A comparison of the acute hemodynamic effects of inhaled nitroglycerin and iloprost in patients with pulmonary hypertension undergoing mitral valve surgery.

BACKGROUND: Since the presence of pulmonary hypertension (PHT) affects the prognosis of the patients, it is important to manage and evaluate PHT. The aim of this study was to compare the hemodynamic effects of inhaled nitroglycerin and iloprost during early postoperative period, in patients with PHT undergoing mitral valve replacement surgery. MATERIALS AND METHODS: One hundred patients with PHT (mean pulmonary artery pressure (MPAP) >25 mmHg at rest), were randomized to receive either inhalation of nitroglycerin (group I; n=50) or iloprost (group II; n=50) in the postoperative period. In both groups, baseline hemodynamic parameters were recorded before the treatment (T(0)). Then, patients in group I received 20 microg.kg(-1) nitroglycerin and those in group II received 2.5 microg.kg(-1) iloprost. The same parameters were recorded immediately after the end of the treatment (T(1)). RESULTS: In both study groups MPAP and pulmonary vascular resistance (PVR) were found to be significantly lower at T(1) when compared to that of T(0) period (p<0.05). MPAP and PVR were significantly lower and mean arterial pressure (MAP) was significantly higher in group II when compared to group I at T(1) period (p<0.05). In addition to decreases in PVR and MPAP, iloprost also increased cardiac output (CO)(4.9+/-1.3 vs 5.1+/-0.9, p<0.05) and stroke volume (SV)(48+/-13 vs 56+/-13, p<0.05). CONCLUSION: Inhaled iloprost and nitroglycerin, both effectively reduce MPAP and PVR without affecting MAP, systemic vascular resistance (SVR) and CO. However, iloprost seems to be a more powerful pulmonary vasodilator, therefore we suggest iloprost inhalation in patients with severe PHT.     

Iloprost improves hemodynamics in patients with severe chronic cardiac failure and secondary pulmonary hypertension

PURPOSE: Significant pulmonary hypertension is a predictor of postoperative right heart insufficiency and increased mortality in patients undergoing orthotopic heart transplantation. Since the use of iv vasodilators is limited by their systemic effects, we evaluated the pulmonary and systemic hemodynamic effects of inhaled aerosolized iloprost (IP) in heart transplant candidates with elevated pulmonary vascular resistance (PVR). METHODS: Twenty-nine male heart transplant candidates because of dilated or ischemic cardiomyopathy with elevated PVR were included in the study. After assessing baseline hemodynamics, 50 micro g aerosolized IP were administered by inhalation. RESULTS: Inhalation of iloprost reduced PVR index (PVRI; 416 +/- 180 vs 349 +/- 173 dyn x sec(-1) x m(-2) x cm(-5); P < 0.01) and mean pulmonary artery pressure (MPAP; 28.6 +/- 9 vs 24.2 +/- 9.1 mmHg; P < 0.01), but did not affect blood pressure or systemic vascular resistance. An additional improvement of ventricular performance with an increase of cardiac index (CI; 2.8 +/- 0.7 vs 2.6 +/- 0.7 L x min(-1) x m(-2); P < 0.05) and a decrease of pulmonary capillary wedge pressure (PCWP; 15.6 +/- 6.8 vs 12.8 +/- 7.1 mmHg; P < 0.01) was observed after inhalation of IP. CONCLUSIONS: Inhaled aerosolized iloprost effectively reduces MPAP and is accompanied by an increase in CI and stroke index. Further advantages of iloprost inhalation are the lack of adverse reactions and ease of administration. Iloprost may be a useful drug to screen for vascular reactivity in cardiac transplantation patients.     

Inhaled iloprost in eight heart transplant recipients presenting with post-bypass acute right ventricular dysfunction

BACKGROUND: During heart transplantation, weaning from cardiopulmonary bypass may be particularly laborious as a result of superimposed acute right ventricular dysfunction in the setting of pre-existing pulmonary hypertension. Research in recent years has focused on inhaled vasodilatory treatment modalities which selectively target the pulmonary circulation. METHODS: We present a series of eight patients in whom inhaled iloprost, a synthetic prostacyclin analog, was used to treat pulmonary hypertension and right ventricular dysfunction detected by transesophageal echocardiography during a heart transplant procedure. In addition to conventional inotropic support, 20 mug of inhaled iloprost was administered via nebulized aerosol for a 20-min period. Complete sets of hemodynamic measurements were obtained before inhalation and during and after cessation of the inhalation period. RESULTS: Inhaled iloprost decreased the transpulmonary gradient at the end of the inhalation period relative to baseline (8.2 +/- 1.6 mmHg vs. 11.2 +/- 0.9 mmHg, P < 0.05). The mean pulmonary artery pressure to systemic artery pressure ratio decreased over this period (0.24 +/- 0.07 vs. 0.44 +/- 0.09, P < 0.05). A statistically significant decrease in the pulmonary vascular resistance to systemic vascular resistance ratio was also observed (0.10 +/- 0.02 vs. 0.19 +/- 0.02, P < 0.05). Improved indices of right ventricular function were observed in echocardiographic monitoring. CONCLUSION: During heart transplantation procedures, episodes of pulmonary hypertension can be successfully treated with inhaled iloprost administration, without untoward side-effects or significant systemic impact.     

