Left ventricular function in adult patients with atrial septal defect: implication for development of heart failure after transcatheter closure

Despite advances in device closure for atrial septal defect (ASD), post-closure heart failure observed in adult patients remains a clinical problem. Although right heart volume overload is the fundamental pathophysiology in ASD, the post-closure heart failure characterized by acute pulmonary congestion is likely because of age-related left ventricular diastolic dysfunction, which is manifested by acute volume loading with ASD closure. Aging also appears to play important roles in the pathophysiology of heart failure through several mechanisms other than diastolic dysfunction, including ventricular systolic and vascular stiffening and increased incidence of comorbidities that significantly affect cardiovascular function. Recent studies suggested that accurate assessment of preclosure diastolic function, such as test ASD occlusion, may help identify high-risk patients for post-closure heart failure. Anti–heart failure therapy before device closure or the use of fenestrated device appears to be effective in preventing post-closure heart failure in the high-risk patients. However, the long-term outcome of such patients remains to be elucidated. Future studies are warranted to construct an algorithm to identify and treat patients at high risk for heart failure after device closure of ASD.     

Left ventricular conditioning in the elderly patient to prevent congestive heart failure after transcatheter closure of atrial septal defect.

Transcatheter closure of atrial septal defects (ASDs) is a safe and effective treatment. Over the past years, an increasing number of elderly patients (age > 60 years) have been admitted for transcatheter closure to prevent ongoing congestive heart failure from volume overload. However, recent data point to the risk of serious acute left ventricular dysfunction leading to pulmonary edema immediately after surgical or transcatheter ASD closure in some patients. In this study, we used a technique described before to recognize in advance patients at risk of left heart failure after ASD closure. Those patients at risk were then treated with preventive conditioning medication for 48-72 hr before definitive transcatheter ASD closure was performed. Fifty-nine patients aged over 60 years (range, 60-81.8 years; median, 68 years) were admitted to our institution for transcatheter closure of an atrial septal defect. All patients received evaluation of atrial pressures before and during temporary balloon occlusion of the ASD. Patients with left ventricular restriction due to increased mean atrial pressures (> 10 mm Hg) during ASD occlusion received anticongestive conditioning medication with i.v. dopamine, milrinone, and furosemide for 48-72 hr before definitive ASD closure with an Amplatzer septal occluder was performed. In 44 patients without any signs of left ventricular restriction, ASD closure was performed within the first session. Fifteen (25%) out of 59 patients showed left ventricular restriction. In the majority of patients with LV restriction, the mean left atrial pressures with occluded ASD were significantly decreased after 48-72 hr of conditioning medication. Definitive ASD closure was then performed in a second session. Only two patients received a fenestrated 32 mm Amplatzer occluder due to persistent increased atrial pressures > 10 mm Hg even after conditioning medication. There were no significant differences in shunt, device size, or defect size between the two groups. Balloon occlusion of atrial septal defects identifies patients with left ventricular restrictive physiology before ASD closure. Intravenous anticongestive conditioning medication seems to be highly effective in preventing congestive heart failure after interventional closure of an ASD in the elderly patient with a restrictive left ventricle.     

老年先天性心脏病心房间隔缺损患者左心室舒张功能受限的诊断和介入治疗前的预适应治疗

目的:探讨诊断和预防老年(>60岁)房间隔缺损(ASD)患者内科介入治疗后发生急性左心衰竭(心衰)至肺水肿风险的方法和手段。方法:术前进行常规经胸超声心动图检查(TTE),术中先行球囊封堵ASD,测量左心房压力。如果球囊封堵ASD后,左心房平均压升至10 mm Hg(1 mm Hg=0.133kPa)以上时,定义为左心室舒张受限(LVR)。对于此类患者暂停此次介入,并给予左心室预适应治疗(LVPCT)48 h,然后进行第2次介入治疗。术后将有创血流动力学指标与TTE结果进行对比。结果:23例患者,15例患者在第1次介入治疗过程中,没有发现LVR,ASD介入治疗1次完成。8例患者(34.8%)在第1次介入治疗过程中,被诊断LVR。其中6例患者的左心房平均压在经过48 h的LVPCT后显著下降,第2次介入治疗时封闭ASD。其余2例患者在接受48 h LVPCT后,球囊导管测量ASD封堵后左心房平均压仍>10 mm Hg,其中1例患者在术后发生急性左心衰竭。通过与有创血流动力学指标对比,胸骨旁长轴M型超声测量左心室舒张末期直径(LVEDD)≤40 mm和右心室舒张末期直径(RVEDD)≥30 mm合并心室间隔矛盾运动可预见LVR的存在(P<0.05)。结论:术前超声心动图可以预测左心室舒张受限的存在。介入治疗术中使用球囊封堵ASD后测量左心房压有助于诊断LVR。术前静脉LVPCT可以有效预防术后充血性心衰的出现。     

