|
 
 |
| LETTER TO THE EDITOR |
|
| Year : 2022 | Volume
: 8
| Issue : 1 | Page : 65-67 |
|
Post-COVID-19 cardiovascular syndrome: What does the evidence tell us?
Ivan David Lozada-Martinez1, Geiro Alfonso Pava-Barrios2, Andres Yoli-Garrido3, Anderson Leal-Buitrago4, Nicolas Rodriguez-Medina5
1 Department of Medicine, Grupo Prometheus y Biomedicina Aplicada a las Ciencias Clinicas, Universidad de Cartagena; Medical and Surgical Research Center, St Mary's Medical Group, Barranquilla, Colombia
2 Department of Medicine, School of Medicine, Universidad del Sinu, Cartagena, Colombia
3 Department of Medicine, School of Medicine, Universidad Metropolitana, Barranquilla, Colombia
4 Department of Medicine, School of Medicine, Universidad de Santander, Bucaramanga, Colombia
5 Department of Medicine, School of Medicine, Universidad del Rosario, Bogotá, Colombia
| Date of Submission | 12-Dec-2021 |
| Date of Decision | 12-Feb-2022 |
| Date of Acceptance | 15-Mar-2022 |
| Date of Web Publication | 26-Apr-2022 |
Correspondence Address:
Ivan David Lozada-Martinez
MS, Department of Medicine, Grupo Prometheus y Biomedicina Aplicada a las Ciencias Clinicas, Universidad de Cartagena, 130004 Cartagena
Colombia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jpcs.jpcs_69_21
How to cite this article:
Lozada-Martinez ID, Pava-Barrios GA, Yoli-Garrido A, Leal-Buitrago A, Rodriguez-Medina N. Post-COVID-19 cardiovascular syndrome: What does the evidence tell us?. J Pract Cardiovasc Sci 2022;8:65-7 |
How to cite this URL:
Lozada-Martinez ID, Pava-Barrios GA, Yoli-Garrido A, Leal-Buitrago A, Rodriguez-Medina N. Post-COVID-19 cardiovascular syndrome: What does the evidence tell us?. J Pract Cardiovasc Sci [serial online] 2022 [cited 2023 Mar 30];8:65-7. Available from: https://www.j-pcs.org/text.asp?2022/8/1/65/344137 |
Sir,
Despite the avalanche of literature emerging from the course of the COVID-19 pandemic, there are still unknowns regarding the pathophysiology, management, and sequelae of this disease.[1],[2],[3] The post-COVID-19 syndrome is one of those questions about the pathophysiology and sequelae that occur during the acute phase of COVID-19 and that has been observed not to depend on the phenotype developed.[1],[2] Among studies that have reported the prevalence of manifestations presented in post-COVID-19 syndrome, neurological, cardiovascular, and pulmonary manifestations stand out.[1],[2],[3],[4],[5] However, an important bias to consider in the current evidence is the cutoff scores between the time from what is recognized as the acute phase and post-COVID syndrome, which may alter the certainty of the prevalence and correlation between target organ injury and organ manifestation.[2] The time between the two phases has not yet been clearly defined.
When trying to analyze the current evidence, a question arises: why, if cardiovascular manifestations have a high prevalence in this phase and there are studies that have shown vascular injury in COVID-19 patients, even with the mild phenotype of the disease (which suggests the development of a sequela sometime later),[5] has a post-COVID-19 cardiovascular syndrome not been defined to redirect the management of these patients? Is there not enough evidence to suggest myocardial injury during the acute phase of COVID-19? Within the published literature, post-COVID-19 syndrome has been identified as a risk period where a variable mortality rate has been found with a tendency to be high, even in those without relevant pathological antecedents.[5] Now, what does the most updated evidence say about it?
