Dr. Vincent M. Dor presented this lecture on his experience with left ventricular reconstruction (LVR) for ischemic congestive heart failure (CHF), which he has practiced since 1984 when it was first used to treat refractory ventricular tachycardia (VT). The procedure used by Dor for LVR, called endoventricular circular patch plasty (EVCPP), involves resection-exclusion of the asynergic scar that forms after myocardial infarct (MI). LV dilatation following MI is directly linked to the size of the scar, which persists in 80% of patients even after efficient coronary recanalization. Severe remodeling occurs in about 27% of patients with thrombolysis in MI (TIMI) 3 grade flow.

According to Dor, LVR can reverse post-MI severe ventricular remodeling. LV remodeling occurs when ischemic myocardium becomes dysfunctional or is replaced by fibrosis, known as asynergy, in about 20% to 25% of the LV surface area (Gorlin 1967) or 40% to 50% of the LV circumference (McKay 1986). When this occurs, the extent of shortening required of the remaining functioning heart exceeds physiological limits. There are two types of asynergy—regional akinesis (total lack of wall motion), and regional dyskinesis (paradoxical systolic expansive wall motion). Yoshida and Gould (JACC 1993) reported a 3-year mortality rate of 43% when the post-MI scar involves more than 23% of the LV.

Coronary recanalization changes the size and depth of necrosis but once infarcted, the LV wall remains scarred. Recanalization can result in improvement (TIMI 3 flow) with a limited or no scar; no improvement (TIMI 3) with no reflow, a large scar, and progressive remodeling; or impairment (TIMI 3) with extension of the necrotic area, known as myocardial reperfusion injury.

Magnetic resonance imaging (MRI) is the best tool for evaluating the asynergic scar. The anatomy, function, and viability of the LV can be determined with MRI, including the LV ejection fraction (LVEF), end-diastolic volume index (EDVI), end-systolic volume index (ESVI), and stroke volume (SV). MRI can reveal the type of asynergy, which depends on the depth of the scar. Dyskinesia occurs with a thrombosed LAD and transmural necrosis, while akinesia occurs in the recanalized LAD with a partially necrotic wall. Akinesia is the most common type of asynergy. The percentage of asynergy extension is determined using gadolinium late enhancement (GLE), which provides results comparable to the centerline method but which are more complete and visible.

The goals of LVR for ischemic failing ventricles (IFV) are to treat the lesion, resect-exclude the asynergic scar, restoring ventricular curvature, and preserve the physiologic diastolic volume. The asynergic scar is resected when possible and excluded by positioning a suture in the ventricle between the normal and scarred tissue, on the “contractility trail” outlined by the scar and/or shown by the pre-operative GLE cartography. The suture is tied on a balloon inflated at the normal diastolic volume (50-60 mL/m2 body surface area [BSA]). When tied, the suture restores the curvature of the ventricle and excludes the non-resectable area. A dacron patch is sutured on to close the defect and exclude the scar, and the ventricle is closed. Dor performed this procedure on a series of 104 patients with IFV between February 2002 and August 2006. Even patients with extensive areas of necrotic ventricle had improved LVEF, EDVI, and ESVI following LVR.

The technical keys to success of LVR by EVCPP are:

• Performing coronary revascularization (done in 97% of patients).
• Mitral regurgitation repair when needed (25% of patients).
• Endocardectomy for ventricular arrhythmias (30% of patients).
• Asynergic wall resection or exclusion.
• Keeping the diastolic volume balloon at 50-60 mL/m2/BSA.

Dor stressed that it is critical to precisely place the endoventricular patch to exclude the scar, guided by GLE cartography of the scar, and not by the geometric shape. With regard to diastolic volume balloon sizing (DVBS), it is more important to normalize the stroke volume than to restore the LV shape. Dor studied the influence of DVBS in two series of patients who underwent LVR. In a group of 245 patients who had LVR before the balloon era (1991-1996), immediate mortality was 8.1% and late mortality was 13%. In comparison, a group of 252 patients who had LVR with DVBS (1998-2003) had a 4.8% immediate mortality and 5.5% late mortality. Post-operative recurrence of remodeling occurred in 25% of the patients who did not have DVBS compared to 10% of patients who did have DVBS.

The results of these studies demonstrate that in patients with severe ventricular remodeling LVR with EVCPP:

• Restores LV wall curvature and contractility
• Improves systolic function, generally for a minimum of 15 points
• Improves diastolic function, with a decrease of almost 12 mL/m2
• Improves global cardiac performance. 

In a series of 31 consecutive patients with LVEF <30%, 26 underwent LVR alone and 5 had LVR plus mitral valve repair. After LVR, EDVI, ESVI, and left atrial volume index (LAVI) were significantly improved:

• EDVI improved from 98.4 ± 33.5 mL/m2 pre-op to 65.4 ± 19.3 mL/m2 post-op (p <0.001)
• ESVI improved from 63 ± 30 mL/m2 pre-op to 35.8 ± 14.2 mL/m2 post-op (p <0.001)
• LAVI improved from 39.8 ± 22.3 mL/m2 pre-op to 27.4 ± 14.7 mL/m2 post-op (p <0.05).

Endocardectomy decreases the occurrence of ischemic ventricular arrhythmias. Of 101 patients with spontaneous pre-op VT, only 2 of 92 (9 hospital deaths) had post-op recurrent VT. Of 137 patients with pre-op inducible VT, 13 of 128 (9  hospital deaths) had post-op recurrent VT. Mortality in patients operated on between 1997 and 2001 ranged from 6% to 8%. However, 80% of the patients remained stable and showed progressive improvement following LVR.

Follow-up of the 104 patients who had LVR between February 2002 and August 2006 showed that 80% (n=85) of the patients improved, 9 in-hospital deaths occurred, and 10 patients did not improve, with 5 late deaths. The causes of secondary failure included diastolic incompliance (related to balloon sizing), neglected mitral insufficiency, continuum in remodeling, and evolution of coronary disease. Of the 85 improved patients, LVEF was 26% ± 5 at pre-op, 40% ± 7 at one month post-op (p=0.0001 vs pre-op), and 45% ± 8 at 1 year (p=0.0001 vs one month post-op); EDVI was 125 ± 37 mL/m2 at pre-op, 83 ± 23 mL/m2 at one month post-op (p=0.0001 vs pre-op), and 81 ± 20 at one year; ESVI was 93 ±29 mL/m2 at pre-op, 51 ± 18 mL/m2 at one month post-op (p=0.0001 vs pre-op), and 46 ± 17 mL/m2 at one year (p=0.004 vs one month post-op).

The results of these studies show that post MI remodeling is progressively reversible by LVR surgery with EVCPP for the following reasons:

• EVCPP excludes the scarred wall
• Restores concentric systolic motion of the contractile wall regardless of whether the shape of the rebuilt LV is elliptical or spherical
• Maintains a normal physiological diastolic volume.

Dr. Dor stressed that LVR is not an elliptic reshaping or a volume reduction technique. He concluded that LVR of IFV is guided by the limit between scarred and contractile myocardium and that the procedure must be customized for each patient. An imposed shape and/or preformed patches should not be used for this technique.