Five dogs were instrumented with a left ventricular (LV) micromanometer, pairs of ultrasonic crystals to measure L V short axis and L V wall thickness and an inflatable cuff around the ascending aorta. Wall stress, midwall strain and strain rate were calculated at rest, after acute pressure elevation, and one, two and three weeks as well as 24 h after release of aortic constriction. Myocardial wall stiffness and viscosity were determined from a viscoelastic stress-strain model. Reference values at zero pressure were determined in all five dogs. LV end-diastolic pressure increased from 7 mm Hg at rest to 25 mm Hg after acute pressure elevation, to 18 mm Hg after two weeks and decreased to 16 mm Hg after three weeks of pressure elevation, and 11 mm Hg at release of aortic constriction. L V peak systolic pressure increased from 140 mm Hg at rest to 218 mm Hg after acute pressure elevation, to 227 mm Hg after three weeks of pressure elevation and returned to normal (143 mm Hg) after cuff release. Diastolic myocardial wall stiffness showed no change from 23 at rest to 19 after acute pressure elevation, but increased to 47 after one and 81 after two weeks, and it decreased to 50 after three weeks and 45 after cuff release. Myocardial viscosity increased from 0.1 at rest to 3.0 after acute pressure elevation and remained elevated during chronic pressure elevation. The reference values at zero filling pressure showed an increase in LV short axis (creep) from 25.6 mm at rest to a maximum of 28.9 mm after one and two weeks of pressure elevation and then decreased to 27.0 mm after three weeks. LV wall thickness at zero pressure increased from 12.8 mm at rest to 13.7 mm after three weeks of pressure elevation and remained elevated after cuff release (13.8 mm). Thus, diastolic myocardial wall stiffness increased during the initial stages of chronic pressure overload during ventricular dilatation, but decreased when dilatation regressed and concentric hypertrophy developed. Myocardial viscosity was increased during both acute and chronic pressure overload. It is suggested that the early increase in myocardial stiffness may be more importantly related to ventricular dilatation with creep than to wall hypertrophy per se.
A conscious animal model was developed in which coronary stenosis could be produced while regional myocardial function and local surface electrocardiograms were measured. Responses to isoprenaline stress in the presence of mild (latent) coronary stenosis were then examined. In the absence of coronary stenosis, isoprenaline produced increases in regional function and no change in the surface VCG; at higher doses, increases in the endocardial ST segments occurred. After partial coronary stenosis, which produced no apparent regional dysfunction or electrocardiographic changes, isoprenaline infusion for 3 min (0.02 microgram . kg-1 . min-1) rapidly produced decreases in percentage wall thickening (average 17 +/- 4%, mean +/- SE, P < 0.01) and increases in the mean sum of VCG ST segments by 0.23 +/- 0.06 mV (P < 0.05). 1 min after stopping isoprenaline, most dogs showed further significant deterioration of both measures of ischaemia, but by 5 min there was no significant mean change from control. We conclude that in the presence of latent partial coronary stenosis, stress due to mild sympathomimetic stimulation alone can rapidly induce regional myocardial ischaemia. Deterioration of regional myocardial contractile function during such stress can provide as sensitive means of detecting latent coronary obstruction.
Sonomicrometry was used in 10 conscious dogs to measure regional segment length and dynamic wall thickness by telemetry in a zone supplied by the left circumflex coronary artery after implantation of an ameroid constrictor. When coronary obstruction was nearly complete and collaterals had developed (24-42 days), control exercise and exercise runs after oral isosorbide dinitrate were carried out. During control runs, significant increases occurred in hemodynamic parameters, and percent shortening in normal segments increased (P < 0.01). During the repeat runs after isosorbide dinitrate, there were smaller increases in left ventricular systolic and end-diastolic pressures and significantly reduced end-diastolic dimensions. In addition, percent wall thickening and percent segment shortening in the ischemic zone did not deteriorate significantly during exercise. In this animal model, which appears to mimic chronic single-vessel coronary heart disease, isosorbide dinitrate can prevent exercise-induced deterioration of regional myocardial function.
We developed a new ultrasonic triangulation technique to measure regional wall thickness and shear motion of the left ventricular wall under normal conditions and during complete and partial coronary occlusions.In 10 open-chest dogs, a left ventricular micromanometer was inserted, and a screw-driven arterial clamp and flowmeter were placed around the left circumflex coronary artery.A single miniature ultrasonic crystal was placed in the subendocardium of the left ventricular free wall in a region to be made ischemic, and three receiving crystals were sutured to the opposing epicardium at the corners of a 45-degree right triangle.By the trigonometric combination of three measured lengths from ultrasonic dimension gauges, the exact position of the endocardial crystal in X, Y, and Z coordinates could be displayed by computer.The endocardial surface moved in a longitudinal direction relative to the epicardial surface during normal systole [0.58 ± 0.26 (mean ± SEM) mm].With coronary occlusion, this myocardial shear became less marked (0.11 ± 0.12 mm), and systolic wall thickening changed to thinning.When coronary occlusion was released, end-diastolic wall thickness and percent wall thickening rapidly increased to 104.8% and 141.7% of control, respectively, concurrent with the reactive hyperemia.With partial coronary constriction, these postreperfusion changes were markedly reduced, suggesting a role for reactive hyperemia in postreperfusion wall thickness dynamics.These techniques allow measurement of shear and three-dimensional display of dimensions and thereby permit documentation of true wall thickness dynamics both during and after coronary occlusion.
