# Chronic Cardiovascular Disorders Associated With COVID-19: A Literature Review

**Authors:** Adam Dudek, Marcin Bursy, Wojciech Szkudlarek, Jan Linkiewicz, Zbigniew Fabiszewski, Piotr Starosta

PMC · DOI: 10.7759/cureus.93271 · 2025-09-26

## TL;DR

This paper reviews chronic cardiovascular issues like heart fibrosis and hypertension that can occur after recovering from COVID-19, highlighting the need for better understanding and treatment.

## Contribution

The paper systematically reviews chronic cardiovascular outcomes of long COVID, emphasizing shared mechanisms and gaps in treatment.

## Key findings

- Heart fibrosis, POTS, hypertension, and coagulopathy are common chronic cardiovascular issues after SARS-CoV-2 infection.
- Shared mechanisms include endothelial inflammation, RAAS disruption, immune damage, and clotting promotion.
- Current management focuses on symptom relief and repurposed drugs, with experimental treatments needing further study.

## Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), responsible for the COVID-19 pandemic, is now widely recognized for causing several long-term effects known as post-COVID-19 syndrome (PCS) or long COVID (LC). This presents a growing challenge for healthcare systems worldwide. This narrative review summarizes original peer-reviewed studies indexed in PubMed and published between January 2020 and August 2025. It focuses on adult populations unless stated otherwise. We included studies that provided primary clinical or imaging data on chronic cardiovascular outcomes after confirmed SARS-CoV-2 infection. We excluded case reports, pediatric-only cohorts, and non-peer-reviewed sources. Among the various cardiovascular issues related to LC, we focused on heart fibrosis (HF), postural orthostatic tachycardia syndrome (POTS), new-onset hypertension (HT), and coagulopathy. These conditions consistently show up in the reports and are significant in terms of illness, potential long-term disability, and public health impact. Although these issues are distinct in their underlying causes, they share common mechanisms. These include ongoing inflammation of the endothelium, disruption of the renin-angiotensin-aldosterone system (RAAS), immune-related tissue damage, and an ongoing state that promotes blood clots.

These processes can lead to measurable myocardial fibrosis that cardiac magnetic resonance imaging can detect, autonomic dysfunction often seen as POTS, a greater risk of developing hypertension shortly after infection, and a long-term rise in thromboembolic events due to increased clotting and resistant microclots. Current management is mostly focused on relief of symptoms and involves a team approach. It uses repurposed medications and tailored physical rehabilitation since no specific cure is available yet. Promising but still experimental methods, such as endothelial-protective agents like sulodexide and targeting inflammatory pathways, need thorough testing. There are significant gaps in our understanding of the long-term risk of hypertension, the natural progression of fibrosis, and the best treatment for POTS. This highlights urgent needs for future research. Beyond caring for individual patients, these ongoing cardiovascular problems raise important public health concerns. They include higher healthcare use, long-term disability, and economic costs. This situation requires increased clinical attention and proactive cardiovascular monitoring for those recovering from COVID-19.

## Linked entities

- **Diseases:** postural orthostatic tachycardia syndrome (MONDO:0011479), coagulopathy (MONDO:0001531), COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}
- **Diseases:** coagulopathy (MESH:D001778), immune (MESH:D007154), autonomic dysfunction (MESH:D001342), inflammation (MESH:D007249), POTS (MESH:D054972), thromboembolic (MESH:D013923), LC (MESH:D000094024), HT (MESH:D006973), HF (MESH:D005355), cardiovascular problems (MESH:D002318), Chronic Cardiovascular Disorders (MESH:D018376), infection (MESH:D007239), COVID-19 (MESH:D000086382), tissue damage (MESH:D017695)
- **Chemicals:** sulodexide (MESH:C007858), aldosterone (MESH:D000450)
- **Species:** Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606]

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Source: https://tomesphere.com/paper/PMC12554255