Fate of a modified fenestration of atrial septal occluder device after transcatheter closure of atrial septal defects in elderly patients

Background: Data on closure of atrial septal defects (ASD) in elderly patients with a fenestrated Amplatzer septal occluder (ASO) device is limited. Methods: A hemodynamically significant ASD was closed with a fenestrated ASO in 3 patients with ages >62 years. Prior to implant a 4‐mm fenestration was created by balloon dilatation without additional suture fixation just adjacent to the stent part of the device. Indications for fenestration were restrictive left ventricular physiology and/or pulmonary hypertension. Heparin had been administered during and for 48 hours after the procedure. Two patients were maintained on phenprocoumon because of chronic atrial fibrillation, the remaining patient on aspirin and clopidogrel for 3 months after implant. Transesophageal echocardiography (TEE) and hemodynamic evaluation were performed 4–18 months after ASD closure. Results: A trace or small fenestration through the ASO with left‐to‐right shunt was detected by TEE in all 3 patients without any hemodynamic significance. No thrombus formation was observed. Pulmonary hypertension improved in the affected patient. Pulmonary arterial wedge pressure and cardiac index improved in the second patient with improvement in heart failure symptoms and of quality of life in both. The third patient, after initial improvement for 6 months, developed significant comorbidities and clinical deterioration at 18 months follow‐up. Conclusion: The modified fenestration of the ASO decreased significantly in size at follow‐up. Applying this technique to selected patients judged to be at risk for ASD closure avoids acute decompensation and allows gradual diminuition of right ventricular volume overload during mid‐term follow‐up. (J Interven Cardiol 2011;24:485–490)     

Right ventricular failure in patients with preserved ejection fraction and diastolic dysfunction: an underrecognized clinical entity

It is well recognized that patients with severe left ventricular (LV) systolic dysfunction develop pulmonary venous hypertension or postcapillary pulmonary hypertension, which leads to an increase in pulmonary vascular resistance (PVR) and right ventricular (RV) systolic failure. It is often underrecognized, however, that patients with heart failure with preserved LV ejection fraction and diastolic dysfunction may also develop postcapillary pulmonary hypertension with elevated PVR leading to RV systolic failure. This form of biventricular failure is a result of diastolic failure on the left in patients with preserved LV ejection fraction and systolic failure on the right. At this time, there are no randomized trials or guidelines addressing the management of patients with diastolic heart failure with and without resultant RV failure. The authors review the pathophysiology, clinical presentation, and suggested treatment of this underrecognized clinical entity.     

Closure of a moderately large atrial septal defect with a self-fabricated fenestrated Amplatzer septal occluder in an 85-year-old patient with reduced diastolic elasticity of the left ventricle.

Percutaneous closure of an atrial septal defect (ASD) in the elderly with reduced diastolic elasticity of the left ventricle poses a significant management challenge. We report on the case of an 85-year-old patient who was admitted for percutaneous device closure of a moderately large secundum atrial septal defect. Hemodynamic evaluation documented an increase in left atrial pressure from a mean of 12 mm Hg to a mean of 32 mm Hg after balloon test occlusion of the ASD. Two months later, after adequate pretreatment with diuretics and afterload-reducing substances, he underwent successful closure of the ASD using a self-fabricated fenestrated Amplatzer septal occluder, which resulted in a postimplantation left atrial pressure of a mean of 18 mm Hg. Recovery was unremarkable and the fenestration has remained patent for 3 months since implantation of the device. This unique case highlights the feasibility of using a self-fabricated fenestrated Amplatzer septal occluder to close interatrial communications in elderly patients with diastolic dysfunction of the left ventricle.     

