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Effect of intracoronary contrast medium on left ventricular diastolic pressure-volume relationships
Effect of intracoronary contrast medium on left ventricular diastolic pressure-volume relationships The purpose of this study was to investigate the effect of intracoronary injection of the contrast medium sodium-meglumine diatrizoate (CM) on left ventricular (LV) diastolic pressure-volume relationships. Seven closed-chest dogs were instrumented with pressure catheters in the left ventricle and aorta, a balloon transducer to measure pericardial pressure, and an aortic flow meter to determine stroke volume. We estimated LV volume from two diameters by sonomicrometry. Six milliliters of CM was injected into the left main coronary artery. Transmural LV end-diastolic pressure increased from 3.3 +_ 1.1 to 7.2 +_ 0.9 mm Hg and LV end-diastolic volume index from 4 0 . 8 _+ 6.8 to 4 4 . 7 +_ 7.4 ml. There was only a minor increase in pericardial pressure. Stroke volume decreased by 31 _+ 7 % . There was no change in the intracavitary or transmural diastolic pressure-volume relationship, indicating unchanged LV "compliance." increased LV filling pressure by CM reflected reduced systolic function. (AM HEART J 1990:119:59.)
Nils-Einar KlCw, MD, Helge Refsum, MD, PhD, Olav H e v r ~ , MD, and Otto A. Smiseth, MD, PhD. Troms~ and Oslo, Norway The contrast media in current use for coronary arteriography produce multiple hemodynamic changes. 1-3 Initial short-term depression of myocardial function with the high-osmolality contrast medium sodiummeglumine diatrizoate (CM) is well known. Although new low-osmolality contrast media cause less myocardial depression, CM is still widely used. During coronary arteriography with CM, a decrease in left ventricular (LV) function is accompanied by an increase in intracavitary LV end-diastolic pressureJ -6 A greater increase has been demonstrated in patients with coronary artery disease than in control subjects. 7 Many explanations for the increased diastolic pressure have been proposed, such as increased myocardial stiffnesss and increased diastolic pressure as a compensatory mechanism according to the Frank-Starling mechanism. 9 The possible role of the pericardium in mediating the effect of contrast media on LV diastolic pressure has not been evaluated previously. During static equilibrium conditions, LV intracavitary pressure equals the sum of LV transmural pressure and pericardial From the Departments of Radiology and Physiology, Institute of Medical Biology, University of Tromsr and the Department of Medicine, National Hospital, Oslo. Received for publication June 20, 1989; accepted Aug. 1, 1989. Reprint requests: Nils-Einar Kl~w, Department of Radiology, National Hospital, N-0027 Oslo 1, Norway. 4/1/16537
surface pressure. An increase in intracavitary LV pressure may therefore represent an increase in LV transmural pressure, an increase in pericardial pressure, or a combination of the two. Our study was designed to determine the effect of intracoronary injection of CM on LV diastolic pressure volume relationships. The experiments were carried out in anesthetized dogs in which we recorded pericardial pressure by a balloon transducer 1~and LV dimensions by sonomicrometry. METHODS Animal p r e p a r a t i o n . Seven overnight-fasted mongrel dogs of both sexes, weighing 15 to 29 kg, were used. Anesthesia was induced with 30 mg/kg pentobarbital intravenously followed by a continuous infusion of 3.5 mg/kg/hr.ll The dogs were placed in the right supine position, and the lungs were mechanically ventilated through a cuffed endotracheal tube with a volume-controlled respirator (Servo Ventilator 900, Siemens Elema AB, Stockholm, Sweden), Body temperature was maintained by means of a warming lamp. The heart was exposed through a left-sided thoracotomy. An electromagnetic flow meter probe was placed around the root of the aorta (Scalar Instruments, Delft, The Netherlands). LV anteroposterior and apex-to-base dimensions were measured by transmission of ultrasound (5 MHz) between two pairs of endocardially placed discoid piezoelectric crystals (diameter 3 mm) connected to an ultrasound dimension meter (Schuessler and Associates, Cardiffby the Sea, Calif.). The crystals were placed through a stab incision.12 A silicone rubber, flat, fluid-containing balloon
59
January 1990
60
Kl~tw et al.