Inhaled iloprost to control pulmonary artery hypertension in patients undergoing mitral valve surgery: a prospective, randomized-controlled trial

Background: Pulmonary hypertension (PHT) is common in patients undergoing mitral valve surgery and is an independent risk factor for the development of acute right ventricular (RV) failure. Inhaled iloprost was shown to improve RV function and decrease RV afterload in patients with primary PHT. However, no randomized‐controlled trials on the intraoperative use of iloprost in cardiac surgical patients are available. We therefore compared the effects of inhaled iloprost vs. intravenous standard therapy in cardiac surgical patients with chronic PHT. Methods: Twenty patients with chronic PHT undergoing mitral valve repair were randomized to receive inhaled iloprost (25 μg) or intravenous nitroglycerine. Iloprost was administered during weaning from cardiopulmonary bypass (CPB). Systemic and pulmonary haemodynamics were assessed with pulmonary artery catheterization and transoesophageal echocardiography. Milrinone and/or inhaled nitric oxide were available as rescue medication in case of failure to wean from CPB. Results: Inhaled iloprost selectively decreased the pulmonary vascular resistance index after weaning from CPB (208 ± 108 vs. 422 ± 62 dyn·s/cm⁵/m², P<0.05), increased the RV‐ejection fraction (29 ± 3% vs. 22 ± 5%, P<0.05), improved the stroke volume index (27 ± 7 vs. 18 ± 6 ml/m², P<0.05) and reduced the transpulmonary gradient (10 ± 4 vs. 16 ± 3 mmHg, P<0.05). In all patients receiving inhaled iloprost, weaning from CPB was successful during the first attempt. In contrast, three patients in the control group required re‐institution of CPB and had to be weaned from CPB using rescue medication. Conclusions: In patients with pre‐existing PHT undergoing mitral valve surgery, inhaled iloprost is superior to intravenous nitrogylycerine by acting as a selective pulmonary vasodilator, reducing RV afterload and moderately improving RV‐pump performance.     

Inhaled aerosolized iloprost in the evaluation of heart transplant candidates--experiences with 45 cases

PURPOSE: Pulmonary hypertension represents a significant predictor of postoperative right heart insufficiency and increased mortality in patients undergoing orthotopic heart transplantation. As the use of intravenous vasodilators is limited by their systemic effects, we evaluated the pulmonary and systemic hemodynamic effects of inhaled aerosolized iloprost in heart transplant candidates with elevated pulmonary vascular resistance. METHODS: Forty-five male heart transplant candidates with dilated or ischemic cardiomyopathy were included in the study. After assessing baseline hemodynamics, 20 microg of aerosolized iloprost was administered by ultrasonic inhalation. All patients were breathing spontaneously. RESULTS: Inhalation of iloprost reduced pulmonary vascular resistance index (395 +/- 205 vs 327 +/- 222 dyne.s.cm(-5).m(-2); P < 0.05) and mean pulmonary arterial pressure (28.7 +/- 10 vs 24.3 +/- 10 mm Hg; P < 0.05). An additional improvement of ventricular performance with an increase of cardiac index (2.7 +/- 0.7 vs 3.0 +/- 0.8 L.min(-1).m(-2); P < 0.05) and a decrease of pulmonary capillary wedge pressure (16.6 +/- 7.7 vs 13.4 +/- 7.3 mm Hg; P < 0.05) was accompanied by a slight decrease of systemic vascular resistance (1280 +/- 396 vs 1172 +/- 380 dyne.s.cm(-5); P < 0.05). However, the mean arterial pressure remained uninfluenced. CONCLUSIONS: Inhaled aerosolized iloprost effectively reduces mean pulmonary arterial pressure and also induces an increase in cardiac index. Further advantages of iloprost inhalation are the lack of adverse reactions and ease of administration. Iloprost represents a useful drug to screen for vascular reactivity in cardiac transplantation patients.     

Inhaled nitric oxide for pulmonary hypertension after heart transplantation.

