Cavitation phenomenon in a patient with mechanical aortic valve prosthesis – a rare mechanism of ischemic stroke and the question of re-operation in a young adult

K. Wosgien (Berlin)1, S. Kische (Berlin)2, A. Bärisch (Berlin)2, D. O h-Ici (Berlin)2, I. Siegel (Berlin)2
1Vivantes Friedrichshain Kardiologie Berlin, Deutschland; 2Vivantes Klinikum im Friedrichshain Klinik für Innere Medizin - Kardiologie und konserv. Intensivmedizin Berlin, Deutschland
Background:
Mechanical heart valves are associated with an increased risk of thromboembolic events. In addition to thrombus and endocarditis, the cavitation phenomenon has been increasingly recognized as a potential mechanism. Cavitation refers to the formation and implosion of microbubbles caused by turbulent flow and pressure fluctuations near mechanical valves. These bubbles may cause hemolysis and microembolic events. Recent studies indicate that cavitation is frequent, enhanced at higher heart rates, and often misinterpreted as thrombus or vegetation.

Case report:
A 27-year-old man with a mechanical aortic valve (St. Jude Medical 25 mm, implanted 2018) presented with acute dysarthria and visual field loss. Brain MRI revealed multiple acute right occipital infarctions and older left-sided lesions. Despite adequate anticoagulation (INR 2.2–2.4), TEE repeatedly demonstrated fine, echo-bright structures in the LVOT below the prosthesis, initially interpreted as possible thrombus or endocarditis but ultimately consistent with a cavitation phenomenon. Blood cultures were negative, and fluoroscopy confirmed normal leaflet motion. After multidisciplinary evaluation involving Cardiac Surgery, the diagnosis of valvular cavitation was made. The patient remains clinically stable, with follow-up planned for November 2025; surgical re-operation is being discussed to prevent recurrent embolic events.

Discussion:
Cavitation is a rare but clinically significant differential diagnosis for echogenic structures near mechanical valves. Implosion of microbubbles generates shear stress that may damage erythrocytes and endothelium and activate coagulation. In-vivo data (Andersen et al., Ann Thorac Surg 2006) confirmed high-frequency acoustic energy as a marker of cavitation. A larger echocardiographic study (Vriz et al., Echocardiography 2020) showed frequent gas emboli associated with higher heart rate. While a direct causal link to clinical stroke remains unproven, the mechanism is biologically plausible. The key clinical question raised by this case is whether persistent cavitation despite adequate anticoagulation justifies valve re-operation to prevent recurrence.

Conclusion:
In young patients with mechanical valves presenting with ischemic stroke, cavitation should be considered as a potential mechanism. In such patients, the question of whether valve re-operation is warranted gains particular clinical relevance. This case highlights the need to define evidence-based criteria for surgical intervention in persistent cavitation.