Contractile function and reserve during acute ischaemia in the canine lateral border zone.

The hypothesis that there is a lateral border zone with function intermediate to adjacent ischaemic and non-ischaemic tissue was tested in 10 open chest anaesthetised dogs. Four pairs of segment length crystals were placed in parallel so as to span the ischaemic and non-ischaemic zones. Graded occlusion was produced with a screw clamp applied to a carotid to left anterior descending artery cannulation system. Contractile reserve was assessed using postextrasystolic potentiation. A balloon perfusion labelling system was used to label negatively the potentially ischaemic zone and quantify the admixture of ischaemic and non-ischaemic tissue in the lateral border zone, defined by the fraction of normal zone tissue. When the 40 crystal pairs from the 10 dogs were grouped according to fraction of normal zone tissue (FNZT), 13 were in the central ischaemic zone (FNZT less than 0.1), seven were in the border ischaemic zone (FNZT 0.1-0.5), five were in the border non-ischaemic zone (FNZT 0.5-1.0), and 15 were in the non-ischaemic zone (FNZT 1.0). When the lateral border zone is predominantly non-ischaemic tissue, the tissue behaves as though it is non-ischaemic. Segmental shortening before and after postextrasystolic potentiation in the border non-ischaemic zone and non-ischaemic zone did not change with ischaemia. When tissue in the lateral border zone is predominantly ischaemic, it behaves as though it is ischaemic. Segmental shortening decreased in parallel with progressive ischaemia in the border ischaemic zone and ischaemic zone. At total occlusion, segmental shortening in the border ischaemic zone was -2.3(5.9%) and in the ischaemic zone -3.5(3.6)% (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Relation between left ventricular global and regional function and extent of myocardial ischemia in the canine heart.

To develop a quantitative relation between the overall severity of acute ischemia and left ventricular global and regional function, two minor axis internal diameters and myocardial wall thickness were determined using ultrasonic crystals in 10 open chest dogs with carotid-left anterior descending artery cannulation. The overall extent of ischemia produced by graded stenosis of the cannulation system was estimated by total myocardial blood flow deficit, calculated using radioactive microspheres and a balloon-reservoir perfusion technique permitting precise separation of ischemic from nonischemic tissue. Although cardiac output and left ventricular stroke work were maintained through chamber enlargement until total myocardial blood flow deficit was about 10%, ejection indexes of left ventricular function decreased progressively with increasing ischemia and correlated inversely with total myocardial blood flow deficit (r = -0.55 to -0.73). Ejection indexes of left ventricular global function correlated directly with regional function in the ischemic zone (r = 0.67 to 0.83), although global function decreased at a far slower rate than regional contraction during progressive coronary stenosis with an ischemic region comprising about 25% of total left ventricular weight. During myocardial ischemia, regional dysfunction resulted in progressive global contractile dysfunction; left ventricular hemodynamic status was maintained until ischemia was severe.

Sinus rhythm mapping in healed experimental myocardial infarction: contrasting activation patterns for inducing ventricular tachycardia versus fibrillation.

The inducibility of ventricular tachycardia (VT) and fibrillation (VF) is variable in healed myocardial infarction (MI) in the dog. To better understand the electrophysiologic basis for these arrhythmias, MI was produced in dogs by ligating the left anterior descending artery. One week later, epicardial mapping was performed with the dog in sinus rhythm using a hand-held bipolar electrode. Transmural mapping was performed with the dog in sinus rhythm with 4 pairs of bipolar electrodes mounted on a #14 needle. Ventricular arrhythmias were induced by the S1S2S3 technique or 3- to 5-beat burst pacing at twice diastolic threshold. Only VF could be induced in 11 dogs, while sustained VT was induced in 6 dogs. Significantly more marked and more extensive delay in activation was seen both in the epicardium and transmurally in dogs with VT than in dogs with VF. In addition, dogs with VT had morphologic evidence of a large transmural MI, whereas dogs with VF had only a subendocardial MI. It is concluded that inducible sustained VT in the dog is usually associated with a large transmural MI and an activation sequence in sinus rhythm characterized by an extensive area of marked delay in activation. This activation pattern in sinus rhythm presumably is necessary to provide the underlying electrophysiologic milieu for sustained reentry.

Epicardial, endocardial and transmural mapping in assessing electrophysiological effects of 14-C lidocaine and 14-C propafenone on activation times in experimental chronic myocardial infarction. Correlations with myocardial drugs concentrations.

The electrophysiological effects of lidocaine (L) and propafenone (P) in chronic myocardial infarction in relation to tissue drug concentrations (TDC) are unknown. Thus of 16 dogs with one week old myocardial infarction, 8 received propafenone 2 mg/kg and 8 lidocaine 5 mg/kg followed by 0.2 mg/kg/min of either drug for 60 min. Epicardial (EPI) mapping (greater than 30 points) was performed with a bipolar electrode. Endocardial (ENDO) and transmural (TRANS) mapping (greater than 20 points) were performed with 4 pairs of needle mounted bipolar electrodes. The % change in activation times (% delta AT) in EPI, ENDO and TRANS was evaluated in normal (N) and infarcted (I) zones at control and 60 min after drugs. Ventricular arrhythmias (VA) were studied with programmed extra stimulation. Results (P less than 0.01 to L, P less than 0.01 to N zone, # P less than 0.05 to ENDO): (Table: see text) At 60' ventricular tachycardia and ventricular fibrillation were both still inducible in 50% in the lidocaine group (37% in control), while only in 16% in the propafenone group (62% in control). Despite lower drug concentrations in the infarct, the effects on AT are comparable to normal zones for both drugs. In conclusion lidocaine reduces and propafenone increases AT, affecting in opposite directions the inducibility of reentrant ventricular arrhythmias.

Evaluation of "ischemia at a distance": effects of coronary occlusion on a remote area of left ventricle.

The effect of coronary occlusion on blood flow and function in a remote zone of the left ventricle was studied in 21 open-chest dogs. Group A consisted of 6 dogs not undergoing left circumflex (LC) coronary artery cannulation. The other 15 dogs underwent cannulation of the LC artery followed by partial occlusion to 40 mm Hg diastolic perfusion pressure. Of these dogs, 7 with constant perfusion pressure (group B) were separately evaluated from 8 with declining perfusion pressure (group C). Sequentially more proximal left anterior descending (LAD) occlusions were performed in each group. Blood flow in the LC zone remained unchanged in group A after sequential LAD occlusions, whereas in groups B and C distal and proximal LAD occlusions caused progressive reduction in LC flow. Although in group A segment shortening improved in the LC zone after distal LAD occlusion, in groups B and C progressive impairment in segmental shortening was observed in the LC zone after distal and proximal LAD occlusions. Thus, in the setting of critical coronary stenosis in a zone, total occlusion in another coronary artery can initiate a series of events leading to decreased blood flow in the territory of the stenotic coronary artery, resulting in ischemia and impaired segmental function.