Abstract
A 71-year-old woman was diagnosed with a subacute myocardial infarction caused by an obstruction in the middle segment of the right coronary artery. Two hours after successful percutaneous coronary intervention, bedside transthoracic echocardiography revealed an interventricular septal perforation. Three hours later, the patient developed cardiac tamponade. An emergency pericardiocentesis was performed, which promptly restored hemodynamic stability. Echocardiographic findings suggested oozing from a minor perforation of the postinfarct inferior wall. Subsequent cardiac magnetic resonance imaging identified a basal inferoposterior septal perforation connected with an intramyocardial dissection. After intensive medical management, the patient gradually recovered and was discharged on the 135th day of admission. Five years of follow-up were uneventful with optimal medication therapy.
Learning objective
– Ventricular septal perforation following a myocardial infarction can result in intramyocardial dissection, which may extend to the epicardium and eventually lead to cardiac tamponade.
– Physicians should individualize treatment strategies for each patient based on various factors, especially in cases with rare and complex post-infarct complications.
– Advanced imaging techniques are recommended for assessing complex mechanical complications following a myocardial infarction.
Introduction
Ventricular septal perforation (VSP) associated with intramyocardial dissection is an extremely rare yet potentially fatal complication of myocardial infarction (MI), with many cases being identified solely through post-mortem investigations [ ]. Early detection using transthoracic echocardiography (TTE) is crucial for improving patient prognosis. Typically, patients present with early hemodynamic deterioration resulting from cardiogenic shock despite previous successful interventions for coronary artery lesions. Emergency surgical repair is generally required. However, postoperative outcomes remain poor [ ].
Case report
A 71-year-old woman was transferred to our emergency department due to severe fatigue and disturbance of consciousness. She also reported experiencing vomiting and lightheadedness for the previous three days. Her comorbidities included poorly controlled type 2 diabetes mellitus (HbA1c 10.9 %), and her body mass index was 17.36. Upon arrival, her blood pressure was 114/68 mmHg. An electrocardiogram (ECG) showed sinus arrest with an atrioventricular junctional rhythm at a rate of 34 beats per minute, as well as ST-segment elevation in leads II, III, and aVF. On admission, the troponin-I level was 96.40 ng/ml, the peak creatine kinase (CK) level was recorded at 1029 IU/l, and the peak CK-MB level was 31.7 ng/ml, confirming the diagnosis of subacute MI with an onset three days previously. A TTE showed a left ventricular ejection fraction (LVEF) of 39 % and akinesis of the inferior wall. Temporary transvenous cardiac pacing was initiated, and subsequent coronary angiography revealed an obstruction in the middle segment of the right coronary artery. A diagnosis of subacute MI was made, and a percutaneous coronary intervention (PCI) was promptly performed. Following the removal of the thrombus using an aspiration catheter, a sirolimus-eluting cobalt chromium stent (Ultimaster™ 4.0 mm / 24 mm; Terumo, Tokyo, Japan) was successfully deployed.
Two hours after PCI, the patient’s blood pressure dropped to 75/55 mmHg, and a bedside TTE revealed a left-to-right shunt flow through an interventricular septal perforation ( Fig. 1 A ). Therefore, an intra-aortic balloon pump (IABP) was inserted. Partial oxygen pressure measurements obtained via a Swan-Ganz catheter indicated a step-up in oxygen saturation at the right ventricular (RV) apex, with a pulmonary-systemic blood flow ratio (Qp/Qs) of 1.13. The hemodynamic instability was temporarily managed through the use of the IABP and catecholamines.
However, three hours after the insertion of the IABP, her blood pressure dropped again to 50/31 mmHg, and a TTE revealed a significant pericardial effusion. An emergency pericardiocentesis was performed, which evacuated 250 ml of sanguineous fluid from the pericardial space and promptly restored hemodynamic stability. Subsequent TTE assessments showed no visible ventricular or atrial wall perforation. A careful review of coronary angiograms revealed no signs of contrast extravasation that suggested coronary perforation. The hemopericardium could be attributed to oozing from a minor perforation in the post-infarct inferior wall or, less likely, to mechanical stress induced by the temporary pacemaker electrode catheter. A pericardial drainage catheter subsequently drained 5-10 ml/h of serosanguinous to serous fluid, and the patient gradually reached a stable condition.
A TTE at 2 days identified a basal inferoposterior septal perforation connected with intramyocardial dissection ( Fig. 1 B).
The IABP, pericardial drain, and temporary cardiac pacing catheter were removed on day 7, catecholamines were discontinued on day 28, and the patient was discharged from the intensive care unit on day 33 of admission. The patient made a significant recovery over the following weeks, becoming symptom-free and capable of performing daily self-care tasks. Cardiac magnetic resonance imaging (CMR) at one month confirmed similar findings ( Fig. 2 A,B ). Left ventriculography at two months demonstrated contrast inflow into the dissection cavity, with subsequent leakage into the RV lumen through the RV exit site ( Fig. 2 C). Additionally, concurrent measurements obtained from a Swan-Ganz catheter reported a Qp/Qs ratio of 1.20. She was subsequently discharged from the hospital on the 135th day of admission. However, without surgical intervention, she remains at risk of death from a sudden ventricular rupture. Following extensive discussions concerning her stable condition, limited capacity for daily living activities, fragility, reduced mobility while using a wheelchair, and poorly controlled diabetes mellitus, the patient and her family decided to refuse elective surgery. Five years of follow-up were uneventful with optimal medication therapy. Serial TTEs showed the persistence of the dissection tract but an improved LVEF to 51 %, without significant change in the estimated Qp/Qs ratio. A contrast-enhanced computed tomography at five years indicated a slight enlargement of the dissection cavity, but no significant changes in its morphology were observed ( Fig. 3 ).
