·640 per patient-year) in 503 patients in the control group (hazard ratio [HR] 0·88, 95% CI 0·74-1·05; p=0·16). A prespecified COVID-19 sensitivity analysis using a time-dependent variable to compare events before COVID-19 and during the pandemic suggested a treatment interaction (pinteraction=0·11) due to a change in the primary endpoint event rate during the pandemic phase of the trial, warranting a pre-COVID-19 impact analysis. In the pre-COVID-19 impact analysis, there were 177 primary events (0·553 per patient-year) in the intervention group and 224 events (0·682 per patient-year) in the control group (HR 0·81, 95% CI 0·66-1·00; p=0·049). This difference in primary events almost disappeared during COVID-19, with a 21% decrease in the control group (0·536 per patient-year) relative to pre-COVID-19, virtually no change in the treatment group (0·597 per patient-year), and no difference between groups (HR 1·11, 95% CI 0·80-1·55; p=0·53). The cumulative incidence of heart failure events was not reduced by haemodynamic-guided management (0·85, 0·70-1·03; p=0·096) in the overall study analysis but was significantly decreased in the pre-COVID-19 impact analysis (0·76, 0·61-0·95; p=0·014). 1014 (99%) of 1022 patients had freedom from device or system-related complications. INTERPRETATION: Haemodynamic-guided management of heart failure did not result in a lower composite endpoint rate of mortality and total heart failure events compared with the control group in the overall study analysis. However, a pre-COVID-19 impact analysis indicated a possible benefit of haemodynamic-guided management on the primary outcome in the pre-COVID-19 period, primarily driven by a lower heart failure hospitalisation rate compared with the control group. FUNDING: Abbott.


Subject(s)
Electrodes, Implanted , Heart Failure , Hemodynamics , Hospitalization/statistics & numerical data , Pulmonary Artery , Aged , COVID-19 , Female , Heart Failure/classification , Heart Failure/physiopathology , Hemodynamics/physiology , Hospitalization/trends , Humans , Male , Mortality/trends , Remote Sensing Technology
4.
Ochsner J ; 21(2): 181-186, 2021.
Article in English | MEDLINE | ID: covidwho-1296380

ABSTRACT

Background: The incidence of myocarditis in patients with coronavirus disease 2019 (COVID-19) remains unknown; however, increasing evidence links COVID-19 to cardiovascular complications such as arrhythmias, heart failure, cardiogenic shock, fulminant myocarditis, and cardiac death. We present a case of suspected COVID-19-induced myopericarditis and discuss the diagnostic implications, pathophysiology, and management. Case Report: A 72-year-old female was admitted to the hospital with acute on chronic respiratory failure in the setting of COVID-19. The next day, she developed pressure-like retrosternal chest pain. Laboratory findings revealed elevated cardiac enzymes and inflammatory markers consistent with myocardial injury. Electrocardiogram revealed diffuse ST segment elevations without reciprocal changes, concerning for myopericarditis. Transthoracic echocardiography showed new findings of severely reduced left ventricular (LV) systolic function, with an estimated ejection fraction (EF) of 20%. Her hospital course was further complicated by cardiogenic shock that required treatment in the intensive care unit with vasopressors and inotropes. During the next few days, she had almost full recovery of her LV function, with EF improving to 50%. However, her clinical status deteriorated, likely the result of a bowel obstruction. She was transitioned to comfort care at the request of her family, and she died shortly after. Conclusion: This case highlights diagnostic and therapeutic challenges that physicians may encounter when managing acute cardiac injury in the setting of COVID-19. The multiple mechanisms of COVID-19-related myocardial injury may influence the approach to diagnosis and treatment.

5.
Curr Probl Cardiol ; 46(10): 100845, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1230421

ABSTRACT

Coronavirus disease 2019 (COVID-19) has high infectivity and causes extensive morbidity and mortality. Cardiovascular disease is a risk factor for adverse outcomes in COVID-19, but baseline left ventricular ejection fraction (LVEF) in particular has not been evaluated thoroughly in this context. We analyzed patients in our state's largest health system who were diagnosed with COVID-19 between March 20 and May 15, 2020. Inclusion required an available echocardiogram within 1 year prior to diagnosis. The primary outcome was all-cause mortality. LVEF was analyzed both as a continuous variable and using a cutoff of 40%. Among 396 patients (67 ± 16 years, 191 [48%] male, 235 [59%] Black, 59 [15%] LVEF ≤40%), 289 (73%) required hospital admission, and 116 (29%) died during 85 ± 63 days of follow-up. Echocardiograms, performed a median of 57 (IQR 11-122) days prior to COVID-19 diagnosis, showed a similar distribution of LVEF between survivors and decedents (P = 0.84). Receiver operator characteristic analysis revealed no predictive ability of LVEF for mortality, and there was no difference in survival among those with LVEF ≤40% versus >40% (P = 0.49). Multivariable analysis did not change these relationships. Similarly, there was no difference in LVEF based on whether the patient required hospital admission (56 ± 13 vs 55 ± 13, P = 0.38), and patients with a depressed LVEF did not require admission more frequently than their preserved-LVEF peers (P = 0.87). A premorbid history of dyspnea consistent with symptomatic heart failure was not associated with mortality (P = 0.74). Among patients diagnosed with COVID-19, pre-COVID-19 LVEF was not a risk factor for death or hospitalization.


Subject(s)
COVID-19 , Heart Failure , COVID-19 Testing , Humans , Male , SARS-CoV-2 , Stroke Volume , Ventricular Function, Left
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