Effective antiretroviral therapy (ART) has transformed Human Immunodeficiency Virus (HIV) infection into a manageable, chronic condition, significantly extending life expectancy. However, as people living with HIV (PLWH) age, they face an increased risk of complications, including the formation of blood clots, known as thrombosis. Thrombosis underlies serious events like heart attacks, strokes, and dangerous blockages in the lungs. It is now well-established that HIV creates a prothrombotic state in the body, meaning the biological environment is more prone to clot formation. Understanding the specific risk factors and biological mechanisms is a key part of modern HIV care.
Confirming the Increased Risk
The heightened risk of thrombosis in people living with HIV extends across both the venous and arterial systems. Venous thromboembolism (VTE) encompasses deep vein thrombosis (DVT), typically in the legs, and pulmonary embolism (PE), which occurs when a DVT travels to the lungs. Studies indicate that the risk of VTE is elevated by two to tenfold in PLWH compared to the general population, establishing HIV as an independent risk factor.
Arterial thrombosis is equally concerning, as it involves clots that block blood flow in the arteries, leading to myocardial infarction (heart attack) or ischemic stroke. The overall incidence of cardiovascular events, including these arterial clots, is significantly higher in PLWH. This increased risk profile for both VTE and arterial events persists even in individuals whose virus is effectively suppressed and controlled by ART.
While effective ART is essential and significantly lowers the overall risk compared to untreated HIV, it does not completely eliminate the predisposition to clotting. The residual risk suggests that the underlying biological changes initiated by the virus are not entirely reversed by treatment alone. Recognizing this persistent, elevated risk is necessary for long-term health management in this population.
How HIV Promotes Clot Formation
Chronic systemic inflammation is a primary driver of the prothrombotic state in people living with HIV. Even with effective viral suppression, the presence of the virus maintains a low-grade immune activation that constantly stimulates the body’s clotting factors. This ongoing inflammatory state, marked by elevated levels of certain inflammatory molecules, promotes the activation of the coagulation cascade.
The endothelial lining, the layer of cells covering the inside of blood vessels, suffers damage from this persistent inflammation and direct exposure to HIV proteins. Endothelial dysfunction occurs when this lining loses its ability to regulate blood flow and prevent clotting, instead becoming activated and expressing procoagulant factors. This damage makes the vessel wall a receptive surface for clot formation.
HIV infection also contributes to the hyperactivation of platelets, which are cell fragments central to forming a clot. These platelets become more reactive and prone to clumping together. Furthermore, activated monocytes, a type of white blood cell, express tissue factor, a powerful initiator of the clotting cascade.
Additional Risk Multipliers
Traditional cardiovascular risk factors compound the clotting risk already present due to the HIV infection itself. Co-occurring health issues like high blood pressure, elevated cholesterol, diabetes, and obesity are often more prevalent in the HIV population, significantly amplifying the chances of a thrombotic event. Smoking, a major risk factor for the general population, interacts with the inflammatory state of HIV to further accelerate vascular damage.
The choice of antiretroviral therapy (ART) also requires consideration, even though treatment is necessary to preserve health. While newer regimens are generally well-tolerated, some older or specific classes of drugs, such as certain protease inhibitors (PIs), have been associated with metabolic side effects like hyperlipidemia. These metabolic changes can increase the risk of atherosclerosis, which in turn contributes to the likelihood of arterial clot formation.
Acute illness, hospitalization, and opportunistic infections dramatically increase the risk of blood clots. Prolonged immobility, such as during a hospital stay, is a known clot risk factor, but this is amplified in PLWH. Infections like Cytomegalovirus (CMV) or Pneumocystis pneumonia (PCP) contribute significantly to the hypercoagulable state, especially in individuals with low CD4+ T-cell counts.
Monitoring and Clinical Strategies
Given the established elevated risk, clinical awareness and proactive risk management are necessary components of care for people living with HIV. Healthcare providers should prioritize screening for both traditional and HIV-specific risk factors, recognizing the higher baseline risk for thrombosis. Monitoring certain biomarkers, such as D-dimer, may help identify individuals in a prothrombotic state, though specific screening guidelines are still evolving.
Lifestyle modifications remain a cornerstone of risk reduction, particularly focusing on controlling the traditional cardiovascular multipliers. Smoking cessation, achieving a healthy weight, and managing blood pressure and cholesterol levels are essential actions that can mitigate the overall risk profile. These measures directly address factors that compound the underlying inflammation caused by the virus.
For patients who experience a thrombotic event, the treatment approach with anticoagulation is generally the same as for those without HIV. However, ART requires careful attention due to potential drug-drug interactions. Many antiretroviral agents can affect the metabolism of blood thinners like warfarin or direct oral anticoagulants, necessitating close monitoring and dose adjustments. Patients must ensure their healthcare providers are fully aware of their current ART regimen when discussing treatment for clotting events.