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Page 6 of 17 Cannata et al. Mini-invasive Surg 2020;4:53 I http://dx.doi.org/10.20517/2574-1225.2020.41

Extremely rare etiologies include chest traumas, systemic inflammatory diseases or acute rheumatic fever
[8,9]
which remains a serious concern in endemic areas .

Ischemic papillary muscle rupture is another major cause of acute massive MR, with more frequent
involvement of the posterior papillary muscle during inferior myocardial infarctions.

Acute myocardial ischemia or infarction may cause acute functional MR with systolic symmetrical or
asymmetrical leaflet tethering, due to global or regional ventricular systolic dysfunction.

Another functional cause of MR is systolic anterior motion (SAM) of mitral leaflets in hypertrophic
[2]
obstructive cardiomyopathy or Takotsubo cardiomyopathy .

Echocardiography
Diagnosis of acute MR
Echocardiography is essential for diagnosis. As opposed to chronic MR, left atrial and ventricular sizes
are usually normal in acute MR, except for preexisting conditions influencing chambers’ dimension,
compliance and hemodynamic tolerance. For instance, patients with a history of chronic MR and preserved
ventricular systolic function have enlarged cardiac volumes and tolerate the further volumetric increase
better than patients with normal sized hearts or with preexisting reduced LVEF. Color Doppler may
underestimate the severity of MR, owing either to rapid equalization of left atrial and ventricular pressures
or to an eccentric direction of the regurgitant jet with “Coanda” effect. Consequently, the use of color
Doppler-based quantitative measures such as regurgitant volume and effective regurgitant orifice area may
be misleading and even challenging, due to severe acute congestive heart failure with tachycardia. Vena
contracta width and continuous wave Doppler signal represent reliable semiquantitative tools to quickly
evaluate the significance of MR. A triangular and dense continuous wave Doppler curve supports the
diagnosis of acute MR. It mirrors the rapid decline in late systolic velocity as a consequence of the abrupt
increase in left atrial pressure. Systolic pulmonary venous flow reversal in one or both pulmonary veins
can be found but tachycardia or atrial fibrillation can mask these findings. Any measure or value should
be interpreted in the clinical context, as patients with acute heart failure and acute MR may appear to
have only moderate MR when assessed by semi-quantitative and quantitative methods. Indeed, an acute
significant MR should be suspected in patients with a clinical pattern of acute heart failure, with evidence of
hyperdynamic LV without systolic or diastolic dysfunction, and with anatomic imaging of MV lesions [10,11] .

Trans-thoracic echocardiography is the first-line examination in the assessment of acute dyspnea,
feasible at bedside and sufficient to raise the clinical suspicion, but often inconclusive regarding the
identification of the mechanism of MR, the evaluation of the MV anatomy and preoperative planning,
which all require TEE. As such, three-dimensional (3D) echocardiography should always be adopted, as it
provides anatomical details not detectable with two-dimensional (2D) imaging, enabling a dynamic and
[12]
comprehensive assessment of MV tissue, and seizes dataset for off-line multiplanar reconstructions .
Mechanism and cause of MR
The first step of echocardiographic evaluation of MR mechanism is the distinction between organic/
structural damage and functional alteration of MV [Table 1]. Close assessment of leaflet motion, anatomic
lesions and finally the Color Doppler-based evaluation of convergence area and regurgitant jets are
required.

A structural lesion with normal leaflet motion is generally due to a leaflet perforation. In this case, TEE
should evaluate the position, shape and dimensions of the perforation, detect any sign suggestive of
endocarditis, such as masses, vegetations or abscesses and explore mitral-aortic junction, left ventricular