Magnetic resonance imaging of abnormal ventricular septal motion in heart diseases: a pictorial review

Atrial septal defects and partially anomalous pulmonary venous returns to systemic veins or directly to the right atrium result in left-to-right shunting, which when significant, leads to right atrial and ventricular enlargement and pulmonary artery dilatation. In these patients, the degree of flattening and leftwards septal bowing during diastole (Fig. 3) was related to the degree of volume overload [9].

Surgical closure should be considered in the short term for patients with a ratio of pulmonary-to-systemic blood flow (Qp/Qs) higher than 1.5, irrespective of age. After surgical closure, the persistence of right ventricular dilatation and paradoxical septal motion are common, with older age at surgery, systolic pulmonary artery pressure >40 mmHg and a ratio of pulmonary/systemic blood flow >3 [10].

Ebstein’s anomaly is a common primary cause of tricuspid regurgitation characterised by varying degrees of dysplasia and displacement of the tricuspid valve leaflets into the RV [11]. The major haemodynamic consequence of tricuspid regurgitation is an increase in end-diastolic RV volume that leads to paradoxical septal motion during diastole. Although this abnormal septal motion is not specific to valve regurgitation, its presence is considered to be a distinct indirect echocardiographic and Doppler parameter for severe tricuspid regurgitation [12]. In some cases, right ventricular dilatation is so marked that the ventricular septum bulges leftwards during diastole, compressing the left ventricular chamber (Fig. 4). Episodic left ventricular outflow tract obstruction may be observed in extreme cases [11].

Tetralogy of Fallot (TOF) is the most common form of cyanotic congenital heart disease after the first year of life. Most patients with TOF nowadays undergo total repair early in life via closure of the ventricular septal defect and relief of RV outflow tract (RVOT) obstruction with good results.

Long-term follow-up studies have reported that following TOF repair, these patients have residual haemodynamic abnormalities, such as pulmonary regurgitation after RVOT patch augmentation, which leads to progressive RV dilatation, tricuspid regurgitation and secondary RV volume overload [7, 13]. This abnormal RV volume overload is associated with flattening (Movie 1) or leftwards septal bowing during diastole that causes alterations in left ventricular geometry and function (Fig. 5 and movie 1) [7].

Left ventricular dysfunction in patients following TOF repair was found to be the strongest predictor of poor clinical status. Proposed mechanisms include akinesia resulting from the ventricular septal defect patch, septal fibrosis, chronic volume loading from early palliative shunt creation, progressive mechanical interaction between an enlarged failing RV and the LV that is mediated through paradoxical septal motion, and myocardial injury at the time of repair [7, 13]. Right ventricular restoration in patients with severe right ventricular dilatation and underlying aneurysm or akinesia of the right ventricular outflow tract has proven to be an effective procedure to return the bowed non-functional septum to a central position that improves right-sided function [13].

This paradoxical septal motion may also be observed in asymptomatic postoperative patients following TOF repair without significant right ventricular volume. Prolongation of the QRS duration secondary to right bundle branch block has been related to the degree of reduced regional septal systolic function. Reduced LV systolic function in this group of patients is mainly secondary to diminished regional septal systolic function and the paradoxical septal motion [7].

Valvular pulmonary stenosis is found in patients with RVOT obstruction and is almost always congenital. Pulmonary stenosis, when significant, results in delayed ventricular filling and compensatory RV hypertrophy. RV systolic function is initially preserved with RV pressure overload, but diastolic dysfunction occurs as a consequence of myocardial hypertrophy and remodelling [14].

Cardiac MRI can show normal septal function or septal flattening or leftwards bowing throughout the cardiac cycle with most marked distortion of the left ventricle at early diastole. In addition, it is the gold standard method for quantifying RV size and function, and can provide additional information for assessing pulmonary stenosis and locating the exact area of obstruction [15].

After percutaneous pulmonary valve implantation, an increase in LV end-diastolic volume due to an improvement in early diastolic filling has been reported. This better LV filling correlates with more favourable septal motion [14].