In 10 conscious dogs, a model was developed for studying regional contractile responses in a coronary collateral-dependent bed. Regional myocardial function was compared after terminating a maximum paced rate of 240 beats/min maintained for 3 minutes (postpacing period) with that during telemetry-monitored exercise at comparable heart rates (average 252 +/- 34 beats/min, duration 2.4 minutes) at different times during collateral development. Ultrasonic dimension gauges were used to measure control and ischemic segment (CS and IS) lengths and ischemic zone regional wall thickness (IW). An ameroid constrictor and a Doppler flow probe were placed around the left circumflex coronary artery, and pacing electrodes were sutured to the right ventricle. An average of 23 days postoperatively, coronary obstruction was complete. Studies at that time showed that percent shortening (% delta L) of IS and percent wall thickening (% delta W) of IW decreased after pacing to 57% and 35% of control, respectively, and during exercise to 37% of control. One week later (average 30 days postoperatively), significant depression of regional function no longer occurred postpacing. However, exercise at a comparable heart rate still provoked regional dysfunction in the collateral-dependent zone: Both IS% delta L and IW% delta W decreased to 51% of control. Regional function at rest did not differ during these studies. Thus, the effectiveness of the postpacing response for detecting limited collateral reserve was eliminated by further collateral development, but regional myocardial dysfunction during exercise stress served to detect ischemia despite increased collateral circulation.
The objective of this research was to determine if the ultrasound emissions of the Doppler catheter can be used to locate its position in 3 dimensions by conventional echocardiography. A Doppler catheter has previously been shown to permit nonfluoroscopic retrograde catheterization of the aortic root and left ventricular chamber by using velocity waveform polarity for directional guidance. A significant difficulty in providing ultrasound catheter guidance, however, has been the inability to recognize the Doppler catheter tip, because each point at which a flexible catheter crosses the image plane can be misinterpreted as the catheter tip. Initial in vitro water bath trials were performed using the Doppler catheter attached to a standard velocimeter. Using a 5 MHz imaging transducer and color Doppler methods, the presence or absence of a banded color pattern which could demarcate the Doppler catheter tip was recorded at various angles in and out of the scanning plane. Using Doppler retrograde guidance and transesophageal echocardiography, color Doppler banded patterns, which could identify the Doppler catheter tip, were investigated in the dog aorta. In order to understand the physical mechanisms involved, a series of water bath trials were then conducted using the Doppler catheter attached to a velocimeter which was synchronized to the echo machine. Initial nonsynchronized water bath trials revealed distinct banded color patterns demarcating the Doppler catheter tip when it pointed in any direction within the beam width, except for a 40 degrees blind cone directly away from the imaging transducer.(ABSTRACT TRUNCATED AT 250 WORDS)
Relationships between regional myocardial perfusion and transmural function, both during treadmill exercise and at rest, were examined in conscious dogs with varying degrees of coronary stenosis produced by a hydraulic occluder. In 13 dogs we measured myocardial blood flow with microspheres (10-12 microns in diameter) and regional systolic wall thickening (%). During exercise with coronary stenosis, myocardial blood flow was characterized by nonuniform distribution, and associated with regional dysfunction. The relationships between normalized myocardial blood flow and normalized %wall thickening during exercise with coronary stenosis were linear, with significantly different slopes (mean myocardial blood flow: y = 1.23x - 0.16, r = 0.93; subendocardial myocardial blood flow: y = 1.50x - 0.02, r = 0.86; subepicardial myocardial blood flow: y = 0.83x - 0.18, r = 0.87). To fill the gap between available subendocardial and subepicardial data during exercise with coronary stenosis and control points, however, would require nonlinear components. In 10 of the dogs, coronary stenosis at rest was also produced to compare regional myocardial blood flow - %wall thickening relations at rest with those during steady state exercise. The absolute mean myocardial blood flow - %wall thickening relation during exercise with coronary stenosis (y = 11.6x - 1.9, r = 0.90) was significantly shifted rightward from the resting relation (y = 25.3x -2.1, r = 0.80). However, when changes in %wall thickening were plotted vs. myocardial blood flow per beat, the relationships at rest and exercise were nearly superimposable. Likewise, relations between normalized myocardial blood flow and changes in %wall thickening at rest and exercise were not significantly different. We conclude: %wall thickening during exercise is directly related to changes in mean myocardial blood flow but is related in nonlinear fashion to changes in subepicardial and subendocardial myocardial blood flow; %wall thickening may provide a reliable index of the relative transmural flow distribution during exercise as well as at rest; during brief bouts (5-8 minutes) of exercise with coronary stenosis, the relationship between stabilized regional contractile dysfunction and level of myocardial blood flow per beat is the same as that during coronary stenosis at rest.