Home-made fenestrated amplatzer occluder for atrial septal defect and pulmonary arterial hypertension

We report the management of a patient with secundum atrial septal defect (ASD) and severe pulmonary hypertension. A 65-year-old male with recently diagnosed atrial septal defect was referred to our centre for decompensated right heart failure with rest and exercise induced dispnea and severe pulmonary hypertension. Right heart catheterization confirmed a mean pulmonary pressure of about 55 mmHg and a Qp/Qs of 2.7. An occlusion test with a compliant large balloon demonstrated partial fall of pulmonary arterial pressure. The implantation of a home-made fenestrated Amplatzer ASD Occluder (ASO) was planned in order to decrease left-to-right shunt and promote further decrease of pulmonary arterial pressure in the long-term. Thus, by means of mechanical intracardiac echocardiography study with a 9F 9 MHz UltraIce catheter (Boston Scientific Corp.), we selected a 34 mm ASO for implantation. Four millimeter fenestration was made inflating a 4 mm non-compliant coronary balloon throughout the waist of the ASO, which was successfully implanted under intracardiac echocardiography. After six months, a decrease of pulmonary arterial pressure to 24 mmHg and full compensated right heart failure was observed on transthoracic echocardiography and clinical examination. This case suggests that transcatheter closure with home-made fenestrated ASD in elderly patients with severe pulmonary hypertension is feasible.     

Evaluation of right ventricular pressure by two-dimensional echocardiography

To estimate the severity of right ventricular hypertension noninvasively, the two-dimensional echocardiograms of 86 patients were examined--26 patients with atrial septal defect (ASD group), 22 with rheumatic valvular heart disease (VHD group), 12 with primary pulmonary hypertension (PPH group) and 26 with tetralogy of Fallot (Fallot group)--and data were compared with those of 20 normal persons. The interventricular septal (IVS) curvature index (delta r) from short axis view correlated well with the ratio of right to left ventricular systolic pressure (RVP/LVP). When IVS became convex towards the right ventricular cavity, the correlative coefficient between delta r and RVP/LVP was r = 0.75 in the ASD group, r = 0.83 in the VHD group, r = 0.71 in the PPH group and r = 0.77 in the Fallot group. The RVP/LVP approached a plateau when IVS became straight or convex towards the left ventricular cavity. Two-dimensional echocardiography provides a useful means to assess the right ventricular systolic pressure non-invasively.     

国产封堵器介入治疗房间隔缺损后心功能变化的研究

目的探讨国产封堵器介入治疗房间隔缺损(ASD)后心脏形态和功能的变化规律。方法全组60例,年龄5～35(16.10±10.71)岁,体重17～7(243.91±13.21)kg,经胸超声心动图(TTE)示ASD最大径7～3(618.3±7.2)mm,选用封堵器型号为10～4(026±3)mm。术后3d、3个月、6个月和12个月行TTE追踪测量。采用心尖四腔切面面积-长度法计算左右心室容积及射血分数。结果术后3d,右心房上下径、左右径,右心室舒张末期前后径、左右径均逐渐减小(与术前比较,P<0.05);右室舒张末期容积(RVEDV),右室收缩末期容积(RVESV),及右室射血分数(RVEF)均逐渐减小(与术前比较,P<0.05)。3～6个月随访,右心功能进一步改善。至12个月随访时,右心房、右心室大小及右心功能恢复正常(与术前比较,P<0.01)。术后3d,左室舒张末期前后径(LVEDD),左室舒张末期容积(LVEDV)均逐渐增大(与术前比较,P<0.05);左室收缩末期容积(LVESV),左室每搏量(LVSV)及左室射血分数(LVEF)均逐渐增大(与术前比较,P<0.05)。3～6个月随访,左心功能进一步改善。至12个月随访时,左心房、左心室大小及左心室功能恢复正常(与术前比较,P<0.01)。结论国产封堵器介入封堵ASD,既阻断了异常分流,又改善了左心室及右心系统功能及其几何构型。     

Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling.

