**6. Contrast-enhanced MRI**

**3. Results**

**3.1. Survival rate**

mortality are shown in Table 2.

326 Principles and Practice of Cardiothoracic Surgery

**4. Cardiac function**

ative hemodynamic values.

ml/m2

increased on average up to 118 ml/m2

parameters were: LV EDVI - 114 ml/m2

**Causes of postoperative mortality LVR with EE**

Low cardiac output syndrome 1 2

Progressing HF 3 4

Acute myocardial infarction 2 1

Stroke - 2

Sudden cardiac death - 4

Non-cardiac reason 1 1

were 52% and 49% of the entire myocardial perimeter in the groups.

up to 49% и 52%, decreased EDVI down to 79 and 77 ml/m<sup>2</sup>

Thus, in the study group patients left ventricular end-diastolic volume index (LV EDVI) was

phase in synchronizing mode showed perimeters of affected myocardium; on average they

EchoCG performed in 2 weeks after the surgical intervention showed statistically signifi‐ cant (p<0,01) change of the values in comparison with preoperative data: increased EF

the patients of the study group and control group correspondingly. There were no statis‐ tically significant differences found between the groups as for preoperative and postoper‐

, LV ejection fraction (EF) was lowered to 38% and in the control group patients these

, LV ESVI – 69 ml/m2

**Table 2.** Surgical outcomes of the patients in 1 year after the intervention.

Intraoperative mortality for the patients underwent LVR comprised 5% (9/188). For the pa‐ tients of the study group (LVR with EE) mortality was 4% (3/84), for the patients of the con‐ trol group (LVR without EE) – 6% (6/104). One year survival was 92% (77/84) for the patients subjected to LVR with EE and 87% (90/104) for those from the control group. The causes of

**(N=7 from 84)**

, end-systolic volume index (LV ESVI) – up to 74

, EF - 40%. MRI of diastolic

, ESVI to 49 and 48 ml/m2 in

**LVR without EE (N = 14 from 104)**

> Analyzing the obtained MRI values characterizing local morphological condition of the my‐ ocardium with values of local electrical myocardial potential we found a significant differ‐ ence as for the thickness of viable myocardium (i.e. myocardium which does not accumulate contrast paramagnetic agent) in comparable segments. Thus in the zones with normal po‐ tential (0 decrease) the thickness of viable myocardium was more than 7 mm - on average 9,8mm; in transient zone (lowered potential 1) it was 6,2mm; in low potential zone (lowered potential 2) – 5,3mm and in "electrical scar" zone (lowered potential 3) – 2,8 mm. In the lat‐ ter case viable myocardium was thinner than 3,5mm in all the segments. Figure 4 shows an example of a typical MR image in a patient with a previous acute myocardial infarction and affected lateral LV wall.

> In the segments 10,11, 12 the uptake of contrast with the index of transmurality ranging from 0,20 to 0,55 is obviously seen. Later on during the electrophysiological study the activi‐ ty of proarrhythmogenic type 2 was revealed. (original data)

> Besides, the value of transmural index (TI) of paramagnetic contrast agent accumulation in myocardium differed significantly between unaffected segments with 0 degree potential lowering and segments with the 1st and 2nd degrees of potential lowering –the most arrhyth‐ mogenic degrees (Figure 4). In electrically normal myocardial segments, in particular, TI val‐ ue was 0,072 ± 0,020. In the group of segments in transient zone TI was 0,46 ± 0,046, and in the low potential zone - 0,32 ± 0,052. Finally, the most affected myocardium with TI of 0,32 ± 0,052 was found in the area of an "electrical scar" with no electrical potential.

> By the data of ROC analysis and discriminative analysis the most appropriate breaking val‐ ue allowing to differentiate segments with abnormal electrical activity became TI value of 0,27. In other words, when TI ≥ 0,27 one should consider probable arrhythmogenic activity in such a segment and pay closer attention to such areas during EPhS.

surgery we performed epicardial EPhS with overdriving stimulation of 200 impulses a mi‐ nute; VT was induced. In conditions of CP bypass and cardioplegia mammary-coronary ar‐ tery bypass grafting of the LAD artery, LV aneurysm dissection, endocardectomy of the apex, ventricular septum, anterior and lateral LV walls along RF tags were performed as well as SVR including endoventricular circular repair with a synthetic patch by the method of V.Dor. Postoperatively the patient received routine care. Postoperative period was un‐ eventful. By EChoG done in 3 weeks after the surgery one could notice better contractile car‐ diac function – LV EF grew up to 40% (B-made), LV sizes became smaller – EDVI was 70ml, ESVI – 48ml. The data of 24-hour ECG monitoring did not reveal any signs of ventricular rhythm disturbances. Postoperative mapping (Figure 5) showed significantly smaller transi‐

Diagnostics and Surgical Treatment of Left Ventricular Aneurysm with Ventricular Tachycardia

http://dx.doi.org/10.5772/54126

329

**Figure 5.** Patient T, 56 year old. EPhS with LV reconstruction of the patient after LV aneurysmectomy (LVR) : electrical scar in the area of the patch. Low-potential areas with the potential from 0,5 mV and transient zones (from 0,5 to1,5 mV) take a limited area with no possibility of re-entry and VT induction. Front view, right oblique view. (original data)

In 1956 Couch O.A. performed LV aneurysm resection in a patient with VT thus beginning

It has been more than 50 years since; nevertheless the issue of complications and approaches of surgical treatment associated with the appearance of VT in patients with remodelled LV after previous MI is still quite challenging [14]. It was at that time already when specialists were aware of the fact that LV myocardium affected by infarction was a source of fatal ven‐ tricular rhythm disorders. Initially there were offered methods of indirect surgical interven‐

The patient was discharged from the hospital in satisfactory condition.

an era of surgical treatment of ventricular rhythm disorders [13].

ent zone, lack of re-entry and VT.

**8. Discussion**

**Figure 4.** Patient K, has had an acute MI in the circulation of a left circumferential artery with a long area of subendo‐ cardial lesion of a lateral wall. Fig.4а – Т1- weighed spin-echo ECG-gated MRI study before injection of paramagnetic contrast; Fig. 4b – T1-weighted spin-echo ECG-gated MRI 15 min after injection of paramagnetics, as 2ml of 0,5M sol‐ ution per 10 kg of BW. Fig. 4c – the same as 4b, after semi-automatic bordering of subendocardial contrast uptake.