In search of general findings on the impact of the sequelae that occur during the post-COVID-19 syndrome, authors such as Tabacof et al.[6] evaluated the impact of this syndrome on the physical and cognitive function and quality of life of those affected, showing that of a total of 156 patients (all prevaccinated), on average 1 year after suffering the symptoms of COVID-19, 82% presented fatigue (affecting the performance of activities of daily living), 67% cognitive impairment, and 60% persistent headache.[6] The events that exacerbated these symptoms most frequently were physical exercise (86%), distress (69%), and dehydration (49%). When reviewing the Neuro-QoL questionnaire, 63% had moderate cognitive impairment.[6] Sivan et al.[7] conducted a study where they included 370 patients who were in the rehabilitation process during the post-COVID-19 phase, to whom they applied the COVID-19 Yorkshire Rehabilitation Scale and classified the severity of these symptoms (by phenotypes).[7] The authors found that during an average symptom duration of 211 days, moderate (n = 186) and severe (n = 94) phenotypes were the most frequent, and symptom intensity was positively correlated with decreased functional capacity.[7] This allowed the authors to conclude that knowing the phenotypes of post-COVID-19 syndrome would help to stratify patients and thus be more precise when defining an intervention and planning the care pathway in the medium and long term.[7] These types of results reported in the literature have allowed synthesizing evidence such as that published by Kunal et al.,[8] where they describe phenotypes as spectra, focusing mainly on pulmonary, cardiovascular, neurological, and musculoskeletal sequelae. Interestingly, they also summarized the clinical and preclinical trials currently underway on the use of antifibrotic therapy to reduce the risk of developing complications or de novo disease during the post-COVID-19 phase.[8] Other studies that established a 6-month cutoff score to assess post-COVID-19 sequelae found that fatigue or muscle weakness, as well as anxiety or depression, were the most common symptoms. However, there are patients who had moderate disease and presented altered pulmonary diffusion and radiographic alterations, which could influence the physiology of cardiac perfusion and hemodynamics.[9],[10],[11] This was particularly evaluated by Puntmann et al.[9] who evidenced elevation of troponins, myoglobin, and other cardiac markers, even after 2 months of the acute phase of COVID-19, suggesting that in some cases, the neuropsychiatric or pulmonary symptomatology could have a mixed component, with the main origin at the cardiovascular level.[9]
Now, focusing on the results reported by studies that evaluated cardiovascular sequelae, Giurgi-Oncu et al.[12] conducted a study where they evaluated hospitalized (n = 64) and nonhospitalized (n = 79) patients by means of transthoracic echocardiography, mental health examination, quality of life questionnaire, and Functional Status scale post-COVID-19, where they found that all hospitalized patients had mild or moderate pulmonary sequelae, with lower functional status and quality of life scores.[12] A significant finding was the increase in pulmonary artery pressure (28.11% in hospitalized vs. 17.72% nonhospitalized) and the prevalence of diastolic dysfunction (28.12% in hospitalized vs. 20.25% nonhospitalized; P = 0.02). The prevalence of altered systolic function was approximately 10% in both groups and of neuropsychiatric disorders was greater than 30%, being higher in hospitalized patients.[12] Kotecha et al.[13] performed a study using multi-parametric cardiovascular magnetic resonance imaging in 148 post-COVID-19 patients, all of whom developed the severe phenotype and were hospitalized, showing that 54% had late gadolinium enhancement and/or an ischemic pattern.[13] Myocarditis-like injury was limited to two or three myocardial segments in 88% of the cases that were not associated with ventricular dysfunction, and of these, 30% had active myocarditis. Myocardial infarction was found in 19% of the total cases and induced ischemia in 26%. An important aspect to highlight is that 66% of those with ischemic findings had no history of coronary artery disease.[13] A similarly aimed pilot study was performed by Drakos et al.,[14] who by means of the same technique evaluated microvascular coronary artery disease, but in patients in the acute phase of COVID-19 versus control group, finding that coronary sinus flow was lower during stress in the COVID-19 group (3.33 ml/min [2.76–4.20 ml/min] vs. 5.32 ml/min [3.66–5.52 ml/min], P = 0.05).[14] Myocardial global perfusion reserve was significantly reduced in the COVID-19 group compared to the control group (2.73 [2.10-4.15-11] vs. 4.82 [3.70–6.68], P = 0.005). This led to the conclusion that COVID-19 patients have a considerably reduced myocardial global perfusion reserve,[14] which, together with atherosclerotic coronary artery disease or other opportunistic thromboembolic condition, could trigger a major cardiovascular event and leave a serious sequela that can manifest itself in an intense form during the post-COVID-19 phase.