To compare the effects of isolated right ventricular pressure and volume overload on left ventricular diastolic geometry and filling, 11 patients with primary pulmonary hypertension, 11 patients with severe tricuspid regurgitation due to tricuspid valve resection and 11 normal subjects were studied with use of Doppler echocardiographic techniques. Right ventricular systolic overload in primary pulmonary hypertension resulted in substantial leftward ventricular septal shift that was most marked at end-systole and early diastole and decreased substantially by end-diastole. Right ventricular diastolic overload after tricuspid valve resection resulted in maximal leftward ventricular septal shift at end-diastole sparing end-systole and early diastole. The early diastolic distortion of left ventricular geometry associated with right ventricular pressure overload resulted in prolongation of isovolumetric relaxation of the left ventricle (129 +/- 39 ms) and a reduction in early diastolic filling compared with values in normal subjects. Late diastolic distortion of left ventricular geometry associated with right ventricular volume overload had no influence on the duration of left ventricular isovolumetric relaxation (52 +/- 32 ms) but caused a reduction in the atrial systolic contribution to late diastolic filling of the left ventricle compared with values in normal subjects. In patients with right ventricular pressure overload, 52 +/- 16% of left ventricular filling occurred in early diastole compared with 78 +/- 11% in patients with right ventricular volume overload (p less than 0.001). The differential effects of systolic and diastolic right ventricular overload on the pattern of left ventricular filling appear to be related to the timing of leftward ventricular septal displacement.     

Tissue Doppler assessment of longitudinal right and left ventricular strain and strain rate in pulmonary artery hypertension

Tissue Doppler imaging (TDI) in 38 adult patients with pulmonary artery hypertension of varied etiology and normal left ventricular systolic function by two-dimensional transthoracic echocardiography showed significantly reduced peak systolic strain (SS) in all three segments of left ventricular free wall and ventricular septum and two of three segments of right ventricular free wall when compared to 29 adults with no clinical or echocardiographic evidence of heart disease and normal left and right ventricular systolic function. A similar reduction in peak diastolic strain (DS) was also noted in all three segments of left ventricular free wall and ventricular septum and one of three segments of right ventricular free wall. This reduction in strain indices in patients with pulmonary hypertension was noted irrespective of whether right ventricular systolic function was normal or reduced as assessed by two-dimensional transthoracic echocardiography. SS and DS rates also showed reductions in patients with pulmonary artery hypertension. Our study shows the potential value of TDI indices in identifying reduced regional left ventricular systolic and diastolic longitudinal function in patients with pulmonary artery hypertension and normal left ventricular systolic function by two-dimensional transthoracic echocardiography. This reduction in left ventricular function was noted in patients with both normal and reduced right ventricular systolic functions by two-dimensional echocardiography.     

Left ventricular function in pulmonary hypertension

To elucidate left ventricular function in pulmonary hypertension, we measured parameters of left ventricular as well as right ventricular function by echocardiography in 11 patients with pulmonary hypertension (idiopathic pulmonary artery hypertension in 4, chronic thromboembolic pulmonary hypertension in 5, and other pulmonary hypertension in 2). The percent change in these parameters 6 months after treatment with pulmonary artery vasodilators (beraprost in 8 and sildenafil in 3) was assessed. There was a correlation between the relative change in right ventricular systolic pressure (RVSP) and the relative changes in left ventricular outflow tract velocity–time integral (r = ?0.730, P = 0.011) and mitral valve velocity–time integral (r = ?0.621, P = 0.041). However, there was no correlation between the relative change in RVSP and the relative changes in left ventricular ejection fraction, left ventricular diastolic dimension, and systolic blood pressure. The relative change in RVSP was also correlated with the relative change in early diastolic myocardial velocity at the medial mitral annulus (r = ?0.675, P = 0.023). Reduction of RVSP by pulmonary artery vasodilators might increase left ventricular preload, leading to an increase in stroke volume. Right ventricular load reduction might improve left ventricular diastolic function in patients with pulmonary hypertension, possibly through altered interventricular septal performance.     

