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1.
Heart Fail Clin ; 19(2): 197-204, 2023 Apr.
Article in English | MEDLINE | ID: covidwho-2260510

ABSTRACT

The Coronavirus disease 2019 (COVID-19) pandemic has led to a significant increase in worldwide morbidity and mortality. Patients with COVID-19 are at risk for developing a variety of cardiovascular conditions including acute coronary syndromes, stress-induced cardiomyopathy, and myocarditis. Patients with COVID-19 who develop ST-elevation myocardial infarction (STEMI) are at a higher risk of morbidity and mortality when compared with their age- and sex-matched STEMI patients without COVID-19. We review current knowledge on the pathophysiology of STEMI in patients with COVID-19, clinical presentation, outcomes, and the effect of the COVID-19 pandemic on overall STEMI care.


Subject(s)
COVID-19 , ST Elevation Myocardial Infarction , Humans , COVID-19/complications , COVID-19/epidemiology , Pandemics , ST Elevation Myocardial Infarction/diagnosis , ST Elevation Myocardial Infarction/epidemiology , ST Elevation Myocardial Infarction/physiopathology , ST Elevation Myocardial Infarction/therapy
2.
Curr Cardiol Rep ; 24(6): 659-665, 2022 06.
Article in English | MEDLINE | ID: covidwho-2265117

ABSTRACT

PURPOSE OF THIS REVIEW: We discuss the role of observational studies and cardiac registries during the COVID-19 pandemic. We focus on published cardiac registries and highlight contributions to the field that have had clinical implications. RECENT FINDINGS: We included observational studies of COVID-19 patients published in peer-reviewed medical journals with defined inclusion and exclusion criteria, defined study design, and primary outcomes. A PubMed and MEDLINE literature review results in 437 articles, of which 52 include patients with COVID-19 with cardiac endpoints. From July 2020 to December 2021, the average time from last data collected to publication was 8.9 ± 4.1 months, with an increasing trend over time (R = 0.9444, p < 0.0001). Of the 52 articles that met our inclusion criteria, we summarize main findings of 4 manuscripts on stroke, 14 on acute coronary syndrome, 4 on cardiac arrest, 7 on heart failure, 7 on venous thromboembolism, 5 on dysrhythmia, and 11 on different populations at risk for cardiovascular. Registries are cost effective, not disruptive to essential health services, and can be rapidly disseminated with short intervals between last data point collected and publication. In less than 2 years, cardiac registries have filled important gaps in knowledge and informed the care of COVID-19 patients with cardiovascular conditions.


Subject(s)
COVID-19 , Heart Failure , COVID-19/epidemiology , Humans , Pandemics , Registries , SARS-CoV-2
3.
Physiol Rep ; 10(16): e15430, 2022 08.
Article in English | MEDLINE | ID: covidwho-2002702

ABSTRACT

Although acute COVID-19 is known to cause cardiac damage in some cases, there is still much to learn about the duration and relative permanence of the damage that may occur. Long COVID is a condition that can occur when COVID-19 symptoms remain in the postviral acute period. Varying accounts of long COVID have been described across the literature, however, cardiac impairments are sustained in many individuals and cardiovascular assessment is now considered to be an expected follow-up examination. The purpose of this review and proof of concept is to summarize the current research related to the assessment of cardiac function, including echocardiography and blood biomarker data, during the follow-up period in patients who recovered from COVID-19. Following a literature review, it was found that right ventricular dysfunction along with global longitudinal strain and diastolic dysfunction are common findings. Finally, more severe acute myocardial injury during the index hospitalization appears to exacerbate cardiac function. The available literature implies that cardiac function must be monitored in patients recovered from COVID-19 who remain symptomatic and that the impairments and severity vary from person-to-person. The proof-of-concept analysis of patients with cardiac disease and respiratory disease in comparison to those with sustained symptoms from COVID-19 suggests elevated systolic time interval in those with sustained symptoms from COVID-19, thus reducing heart performance indices. Future research must consider the details of cardiac complications during the acute infection period and relate this to the cardiac function in patients with long COVID during mid- and long-term follow-up.


Subject(s)
COVID-19 , Ventricular Dysfunction, Right , COVID-19/complications , Echocardiography , Humans , Systole , Post-Acute COVID-19 Syndrome
4.
J Soc Cardiovasc Angiogr Interv ; 1(5): 100404, 2022.
Article in English | MEDLINE | ID: covidwho-1936877

ABSTRACT

Background: In-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is higher in those with COVID-19 than in those without COVID-19. The factors that predispose to this mortality rate and their relative contribution are poorly understood. This study developed a risk score inclusive of clinical variables to predict in-hospital mortality in patients with COVID-19 and STEMI. Methods: Baseline demographic, clinical, and procedural data from patients in the North American COVID-19 Myocardial Infarction registry were extracted. Univariable logistic regression was performed using candidate predictor variables, and multivariable logistic regression was performed using backward stepwise selection to identify independent predictors of in-hospital mortality. Independent predictors were assigned a weighted integer, with the sum of the integers yielding the total risk score for each patient. Results: In-hospital mortality occurred in 118 of 425 (28%) patients. Eight variables present at the time of STEMI diagnosis (respiratory rate of >35 breaths/min, cardiogenic shock, oxygen saturation of <93%, age of >55 â€‹years, infiltrates on chest x-ray, kidney disease, diabetes, and dyspnea) were assigned a weighted integer. In-hospital mortality increased exponentially with increasing integer risk score (Cochran-Armitage χ2, P â€‹< â€‹.001), and the model demonstrated good discriminative power (c-statistic â€‹= â€‹0.81) and calibration (Hosmer-Lemeshow, P â€‹= â€‹.40). The increasing risk score was strongly associated with in-hospital mortality (3.6%-60% mortality for low-risk and very high-risk score categories, respectively). Conclusions: The risk of in-hospital mortality in patients with COVID-19 and STEMI can be accurately predicted and discriminated using readily available clinical information.

