JORGE GASPAR, M.D., F.A.C.C., and JULIO SANDOVAL, M.D., F.A.C.C.. Department of ... Vargas-Barron, Department of Echocardiography, Insti- tuto Nacional ...
Echocardiographic Evaluation of Patients with Primary Pulmonary Hypertension Before and After Atrial Septostomy NILDA ESPINOLA-ZAVALETA, M.D., JESUS VARGAS-BARRON, M.D., JORGE ISAAC TAZAR, M.D., JOSE MIGUEL CASANOVA, M.D., CANDACE KEIRNS, M.D., ANGEL ROMERO CARDENAS, M.D., JORGE GASPAR, M.D., F.A.C.C., and JULIO SANDOVAL, M.D., F.A.C.C. Department of Echocardiography, Instituto Nacional de Cardiologia “Ignacio Chavez,” Mexico, D.F., Mexico Objectives: To characterize the early changes i n right ventricular [right ventricle (RV)lgeometry and function, as assessed by two-dimensional (2-D)and Doppler echocardiography, after balloon-dilation atrial septostomy (BDAS) i n patients with severe primary pulmonary hypertension (PPH).Background. Suruival in PPH is to a great extent dependent on the functional status of the RV. BDAS recently has been shown to improve functional class and hemodynamics in patients with PPH nonresponsive to conventional vasodilator treatment. Methods: Ten patients with severe PPH who underwent BDAS were studied with transthoracic and transesophageal 2-0 and Doppler echocardiogra,phy. RV dimensions were measured in the apical four-chamber view. Continuous-waveDoppler echocardiography was used to obtain peak velocity of tricuspid regurgitation. Transesophageal echocardiography (TEE) primarily was used for the follow-up of the atrial septa1 defects (ASDs). Results: I n the early post-BDAS studies, right atrial and ventricular dimensions significantly decreased in all patients (P< 0.05). Global right ventricular wall motion ( R W M ) also improved. RV percent change in area after septostomy inversely correlated with the changes i n RV systolic area ( r = -0.75; P < 0.05) and also with the baseline (preprocedure) values of RVpercent change in area (r = - 0.77; P < 0.05).Neither RV wall thickness nor the degree of tricuspid regurgitation were modified significantly after the procedure. Conclusions: BDAS in the setting of severe PPH results in moderate and salutary changes i n geometry and function of the RV as assessed by 2 - 0 echocardiography. These changes mainly appear to be the result of the decompression effect of atrial septostomy. (ECHOCARDIOGRAPHY, Volume 16, No. 7, Part 1, October 1999) atrial septostomy, primary pulmonary hypertension, tramesophageal echocardiography. Severe pulmonary hypertension invariably results in abnormalities in cardiac structure and function. Progressive right ventricular (RV) dysfunction in patients with primary pulmonary hypertension (PPH) is associated with a poor short-term progno~is.l-~ Contemporary
Address for correspondence and reprint requests: Dr. Jesus Vargas-Barron, Department of Echocardiography, Instituto Nacional de Cardiologia “Ignacio Chavez,” Juan Badia n o No. 1, Colonia Seccion XVI, Tlalpan 14080, MCxico. Fax: 525-573-0994.
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medical treatment of PPH mainly is directed to alleviate the existing pulmonary microvascular obstruction (ie., anticoagulants, oral vasodilators, chronic infusion of prostacyclin, and lung transplant) with an improvement in RV dysfunction as a secondary g ~ a l .Although ~-~ prostacyclin and transplant are effective for patients who are nonresponders to oral vasodilators, the worldwide application of these interventions is limited by technical difficulties and cost. Several recent studiess-I2have evaluated the
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potential role of atrial septostomy in the treatment of selected patients with PPH. These studies have shown that both blade-balloon atrial septostomy (BBAS) and/or balloon-dilation atrial septostomy (BDAS) can be performed successfully in patients with advanced disease and can bring about significant clinical and hemodynamic impr0vement.~-'4In the initial report from our institution,12 a significant improvement in RV hernodynamics and exercise tolerance was documented after the BDAS procedure. However, the extent to which chronic RV compensatory changes regress after BDAS has not been defined. Accordingly, the present study was designed t o evaluate the early changes in RV geometry and function in patients with severe pulmonary hypertension after BDAS as assessed by the echocardiographic findings before and after this procedure.
Methods Study Patients
From November 1994 to September 1997 we performed 22 procedures of BDAS in 15 consecutive patients with established diagnosis of PPH. The BDAS procedure and the clinical response in these patients have been reported elsewhere.12 The ten patients reported here represent those in whom a technically adequate two-dimensional (2-D) and/or transesophageal echocardiographic (TEE) studies before and after the procedure were available. The patients underwent BDAS as part of their treatment on the basis of severe and symptomatic pulmonary arterial hypertension with RV dysfunction or recurrent syncope despite medical therapy (including diuretic drugs, anticoagulation therapy, and digoxin). Also, during their diagnostic study, all patients had and did not respond to an acute vasodilator trial with adenosine and nifedipine.l5 Before the procedure, an anatomic atrial septal defect (ASD) or a patent foramen oval and a poor left ventricular (LV) function in these patients were ruled out by 2-D echocardiography. Also, patients considered candidates for the procedure had to have a baseline arterial oxy626
gen saturation (SaO,) greater than 80% at rest and have a hematocrit greater than 35% to enable them to maintain adequate systemic oxygen transport after the procedure. The exercise endurance of the patients was assessed through a 6-minute walk test16 before and after (i.e., before discharge) the procedure. All procedures were approved by our Institutional Committee for Clinical Investigation. The risks involved and the potential benefits of BDAS were explained to the patients and their written consent was obtained.
