Ventricular septal rupture (VSR) is a rare but critical complication that usually occurs within 1 week after acute myocardial infarction (AMI) [1]. Patients without surgical repair of VSR show a high mortality rate of 76% within 1 month, and emergency surgical repair is necessary. However, the in-hospital mortality rate is still high at 47%, and depends on the patient's preoperative condition [2,3]. Here, we describe the successful transcatheter closure of a recurrent post-infarction VSR using an Amplatzer duct occluder (ADO) in a patient who had undergone emergency surgical repair. Case report A 78-year-old woman was referred to our hospital with cardiogenic shock 2 days after the first episode of chest pain. Upon hospital admission, her blood pressure was 78/52 mmHg and her pulse rate was 104 beats/min. Physical examination revealed internal jugular venous dilatation and a grade 3 pan-systolic murmur at the apex. Her 12-lead electrocardiogram showed ST elevation in leads V2-V5. Echocardiography in the emergency room revealed akinesis in the mid anterior septum and apex, and VSR in the apical interventricular septum with left-to-right shunt
Background:
Cardiomyocyte injury is a key pathological pathway in the progression of heart failure that predicts a poor prognosis; therefore, combined assessment of myocardial fibrosis and cardiomyocyte DNA damage from endomyocardial biopsy (EMB) samples may be of great importance. Meanwhile, cardiovascular magnetic resonance (CMR) native T1 reflects a composite of both intra- and extracellular compartments in the whole myocardium. We sought to assess the performance of native T1 mapping and EMB results to predict left ventricular reverse remodeling (LVRR) in recent-onset dilated cardiomyopathy (DCM).
Methods:
A total of 29 patients with DCM underwent cine CMR and triple-slice T1 mapping using the MOLLI sequence at 3T, and EMB before receiving guideline-directed medical therapy. Poly ADP-ribose (PAR) nuclear and sirius-red staining were used for quantification of DNA damage and collagen volume fraction (CVF), respectively. LVRR was defined as an increase in LV ejection fraction of ≥10% to the final value of >35%, accompanied by a decrease in LV end-diastolic volume ≥10% at the follow-up CMR.
Results:
Fifteen patients (52%) achieved LVRR. The mean native T1, histological CVF, and proportion of PAR-positive nuclei were 1376 ± 55 ms, 0.13 ± 0.05, 25 ± 15%, respectively. Native T1 correlated well with CVF (p=0.004) and trended to be higher in DCM patients with increased DNA damage (p=0.17). There was no significant association between CVF and %PAR-positive nuclei. Native T1 <1400 ms provided 86% sensitivity and 67% specificity, with the C-statistic of 0.82 (95% CI 0.67-0.98) for predicting LVRR. By contrast, C-statistic of %PAR nuclei, CVF, and combined assessment of %PAR nuclei and CVF were 0.59, 0.61 and 0.66, respectively.
Conclusion:
CMR T1 mapping may be a promising strategy for noninvasive biopsy of the whole heart and provide a better prediction of LVRR in recent-onset DCM than comprehensive histological analysis of EMB.
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