Valve-Specific Anatomy and Structural Determinants of Susceptibility to Infective Endocarditis: A Review

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Background/Objectives: Infective endocarditis (IE) is a life-threatening cardiovascular infection with in-hospital mortality of 15–30% despite modern therapy. Contemporary IE demonstrates non-random valve involvement: aortic and mitral 35–45%, tricuspid 5–10% (30–50% in intravenous drug users [IVDU]), and pulmonary < 1%. These patterns implicate valve-specific anatomy and hemodynamics as central determinants of susceptibility. This narrative review examines the reported distribution of IE across the aortic, mitral, tricuspid and pulmonary valves and summarises the anatomical, haemodynamic, structural, microbial and patient-related factors associated with valve-specific susceptibility. Methods: A structured narrative review of English-language literature was conducted using PubMed/MEDLINE, Embase, Scopus, and Google Scholar (January 1990–March 2026). Search terms included “infective endocarditis,” “valve anatomy,” “hemodynamics,” “bicuspid aortic valve,” “prosthetic valve endocarditis,” and “transcatheter aortic valve replacement (TAVR) endocarditis.” We included anatomical studies, clinical cohorts, surgical series, imaging research, and international guidelines. Evidence was synthesized narratively using Oxford Centre for Evidence-Based Medicine (CEBM) levels. Results: IE susceptibility follows a biologically coherent gradient determined by the interaction between valve anatomy, hemodynamic stress, endothelial injury, and structural substrate. The aortic valve is most vulnerable because of high shear stress, congenital abnormalities such as bicuspid aortic valve, and direct continuity with the cardiac fibrous skeleton, predisposing to peri-annular extension. Mitral valve IE is largely conditional upon pre-existing structural disease, particularly mitral valve prolapse, rheumatic heart disease, and mitral annular calcification, and is characterized by a high risk of systemic embolization. Tricuspid valve IE reflects the interaction between low-pressure hemodynamics and acquired patient-specific modifiers, including intravenous drug use, cardiovascular implantable electronic devices, and congenital heart disease. Pulmonary valve IE remains uncommon because of favorable native hemodynamics but occurs predominantly in repaired congenital heart disease, right ventricular outflow tract reconstruction, and prosthetic pulmonary valves. Across all valve types, multimodality imaging and anatomical assessment consistently influence complication detection, surgical planning, and long-term surveillance. Conclusions: IE involvement is unevenly distributed among the cardiac valves. Aortic and mitral involvement predominate, tricuspid involvement is strongly influenced by injection drug use and intracardiac devices, and pulmonary-valve IE remains rare and is principally associated with congenital abnormalities or prosthetic material. These patterns highlight the possible contributions of haemodynamic stress, pre-existing structural abnormalities, and age-related valvular changes to the greater susceptibility of left-sided valves.