An aneurysm is a localized, abnormal bulging or ballooning that forms in the wall of a blood vessel. This weakening creates an outpouching that can expand over time, potentially leading to rupture and life-threatening internal bleeding. While many aneurysms develop due to long-term conditions like atherosclerosis or high blood pressure, certain drugs can significantly increase the risk or directly facilitate their formation. These substances compromise the structural integrity of the arteries, leading to dangerous vascular defects.
Specific Substances Linked to Aneurysm Formation
Illicit stimulants that powerfully affect the cardiovascular system are most strongly associated with aneurysm formation. Cocaine and methamphetamine, in particular, are repeatedly linked to the development of aneurysms, especially those found in the brain. The use of these substances introduces an immediate and intense strain on the arterial system, accelerating the degradation of vessel walls.
Prescription and over-the-counter medications that cause sudden increases in blood pressure also contribute to vascular wall stress. For example, certain decongestants containing sympathomimetic agents can trigger acute hypertensive spikes. Some antidepressant medications, such as venlafaxine, and specific hormonal therapies are also noted to elevate blood pressure, increasing the background risk of aneurysm formation or rupture.
Intravenous drug use presents a different, serious pathway to aneurysm development. This practice introduces bacteria into the bloodstream, which can lodge in the arterial wall. The resulting infection weakens the vessel structure, leading to a specific defect known as a mycotic aneurysm. These infectious aneurysms can occur in various locations, including the brain and peripheral arteries.
Mechanisms of Vascular Damage
The primary way substances trigger aneurysm formation is through the sudden, extreme elevation of blood pressure and the constriction of blood vessels. Stimulants cause a massive release of catecholamines, leading to powerful, transient spikes in systolic blood pressure. This acute hypertension places an enormous mechanical strain on the artery walls, especially at vulnerable points like arterial bifurcations where aneurysms commonly originate.
The rapid and forceful constriction of blood vessels, known as vasospasm, is another powerful mechanism of damage. This intense narrowing can cause microscopic tears and injury to the endothelium, the inner lining of the artery. Repeated episodes of this trauma and subsequent extreme pressure weaken the vessel’s structural layers, facilitating the characteristic ballooning effect.
Certain drugs also induce vasculitis, which is the inflammation of the blood vessel walls. This inflammatory response degrades the structural components of the vessel, specifically collagen and elastin, which provide strength and elasticity. The resulting necrosis, or death of the vessel wall tissue, leads to a profound loss of integrity, creating an area that easily balloons outward.
Some substances exert direct toxicity on the vascular smooth muscle cells that form the middle layer of the artery wall. This toxicity can cause the programmed death of these cells (apoptosis), further compromising the structural scaffolding of the vessel. The combination of intense pressure, inflammation, and cellular degradation creates an environment where the artery wall cannot withstand normal blood flow, culminating in aneurysm development.
Characteristics of Drug-Related Aneurysms
Aneurysms resulting from substance use often exhibit distinguishing features compared to those caused by congenital defects or chronic conditions like atherosclerosis. A significant proportion of aneurysms linked to stimulant use are found in the brain, presenting as saccular or “berry” aneurysms. These defects tend to be smaller and located more distally on the small arteries of the brain than typical aneurysms found in the general population.
This location in the brain’s smaller vessels is a hallmark of stimulant-associated vascular injury, contrasting with aneurysms found at the base of the main arteries. This pattern suggests the damage relates to the intense, localized vasospasm and high pressure surges induced by these substances. Patients presenting with drug-related aneurysms are also often notably younger than those with aneurysms from other causes.
A separate category is the mycotic aneurysm, which arises from infection introduced through unsterile drug administration. These aneurysms are caused by the destruction of the vessel wall by bacteria, making them structurally distinct and often more fragile. While they can occur in the brain, mycotic aneurysms are also frequently found in peripheral arteries, such as those in the abdomen or limbs, reflecting the systemic spread of the infection.
It is important to differentiate a true aneurysm from a pseudoaneurysm (false aneurysm). A true aneurysm involves the dilation of all three layers of the arterial wall. In contrast, a pseudoaneurysm is a collection of blood leaking from the artery but contained by the surrounding tissue. Although needle trauma can cause a pseudoaneurysm at an injection site, the chemical effects of the substance itself typically result in a true aneurysm, particularly the saccular type in the cerebral circulation.

