How to Prevent Heart Disease After a Stroke

Abstract：This article explores the direct causal link between cerebrovascular diseases (stroke) and heart diseases. While both conditions share common lifestyle risk factors, recent studies suggest a deeper biological connection. A groundbreaking 2024 study revealed that strokes can trigger immune system dysfunction, particularly in bone marrow, leading to excessive monocyte activity that damages heart tissue, causing fibrosis and cardiac dysfunction. Experiments with mice confirmed this, showing heart complications post-stroke. The study identified the cytokine IL-1b as a key trigger and demonstrated that blocking IL-1b with drugs like cenicriviroc could prevent heart damage. This research emphasizes the importance of holistic health approaches, combining lifestyle adjustments and targeted immunotherapies for effective cardiovascular prevention.

We are going to explore a significant yet complex medical question: Is there a direct causal relationship between cerebrovascular diseases and heart diseases?

The Dangers and Connection Between Cardiovascular and Cerebrovascular Diseases

The reason for discussing this topic is that cardiovascular and cerebrovascular diseases have become the most critical global health threats. They refer to conditions caused by bleeding or ischemia in the heart, brain, and other body tissues, characterized by high incidence, high disability, and high mortality rates. According to a 2020 study by the World Economic Forum, ischemic heart disease (like myocardial infarction) caused 8.9 million deaths worldwide in 2019, while stroke caused 6.2 million deaths. These two conditions ranked as the top two causes of death globally and both fall under the category of cardiovascular and cerebrovascular diseases.

Given these staggering figures, identifying the relationship between cerebrovascular diseases and heart diseases could offer a critical opportunity for early intervention and reducing global mortality rates.

Why Consider These Two Diseases Together?

Clinically, a pattern often emerges where patients experience both heart and cerebrovascular diseases simultaneously. For example, myocardial infarction and stroke frequently occur together. Many have explained this correlation by attributing it to similar risk factors, such as unhealthy lifestyle habits. High sugar, fat, and salt consumption, physical inactivity, smoking, and excessive alcohol intake are all modern lifestyle factors that can disrupt the body’s metabolic balance, leading to chronic conditions such as hypertension, hyperglycemia, and atherosclerosis. Over time, vital blood vessels, like the coronary arteries supplying the heart and cerebral arteries supplying the brain, can narrow, become blocked, or rupture, causing life-threatening cardiovascular and cerebrovascular events.

However, could the relationship be more direct than just shared risk factors?

Beyond lifestyle influences, there are indications that stroke and myocardial infarction may have a more direct causal link. For instance, clinical observations show that 10-20% of stroke patients develop severe cardiovascular complications within a month after a stroke. The more severe the stroke, the greater the likelihood of heart complications. In 2018, a new term was even coined for this phenomenon: stroke-heart syndrome.

Yet, for a long time, the specific mechanisms linking these conditions remained unclear, limiting any practical advancements in prevention or treatment.

A Breakthrough in 2024: The Role of the Immune System

In August 2024, a groundbreaking study published in Cell shed light on this issue. Using animal models and patient data, researchers identified a new mediator between stroke and heart disease: dysfunction in the innate immune system.

Revealing the Mechanism Through Mouse Experiments

The study involved inducing stroke in mice to observe how their bodies responded post-stroke, specifically in cases where the mice developed heart disease afterward.

Researchers at Ludwig Maximilian University in Munich induced stroke in mice by inserting a filament into the middle cerebral artery through the carotid artery, simulating ischemic stroke. Despite physical recovery after 1-2 weeks due to neural plasticity, researchers suspected long-term systemic impacts from the stroke.

Upon analyzing immune cells from various organs (heart, lungs, liver, spleen), they performed approximately 30,000 single-cell RNA sequencing tests. Results showed persistent immune activity a month after the stroke, particularly increased activity in monocytes and macrophages, cells known for their role in inflammation.

Significantly, the presence of hyperactive monocytes in heart tissue surged from a normal 1.27% to 10.27% post-stroke, indicating a tenfold increase. This hinted that these cells could be directly contributing to post-stroke heart complications.