Which statement about peripartum cardiomyopathy (PPCM) is correct regarding its molecular pathogenesis and treatment implications?
- A PPCM is caused by cleaved 16 kDa prolactin fragment (vasoinhibin) damaging cardiomyocytes; bromocriptine is an adjunct treatment to suppress prolactin ✓
- B PPCM arises from autoantibodies against cardiac troponin-I and is treated with IV immunoglobulin
- C PPCM is a form of dilated cardiomyopathy caused by viral myocarditis exclusive to the postpartum period
- D PPCM pathogenesis involves placental anti-angiogenic factors identical to pre-eclampsia
Explanation
Current evidence supports a key role for cathepsin D-cleaved 16 kDa prolactin fragment (vasoinhibin) in PPCM pathogenesis. This fragment is cardiotoxic, inducing cardiomyocyte apoptosis and microvascular damage. Based on this, the German PPCM Network initiated trials of bromocriptine (a D2 agonist that suppresses prolactin secretion) as adjunct to standard heart failure therapy. The BOARD trial (2021) demonstrated non-inferiority of short-course (8-week) versus long-course (52-week) bromocriptine, both superior to standard care for recovery of EF. Current recommendation: bromocriptine 2.5 mg BD for 2 weeks added to guideline-directed heart failure therapy if no contraindication.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.