Abrupt homeostatic responses to transient intracardiac occlusion during balloon valvuloplasty

VALVULAR HEART MSEASE

Abrupt Homeostatic Responses to Transient Intracardiac Occlusion During Balloon Valvuloplasty Jose Su5rez de Lezo, MD, Pedro Mantilla, MD, Manuel Pan, MD, Miguel Romero, MD, Manuel Sancho, MD, Joaquin Ruiz de Castroviejo, MD, lnmaculada Tejero, MD, Jose Arizb, MD, and Jose Luis Carrasco, MD, with the technical assistance of Ana Rejano and Carlos Martinez

The present study analyzes the hemodynamics of intracardk occluske periods during balloon mitral or aortic vatvuloplasty and compares them with immedlate plasma levels of atrial natriuretic factor (ANF), v-n and renin activity. Forty-nine patients were m 33 of them had mitral stenosis and 16 had aortic stenosis. The mean age was 92 f 17 years. During dilations pressures were monitored from the ascending aorta and left atrium. Plasma levels of ANF, vasopressin and renin were serially determined at baseline, after diagnostic prombes, within 15 to 30 seconds after the fb-st 2 occlusive dilations, and 1 and 7 hours later. There were no slgniffcant changes in plasma renin throughout the study stages. ANF and vasopressin sigMcantly lnereased after the dilations. These hormonal changes were related to the signiffcant hemodynfuni changes observed during intracardiac occksmn. The left atrial pressure correlated directly and signifkntly (r = 0.54, p
From the Servicio de Cardiologfa, Hospital “Reina Soffa,” and the University of Cbrdoba, Cbrdoba, Spain. Manuscript received March 20,1989; revisedmanuscript receivedand acceptedMay 30,1989. Addressfor reprints: Jo& SuSlrezde Lezo, MD, Serviciode Cardiologfa, Hospital “Reina Soffa,” Avenida Men6ndezPidal 1, 14004C6rdoba, Spain.

he developmentof percutaneousballoon valvuloplasty for the treatment of stenotic cardiac valves has allowed observationson the adaptation of the intact heart to sudden and transient intracardiac occlusion.’ During aortic valvuloplasty, dramatic decreasesin systemic pressure coexist with significant increases in left ventricular and atria1 pressures.Changesin myocardial perfusion and metabolism have been detected during the inflation periods.* Similar findings also can be observedduring inflow ventricular occlusion at the time of mitral balloon valvuloplasty. These occlusive periods could be a potential model for further studying the physiopathologic consequencesof temporarily stopping cardiac output in the intact circulation. Such transient pressurechangescould stimulate the homeostaticreceptors involved in the immediate intravascular pressure and volume regulation. The present study investigates the possiblehormonal responsesto transient intracardiac occlusion periods at the time of mitral or aortic balloon valvuloplasty.

T

METHODS

We prospectivelystudied in 49 patients the hemodynamics and serial plasma levels of immunoreactive atrial natriuretic factor (ANF), arginine vasopressinand renin activity at the time of mitral (33 patients) or aortic (16 patients) balloon valvuloplasty. Each patient gave written informed consent. Ages ranged from 8 to 83 (mean 52 f 17); 15 patients were men and 34 women. Thirty patients were in sinus rhythm; 19 had chronic atria1 fibrillation. All patients had normal renal function at the time of the study. Twenty-sevenof them were in functional class III or IV, and 22 were in class II. Whenever possible (30 patients), all medications were withheld 24 hours before the study. We performed cardiac catheterization under mild sedation and heparin (1 mg/kg). No other medication, blood or fluid infusion was administered during the study. Patients who had blood loss or any other complication during the procedure were excluded from the study. We introduced 3 catheters percutaneously (2 arterial, 1 venous) in our aortic patients and 4 (2 arterial, 2 venous) in the mitral patients. The diagnostic procedures always included ventricular, aortic and coronary angiograms in aortic patients, and left ventricular, pulmonary trunk and cor-