AmericanHeartJournal
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1. Example of early effect of contrast medium on LV pressure-volume relationship. Values.before
(solid line) and 10 seconds after (dotted line) coronary arteriography. T a b l e I. Hemodynamic effect of CM: Mean values + SEM
before and 10 seconds after coronary artery injection (n = 7)
Hemodynamics
Before
After
HR (beats - min-1) SV (ml) AOP (mm Hg) LVSP (mm Hg) LV dp/dtmax (mm Hg 9 sec-1) LV dp/dtmin (mm Hg 9 sec-1) LVEDP (mm Hg) LVEDPtm (mm Hg) Ppericard (mm Hg) LVEDV (ml)
141 _+ 8 11.1 _+ 1.3 123 _+ 6 129 _+ 5 1,980 _+ 150
141 _+ 9 7.5 _+ 1.1" 92 _+ 7* 98 _+ 6* 1,250 _+ 130"
2,440 _+ 180
1,250 _+ 180"
7.1 3.3 3.8 40.8
_+ 1.8 -+ 1.1 + 1.0 _+ 6.8
12.2 _+ 1.6" 7.2 -+ 0.9* 5.0 + 1.2" 44.7 _+ 7.4*
HR, heart rate; SV, stroke volume; AOP, aortic pressure; LVSP, left ventricular systolic pressure; LV dp/dtmax/min, maximum and minimum derivatives of left ventricular pressure; LVEDP and LVEDPtm, intracavitary and transmural left ventricular end-diastolic pressure; Ppericard, pericardial pressure; LVEDV, left ventricular end-diastolic volume. *p < 0.05 vs control value.
(diameter 3 cm) was positioned on the anterolateral surface of the left ventricle. Before insertion the balloon was calibrated by a previously described procedure. 13 After the completion of the cardiac i n s t r u m e n t a t i o n the pericardium was loosely adapted. The chest was then closed leaving a pleural drain for continuous suction. H e m o d y n a m i c m e a s u r e m e n t s . LV pressure was determ i n e d by a microtip catheter (Scalar Instruments) inserted via the left carotid artery. Aortic pressure was recorded through a fluid-filled polyvinyl catheter positioned in the thoracic aorta via the left femoral artery. Aortic pressure and pericardial pressure were connected to a Statham P23 ID transducer (Spectramed Inc, Oxnard, Calif.). ECG, pressures, aortic flow, and dimensions were recorded on a Dynograph recorder (type R 411, Beckman I n s t r u m e n t s
Inc, Schiller Park, Ill.) and digitized to an on-line connected computer by means of a commercially available program (Asystant, Macmillan Software Company, New York, N.Y.). Mean values from one respiratory cycle during sinus rhythm are presented. Calculations. T r a n s m u r a l LV pressure was obtained by subtracting pericardial pressure from intracavitary LV pressure. LV end diastole was defined as the time when the third-order derivative of LV pressure was maximum. An estimated LV volume was calculated from the two internal dimensions, assuming an ellipsoid model with the formula: LV volume index = ap 2 9 la 9 pi/6, where ap is the anteroposterior and la is the apex-to-base dimension.14-16 Experimental procedure. Six milliliters of s o d i u m meglumine diatrizoate, 370 mg/ml (Renografin, Squibb Diagnostics, New Brunswick, N.J.), was injected into the left main coronary artery over 10 seconds. The animal was then allowed to recover over a period of 30 minutes. To obtain a range of cardiac volumes, saline solution was infused into the vena jugularis and terminated when the intraluminal left ventricular end-diastolic pressure (LVEDP) reached 20 m m Hg. During the infusion of saline solution, hemodynamic variables were recorded at LVEDP intervals of 3 to 5 mm Hg. Statistics. Mean values + SEM were used to express data. Two-tailed Student's t test for paired observations was used for comparison of means. RESULTS
The effect of CM on the LV pressure-volume relationship in one heart beat is shown in Fig. 1. Intracoronary injection of CM caused a decrease in stroke volume from 11.1 + 1.3 ml to a minimum value of 7.5 _+ 1.1 ml after about 10 seconds (Table I). Heart rate was unchanged. The reduction in stroke volume was accompanied by a reduction in aortic pressure and LV systolic pressure. The maximum rate of increase in LV pressure, LV dp/dtmax, was also reduced.