Therapy for diastolic heart failure

There is little objective to guide the therapy of patients with diastolic heart failure. Because of the similarities of pathophysiology abnormalities in diastolic and systolic heart failure, it is a reasonable inference to suggest that the proven therapy for systolic heart failure may also be of benefit in patients with diastolic heart failure. Treatment of underlying or exacerbating conditions in diastolic heart failure, such as hypertension, left ventricular hypertrophy, ischemia, diabetes, anemia, obesity and pulmonary disease is an important means of managing diastolic heart failure. Control of systolic blood pressure is effective in improving and preventing the development of diastolic heart failure. Treatment of diastolic heart failure is most effective when it is associated with hypertension. Production of systolic arterial pressure acutely reduces pulmonary congestion, ischemia, and chronically may lead to regression of left ventricular hypertrophy. Patients with diastolic heart failure in the absence of hypertension are very difficult to treat.     

Analysis of ventricular septal motion by doppler tissue imaging in atrial septal defect and normal heart

The aortic root and the upper part of the ventricular septum moves anteriorly in early systole, while the lower part moves posteriorly. The hinge of the counterpart motion of the ventricular septum is called pivot point. Using Doppler tissue imaging (DTI), we attempted to clarify the location of the pivot point of the ventricular septum in children with normal heart and with atrial septal defect (ASD), and to investigate the relation between the degree of the downward shift of the pivot point and that of volume overload of the right ventricle in patients with ASD. Study subjects consisted of 20 healthy children and 36 patients with ASD, aged from 1 to 15 years (mean 5.7+/-3.4) in the normal group and 6 months to 12 years (mean 4.4+/-3.2) in the ASD group, respectively. The pivot point was designated as a border of the color signal of DTI of the ventricular septum in early systole. Measurements were then obtained on cross-sectional echocardiography and DTI: septal length in the parasternal long-axis view, distance from aortic valve to pivot point in early systole, diastolic left ventricular internal dimension, and diastolic right ventricular internal dimension. In the normal group, the ratio of distance from aortic valve to pivot point/septal length was 0.13+/-0.049, whereas it was 0.26+/-0.168 in the group with ASD (p <0.001). In the ASD group, the distance from aortic valve to pivot point normalized by body surface area (mm/m2) correlated with the ratio of diastolic right/left ventricular internal dimension and with the ratio of pulmonary to systemic flow (Qp/Qs) (r = 0.63 and 0.50, respectively). The ratio of the distance from aortic valve to pivot point/septal length correlated with the ratio of diastolic right/left ventricular internal dimension and Qp/Qs (r = 0.56 and 0.44, respectively). By DTI, the pivot point was located at the upper 13+/-5% of the total length of the ventricular septum in normal children, and was located at 26+/-17% in patients with ASD (p < 0.001). The degree of this displacement in ASD correlated with that of volume overload of the right ventricle. The paradoxic motion of the ventricular septum shown in the ASD could be explained by this downward shift of the pivot point.     

房间隔缺损并发畸形的介入治疗

目的 :评价同期应用介入治疗房间隔缺损 （ASD）及其并发心脏其它畸形的可行性和治疗效果。方法 :全组 7例 ,年龄 2～ 6 5 （34± 2 8）岁。经临床、心电图、X线及超声心动图诊断为 ASD并发其他心脏畸形 ,其中 3例为肺动脉瓣狭窄 ,2例为二尖瓣狭窄 （L utembacher综合征 ） ,2例为动脉导管未闭 （PDA ）。应用 Amplatzer封堵器经导管关闭ASD前 ,先纠正其它畸形 （包括瓣膜成形术及 PDA封堵术 ）。术后 3d,1～ 6月分别行经胸超声心动图 （TTE）、心电图、X线检查评价治疗效果。结果 :7例同期介入治疗均获得成功 ,术中未发生任何重要并发症。术后 3d,1～ 6月TTE显示房间隔无残余分流。并发肺动脉瓣狭窄患者 ,术后即刻跨肺动脉瓣压差得到满意的下降 ;L utembacher综合征患者 ,二尖瓣瓣口面积分别由术前 1.0 ,1.2 cm2增加到术后 1.9,2 .0 cm2 ,左房平均压分别由 2 9,2 6 m m Hg（1mm Hg=0 .133k Pa）降至 8,7m m Hg;并发 PDA患者 ,应用 Amplatzer封堵器 PDA关闭术后 10 min降主动脉侧位造影 ,无残余分流。术后 6月 X线检查显示肺血减少 ,心脏房、室缩小。结论 :同期介入治疗 ASD并发某些心脏畸形是一种有效、安全、简便可行的方法。     