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onary (for those older than 40 years) angiogramsin mitral patients. Hemodynamic data and cardiac output (dye dilution technique) were recorded at baseline and after the procedures. Balloon size selection always was basedon echocardiographic and angiographic measurements of the anulus. Mitral valvuloplasty: The procedure was always a retrograde approach as describedby Babic et al.3 A single multiballoon catheter ranging in total diameter from 30 to 38 mm (mean 36 f 3) was inserted percutaneously from the left femoral artery over a long guidewire and advanced to the level of the mitral valve. The wire had previously been introduced through a catheter into the right femoral vein and advanced transseptally through a Brockenbrough catheter to the left ventricle and aorta, where it was subsequently drawn out of the body through the left femoral artery using an intravascular retrieval set. Once the catheter stabilized within the mitral valve, the balloon was inflated 1 to 4 times at 3 to 5 atmospheres.During dilation, the left additional catheter always monitored the pressurein the ascending aorta while the right catheter monitored the pressure changesfrom the left atrium or wedged pulmonary ar-

tery. Occasionally, we simultaneously monitored the pressuresin the pulmonary artery, left atrium and aorta during occlusion and recovery (Figure 1). Aortic valvulopiasty: For adult patients, we extended our protocol from that used in congenital aortic ste nosis and described elsewhere.4y5A retrogradely advanced single or multiballoon catheter, ranging in total diameter from 15 to 38 mm (mean 26 f 5), was introduced percutaneously through the right femoral artery and positioned within the stenosis.Once the systemic pressurestabilized, the balloon was fully inflated 1 to 4 times. During dilation the left additional catheter always monitored the pressure changes from the aorta, while the right catheter was positionedin the left atrium or wedged pulmonary artery (Figure 2). FIow oeelusion: Flow occlusion was defined as the situation following technically correct tentative dilations. The situation included a fxed inflated balloon during predominant sinus rhythm, accompaniedby dramatic hemodynamic changes.Incomplete or interrupted occlusions(unfixed balloon) were excluded from analysis. The inflation-deflation time always was monitored during dilation and measuredfrom the record tracings.

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Pressureswere obtained through standard fluid-filled catheters connected to Statham P23D transducers and recorded through a Hewlett-Packard 4588 B system. We only considered the 2 first occlusive dilations for comparison with hormone determination. Hommnal study: Plasma hormone levels of ANF, vasopressin and renin were serially determined from blood samples(12 ml) obtained as follows: (1) at baseline, once the catheters were introduced; (2) after the diagnostic procedures;(3) and (4) within 15 to 30 seconds after the first 2 occlusive dilations; (5) 1 hour later; and (6) 7 hours later. Blood samples were drawn through a catheter from the ascending aorta under all hemcdynamic conditions, whereas the last 2 samples were obtained from a peripheral vein. The sampleswere immediately placed in 3 ice-chilled disposable tubes containing ethylenediaminetetraacetate(1 mg/ml). The plasma was separatedby centrifugation for 20 minutes at 4OC.We then mixed 200 kallikrein inhibitor units of aprotinin (Trasylol, Bayer) per ml with that part of the plasma used for ANF determination. All 3 tubes were immediately frozen and stored at -4O’C. The ANF was isolated using column chromatography on Sep-Pak Cis cartridges (Waters Assoc.). The vasopressinwas extracted with ethanol. Plasma renin was determined by quantification of generated angiotensin I. Radioimmunoassay methods were applied for measurements of ANF, vasopressinand angiotensin I.6,7 StatIstIeal study: Data are expressed as mean f standard deviation unless otherwise stated. Differences in group meanswere analyzed using the unpaired t test. The l-way analysis of variance was used to determine whether there were differences between the conditions; individual comparisons were performed by Scheffe’s test. Hormonal determinations were plotted against left atria1 and aortic pressures,and their respectivecorrelations were determined by linear and exponential regression analysis. Correlation coefficients (r) were obtained for each comparison.The slopesof the regressioncurves were compared using the Student t test through their corresponding standard error allowed by automatic lit. Significance was established at the level of p <0.05.