Volume 119 Number 1
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Fig. 2. Effect of contrast medium on LV diastolic pressure-volume relationships. Left panels, intracavitary pressure; right panels, transmural pressure; two solid curves, recordings before and after volume loading; dotted curve, recordings after injection of contrast medium.
In addition, the maximum rate of reduction in LV pressure during isovolumic relaxation, LV dp/dtmin, decreased. Mean control values of intracavitary LVEDP for the total group were 7.1 + 1.8 mm Hg. After selective left coronary arteriography, mean values increased by 5.1 + 1.2 mm Hg (Table I). LVEDP increased in
all dogs, usually at the end of or a few seconds after the completion of the CM injection. Increased intracavitary LVEDP represented mainly increased transmural LVEDP (+3.9 + 1.1) but also a slightly increased pericardial pressure (+1.2 +_ 0.3 mm Hg). Left ventricular end-diastolic volume (LVEDV) increased by 3.9 _+ 1.0 ml.
62
January 1 9 9 0 American Heart Journal
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transmural LVEDP(mmHg) Fig. 3. E•ect•fc•ntrastmedium•nstrokevolume-transmuralLVEDPrelationshipbef•re(•pencircles)
and 10 seconds after (closed circles) contrast medium was injected in each of seven experiments.
In five of the dogs transmural L V E D P was increased more than 2 mm Hg after injection of CM. Fig. 2 shows the effect of intracoronary injection of CM and intravenous infusion of saline solution on intracavitary and transmural LV diastolic pressurevolume curves in these five experiments. The pressure-volume curves after injection of CM are compared to control curves obtained during baseline and after intravenous infusion of saline solution. The diastolic portion of the pressure-volume curves after injection of CM fell close to control curves indicating unchanged intracavitary and transmural LV diastolic pressure-volume relationships. Effect of CM on transmural L V E D P varied considerably and was related to the degree of depressed systolic function. Fig. 3 shows the correlation between stroke volume and transmural L V E D P before and after injection of CM. DISCUSSION
Results of the present study show that during coronary arteriography in dogs with closed pericardium the initial increase in intracavitary LVEDP comprised both increased transmural L V E D P and increased pericardial pressure. The increase in pericardial pressure was accounted for by an increase in LVEDV. There was no change in the intracavitary or transmural LV diastolic pressure-volume relationship, indicating that neither apparent LV compliance nor myocardial compliance per se was affected by CM. After injection of C M there was a marked decrease in stroke volume at increased end-diastolic volume, suggesting a substantial depression of myocardial contractile function. Results of previous studies in humans and animal
models have shown that intracavitary LVEDP is increased during injection of sodium-meglumine diatrizoate into the coronary artery. 47 However, little attention has been paid to the change in transmural filling pressure, which is intracavitary pressure minus pericardial pressure. This is because determination of transmural filling pressure in the heart has been complicated by difficulty in measuring pericardial pressure. It has been shown that pericardial constraint can accurately be measured by a flat, fluidcontaining balloon. 13 In the present study such a balloon transducer was used to measure pericardial pressure. The increase in pericardial pressure with the injection of CM was rather modest in the present study. This is probably related to the fact that baseline filling pressures were close to normal and hence pericardial pressure was changing along the shallow part of the pericardial pressure-volume curve.17 However, in the diseased and dilated heart, when operating on the steep part of the pericardial pressurevolume curve, is we would expect a more marked increase in pericardial pressure for a given increase in cardiac volume. To explain the mechanism of a possible shift in the LV diastolic pressure-volume curve by CM, we established a control LV diastolic pressure-volume relationship by volume loading the animals. After intracoronary injection of CM, intracavitary LVEDP and LVEDV increased significantly, but LV end-diastolic pressure-volume points did not deviate from the control curve. This implies that CM did not affect apparent LV compliance. To determine the effect on myocardial compliance as such, the transmural pressure-volume curves before and after in-
Volume 119
Number
Contrast medium and diastolic function
1