The most distinctive feature of constrictive pericarditis is increased pericardial stiffness, leading to impaired ventricular filling with a subsequent rise in filling pressures. Although a pericardial width of more than 4 mm has been used as a morphological criterion to diagnose constrictive pericarditis, a significant number of patients with pericardial constriction are found to have a minimally increased or even normal pericardial width during surgery. In such cases, one of the most useful criteria for differentiating constrictive pericarditis from other entities with increased filling pressure, such as restrictive cardiomyopathy, is the presence of abnormal septal bowing towards the LV during early diastole (Movie 3 and Fig. 8) [3]. Early diastolic leftwards ventricular septal bowing can be enhanced at the onset of inspiration as the changes in intrathoracic pressure are not transmitted to the cardiac chambers, because the non-compliant pericardium impedes the outward movement of the ventricular free wall (Movie 3). Therefore, during inspiration, the pulmonary venous left atrial pressure gradient decreases, reducing flow to the left heart, with a concomitant increase in flow to the right chambers, a sign of pathological ventricular interdependence [3, 18].

Inspiratory septal bowing during early diastole can also be seen in inflammatory pericarditis (Fig. 9) because the inflammatory thickened pericardial layers may lower pericardial compliance and lead to transient pericardial constriction [18]. Late enhancement of the inflamed pericardium after the administration of gadolinium-based contrast material is useful to differentiate inflammatory pericarditis from fibrosing forms of chronic pericarditis (Fig. 9b).

Left anterior descending artery occlusion produces necrosis of the apex and anterior septum.

Septal myocardial infarction has many deleterious effects, among which are the loss of contractile function, impairment of electrical conduction and loss of ventricular synchrony [21].

Left bundle branch block is commonly associated with atherosclerotic coronary artery disease, and its identification in these patients is important to stratify the risk and manage the therapy [22].

Patients with antero-septal myocardial infarction and left bundle branch block exhibit similar paradoxical systolic movement of the IVS (Fig. 10), which may limit the interpretation of non-invasive stress tests [23]. Moreover, myocardial perfusion studies often suffer from false-positive antero-septal or septal perfusion defects in the absence of left anterior descending artery stenosis [22].

Only myocardial contrast echocardiography with adenosine and 64-slice computed tomography seems to improve diagnostic accuracy [22].

Recent studies have shown that tagging cardiac MRI combined with viability data obtained by late gadolinium enhancement may be a valuable adjunct for the assessment of myocardial viability in patients with regional wall motion abnormalities and left bundle branch block or myocardial infarction (Fig. 10c) [23].

The septum plays a central role in the understanding and management of the RV failure seen in RV dysplasia. The disease involvement is not limited only to the RV as LV has also been reportedly affected. Right ventricular free wall is replaced by a fatty deposition that allows the free wall to dilate and become aneurysmal. These right ventricular changes exist despite normal pulmonary artery pressure. Left ventricular involvement is associated with increased myocardial mass, inflammatory infiltrates, clinical arrhythmic events and more severe right ventricular wall thinning and heart failure [24].

Cardiac MRI can show normal septal function or septal flattening or leftwards bowing during early diastole, which may lead to left ventricular dysfunction. Understanding septal function and its contribution to RV performance has allowed for a rational design of a procedure to treat this disease. The treatment goals are to limit free wall aneurysm, as reported experimentally, and restore the midline septal position [25].

Systolic movement of the interventricular septum towards the LV despite normal thickening is assumed to be a usual and inevitable event after uncomplicated heart valve surgery, coronary artery bypass grafting and cardiac transplantation. The cause is uncertain but is likely to be related to alterations in heart mobility in the chest due to postoperative adhesions, conduction abnormalities and some mechanism that injures the IVS. In general, PSM is typically transient, not due to septal ischaemia or infarct, and resolves within the first year as pericardial adhesions form or as conduction abnormalities [5].

Leftwards septal bowing during systole can also be seen in cardiac transplant patients (Fig. 11) with RV pressure overload in the donor heart secondary to the effect of the recipient’s increased pulmonary resistance by chronic LV failure of the excised heart [26].