TABLE I Global Data Mitral Valvuloplasty (n = 33) Age 6-d Sex (F) (%) Functional class II (%) III-IV (“x9) Pulmonary wedge pressure (mm Hg) Basal After Gradient (mm Hg) Basal After Valvular area (cm2) Basal After Pulmonary resistance (WU/m2) Basal After Ejection fraction (%) Basal After Anulus diameter (mm) Balloon size (mm)

Aortic Valvuloplasty (n = 16)

5OflO 85

55 f 25 37

15 (45) 18 (55) 21 f7 10f7 17 f 7 5f3

7 (44 9 (56) 14i6 lOf8 111 f41 45f20

1.08 f 0.38 2.30 f 0.80

0.54f0.19 0.91 f 0.30

4.9 f 5.5 4.9 f 5.8

3.5 f 3.2 3.7 f 3.1

57f9 57f7 41zk.6 36f3

58f 13 63f 10 24f5 26f5

systemic pressurewas observedmore frequently during aortic valvuloplasty (Figure 2), the dilation of the mitral valve frequently was associatedwith similar decreasesin aortic pressurebut with preservedpulsatility, which led to incomplete but more prolonged occlusive periods (Figure 1). The occlusion time was significantly shorter in aortic patients (29 f 18 vs 43 f 18 s, p
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DISCUSSION The inflation of a balloon within a cardiac valve provokes a hitherto unrecorded situation that maximizes, during a short period, the conditions of acute heart failure.’ The changesin pressureare dramatic and lead to an anterograde reduction in flow concomitant with a retrograde stagnant flow. The intact circulation has to suddenly adapt to such transient episodesof acute forward and backward failure induced by the mechanical occlusion of the heart during dilation. Thus, thesetherapeutic proceduresrepresenta potential model to further investigate the conditions of acute heart failure. The function of the circulation is to perfuse the tissues,and the body monitors the adequacyof its perfusion mainly by sensingthe arterial pressure.In the short term this is achieved by pressure and volume regulation, not only during physiologic pressurechangesbut also during exercises and failure.8-10Our findings show that abrupt releasesof ANF and vasopressinoccur immediately after the intracardiac occlusive periods. These homeostatic responsesare related to the pressurechangesobserved during dilation, which in fact represents the stimulus evoking such releases.

Atrial natriuretk factor: Increasesin the plasma levels of ANF can be elicited by atria1 stretch caused by volume expansion,’t constrictive agents that increase atria1 pressure,l*immersion in water13and atria1 tachycardia.r4J5 These conditions provide models that have beenusedto study acutely ANF release.The increasein atria1 pressureis the mediatory mechanismin hormonal release induction.16 High plasma ANF concentrations also occur in pathologic states such as heart, renal and liver failure.9J7-20These increased concentrations decreasetoward normal values after successfultherapy.**23Dussaule,**Waldman23and their co-workershave recently studied the responsivenessof plasma ANF to short-term changesin left atria1 pressureafter percutaneousballoon mitral valvuloplasty. They observedan inhibitory responseon ANF secretion to successfulreduction in left atria1 stretch. Both studies also found an unexplained increasein ANF within 1 to 10 minutes after valvuloplasty. They postulated that it could reflect a transient elevation of left atria1 pressureduring balloon occlusion, although their observations were not related to pressurechanges.Our study confirms this hypothesis. The mechanical occlusion of the heart at the time of balloon valvuloplasty also can provide a model to study the acutely hormonal release.The intensity of the stim-

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TABLE III Factors Influencing Basal and Postocclusive Arginine Vasopressin Plasma Levels

TABLE II Factors Influencing Basal and Postocclusive Plasma Atrial Natriuretic Factor Levels

Ox/ml)

After Occlusion (ix/ml)

42 f 23 61 f33

112f61 171*91

49f21 64438

178 f 143 134 f 65

57f34 53 h 23

192 f 136* 107 f 45

63f28 60*38

143 f 62 197 f 177

49 f 27t

72 f 37

172 f 135 131 f 62

49 f 26* 78f39

174f 135 125 f 53

71 f36 51 f28

143f66 173 f 147

60f35 50f25

190f 143 124f67

51 f27 63f34

130f62 193 f 156

Basal

sex M F Functional class II III-IV Rhythm Sinus Atrial fibrillation PR WU/m2) <4 >4 PR/SR <0.13 20.13 EF (%) 554 >54 Type of occlusion Mitral Aortic Occlusion time (s) <35 235

Sex

M F Functional class II III-IV Rhythm Sinus Atrial fibrillation LA dimension (cm) 25 <5 PR (WU/m2) <4 24 PR/SR <0.13 to.13 EF (%) a4 X4 Type of occlusion Mitral Aortic Occlusion time (s) <35 235

Basal (rx/mO

After Occlusion @g/ml)