jection of CM were compared. The transmural pressure-volume relationship was unchanged after injection of CM indicating that myocardial compliance was also unchanged. It is important to note, however, that the present study was performed in nonischemic hearts. In the presence of coronary artery disease it is theoretically possible that CM might aggravate myocardial ischemia and thereby affect myocardial compliance. Increases in LVEDP and LVEDV after injection of CM were probably a consequence of a decrease in myocardial contractility. 19,2~ The increased preload would tend to compensate for the decrease in systolic function after injection of CM. In conclusion, in the nonischemic heart increased LVEDP after intracoronary injection of CM was mainly a reflection of increased transmural LVEDP (preload). CM caused only a small increase in pericardial pressure. The LV diastolic pressure-volume relationship was unaffected by CM, indicating no change in LV compliance. The skilled technical assistance of Knut Steinnes is gratefully acknowledged. REFERENCES
1. Higgins CB, Sovak M, Schmidt WS, Kelley MJ, Newell JD. Direct myocardial effects of intracoronary administration of new contrast materials with low osmolality. Invest Radiol 1980;15:39-46. 2. Deutsch AL, Gerber KH, Haigler FH, Higgins CB. Effects of low osmolality contrast materials on coronary hemodynamics, myocardial function, and coronary sinus osmolality in normal and ischemic states. Invest Radiol 1982;17:284-91. 3. Gerber KH, Higgins CB, Yuh YS, Koziol JA. Regional myocardial hemodynamic and metabolic effects of ionic and nonionic contrast media in normal and ischemic states. Circulation 1982;65:1307-14. 4. Kavanagh-Gray D. Left ventricular end-diastolic pressures following selective coronary arteriography. AM HEART J 1972;84:629-33. 5. Higgins CB, Schmidt W. Direct and reflex myocardial effects of intracoronary administered contrast materials in the anesthetized and conscious dog: comparison of standard and newer contrast materials. Invest Radiol 1978;13:205-16. 6. Hirshfeld JW, Laskey W, Martin JL, Groh WC, Untereker W,
7. 8. 9. 10.
11.
12.
13. 14.
15.
16. 17.
18. 19. 20.
63
Wolf GK. Hemodynamic changes induced by cardiac angiography with ioxaglate: comparison with diatrizoate. J Am Coll Cardiol 1983;2:954-7. Gensini GG, Dubiel J, Huntington PP, Kelley AE. Left ventricular end-diastolic pressure before and after coronary arteriography. Am J Cardiol 1971;27:453-9. Palik I, Szente A, KSszfighy GA, Koltai MZ, Kiss V, Pog~tsa G. Direct cardiac effects of an ionic and a non-ionic contrast medium in dogs. Eur J Radiol 1986;6:296-300. Newell JD, Schmidt W, Higgins CB. Effects of intracoronary administration of contrast materials on left ventricular dimensions and rate of relaxation. Invest Radiol 1979;14:233-8. Smiseth OA, Kingma I, Refsum H, Smith ER, Tyberg JV. The pericardial hypothesis: a mechanism of acute shifts of the left ventricular diastolic pressure-volume relation. Clin Physiol 1985;5:403-15. Hotvedt R, Platou ES, Koppang ER, Refsum H. Pentobarbital plasma concentrations and cardiac electrophysiology during prolonged pentobarbital infusion anaesthesia in the dog. Acta Anaesth Scand 1982;26:638-42. Goto Y, Yamamoto J, Saito M, Haze K, Sumiyoshi T, Fukami K, Hiramori K. Effects of right ventricular ischemia on left ventricular geometry and the end-diastolic pressure-volume relationship in the dog. Circulation 1985;72:1104-14. Smiseth OA, Frais MA, Kingma I, Smith ER, Tyberg JV. Assessment of pericardial constraint in dogs. Circulation 1985; 71:158-64. Rankin JS, McHale PA, Arentzen CE, Ling D, Greenfield JC, Anderson RW. The three-dimensional dynamic geometry of the left ventricle in the conscious dog. Circ Res 1976;39:30413. Mirsky I, Tajimi T, Peterson KL. The development of the entire end-systolic pressure-volume and ejection fraction-afterload relations: a new concept of systolic myocardial stiffness. Circulation 1987;76:343-56. Dodge HT, Sandler H, Baxley WA, Hawley RR. Usefulness and limitations of radiographic methods for determining left ventricular volume. Am J Cardiol 1966;18:10-24. Refsum H, Jtinemann M, Lipton MJ, SkiSldebrand C, Carlsson E, Tyberg JV. Ventricular diastolic pressure-volume relations and the pericardium. Effects of changes in blood volume and pericardial effusion in dogs. Circulation 1981;64:997-1004. Lee M-C, Fung YC, Shabetai R, LeWinther MM. Biaxial mechanical properties of human pericardium and canine comparisons. Am J Physiol 1987;253:H75-82. Boettcher DH, Vatner SF, Hayndrickx GR, Braunwald E. Extent of utilization of the Frank-Starling mechanism in conscious dogs. Am J Physiol 1978;234:H338-45. Ross Jr J. Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function. Prog Cardiovasc Dis 1976;18:255-64.
