A 61 year old patient with sudden onset of typical angina pectoris, sweat and a sinus bradycardia of 40 beats per minute was admitted at intensive care unit. It was known, that he had an elective coronary angiography at the same day because of suspected coronary artery disease with typical chest pain and exercise induced dyspnoea as well as paroxysmal atrial fibrillation. His baseline treatment was for arterial hypertension metoprolol (150 mg/d) and ramipril (2,5 mg/d), for atrial fibrillation dalteparin (3 × 5.000 IU/d) and for expected angioplasty aspirin (100 mg/d) and loading dose of clopidogrel (300 mg at the first day). The coronary angiography report described a severe proximal type B2 stenosis and a medial type B stenosis of the left anterior descending artery (LAD). Intended angioplasty of the LAD and implantation of a special stent was planned for the next day.
At intensive care unit an ECG was performed because of unstable angina pectoris one hour after finishing angiography but without signs of acute myocardial ischemia. Transthoracic echocardiography (ViVid 7, GE Vingmed, Norton, Norway; 7,5 MHz ; very low non destructive transmit power technique, MI 0,12, non triggered mode; contrast agent Sonovue as bolus of 0,1 ml) demonstrated an increase of septum thickness from 13 mm to 26 mm. Septal strain (6%) as well as strain rate (0,45/s) showed an non perfused areal of 2,3 × 3,3 cm in the middle of interventricular septum. (Figure 1 and 2).
These echocardiographic and clinical findings were in accordance with an acute non-ST-segment elevation infarction of the interventricular septum in connection with angiography. Cineventriculography was reviewed again and revealed a contrast enhancement in the interventricular septum after conventional automated high flow contrast medium injection. Tip of pigtail catheter was dislocated in between the trabeculae of the interventricular septum (Figure 3).
CK max value of 1082 U/l and Troponin I I value of 80 ng/ml were observed during the same day. The following day ECG showed ST-segment elevation in V1 (+0.15 mV) and V2 (+0.25 mV) indicating myocardial infarction. No ventricular arrhythmias or atrio-ventricular block caused by the septal infarction were observed. 2 days after contrast agent deposition into interventricular septum CK values decreased dewithin normal range. 2 weeks later, transthoracic echocardiography revealed a maximum of septum thickness with 28 mm, a non-perfused area of 2.6 × 4.7 cm with a strain of -4% and a strain rate of 0,45/s as well as an akinesia in the middle septum.
By magnetic resonance tomography an intramural hematoma was demonstrated 3 weeks after contrast medium injection into interventricular septum (Figure 4 and 5).
6 weeks after contrast agent injection the baseline septum thickness (13 mm) was restored, the non-perfused region was reduced to 0.9 × 1 cm in mid septum with a strain of -7% and a width of 9 mm. 8 weeks after accidental intraseptal contrast agent injection patient underwent an elective angioplasty with successful implantation of two bare metal stents into LAD. At that point a MR-follow-up was performed (Figure 6).
The final pharmacological dobutamin-stressechocardiography 8 month after complicated cineventriculography and 6 month after successfully implanted LAD stents revealed a negative viability (contractile reserve) midseptal but a normal global systolic left ventricular function without regional stress induced myocardial ischemia. (Figure 7 and 8).