In this order of ideas, and reviewing the recent evidence on the imaging, clinical and functional findings of patients with post-COVID-19 syndrome, who specifically present cardiovascular manifestations and quality of life impairment, would it not be ideal for defining a post-COVID-19 cardiovascular syndrome, which would allow redirecting the evaluation at different times of patients with COVID-19, knowing that even those who only develop the mild phenotype and do not need hospitalization, can also present myocardial and vascular lesions? We propose the need to carry out prospective multicenter studies that allow us to know precisely the integrity of the cardiovascular system in this type of patient. The creation of cardiovascular rehabilitation centers specialized in post-COVID-19 syndrome, which facilitate the recording and study of data and the strict follow-up in the short, medium, and long term of those with cardiovascular manifestations during the post-COVID-19 phase. Another point to consider as a future line of research is the impact of vaccines and the prevalence of the omicron variant on the development and severity of post-COVID-19 cardiovascular syndrome. There is no evidence describing the behavior of this syndrome under the influence of these factors, and it is necessary to establish hypotheses of causality to avoid confusion about the appearance or persistence of disabling clinical manifestations.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | |  |
| 1. | Ståhlberg M, Reistam U, Fedorowski A, Villacorta H, Horiuchi Y, Bax J, et al. Post-COVID-19 tachycardia syndrome: A distinct phenotype of post-acute COVID-19 syndrome. Am J Med 2021;134:1451-6.  |
| 2. | Rodríguez-Hernández YA, Villamizar-Gómez FJ, Mantilla-Pardo JC, Robledo-Arias JS, Rahman S, Lozada-Martinez ID, et al. Post-COVID 19 neurological syndrome: The need to define a cut-off score between the acute and post-COVID 19 phases. Ann Med Surg (Lond) 2021;71:102983. |
| 3. | González-Herazo MA, Silva-Muñoz DC, Guevara-Martínez PA, Lozada-Martinez ID. Post-COVID 19 neurological syndrome: A fresh challenge in neurological management. Neurol Neurochir Pol 2021;55:413-4. |
| 4. | Camargo-Martínez W, Lozada-Martínez I, Escobar-Collazos A, Navarro-Coronado A, Moscote-Salazar L, Pacheco-Hernández A, et al. Post-COVID 19 neurological syndrome: Implications for sequelae's treatment. J Clin Neurosci 2021;88:219-25. |
| 5. | Menges D, Ballouz T, Anagnostopoulos A, Aschmann HE, Domenghino A, Fehr JS, et al. Burden of post-COVID-19 syndrome and implications for healthcare service planning: A population-based cohort study. PLoS One 2021;16:e0254523. |
| 6. | Tabacof L, Tosto-Mancuso J, Wood J, Cortes M, Kontorovich A, McCarthy D, et al. Post-acute COVID-19 syndrome negatively impacts physical function, cognitive function, health-related quality of life, and participation. Am J Phys Med Rehabil 2022;101:48-52. |
| 7. | Sivan M, Parkin A, Makower S, Greenwood DC. Post-COVID syndrome symptoms, functional disability, and clinical severity phenotypes in hospitalized and nonhospitalized individuals: A cross-sectional evaluation from a community COVID rehabilitation service. J Med Virol 2022;94:1419-27. |
| 8. | Kunal S, Madan M, Tarke C, Gautam DK, Kinkar JS, Gupta K, et al. Emerging spectrum of post-COVID-19 syndrome. Postgrad Med J 2021;94:1419-27. |
| 9. | Puntmann VO, Carerj ML, Wieters I, Fahim M, Arendt C, Hoffmann J, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:1265-73. |
| 10. | Logue JK, Franko NM, McCulloch DJ, McDonald D, Magedson A, Wolf CR, et al. Sequelae in adults at 6 months after COVID-19 infection. JAMA Netw Open 2021;4:e210830. |
| 11. | Huang C, Huang L, Wang Y, Li X, Ren L, Gu X, et al. 6-month consequences of COVID-19 in patients discharged from hospital: A cohort study. Lancet 2021;397:220-32. |
| 12. | Giurgi-Oncu C, Tudoran C, Pop GN, Bredicean C, Pescariu SA, Giurgiuca A, et al. Cardiovascular abnormalities and mental health difficulties result in a reduced quality of life in the post-acute COVID-19 syndrome. Brain Sci 2021;11:1456. |
| 13. | Kotecha T, Knight DS, Razvi Y, Kumar K, Vimalesvaran K, Thornton G, et al. Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance. Eur Heart J 2021;42:1866-78. |
| 14. | Drakos S, Chatzantonis G, Bietenbeck M, Evers G, Schulze AB, Mohr M, et al. A cardiovascular magnetic resonance imaging-based pilot study to assess coronary microvascular disease in COVID-19 patients. Sci Rep 2021;11:15667. |
|
Search Pubmed for