Nils-Einar KlCw, MD, Helge Refsum, MD, PhD, Olav H e v r ~ , MD, and Otto A. Smiseth, MD, PhD. Troms~ and Oslo, Norway The contrast media in current use for coronary arteriography produce multiple hemodynamic changes. 1-3 Initial short-term depression of myocardial function with the high-osmolality contrast medium sodiummeglumine diatrizoate (CM) is well known. Although new low-osmolality contrast media cause less myocardial depression, CM is still widely used. During coronary arteriography with CM, a decrease in left ventricular (LV) function is accompanied by an increase in intracavitary LV end-diastolic pressureJ -6 A greater increase has been demonstrated in patients with coronary artery disease than in control subjects. 7 Many explanations for the increased diastolic pressure have been proposed, such as increased myocardial stiffnesss and increased diastolic pressure as a compensatory mechanism according to the Frank-Starling mechanism. 9 The possible role of the pericardium in mediating the effect of contrast media on LV diastolic pressure has not been evaluated previously. During static equilibrium conditions, LV intracavitary pressure equals the sum of LV transmural pressure and pericardial From the Departments of Radiology and Physiology, Institute of Medical Biology, University of Tromsr and the Department of Medicine, National Hospital, Oslo. Received for publication June 20, 1989; accepted Aug. 1, 1989. Reprint requests: Nils-Einar Kl~w, Department of Radiology, National Hospital, N-0027 Oslo 1, Norway. 4/1/16537
surface pressure. An increase in intracavitary LV pressure may therefore represent an increase in LV transmural pressure, an increase in pericardial pressure, or a combination of the two. Our study was designed to determine the effect of intracoronary injection of CM on LV diastolic pressure volume relationships. The experiments were carried out in anesthetized dogs in which we recorded pericardial pressure by a balloon transducer 1~and LV dimensions by sonomicrometry. METHODS Animal p r e p a r a t i o n . Seven overnight-fasted mongrel dogs of both sexes, weighing 15 to 29 kg, were used. Anesthesia was induced with 30 mg/kg pentobarbital intravenously followed by a continuous infusion of 3.5 mg/kg/hr.ll The dogs were placed in the right supine position, and the lungs were mechanically ventilated through a cuffed endotracheal tube with a volume-controlled respirator (Servo Ventilator 900, Siemens Elema AB, Stockholm, Sweden), Body temperature was maintained by means of a warming lamp. The heart was exposed through a left-sided thoracotomy. An electromagnetic flow meter probe was placed around the root of the aorta (Scalar Instruments, Delft, The Netherlands). LV anteroposterior and apex-to-base dimensions were measured by transmission of ultrasound (5 MHz) between two pairs of endocardially placed discoid piezoelectric crystals (diameter 3 mm) connected to an ultrasound dimension meter (Schuessler and Associates, Cardiffby the Sea, Calif.). The crystals were placed through a stab incision.12 A silicone rubber, flat, fluid-containing balloon
59
January 1990
60
Kl~tw et al.
AmericanHeartJournal
dog #1
150 ~D
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~
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LV volume (ml) Fig.