BACKGROUND: Recipient pulmonary hypertension due to chronic congestive heart failure is a major cause of right ventricular (RV) dysfunction after heart transplantation. We hypothesized that inhaled nitric oxide (NO), in the postoperative period, would a) selectively reduce pulmonary vascular resistance and improve RV hemodynamics and b) reduce the incidence of RV dysfunction compared with a matched historical group. METHODS: Sixteen consecutive adult heart transplant recipients with lowest mean pulmonary artery (PA) pressures >25 mmHg were prospectively enrolled. Inhaled NO at 20 parts per million (ppm) was initiated before termination of cardiopulmonary bypass (CPB). At 6 and 12 hours after CPB, NO was stopped for 15 minutes and systemic and pulmonary hemodynamics were measured. RV dysfunction was defined as central venous pressure >15 mmHg and consistent echocardiographic findings. The incidence of RV dysfunction and 30-day survival in this group was compared with a historical cohort of 16 patients matched for pulmonary hypertension. RESULTS: Discontinuation of NO for 15 minutes at 6 hours after transplantation resulted in a significant rise in mean PA pressure, pulmonary vascular resistance (PVR), and RV stroke work index. Systemic hemodynamics were not affected by NO therapy. One patient in the NO-treated group, compared with 6 patients in the historical cohort group, developed RV dysfunction (P< .05). The 30-day survival in the NO-treated group and the historical cohort group were 100% and 81%, respectively (P> .05). CONCLUSION: In heart transplant recipients with pulmonary hypertension, inhaled NO in the postoperative period selectively reduces PVR and enhances RV stroke work. Furthermore, NO reduces the incidence of RV dysfunction in this group of patients when compared with a historical cohort matched for pulmonary hypertension. Inhaled NO is a useful adjunct to the postoperative treatment protocol of heart transplant patients with pulmonary hypertension.     

Hemodynamic effects of inhaled aerosolized iloprost and inhaled nitric oxide in heart transplant candidates with elevated pulmonary vascular resistance.

OBJECTIVE: An elevated pulmonary vascular resistance (PVR) is described as a predictor of postoperative right heart failure and increased mortality in patients undergoing orthotopic heart transplantation. The use of intravenous vasodilators is limited by their systemic effects. We evaluated the pulmonary and systemic hemodynamic effects of inhaled nitric oxide (NO) and inhaled aerosolized iloprost (IP) in heart transplant candidates with elevated PVR. METHODS: Fourteen male heart transplant candidates due to dilative or ischemic cardiomyopathia with elevated PVR (> or = 180 dyn s cm(-5)) were included in the study. Increasing concentrations of NO (5, 10 and 30 ppm) and 50 microg aerosolized IP were administered by inhalation. Hemodynamic measurements preceded and followed administration of each agent. RESULTS: Inhalation of IP, 10, and 30 ppm NO reduced PVR and mean pulmonary artery pressure (MPAP), but did not affect blood pressure or systemic vascular resistance. Comparing the effectiveness of 10 ppm NO and IP, we found a significant higher reduction of MPAP in patients treated with IP. An increase of cardiac index and stroke index could only be shown with IP-inhalation. CONCLUSIONS: Inhaled iloprost induces pulmonary vasodilation which is significantly greater than the effects of 10 and 30 ppm NO. The results of our study show, that inhaled iloprost induces a reliable hemodynamic response in the evaluation of heart transplant candidates. Further advantages of iloprost inhalation are the lack of adverse reactions and toxic side effects and an easier administration. Due to this facts we recommend iloprost as a routine screening drug for vascular reactivity in HTx-candidates. Based on our results it would be of great interest to investigate the role of iloprost in management of postoperative right heart insufficiency following cardiac transplantation.     

吸入一氧化氮对室间隔缺损手术后肺动脉高压的疗效观察

目的　观察吸入一氧化氮(nitricoxide,NO)治疗室间隔缺损 (ventricularseptaldefect,VSD)术后肺动脉高压 (pulmonaryhypertension ,PH)的疗效。 方法　 2 0例VSD术后PH病人分别吸入 2 0×10 -6 、6× 10 -6 NO ,监测吸入前后的血流动力学、氧合指标。结果　吸入 2 0× 10 -6 NO后明显降低肺动脉压、肺循环阻力、肺内分流率、肺泡动脉血氧分压差 ,提高动脉血氧分压、氧供指数 ;以上指标停吸NO后恢复吸入NO前水平 ;再吸入 6× 10 -6 NO后恢复吸入 2 0× 10 -6 NO后水平 ,并维持至停吸NO后。吸入前后体循环压及阻力无变化。结论　吸入NO是治疗VSD手术后PH的一种有效的方法。     

Assessment of acute pulmonary vascular reactivity in portopulmonary hypertension.

