Chordae tendineae rupture at 23: post-traumatic acute mitral regurgitation

Severe acute MI in young adults: the role of triggering factors

Severe acute mitral regurgitation (MR) is a rare pathology in young adults, with an etiology generally centered around infectious endocarditis, thoracic trauma, or connective tissue syndromes. While chordal rupture is a classic complication of myxomatous degeneration in elderly subjects, its sudden onset in a 23-year-old patient raises questions about the decompensation kinetics of a latent valvular substrate.

This case report details the management of a 23-year-old patient presenting with massive acute MR with pulmonary edema, characterized by a rupture of the primary chordae of the P2 scallop. The objective is to analyze the temporal convergence between a direct precordial trauma (collision during a football match) and a transient febrile syndrome. The authors explore the hypothesis that these events acted as mechanical and inflammatory catalysts — potentially involving the IL-33/ST2 pathway — on a valve with pre-existing myxoid degeneration, confirmed by histopathological examination. The study thus highlights the importance of the differential diagnosis between pure traumatic injury and rupture on a degenerative background in young subjects.

Study design and subject

This case report documents the diagnostic approach and clinical evaluation of a 23-year-old patient, with no cardiac history, presenting with severe acute mitral regurgitation (MR). The investigation focused on the temporal correlation between a blunt chest trauma occurring seven days prior, a transient febrile episode, and the rupture of valvular chordae.

Evaluation protocol and parameters

The diagnostic protocol included the following steps:

• Clinical and hemodynamic evaluation: Measurement of vital signs upon admission (BP 96/58 mmHg, HR 122 bpm, saturation 88% on room air) and cardiac auscultation.
• Biological analyses: Full blood count (leukocytosis at 13.2 × 10⁹/L), inflammatory markers (CRP at 74 mg/L, procalcitonin at 0.08 ng/mL) and myocardial stress markers (Hs Troponin I at 86/92 ng/L, NT-proBNP at 1,820 pg/mL).
• Infectious work-up: Three sets of blood cultures, streptococcal antigen tests, throat cultures, and nasopharyngeal PCR panels (Influenza A/B, RSV, SARS-CoV-2, EBV, CMV).
• Initial imaging: Chest X-ray, electrocardiogram (ECG) and chest computed tomography (CT) to exclude sternal or rib fractures or pulmonary contusion.

Echocardiographic analyses

The structural evaluation was based on two key imaging modalities:

• Transthoracic echocardiography (TTE): Measurement of ventricular diameters (end-diastolic 51 mm, end-systolic 32 mm), ejection fraction (64%), and left atrial volume (38 mL/m²). MI severity was quantified by the vena contracta (8 mm), EROA (0.48 cm²), and regurgitant volume (72 mL).
• Transoesophageal echocardiography (TOE): Use of two-dimensional multiplane imaging to identify the mechanism of regurgitation (rupture of the primary chordae of the P2 scallop).

Clinical presentation and haemodynamic status

Upon admission, the 23-year-old patient presented with acute respiratory distress, a blood pressure of 96/58 mmHg, and tachycardia at 122 bpm. Oxygen saturation was 88% on room air with a respiratory rate of 28 breaths/min. Cardiac auscultation revealed a grade 4/6 holosystolic murmur at the apex, radiating to the axilla, associated with bibasilar crackles.

Biological analyses and stress markers

The biological assessment revealed an inflammatory response and significant myocardial stress, without confirming an acute infectious etiology. Blood cultures (3 sets) and viral tests (influenza, RSV, SARS-CoV-2, EBV, CMV) remained negative.

Imaging and echocardiography assessment

Chest radiography and CT scan confirmed bilateral pulmonary oedema with slight pleural effusions, without sternal or rib fractures. Transthoracic echocardiography (TTE) showed a non-dilated left ventricle (end-diastolic diameter of 51 mm) with a preserved ejection fraction (64%).

La quantification de l'insuffisance mitrale (IM) a révélé une régurgitation sévère et excentrique :

• Vena contracta width: 8 mm.
• Effective Regurgitant Orifice Area (EROA): 0.48 cm².
• Regurgitant volume: 72 mL.
• Estimated systolic pulmonary arterial pressure: 58 mmHg.

Transesophageal echocardiography (TEE) specified the lesion mechanism: a "flail" appearance of the P2 segment of the posterior mitral valve, secondary to a rupture of the primary chordae tendineae. The leaflets appeared slightly thickened and redundant, suggesting underlying myxoid degeneration, with no signs of vegetation or annular abscess.

Clinical analysis: The crossroads of triggers

This case illustrates the complexity of diagnosing acute mitral regurgitation in young subjects. Here, the patient presented a background of previously asymptomatic myxoid degeneration. The originality of the study lies in the chronology: a direct thoracic impact followed by a transient febrile episode. While mechanical trauma can directly rupture the chordae, the systemic inflammation marked by a CRP of 74 mg/L could also have altered the homeostasis of the valvular extracellular matrix. The authors suggest the IL-33/ST2 pathway, known to activate valvular interstitial cells, as a potential biological link between inflammation and acute rupture.

The highlight of this observation is the rigor in excluding differential diagnoses. Infective endocarditis was ruled out by imaging, negative blood cultures, and histology. Similarly, the absence of pathogenic variants on a panel of 13 genes allows for the exclusion of syndromic connective tissue pathologies such as Marfan or Ehlers-Danlos. The main limitation remains the impossibility of precisely dating the rupture: was it the initial shock or the hemodynamic stress of the fever that precipitated the decompensation? Clinically, the success of the repair by triangular resection and neocords confirms that the conservative approach remains the gold standard, even in emergency settings for this type of valve.

Study summary

This clinical case documents severe acute mitral regurgitation due to chordal rupture (P2 segment) in a 23-year-old patient, occurring after direct thoracic trauma and a febrile episode. Histopathological analysis confirmed underlying myxomatous degeneration, acting as a structural substrate, while surgical management achieved hemodynamic stabilization and complete functional recovery.

In concrete terms, for the practitioner:

• Post-traumatic vigilance: In the event of any rapid-onset dyspnoea following a precordial shock, look for a lesion of the mitral apparatus, even in the absence of thoracic fractures or pulmonary contusions visible on imaging.
• Latent degenerative substrate: Consider that a myxoid valve may remain asymptomatic in young subjects until mechanical stress or an inflammatory process induces an acute rupture.
• Repair efficiency: Early surgical intervention combining chordal reconstruction and annuloplasty is recommended to durably restore valvular function and prevent heart failure.

Technical lexicon of the study

Myxomatous degeneration: Structural alteration of the mitral valve characterized by the accumulation of proteoglycans and the fragmentation of collagen fibers, constituting here the pathological substrate of chordal rupture.

IL-33/ST2 axis: Inflammatory signaling pathway involved in valvular extracellular matrix remodeling, suggested by the authors as a potential biological link between systemic inflammation and mechanical fragility.

EROA (Effective Regurgitant Orifice Area): Effective regurgitant orifice area (measured at 0.48 cm²), a key echocardiographic parameter used to quantify the severity of mitral regurgitation.

Vena contracta: Measurement of the minimum width of the regurgitant jet (8 mm in this case), directly reflecting the significance of the valvular leak orifice.

Flail P2: Echocardiographic appearance of a complete eversion of the central segment of the posterior leaflet into the left atrium, resulting from the rupture of the primary chordae.

NT-proBNP: Biomarker of myocardial wall stress (elevated at 1,820 pg/mL), used to assess the hemodynamic impact of acute mitral regurgitation and pulmonary edema.

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