1. Example of early effect of contrast medium on LV pressure-volume relationship. Values.before
(solid line) and 10 seconds after (dotted line) coronary arteriography. T a b l e I. Hemodynamic effect of CM: Mean values + SEM
before and 10 seconds after coronary artery injection (n = 7)
Hemodynamics
Before
After
HR (beats - min-1) SV (ml) AOP (mm Hg) LVSP (mm Hg) LV dp/dtmax (mm Hg 9 sec-1) LV dp/dtmin (mm Hg 9 sec-1) LVEDP (mm Hg) LVEDPtm (mm Hg) Ppericard (mm Hg) LVEDV (ml)
141 _+ 8 11.1 _+ 1.3 123 _+ 6 129 _+ 5 1,980 _+ 150
141 _+ 9 7.5 _+ 1.1" 92 _+ 7* 98 _+ 6* 1,250 _+ 130"
2,440 _+ 180
1,250 _+ 180"
7.1 3.3 3.8 40.8
_+ 1.8 -+ 1.1 + 1.0 _+ 6.8
12.2 _+ 1.6" 7.2 -+ 0.9* 5.0 + 1.2" 44.7 _+ 7.4*
HR, heart rate; SV, stroke volume; AOP, aortic pressure; LVSP, left ventricular systolic pressure; LV dp/dtmax/min, maximum and minimum derivatives of left ventricular pressure; LVEDP and LVEDPtm, intracavitary and transmural left ventricular end-diastolic pressure; Ppericard, pericardial pressure; LVEDV, left ventricular end-diastolic volume. *p < 0.05 vs control value.
(diameter 3 cm) was positioned on the anterolateral surface of the left ventricle. Before insertion the balloon was calibrated by a previously described procedure. 13 After the completion of the cardiac i n s t r u m e n t a t i o n the pericardium was loosely adapted. The chest was then closed leaving a pleural drain for continuous suction. H e m o d y n a m i c m e a s u r e m e n t s . LV pressure was determ i n e d by a microtip catheter (Scalar Instruments) inserted via the left carotid artery. Aortic pressure was recorded through a fluid-filled polyvinyl catheter positioned in the thoracic aorta via the left femoral artery. Aortic pressure and pericardial pressure were connected to a Statham P23 ID transducer (Spectramed Inc, Oxnard, Calif.). ECG, pressures, aortic flow, and dimensions were recorded on a Dynograph recorder (type R 411, Beckman I n s t r u m e n t s
Inc, Schiller Park, Ill.) and digitized to an on-line connected computer by means of a commercially available program (Asystant, Macmillan Software Company, New York, N.Y.). Mean values from one respiratory cycle during sinus rhythm are presented. Calculations. T r a n s m u r a l LV pressure was obtained by subtracting pericardial pressure from intracavitary LV pressure. LV end diastole was defined as the time when the third-order derivative of LV pressure was maximum. An estimated LV volume was calculated from the two internal dimensions, assuming an ellipsoid model with the formula: LV volume index = ap 2 9 la 9 pi/6, where ap is the anteroposterior and la is the apex-to-base dimension.14-16 Experimental procedure. Six milliliters of s o d i u m meglumine diatrizoate, 370 mg/ml (Renografin, Squibb Diagnostics, New Brunswick, N.J.), was injected into the left main coronary artery over 10 seconds. The animal was then allowed to recover over a period of 30 minutes. To obtain a range of cardiac volumes, saline solution was infused into the vena jugularis and terminated when the intraluminal left ventricular end-diastolic pressure (LVEDP) reached 20 m m Hg. During the infusion of saline solution, hemodynamic variables were recorded at LVEDP intervals of 3 to 5 mm Hg. Statistics. Mean values + SEM were used to express data. Two-tailed Student's t test for paired observations was used for comparison of means. RESULTS
The effect of CM on the LV pressure-volume relationship in one heart beat is shown in Fig. 1. Intracoronary injection of CM caused a decrease in stroke volume from 11.1 + 1.3 ml to a minimum value of 7.5 _+ 1.1 ml after about 10 seconds (Table I). Heart rate was unchanged. The reduction in stroke volume was accompanied by a reduction in aortic pressure and LV systolic pressure. The maximum rate of increase in LV pressure, LV dp/dtmax, was also reduced.
Volume 119 Number 1
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Fig. 2. Effect of contrast medium on LV diastolic pressure-volume relationships. Left panels, intracavitary pressure; right panels, transmural pressure; two solid curves, recordings before and after volume loading; dotted curve, recordings after injection of contrast medium.