9f7 7f5

32 f 39’ 114f46

1016 7f6

101 f 42 113f61

8f6 6f4

83f55 115f54

18f6 6f4

86 f 56 111 f57

8f6 7*5

91 f54 107zt68

6&5 9f6

103 f 68 95f56

7f5 7&4

126A35t 34f36

9f6 654

51 f 43s 124f45

* p
* p
increaseobservedin left atria1 pressure.Besides,repeated stimulations of the ANF secretory system seem to enhanceANF release.24The ANF responsewas significantly greater among our patients in sinus rhythm than ulus is much stronger, albeit shorter, than that provided the responseobservedin patients with atria1 fibrillation. by atria1 tachycardia. In our study, even a slight in- This finding was in accordancewith the observationsof crease in pressure after diagnostic angiography pro- Dussaule et al,** who found an inappropriate response duced a significant increasein ANF. However, the hor- in patients with atria1 fibrillation to changesin left atrimonal responsewas greater during intracardiac occlu- al pressureinduced by successfulmitral balloon valvulosions, and showed a direct relation to the significant plasty. A decreasedresponseto both inhibitory** and l p <0.05 vs atria1 fibrillation; t p <0.05 vs 24 WU/m2; EF = ejection fraction; LA = left atrium; PR = pulmonary resistance.

* p <0.05 vs 20.13. resistance; SR = systemic

SYSTEMICOCCLUSION

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stimulatory (Table II) changes in left atria1 pressure suggests that an endocrine dysfunction of the atria1 myocites could occur in patients with chronic atria1 fibrillation. Vasopressin: The 2 main physiologic stimuli evoking vasopressinsecretion are the increase in plasma osmolarity and the decreaseof extracellular volume. Vasopressin has both antidiuretic and vasoconstrictive properties, although the effects of the latter on arterial pressure are normally canceled by baroreflex mechanisms.25 Over a certain osmolarity threshold (280 mOsm/kg), an increase in plasma osmolarity is followed by an increase in plasma vasopressin levels. Thereafter, the releaseof osmotic vasopressinis directly related to plasma osmolarity. In contrast, the nonosmotic, baroreceptor-mediated, release of vasopressin is mainly evokedby volume depletion.26Situations such as hemorrhage or reduced cardiac output produce an increasein vasopressin,irrespective of plasma osmolarity. In conditions of intracardiac occlusion, the forward decreasein systemic pressuremimics situations like hemorrhage or reduced cardiac output that stimulate an abrupt vasopressinreleasefrom the hypothalamus. The vasopressinreleaseto such stimulus follows an exponen tial type of response(Figure 6) as has been observed in the isotonic volume depletions of rats.27Pathologic states such as acute myocardial infarction have been used to clinically study the nonosmotic releaseof vasopressin. Again, the intensity of the stimulus is greater and shorter during balloon intracardiac occlusion,which provides a mechanical model to further study the immediate neurohumoral responsesto a suddenly diminished pumping capacity of the heart. We did not observeclinical or hemodynamic factors influencing baseline plasma vasopressinlevels. In fact, most patients had normal systemic pressure during baselineconditions. However, we observeda higher hormonal responsein mitral patients compared with that observedin aortic patients, which seemsto be related to more prolonged occlusiveperiods during mitral valvuloplasty. Prolongation of the stimulus (low arterial pressure) generates higher hormonal responsesthan the shorter occlusive periods observedin aortic valvuloplasty. The predominance of female patients in the mitral valvuloplasty group (Table I) also explains the observed differences when compared with the male responses (Table III). Limitations and clinical implications: In the present study, our search for early hormone responsesled us to a design in which blood sampleswere withdrawn from a single site (ascending aorta) and within secondsafter occlusive dilations. This could lead to responseunderestimation or to failure to detect delayed responses.Besides,the total amount of blood samplesalso limited the number of hormone responsesstudied. It is conceivable that other neuroendocrine systemsinvolved in immediate pressure-volumeregulation also might be stimulated during occlusive dilations. Plasma catecholamineswere not measured in this study, although they may be of prime importance in the immediate regulation of vascu496

