Atherosclerosis of the aorta, particularly the aortic arch, is a powerful and often overlooked source of cerebral emboli that can lead to an ischemic stroke. When atherosclerotic plaque builds up in the arch, it creates an unstable surface prone to disruption. This condition is frequently identified in patients who have experienced an Embolic Stroke of Undetermined Source (ESUS), where no other common cause like atrial fibrillation or severe carotid artery stenosis is found.
The mechanism for recurrent stroke involves the complex plaque—defined as lesions 4 millimeters thick or those with mobile components or ulcerations—shedding tiny fragments. These fragments can be small clots (thromboemboli) that form on the plaque surface or cholesterol debris (atheroemboli) that break off and travel to the brain. Given the high risk of recurrent events associated with complex aortic arch atheroma, aggressive medical therapy is necessary to prevent a second stroke. Secondary prevention protocols focus on stabilizing the underlying disease, interrupting the formation of new clots, and controlling the systemic conditions that drive plaque growth.
Stabilizing the Underlying Disease: High-Intensity Statins
High-intensity statin therapy is a foundation of treatment for patients who have experienced a stroke attributed to aortic atherosclerosis, regardless of their initial cholesterol levels. Medications such as atorvastatin (typically 80 mg daily) or rosuvastatin (typically 20-40 mg daily) are prescribed to achieve aggressive lipid-lowering goals. The target for low-density lipoprotein cholesterol (LDL-C) is often a level below 70 mg/dL or a reduction of 50% or more from baseline.
The benefit of statins extends beyond lowering circulating cholesterol; they exert effects directly on the plaque itself. Statins stabilize the atherosclerotic lesion within the aortic wall by reducing inflammation and altering the plaque’s composition. This process makes the plaque surface firmer and less prone to fissuring or rupture, decreasing the likelihood of a clot forming or a fragment breaking off the lesion. Stabilizing the primary source of the emboli reduces the risk of recurrent ischemic stroke.
Interrupting Embolic Risk: Antiplatelet Medications
Medications that prevent platelets from adhering to one another form the primary line of defense against the formation of small clots on the unstable aortic plaque surface. Platelets are activated by a disrupted plaque and aggregate to form a thrombus, which can then embolize to the brain. Common antiplatelet agents used include aspirin and clopidogrel, which inhibit different pathways of platelet activation.
A single antiplatelet agent, such as aspirin or clopidogrel monotherapy, is generally the standard long-term regimen for secondary stroke prevention in patients with aortic arch atheroma. In specific, high-risk scenarios, such as immediately following a minor stroke or a high-risk transient ischemic attack (TIA), a short course of dual antiplatelet therapy (DAPT) using aspirin plus clopidogrel may be prescribed. This dual therapy is time-limited, typically lasting for only the first 21 days, after which the patient transitions back to a single agent to mitigate the elevated risk of major bleeding.
Clarifying the Use of Anticoagulants
A common point of confusion is the role of stronger blood thinners, known as anticoagulants, in treating aortic atherosclerosis. Anticoagulants, such as warfarin or the newer direct oral anticoagulants (DOACs), prevent clot formation by targeting the clotting cascade, a different mechanism from antiplatelet agents. While these medications are the standard for preventing stroke in conditions like atrial fibrillation, they are not typically recommended for stroke caused solely by aortic arch atheroma.
Clinical trials have shown that anticoagulants do not offer a superior benefit over antiplatelet therapy. Furthermore, their use in patients with arch atheroma significantly increases the risk of major bleeding complications, including hemorrhage in the brain. Therefore, unless a patient has a separate, compelling reason for anticoagulation, such as a coexisting diagnosis of atrial fibrillation, the treatment strategy focuses on antiplatelet agents combined with high-intensity statins.
Controlling Systemic Risk Factors
Beyond the targeted therapies that address the plaque and the risk of clotting, secondary prevention must include medications to control the underlying systemic conditions that fuel atherosclerosis. Hypertension is a primary driver of arterial disease and the most important modifiable risk factor for stroke. Medications like Angiotensin-Converting Enzyme (ACE) inhibitors, Angiotensin II Receptor Blockers (ARBs), and certain diuretics are crucial for maintaining a blood pressure goal typically below 140/90 mmHg.
Controlling blood pressure reduces the physical shear stress on the walls of the aortic arch, which helps prevent the existing plaque from becoming unstable and shedding emboli. Similarly, managing diabetes mellitus with appropriate medications is necessary to slow the progression of atherosclerosis throughout the arterial system. Achieving near normoglycemic control, often assessed by a glycated hemoglobin (HbA1c) level below 7%, helps reduce the microvascular damage that contributes to overall vascular risk.