Congenital left ventricular (LV) diverticula (Figs. 3.1 and 3.2) are defined as any outpouching from the ventricle that is lined by ventricular myocardium. Its connection to the ventricle may be wide or narrow [1].

The incidence of congenital ventricular diverticula has been reported to be between 0.04 and 2.2 % in an autopsy series of patients dying of cardiac disease [1–3]. LV diverticula range in size from 0.5 to 9 cm in diameter and have been reported in nearly all LV locations. Most commonly, however, they are found in the left ventricular apex and along the inferior or inferoseptal wall left ventricular walls and at the right ventricular insertion point [4]. When multiple diverticula are present (40 % of the cases, Fig. 3.2), they tend to be in close proximity to each other [1].

The Cantrell syndrome is defined as the association of LV diverticula with congenital midline thoracoabdominal ­abnormalities, sternal and diaphragmatic defects, and partial absence of the inferoapical pericardium [5].

Congenital ventricular diverticula should be differentiated from acquired causes of ventricular aneurysms and pseudoaneurysms such as those that occur after myocardial infarction, myocardial inflammation, or cardiac trauma. These entities may be similar in appearance making differentiation by noninvasive imaging modalities challenging. Often, the correct diagnosis is made using associated clinical history and imaging abnormalities (h/o trauma or myocardial infarction with associated imaging abnormalities like ventricular thinning or calcification). In addition, acquired ventricular aneurysms consist of predominantly fibrous tissue and are associated with abnormal cardiac contour in diastole and myocardial bulging during systole.

Note that muscular ventricular septal defects that spontaneously close by overlapping ventricular trabeculations may also produce diverticular outpouching of the ventricle.

Ventricular noncompaction may have a similar appearance to that of a ventricular diverticulum. The diagnosis of ventricular noncompaction is confirmed by identifying more than three deep intertrabecular recesses and a systolic ratio of noncompacted to compacted layers of >2.2 [6, 7]. Ventricular noncompaction is discussed in detail in Part 4, Chap. 9.

Myocardial bridging (Fig. 3.3) is defined as the presence of an intramyocardial segment of a major coronary artery that normally has an epicardial course. The frequency of myocardial bridging observed by computed tomographic angiography (CTA) is nearly 60 % [8]. Myocardial bridging is typically a benign finding and the vast majority of myocardial bridges are asymptomatic. It is clinically significant only when associated with regional hemodynamic alterations. Hemodynamically significant findings typically occur only when myocardial bridging involves the left anterior descending artery. Even in adult patients with hypertrophic cardiomyopathy, myocardial bridging is not associated with increased risk of death, including sudden cardiac death.

Note that myocardial bridging is almost never seen in the right coronary artery since most of the course of the right coronary artery is not near the myocardium.

Prominent left ventricular trabeculations (Fig. 3.4) have been reported in 323 of 474 autopsies (68 %) in normal human hearts and they occur equally in males and females (72 and 65 %, respectively) [9]. No variation is noted when age is considered [9]. Accordingly, prominent left ventricular trabeculations are considered to be common variants of the normal human heart, frequently visualized during CTA examinations, and these should not to be mistaken for isolated left ventricular noncompaction (described above).

Traditionally, papillary muscles (PM) are depicted as arising directly from the solid portion of the ventricular walls. They are shown to have a broad base connecting them to the ventricular wall. The PM then taper to give rise to the origins of the chordae tendineae. More recently, state-of-the-art multidetector computed tomography (MDCT) has revealed that the base of the PM does not directly contact or join the solid portion of the ventricular heart walls but rather they contact the ventricular wall via a network of trabeculae carneae lining the ventricular cavities (Fig. 3.5) [10]. These trabeculae carneae lie above the actual surface of the solid portion of the heart walls. Both the left ventricular and right ventricular PM demonstrate this relationship [10]. This finding should not be mistaken for left ventricular noncompaction.