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lar resistance after acute systemic hypotension. Although the same mechanism of low systemic pressure mediates renin-angiotensin release,29we did not find significant renin changes throughout the stagesof our study. Increased plasma levels of ANF can inhibit the renin-angiotensin-aldosteronesystem.30During exercise, plasma concentrationsof severalhormonesincreasein a sequential fashion, with catecholamines,vasopressinand ANF followed by renin activity and aldosterone.1°This releasesequencealso could explain the unresponsiveness of renin to a nonmaintained decreasein systemic pressure. The homeostaticeffectsof these abrupt and simultaneoushormone releasesare complex and deservefurther investigation. The pressoreffect of vasopressin,together with a presumable adrenergic response,could provide fast control of the arterial pressure after intracardiac occlusion, which would explain the good tolerance of these procedures.On the contrary, the simultaneousrelease of ANF would produce vasorelaxant and natriuretic effects. In fact, we have detected an increased natriuresis in the hour following aortic dilation in patients with congenital aortic stenosis.Thus, both antagonistic activities of vasopressinand ANF-simultaneously releasedafter intracardiac occlusion-could conflict with each other.

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uretic peptide in spontaneous tachycardias. Br Heart J 1987;58:96-100. 16. Bates ER, Shenker Y, Grekin RJ. The relationship between plasma levels of immunoreactive atria1 natriuretic hormone and hemodynamic function in man. Circulalion 1986;73:1155-1161. 17. Rascher W, Tulassay T, Lang RE. Atrial natriuretic peptide in plasma of volume-overloaded children with chronic renal failure. Lorzcer 1985;2;303-305. 18. Needleman P, Greenwald JE. Atriopeptin: a cardiac hormone intimately involved in fluid, electrolyte, and blood-pressure homeostasis. N Engl J Med 1986;314:828-834. 19. Ding J, Thibault G, Gutkowska J, Garcia R, Karabatsos T, Jasmin J, Gencst J, Cantin M. Cardiac and plasma atrial natriuretic factor in experimental congestive heart failure. Endocrinology 1987;121:248-257. 20. Schrier RW. Pathogen&s of sodium and water retention in high-output and low-output cardiac failure, nephrotic syndrome, cirrhosis, and pregnancy. N Eng/ J Med 1988;319:1065-1072. 21. Creager MA, Hirsch AT, Nabel EC, Cutler SS, Colucci WS, Dzau VJ. Responsiveness of atrial natriuretic factor to reduction in right atria1 pressure in patients with chronic congestive heart failure. JACC 1988;11:1191-1198. 22. Dussaule JC, Vahanian A, Michel PL, Soullier I, Czekalski S, Acar J. Ardaillou R. Plasma atrial natriuretic factor and cyclic GMP in mitral stenosis treated by balloon valvulotomy. Effect of atrial fibrillation. Circulation 1988; 781276-285.

23. Waldman HM, Palacios I, Block PC, Wilkins GT, Homey CJ, Graham RM, Fifer MA. Responsiveness of plasma atrial natriuretic factor to short term changes in left atria1 hemcdynamics after percutaneous balloon mitral valvuloplasty. JACC 1988:12:649-655. 24. Haufe MC, Weil J, Gerzer R, Ernst JE, Theisen K. Effects of repeated increments in right atrial pressure on secretion of atrial natriuretic factor. Am J Cardiol 1988,61:932-934. 25. Aylward PE, Floras JS, Phil D, Leimbach WN, Abboud FM. Effects of vasopressin on the circulation and its baroreflex control in healthy men. Circulation 1986;73:1145-1153. 26. Schrier RW, Berl T, Anderson RJ. Osmotic and nonosmotic control of vasopressin release. Am J Physiol 1979;236:321-322, 27. Dunn FL, Brennan TJ, Nelson AE, Robertson GL. The role of blood osmolality and volume in regulating vasopressin secretion in the rat. J Clin lnuest 1973;52:3212-3219. 28. Schaller MD, Nussberger J, Feihl F, Waeber B, Brunner HR. Perret C, Nicod P. Clinical and hemodynamic correlates of elevated plasma arginine vasopressin after acute myocardial infarction. Am J Cardiol 1987,60:1178-l 180. 29. Skinner SL, McCubbin JW, Page IH. Control of renin secretion. Circ Res 1964;15:64-76. 30. Laragh JH. Atrial natriuretic hormone, the renin-aldosterone axis, and blood pressure-electrolyte homeostasis. N Eng1 J Med 1985;313:1330-1340.

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