Rechtsherzinsuffizienz und Cor pulmonale

Whereas the right ventricle tolerates volume loads without any substantial increase of the pressure in the pulmonary circulation by recruiting capacitance vessels and capillaries, it possesses only small contractile reserves and reacts unadapted with right ventricular dysfunction. Its size and pressure load are relevant factors for prognosis of all forms of pulmonary hypertension, in particular if linked to left-sided heart failure. Differentiation of pulmonary hypertension according to the Venice classification is highly important. Right-sided ventricular heart failure worsens left ventricular hemodynamics due to reduced ejection fraction and in addition due to direct diastolic ventricular interaction in which left ventricular diastolic dysfunction increases even though the left ventricular systolic function is still intact. Right ventricular ejection fraction <40% is an important predictor of prognosis after myocardial infarction or chronic stages of left ventricular heart failure. The most important noninvasive diagnostic method is transthoracic echocardiography with determination of the Tei index and Doppler echocardiographic estimation of pulmonary artery pressure. Chronic obstructive pulmonary disease is the most frequent cause of cor pulmonale. While long-term oxygen therapy in patients with COPD and cor pulmonale and for example the administration of endothelin receptor antagonists in patients with idiopathic pulmonary hypertension is beneficial, the therapeutic use of drugs effective for left-sided heart failure is very limited in patients with right ventricular dysfunction.     

Left ventricular filling characteristics in pulmonary hypertension: a new mode of ventricular interaction.

OBJECTIVE--To examine the effects of pulmonary hypertension on left ventricular diastolic function and to relate the findings to possible mechanisms of interdependence between the right and left sides of the heart in ventricular disease. DESIGN--A retrospective and prospective analysis of echocardiographic and Doppler studies. SETTING--A tertiary referral centre for both cardiac and pulmonary disease. PATIENTS--29 patients with pulmonary hypertension (12 primary pulmonary hypertension, 10 pulmonary fibrosis, five atrial septal defect (ASD), and two scleroderma) were compared with a control group of 10 patients with an enlarged right ventricle but normal pulmonary artery pressure (six ASD, one after ASD closure, one ASD and pulmonary valvotomy, one tricuspid valve endocarditis and repair, and one pulmonary fibrosis). None had clinical or echocardiographic evidence of intrinsic left ventricular disease. MAIN OUTCOME MEASURES--M mode echocardiographic measurements were made of septal thickness, and left and right ventricular internal cavity dimensions. Doppler derived right ventricular to right atrial pressure drop, and time intervals were measured, as were isovolumic relaxation time, and Doppler left ventricular filling characteristics. RESULTS--The peak right ventricular to right atrial pressure gradient was (mean (SD)) 60 (16) mm Hg in pulmonary hypertensive patients, and 18 (5) mm Hg in controls. The time intervals P2 to the end of the tricuspid regurgitation, and P2 to the start of tricuspid flow were both prolonged in patients with pulmonary hypertension compared with controls (115 (60) and 120 (40) v 40 (15) and 45 (10) ms, p values less than 0.001). Pulmonary hypertensive patients commonly had a dominant A wave on the transmitral Doppler (23/29); however, all the controls had a dominant E wave. Isovolumic relaxation time of the left ventricle was prolonged in pulmonary hypertensive patients compared with controls, measured as both A2 to mitral valve opening (80 (25) v 50 (15) ms) and as A2 to the start of mitral flow (105 (30) v 60 (15) ms, p values less than 0.001). The delay from mitral valve opening to the start of transmitral flow was longer in patients with pulmonary hypertension (30 (15) ms) compared with controls (10 (10) ms, p less than 0.001). At the time of mitral opening there was a right ventricular to right atrial gradient of 12 (10) mm Hg in pulmonary hypertensive patients, but this was negligible in controls (0.4 (0.3) mm Hg, p less than 0.001). CONCLUSIONS--Prolonged decline of right ventricular tension, the direct result of severe pulmonary hypertension, may appear as prolonged tricuspid regurgitation. It persists until after mitral valve opening on the left side of the heart, where events during isovolumic relaxation are disorganised, and subsequent filling is impaired. These effects are likely to be mediated through the interventricular septum, and this right-left ventricular asynchrony may represent a hitherto unrecognised mode of ventricular interaction.     