BDAS BDAS at our institution has been previously described.12Briefly, the procedure is performed under standard right and left heart catheterization. The transeptal puncture is performed through the Mullins sheath and dilator with a Brockenbrough needle through which a circular-end Inoue guidewire is passed to the left atrium (LA). Over this guidewire, a first dilation with a 4-mm semirigid dilator is done and then exchanged for successive Mansfield balloons to perform a progressive dilation of the orifice in a step-by-step manner ranging from 8 to 16 mm. At each step (4,8, 12, and 16 mm), we carefully assess the concomitant changes that occur in the following variables: RV enddiastolic pressure (RVEDP), LV end-diastolic pressure (LVEDP), and arterial SaO,%. The final size of the defect is determined by the changes produced in the last two variables; as an endpoint we attempt t o maintain arterial SaO, greater than 75% and to keep LVEDP no higher than 18 mmHg. Cardiac output before and after the procedure are calculated by the indirect Fick principle using assumed oxygen consumption values. All patients are monitored in an intensive care setting for at least 48 hours after the procedure. In the absence of significant bleeding, heparin is started again 6 hours after BDAS and all patients are treated subsequently with oral anticoagulants to maintain an International Normalized Ratio of 2.5-3.0. They also are advised to use long-term nocturnal oxygen therapy as part of their treatment. All survivors were followed clinically and
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ECHOCARDIOGRAPHY AND ATRIAL SEPTOSTOMY
noninvasively with transthoracic echocardiography (TTE) or TEE at our outpatient clinic every 3 months. Exercise tolerance was reassessed at each of these intervals, and during these evaluations, particular care was taken to detect spontaneous closure of the defect based on any of the following findings: (1)reappearance of symptoms or signs of RV failure, (2) spontaneous “improvement” of arterial oxygen saturation, and (3) echocardiographic evidence of closure of the interatrial defect. Echocardiography Transthoracic and transesophageal 2-D Doppler echocardiography were characterized in patients before and after BDAS using a HewlettPackard Sonos 1500 imaging system. Transthoracic studies were performed with a 3.5MHz transducer and transesophageal studies with a 5-MHz biplane or multiplane transducer. Patients were imaged during quiet respiration in the left lateral decubitus position. For TEE examination the oropharynx was anesthetized with 20% lidocaine spray to suppress the gag reflex and retching. Preprocedure echocardiograms were obtained within 2 weeks before BDAS in all patients. Postintervention studies were performed at 5.5 2 3 months after the procedure. In addition, in patients going through follow-up TEE with color flow imaging we used intravenous agitated saline solution contrast injections to evaluate accurately the presence and size of the intracardiac shunts (Fig. 1). Measurements were made on three representative beats and the results were averaged. All echocardiographic studies were recorded on VHS videocassettes for subsequent evaluation by two expert cardiologist-echocardiographers who were unfamiliar with the clinical status of patients. Results were taken by consensus. The following variables were analyzed: (1) Right atrial transverse diameters were measured at 0” in ventricular diastole, and the diameter of the main pulmonary artery (PA) was measured at 70” in systole (Fig. 2). (2) The RVED area (RVEDA) and end-systolic area (RVESA) were measured in a four-chamber view by tracing the endocardial edges of the RV at the plane of Vol. 16, No. 7, Part 1, 1999
Figure 1. Transesophageal image at 62” showing that the diameter of the atrial septostomy is 4.11 m m (arrow). RA indicates right atrium; LA, left atrium.
the tricuspid valve at end-diastole and endsystole (Fig. 3). Both areas were divided by height to correct for differences in body size. Images were considered technically adequate if no dropout in the endocardial outlines along the interventricular septum and RV free wall was observed. RV size was characterized only as a planar area. (3) The RV percent change in area was calculated from the areas of the RV in end-diastole and end-systole as RV percent change in area = 100 X (RVEDA - RVESA)/ RVEDA. This measure correlates closely with RV ejection fraction as measured by radionuclide angiography.l7JS (4)Global RV wall motion (RVWM) was assessed qualitatively. It was considered to be normokinetic if there was obvious normal systolic wall thickness and inward endocardial motion and hypokinetic when abnormal systolic wall thickness and/or inward endocardial motion existed. Hypokinesis was graded as either mild or moderate.17-19 RV wall thickness was measured at end-diastole in a four-chamber view that allowed best definition of the RV free wall. (5) To calculate systolic PA pressure, transthoracic continuouswave Doppler echocardiography positioned from an apical four-chamber image was used to obtain regurgitant tricuspid flow velocity. The Bernoulli equation (V2 X 4,where V = maximum flow velocity) was applied to determine
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regurgitant area was noted; the ratio of the maximal regurgitant jet area to the right atrial area then was obtained. When this ratio was >34% the tricuspid regurgitation was considered severe. If the ratio was