5.
Cardiol Clin ; 40(3): 321-328, 2022 Aug.
Article in English | MEDLINE | ID: covidwho-1763608

ABSTRACT

The Coronavirus disease 2019 (COVID-19) pandemic has led to a significant increase in worldwide morbidity and mortality. Patients with COVID-19 are at risk for developing a variety of cardiovascular conditions including acute coronary syndromes, stress-induced cardiomyopathy, and myocarditis. Patients with COVID-19 who develop ST-elevation myocardial infarction (STEMI) are at a higher risk of morbidity and mortality when compared with their age- and sex-matched STEMI patients without COVID-19. We review current knowledge on the pathophysiology of STEMI in patients with COVID-19, clinical presentation, outcomes, and the effect of the COVID-19 pandemic on overall STEMI care.


Subject(s)
COVID-19 , Percutaneous Coronary Intervention , ST Elevation Myocardial Infarction , COVID-19/complications , Humans , Pandemics , SARS-CoV-2 , ST Elevation Myocardial Infarction/diagnosis , ST Elevation Myocardial Infarction/epidemiology , ST Elevation Myocardial Infarction/therapy
6.
Biol Res ; 54(1): 39, 2021 Dec 14.
Article in English | MEDLINE | ID: covidwho-1577124

ABSTRACT

BACKGROUND: The aim of the study was to investigate the effect of mild cerebral hypoxia on haemoglobin oxygenation (HbO2), cerebrospinal fluid dynamics and cardiovascular physiology. To achieve this goal, four signals were recorded simultaneously: blood pressure, heart rate / electrocardiogram, HbO2 from right hemisphere and changes of subarachnoid space (SAS) width from left hemisphere. Signals were registered from 30 healthy, young participants (2 females and 28 males, body mass index = 24.5 ± 2.3 kg/m2, age 30.8 ± 13.4 years). RESULTS: We analysed the recorded signals using wavelet transform and phase coherence. We demonstrated for the first time that in healthy subjects exposed to mild poikilokapnic hypoxia there were increases in very low frequency HbO2 oscillations (< 0.052 Hz) in prefrontal cortex. Additionally, SAS fluctuation diminished in the whole frequency range which could be explained by brain oedema. CONCLUSIONS: Consequently the study provides insight into mechanisms governing brain response to a mild hypoxic challenge. Our study supports the notion that HbO2 and SAS width monitoring might be beneficial for patients with acute lung disease.


Subject(s)
Cerebrovascular Circulation , Lung Diseases , Adolescent , Adult , Female , Hemoglobins , Humans , Hypoxia , Male , Prefrontal Cortex , Spectroscopy, Near-Infrared , Young Adult
7.
Physiol Rep ; 9(17): e14998, 2021 09.
Article in English | MEDLINE | ID: covidwho-1374672

ABSTRACT

The spread of the novel coronavirus 2019 (COVID-19) has caused a global pandemic. The disease has spread rapidly, and research shows that COVID-19 can induce long-lasting cardiac damage. COVID-19 can result in elevated cardiac biomarkers indicative of acute cardiac injury, and research utilizing echocardiography has shown that there is mechanical dysfunction in these patients as well, especially when observing the isovolumic, systolic, and diastolic portions of the cardiac cycle. The purpose of this study was to present two case studies on COVID-19 positive patients who had their cardiac mechanical function assessed every day during the acute period to show that cardiac function in these patients was altered, and the damage occurring can change from day-to-day. Participant 1 showed compromised cardiac function in the systolic time, diastolic time, isovolumic time, and the calculated heart performance index (HPI), and these impairments were sustained even 23 days post-symptom onset. Furthermore, Participant 1 showed prolonged systolic periods that lasted longer than the diastolic periods, indicative of elevated pulmonary artery pressure. Participant 2 showed decreases in systole and consequently, increases in HPI during the 3 days post-symptom onset, and these changes returned to normal after day 4. These results showed that daily observation of cardiac function can provide detailed information about the overall mechanism by which cardiac dysfunction is occurring and that COVID-19 can induce cardiac damage in unique patterns and thus can be studied on a case-by-case basis, day-to-day during infection. This could allow us to move toward more personalized cardiovascular medical treatment.


Subject(s)
COVID-19/physiopathology , Heart Diseases/physiopathology , Heart/physiopathology , Hemodynamics , SARS-CoV-2/pathogenicity , Ventricular Function , Adult , COVID-19/diagnosis , COVID-19/virology , Diagnostic Techniques, Cardiovascular/instrumentation , Heart/virology , Heart Diseases/diagnosis , Heart Diseases/virology , Host-Pathogen Interactions , Humans , Male , Middle Aged , Predictive Value of Tests , Time Factors , Transducers
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