实验研究发现SARS-CoV-2可导致心脏损伤

概要

日本科学家的一项新研究通过实验证明，心肌病（指损害心脏肌肉及其泵血能力的心脏疾病）患者的心脏可能因COVID-19而受到病毒感染。

研究人员通过人类诱导多能干细胞重建了人类心脏微组织。心脏微组织主要由各种心脏细胞组成，包括负责心脏收缩的心肌细胞以及血管内皮细胞和壁细胞。在心脏微组织感染SARS-CoV-2病毒后，他们发现”病毒感染可导致组织在病毒感染急性期收缩力下降“。研究人员还观察到，抗体水平为轻度至中度的模型在28天后恢复，心脏的收缩能力也得到了恢复。再造心脏组织中的高浓度抗体则会导致收缩力持续下降而无法恢复。研究人员表示，即使是轻度感染，病毒也会持续存在一个月，这表明感染是持续性的。

研究指出，持续感染模型通过实验表明，可能存在一类有轻度SARS-CoV-2感染史的患者，他们会出现轻微的心功能障碍，而且整体心功能会得到代偿，表面上可以维持而不会发展成心力衰竭。然而，这类患者将处于心力衰竭的风险边缘，并可能在额外的心脏压力下出现心脏功能障碍，最终导致心力衰竭。

此外，在对持续感染的实验模型进行缺氧应激诱导时，也会导致心功能不全。研究人员将此归因于心脏中血管紧张素转换酶2（ACE2）的表达高于其他器官。他们认为，心脏易受SARS-CoV-2感染，这在心力衰竭等有害情况下更为明显。

SARS-CoV-2 can lead to heart impairment, experimental study finds

Even mild infections sustained viral presence for a month, indicating persistent infection 

Photo: iStock

Patients with cardiomyopathy could be suffering from viral infections in their hearts due to COVID-19, a new study by Japanese scientists demonstrated through an experiment.

Cardiomyopathy refers to heart disorders that impair the heart muscles and its ability to pump blood.

With a surge in COVID-19 cases worldwide triggered by the variant JN.1, the report raises alarms about COVID-19 triggering a heart failure pandemic of sorts.

The study by the Riken Institute recreated human cardiac microtissues through human-induced pluripotent stem cells. For the most part, cardiac microtissues were composed of various heart cells, including cardiomyocytes responsible for the heart’s contraction as well as vascular endothelial cells and mural cells.

After the cardiac microtissues were infected with SARS-CoV-2, they found that a “viral infection can lead to the reduction of tissue contractility in the acute phase of viral infection”.

The researchers observed that models which had mild to moderate levels of antibodies, recovered at 28 days and restored the heart’s ability to contract. On the other hand, high levels of antibodies in the recreated heart tissues showed a more sustained decrease in contractility without recovery.

Even mild infections sustained viral presence for a month, indicating persistent infection, the researchers said.

According to the investigation, led by senior scientist Hidetoshi Masumoto, this “may indicate a clinical case of the deterioration of cardiac function during the acute phase of COVID-19 requiring heart transplantation”.

“The persistent infection model experimentally indicated that a group of patients with a history of mild SARS-CoV-2 infection who developed slight cardiac dysfunction may exist and that global cardiac function is compensated for and may superficially be maintained without developing heart failure,” the authors of the study noted

“However, such patients would be at marginal risk of heart failure and could opportunistically develop cardiac dysfunction and eventually heart failure under additional cardiac stress,” the study added.

Moreover, when the experimental models with persistent infection were induced with hypoxic stress, it led to cardiac dysfunction.

The researchers attributed this to higher expression of angiotensin-converting enzyme 2 (ACE2) in the heart, as compared to other organs.

"This suggests that the heart is susceptible to SARS-CoV-2 infection, which is more pronounced under detrimental conditions such as heart failure", the researchers said.

ACE2 is a protein found in the epithelial cells in different parts of the body. SARS-CoV-2 virus binds to ACE2 as an entry point through the virus’ spike-like protein on its surface.

According to a 2023 review by the Christ Hospital Health Network in the United States, patients with existing heart failure could get severe COVID-19 symptoms and clinical outcomes. Some complications include myocardial infarction, cardiogenic shock and heart failure.

Another 2022 study that showed the implications of SARS-CoV-2 infections on the heart one year after infection found that 154,000 United States veterans had a range of various cardiovascular risks.

According to the study published in Nature Medicine by the Veterans Affairs St Louis Health Care System, some risks included abnormal heart rhythms, heart muscle inflammation, blood clots, strokes, myocardial infarction, and heart failure. This was present even among those who did not have acute COVID-19 requiring hospitalisation, though patients with more severe disease had a higher risk. This was regardless of age, race, sex, obesity, smoking or preexisting cardiovascular disease and other comorbidities.

Researchers at Johns Hopkins Medicine speculated that these consequences could be the result of a harmful level of cytokines released during an inflammatory response, which overwhelms the body and potentially leads to heart damage.

As of January 1, 2024, the Union Ministry of Health and Family Welfare reported 4,565 active COVID-19 cases, with 1,712 based in Kerala. India reported 573 fresh cases, of which Karnataka reported 296 cases, Kerala 111 cases, Maharashtra 70 cases and Andhra Pradesh 17. Tamil Nadu and Chhattisgarh reported 15 cases each.

India reported 196 cases of the latest COVID-19 variant JN.1, which is soon becoming the dominant COVID-19 lineage worldwide.

Source：

Down To Earth

Published on 2 January, 2024

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