LV systolic dysfunction in MS
Did MS not spare LV?
Many of us got used to hearing during college that mitral stenosis spares the left ventricle, leading us to believe that we should always expect a preserved ejection fraction in those cases of pure MS. However, several studies have shown a high prevalence of systolic dysfunction in patients with MS with values ranging from 30-50%.
Why does this happen?
Initially, we must keep in mind that individuals who develop rheumatic fever can present involvement in any of the three cardiac layers, including the myocardium here. This involvement can occur in an acute form, but also in a chronic form with apoptosis of myocytes and occupation of the intercellular space with fibrosis.
In the 1960s, several cases of MS had segmental changes in left ventricular contractility, corroborating the idea of chronic involvement secondary to acute inflammation in rheumatic fever. Associated with this, the involvement of the subvalvular apparatus could extend to the papillary muscles that presented extensive fibrosis and, therefore, direct involvement in the contractile dynamics of the left ventricle.
A stiffening of the mitral subvalvular apparatus affected by fibrosis secondary to rheumatic involvement associated with endomyocardial fibrosis could be responsible for the substantial drop in left ventricular compliance and, ultimately, a drop in the ejection fraction of the same cavity.
In more advanced cases in which there is a significant increase in pulmonary arterial hypertension, anomalous movement of the interventricular septum may also increase systolic dysfunction of the left ventricle leading to worsening of the condition.
Here it is also worth remembering a recent post here on our platform on mitral stenosis with a low gradient, in which patients underwent PBMV and did not show much improvement in symptoms. In these cases, extensive involvement of LV compliance was also seen due to the increase in ventricular-arterial impedance and diastolic dysfunction, in the same way as paradoxical aortic stenosis.
Another factor to be discussed is the drop in the left ventricular ejection fraction after surgical mitral valve replacement. Ancient techniques involved the extensive removal of the subvalvular apparatus often affected by the disease and this led to a geometric deformity of the left ventricle. Over the years, this irreversibly generated progressive LV systolic dysfunction.
Recent assessments with other diagnostic methods such as strain can further elevate the prevalence of contractile LV dysfunction in these individuals, since it is a parameter of early subclinical dysfunction and may be present in individuals with preserved LVEF.
Thus, mitral stenosis may come with both systolic and diastolic dysfunction of the left ventricle, with the widespread concept that MS saves inadequate LV these days, with what we know of this pathology.