Bidirectional shunt in uncomplicated atrial septal defect

The presence of right to left shunts at atrial level in 40 patients with an uncomplicated atrial septal defect was determined by measuring the pulmonary vein to systemic artery oxygen stepdown . In six patients (group 1) a sizeable right to left shunt was found: left atrial oxygen stepdown was greater than or equal to 0.7 vol%, mean right to left shunt 0.67 1/min/m2 (range 0.36-1.0), and arterial oxygen saturation between 84% and 90.5%. The patients in group 1 did not show any differences from those with left to right shunts alone (group 2) as regards sex, cardiac rhythm, heart rate, "a" wave and mean right atrial pressure, end diastolic right ventricular pressure, morphology of diastolic right ventricular pressure curves, pulmonary to systemic vascular resistance ratio, size of the defect, and coexistence of anomalous pulmonary venous drainage. Patients with coexisting right to left shunts were, however, significantly older and had smaller left to right shunts. Thus an appreciable number of patients with uncomplicated atrial septal defects have major right to left shunts which are unrelated to pulmonary hypertension or right heart failure. These shunts may be detected by the usual oximetric techniques and apparently develop with age, which suggests that they result from changes associated with chronic right volume overload.     

Bidirectional shunt in uncomplicated atrial septal defect.

The presence of right to left shunts at atrial level in 40 patients with an uncomplicated atrial septal defect was determined by measuring the pulmonary vein to systemic artery oxygen stepdown . In six patients (group 1) a sizeable right to left shunt was found: left atrial oxygen stepdown was greater than or equal to 0.7 vol%, mean right to left shunt 0.67 1/min/m2 (range 0.36-1.0), and arterial oxygen saturation between 84% and 90.5%. The patients in group 1 did not show any differences from those with left to right shunts alone (group 2) as regards sex, cardiac rhythm, heart rate, "a" wave and mean right atrial pressure, end diastolic right ventricular pressure, morphology of diastolic right ventricular pressure curves, pulmonary to systemic vascular resistance ratio, size of the defect, and coexistence of anomalous pulmonary venous drainage. Patients with coexisting right to left shunts were, however, significantly older and had smaller left to right shunts. Thus an appreciable number of patients with uncomplicated atrial septal defects have major right to left shunts which are unrelated to pulmonary hypertension or right heart failure. These shunts may be detected by the usual oximetric techniques and apparently develop with age, which suggests that they result from changes associated with chronic right volume overload.     

介入封堵术在老年继发孔型房间隔缺损患者中的临床应用

目的观察老年继发孔型房间隔缺损(ASD)患者进行介入封堵术的中、远期疗效和安全性。方法老年继发孔型ASD患者206例,缺损8～38(26.5±8.1)mm。封堵术前、术后行右心导管检测肺动脉压、右心室压,随访6个月,评价心功能(NYHA)改善情况。结果成功封堵203例,成功率98.5%。封堵器直径12～42(31.5±7.3)mm。与封堵术前比较,患者封堵术后肺动脉收缩压、右心室平均压明显下降(P<0.05,P<0.01);3～6个月随访时,患者右心室容积缩小、LVEF升高、心功能改善明显。术后心包积液1例(0.5%);即刻残余分流10例(4.9%);术后出现心律失常30例(14.8%)、出现急性心功能不全16例(7.9%)。6个月随访,患者均未发现有残余分流、脱落、栓塞。结论老年继发孔型ASD患者行介入封堵治疗中、远期相对安全、有效。