In addition, the maximum rate of reduction in LV pressure during isovolumic relaxation, LV dp/dtmin, decreased. Mean control values of intracavitary LVEDP for the total group were 7.1 + 1.8 mm Hg. After selective left coronary arteriography, mean values increased by 5.1 + 1.2 mm Hg (Table I). LVEDP increased in
all dogs, usually at the end of or a few seconds after the completion of the CM injection. Increased intracavitary LVEDP represented mainly increased transmural LVEDP (+3.9 + 1.1) but also a slightly increased pericardial pressure (+1.2 +_ 0.3 mm Hg). Left ventricular end-diastolic volume (LVEDV) increased by 3.9 _+ 1.0 ml.
62
January 1 9 9 0 American Heart Journal
""-l~lCw et al.
o
15
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transmural LVEDP(mmHg) Fig. 3. E•ect•fc•ntrastmedium•nstrokevolume-transmuralLVEDPrelationshipbef•re(•pencircles)
and 10 seconds after (closed circles) contrast medium was injected in each of seven experiments.
In five of the dogs transmural L V E D P was increased more than 2 mm Hg after injection of CM. Fig. 2 shows the effect of intracoronary injection of CM and intravenous infusion of saline solution on intracavitary and transmural LV diastolic pressurevolume curves in these five experiments. The pressure-volume curves after injection of CM are compared to control curves obtained during baseline and after intravenous infusion of saline solution. The diastolic portion of the pressure-volume curves after injection of CM fell close to control curves indicating unchanged intracavitary and transmural LV diastolic pressure-volume relationships. Effect of CM on transmural L V E D P varied considerably and was related to the degree of depressed systolic function. Fig. 3 shows the correlation between stroke volume and transmural L V E D P before and after injection of CM. DISCUSSION
Results of the present study show that during coronary arteriography in dogs with closed pericardium the initial increase in intracavitary LVEDP comprised both increased transmural L V E D P and increased pericardial pressure. The increase in pericardial pressure was accounted for by an increase in LVEDV. There was no change in the intracavitary or transmural LV diastolic pressure-volume relationship, indicating that neither apparent LV compliance nor myocardial compliance per se was affected by CM. After injection of C M there was a marked decrease in stroke volume at increased end-diastolic volume, suggesting a substantial depression of myocardial contractile function. Results of previous studies in humans and animal
models have shown that intracavitary LVEDP is increased during injection of sodium-meglumine diatrizoate into the coronary artery. 47 However, little attention has been paid to the change in transmural filling pressure, which is intracavitary pressure minus pericardial pressure. This is because determination of transmural filling pressure in the heart has been complicated by difficulty in measuring pericardial pressure. It has been shown that pericardial constraint can accurately be measured by a flat, fluidcontaining balloon. 13 In the present study such a balloon transducer was used to measure pericardial pressure. The increase in pericardial pressure with the injection of CM was rather modest in the present study. This is probably related to the fact that baseline filling pressures were close to normal and hence pericardial pressure was changing along the shallow part of the pericardial pressure-volume curve.17 However, in the diseased and dilated heart, when operating on the steep part of the pericardial pressurevolume curve, is we would expect a more marked increase in pericardial pressure for a given increase in cardiac volume. To explain the mechanism of a possible shift in the LV diastolic pressure-volume curve by CM, we established a control LV diastolic pressure-volume relationship by volume loading the animals. After intracoronary injection of CM, intracavitary LVEDP and LVEDV increased significantly, but LV end-diastolic pressure-volume points did not deviate from the control curve. This implies that CM did not affect apparent LV compliance. To determine the effect on myocardial compliance as such, the transmural pressure-volume curves before and after in-
Volume 119
Number
Contrast medium and diastolic function
1
jection of CM were compared. The transmural pressure-volume relationship was unchanged after injection of CM indicating that myocardial compliance was also unchanged. It is important to note, however, that the present study was performed in nonischemic hearts. In the presence of coronary artery disease it is theoretically possible that CM might aggravate myocardial ischemia and thereby affect myocardial compliance. Increases in LVEDP and LVEDV after injection of CM were probably a consequence of a decrease in myocardial contractility. 19,2~ The increased preload would tend to compensate for the decrease in systolic function after injection of CM. In conclusion, in the nonischemic heart increased LVEDP after intracoronary injection of CM was mainly a reflection of increased transmural LVEDP (preload). CM caused only a small increase in pericardial pressure. The LV diastolic pressure-volume relationship was unaffected by CM, indicating no change in LV compliance. The skilled technical assistance of Knut Steinnes is gratefully acknowledged. REFERENCES
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