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Transcript of Updated results in surgical treatment of recurrent ventricular tachycardia oriented by ventricular...
ABSTRACTS
UPDATED RESULTS IN SURGICAL TREATMENT OF RECURRENT VENTRICULAR TACHYCARDIA ORIENTED BY VENTRICULAR ACTIVATION MAPPING IN 8 PATIENTS WITHOUT CORONARY ARTERY DISEASE.
Robert FRANK, MD, GBrard GUIRAUDON, MD, Guy FONTAINE, MD, Yves GROSGOGEAT, MD, Christian CABROL, MD, Jean FACQUET, MD Hapital de la Salpstrisre Paris France.
Eight patients with refractory ventricular tachy- cardia (VT) and normal coronarography were studied in sinus rhythm and VT I) by endocardial recording and programmed ventricular pacing, 2) by epicardial activa- tion mapping (AM) and in two cases, by plunge electrode technique.
In five cases, VT could be triggered at will and definitely stopped by one, a pair or a burst of stimuli. During AM, localized delayed potentials were constantly found in sinus rhythm and VT. In each case, transmural ventriculotomy was performed at the epicentrum of VT. No VT recurred since, with a background of 24 months for the earliest patient. Macro-reentry was infered as the underlying mechanism.
In the three remaining cases, VT could not be trig- gered nor definitely stopped. During AM no delayed poten- tial was found neither in sinus rhythm nor in VT. In two cases plunge electrode found prepotentials occcuring before QRS complexes. Ventriculotomy at the origin of VT was ineffective, even in one case with myocardial resec- tion (apex). The mechanism was thought to be Ectopic Focus (or focal reentry).
Surgical treatment of "Reentrant VT" seems reliable, "Focal VT" needs still more evaluation for surgical treatment.
INTRAOPERATIVE MYOCARDIAL ISCHEMIA DURING BYPASS SUR- GERY: ITS DEMONSTRATION BY EPICARDIAL MAPPING AND REVERSAL USING A SHUNT TECHNIQUE
Andrew J. Franzone, MD; Simon H. Stertzer, MD, FACC: Eugene Wallsh, MD, FACC
Ten patients with severe proximal left anterior des- cending (LAD) coronary disease underwent bypass grafting. Immediately following incision of the LAD, a plastic tubular shunt was placed intraluminally, both maintain- ing coronary flow and providing local hemostasis during
graft construction.
Epicardial &G's mapped out from the anterolateral left ventricle showed immediate striking injury patterns
following interruption of flow without the shunt in place. These ST-T changes were not noted in the stand- ard surface ECG leads. This change was completely and reproducibly reversed using the intraluminal shunt.
Analysis of discharge ECG's showed no new Q waves in this group of patients.
This study describes the use of a simple intracoronary
shunt which maintains coronary perfusion and prevents the marked injury current ECG changes demonstrated by epicardial mapping during coronary revascularization.
POST OPERATIVE CATHETERIZATION AFTER REPAIR OF VENTRICULAR SEPTAL DEFECTS AND TETPALOGY OF FALLOT IN INFANTS USING DEEP HYPOTHERMIA Michael D. Freed, MD; John F. Keane, MD; Alexander S. Nadas, MD; Aldo R. Castaneda, MD; Children's Hospital Medical Center, Boston, Ma.
Between l/73 and b/74, 35 infants with large ventricular septal defects (VSD) and pulmonary hyperwnsion (21) or tetralogy of Fall& (14) were repaired utilizing deep hypothermia and circulatory arrest (DH). Operative mortality was 14% (3/21) for VSD repair (all deaths in infants weighingL2.5 kq.), and 7% (l/14) for tetralogy of Fallot. Fifty percent (g/18) of the operative sur- vivors of VSD repair and 77% (10/13) of the operative survivors of TOF repair were recatheterized approximately one year after surgery. Among the 9 patients (pts) restudied after VSD closure,
only one has a residual VSD CQp/Qs 1.4). Pulmonary artery pressure, pulmonary vascular resistance and left ventricular function was normal in all. One child had developed subaortic stenosis. None of the 10 pts recatheterized after repair of TOF
utilizing DH had a residual VSD. Residual pulmonary sten- osis (gradient>40 mm. Hg.) was present in 3/10, (30%). Successful reoperation has been performed in the two with the highest gradients. This compares favorably with 76 children operated upon for TOF using normothermic cardio- pulmonary bypass during the same time span. Among 40 children recatheterized in this latter group, 25% (10/40) had significant residual VSD and 23% (q/40) had residual pulmonary stenosis. We conclude that postoperative catheterization data sug-
gests that children operated upon using DH have no greater risk, and better hemodynamic results, than those operated upon usinq normothermic cardiopulmonary bypass.
MYOCARDIAL LACTATE METABOLISM AND CORONARY VENOUS
PHOSPHATE IN CYANOTIC CONGENITAL HEART DISEASE
Beat Friedli, MD ; Pierre Moret, MD ; Lionel Opie, MD,
FACC, HBpital Cantonal, Geneva, Switzerland.
Coronary arterio-venous differences of Lactate (L), inor-
ganic Phosphate (Pi) and Potassium (K) concentration were
measured at rest and after 5 and 10 mm. atria1 pacing
(AP), in 14 patients (pts) with cyanotic congenital heart
disease (CCHD) and seven control pts (no significantheart
disease). Pts ages ranged from 5 to 15 years.
Myocardlal L extraction ratio at rest in pts with CCHD
averaged 29 k 2.0% and was not different from controls
(27 + 4.6%). During AP (150 - 180 min.), L extraction in
controls decreased slightly to 16 ? 4.4'6, (p < 0.05).
Cyanotic pts fell into 2 groups (grp) : nine pts (grp I)
showed a drop in arterial 02 saturation (SaO2) with AP,
from 76 ? 2.5% to 55 f 5.0% ; their L extraction fell
sharply to 3 ? 6.0% (p < 0.001) and L production occured
1.n 5. Five cyanotic pts (grp II) showed no fall in SaO2
with AP, and L extraction remained stable (27 ?- 2.1%). Pi
extraction was noted in all pts at rest (controls : 2.8 ? 0.77 mg/L, CCHD grp I : 3.9 + 1.15 mg/L, grp II : 4.6 i 0.83 mg/L); this dxappeared with AP in controls and
cyanotics grp I, but not in grp II. NO K changes were seen
in any pts. It is concluded that, while myocardlal L meta-
bolism is normal at rest in CCHD, the stress of APinduces
ischemic changes when accompanied by a drop in Sa02 ; cyanotic pts without change in Sa02 during AP seem tohave
less metabolic changes than normals.
136 January 1976 The American Journal of CARDIOLOGY Volume 37