cardiac skeleton

**Components:** - Four fibrous rings (annuli fibrosi) surrounding the aortic, pulmonary, mitral, and tricuspid valves. - Right and left fibrous trigones. The right trigone is the thickest and is formed by the junction of the aortic, mitral, and tricuspid annuli. The left trigone lies between the aortic and mitral annuli. - Membranous part of the interventricular septum. - Tendon of Todaro and conus ligament (tendon of the infundibulum) in some descriptions. - Composition: dense collagenous connective tissue. It may contain cartilage or bone (os cordis) in some species, such as cattle, but not in humans.

**Functions:** 1. **Structural support and anchorage:** it provides attachment for the valve leaflets/cusps and prevents valve annular dilation under pressure. It also gives an origin and insertion for atrial and ventricular myocardium. 2. **Electrical insulation:** it separates atrial and ventricular myocardium, so impulses cannot spread directly between them. The only normal pathway is the AV node → bundle of His, which penetrates the right fibrous trigone (the central fibrous body). This forces the physiologic delay at the AV node, so the atria contract before the ventricles. 3. **Valve integrity:** it maintains valve orifice shape and patency, so the valves open and close correctly.

**Clinical correlations:** - **Wolff-Parkinson-White (WPW):** an accessory pathway (bundle of Kent) crosses the cardiac skeleton and bypasses the AV node. This causes ventricular pre-excitation, with a short PR interval, a delta wave, and a wide QRS. It predisposes to AVRT. In WPW with atrial fibrillation, avoid AV nodal blockers (β-blockers, CCBs, digoxin, adenosine) and use procainamide or cardioversion. Definitive treatment is catheter ablation. - **Infective endocarditis:** extension beyond the valve into the annulus causes a **perivalvular (annular) abscess**, most often with aortic valve involvement and S. aureus. The abscess can damage the conduction system adjacent to the aortic root and AV node/His bundle. This produces a new PR prolongation or AV block, so serial ECGs are needed. It is an indication for surgery. - **Valve annular dilation:** dilated cardiomyopathy or LV/LA enlargement stretches the annulus and can cause functional mitral or tricuspid regurgitation. - **Calcification:** mitral annular calcification and age-related degeneration of the fibrous skeleton (Lev disease and Lenègre disease) can cause conduction block. - **Embryology:** the skeleton develops from endocardial cushions. Endocardial cushion defects (e.g., AV septal defects) are associated with Down syndrome (trisomy 21). - **Arrhythmia/ablation anatomy:** the skeleton defines the boundary of the AV junction. It matters for ablation of accessory pathways and for transcatheter valve procedures (e.g., TAVR can injure the conduction system near the membranous septum, causing LBBB or complete heart block).

**High-yield pearl:** "Fibrous skeleton = insulator + anchor." If the question asks why the atria and ventricles don't depolarize at the same time, or how the ventricles can be excited without passing through the AV node, think of the cardiac skeleton and accessory pathways.