The role of acute pulmonary vasodilator testing in portopulmonary hypertension (PoPH), a current contraindication for orthotopic liver transplantation (OLT), has not been thoroughly elucidated. The purpose of this work was to analyze the results of acute vasodilator testing with inhaled nitric oxide (NO), to compare them with intravenous epoprostenol (PGI(2)), and to investigate the acute effects of the oral vasodilator isosorbide-5-mononitrate (Is-5-MN), in patients with PoPH. A total of 19 patients with PoPH (male/female = 9/10) were studied. Pulmonary hemodynamic measurements were performed at baseline and during NO inhalation (40 ppm); additionally, 15 patients were tested with PGI(2) (2-12 mug/kg/minute) and 8 were tested with Is-5-MN (20-40 mg). Inhaled NO reduced pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) by 5.7% and 11.0%, respectively. PGI(2) elicited greater reductions in PAP (11.8%) and PVR (-24.0%), and produced a 28% drop in systemic vascular resistance (SVR) and a 17% increase in the cardiac index (CI). Is-5-MN reduced PAP by 25.6% and PVR by 21.5%, without systemic changes. There was good agreement between the response to PGI(2) and Is-5-MN: 6 patients of the whole series (32%) decreased PAP >20% from baseline, reaching a final value < or = 35 mmHg, the current limit for OLT. In conclusion, acute vasodilator testing has a relevant role in PoPH, as it identifies one-third of patients able to reach a more favorable hemodynamic situation, which can be determinant for their management. For vasodilator testing, PGI(2) is more suitable than NO in PoPH. Is-5-MN exerts a selective effect on pulmonary circulation in patients who had already responded to PGI(2).     

Is the transpulmonary pressure gradient a predictor for mortality after orthotopic cardiac transplantation?

Elevated pulmonary vascular resistance (PVR) is a well-known risk factor for right ventricular failure after orthotopic cardiac transplantation. The influence of preoperative transpulmonary pressure gradient (TPG) and PVR on post-transplant 30 days mortality was evaluated. To analyze the response of PVR and TPG to cardiac transplantation, we analyzed 718 adult patients undergoing primary cardiac transplantation. Indications for operation were: 35.2% ischemic cardiomyopathy (ICM), 61.2% idiopathic dilated cardiomyopathy (DCM), and 3.3% other diagnosis (e.g. hypertrophic cardiomyopathy). The mean age (51.9) and the mean ischemic time (169.7 min) were comparable between 30 days survivors and nonsurvivors. Student's t-tests and chi-square analysis were used to compare data from 30-day survivors and nonsurvivors. Statistical significance was defined as P < 0.05. Fisher's exact test and multiple logistic regression analysis was performed to evaluate the relationship between hemodynamic parameters and outcome after transplantation. Primary end-point was 30 days mortality and secondary end-point long-term survival of patient groups with different TPG and PVR values. In survivors the mean TPG was 10.3 +/- 5.1 (mean +/- SD) vs. 13 +/- 6.6 in patients who died after transplantation (P = 0.0012). The PVR was 2.6 +/- 1.4 vs. 3.5 +/- 2.2 (P = 0.0012). In multivariate logistic regression, the parameters TPG and PVR exhibit a significant influence between survivors and nonsurvivors after cardiac transplantation within 30 days (TPG: P = 0.0012; PVR: P = 0.0012). The mortality rates in patients with TPG > 11 mmHg and PVR < 2.8 Wood units or TPG < 11 mmHg and PVR > 2.8 Wood units were comparable to those with TPG < 11 mmHg and PVR < 2.8 mmHg. The TPG is an important predictor in nonrejection-related early mortality after orthotopic cardiac transplantation. The determination of TPG in combination with PVR is a more reliable predictor of early post-transplant survival than PVR alone.     

Influence of temperature on tracheal tube cuff pressure during cardiac surgery

BACKGROUND: Lateral wall pressure may cause tracheal injury by affecting tracheal capillary blood flow. Damage to the trachea is less severe when lateral wall pressure exerted by the endotracheal tube cuff does not exceed the mean capillary perfusion pressure of the mucosa. The purpose of this study was to determine the effects of hypothermic and normothermic cardiopulmonary bypass (CPB) on tracheal tube cuff pressure dynamics. METHODS: Twenty-two patients were studied during normothermic CPB (pulmonary artery blood temperature in the CPB period between 36 and 35 degrees C), and 22 patients during hypothermic CPB (pulmonary artery temperature in the CPB period between 32 and 28 degrees C). A Mallinckrodt Medical Lo-Contour Murphy tracheal tube, with high-volume, low-pressure cuff was used without lubricant. Intracuff pressure (ITCP) was recorded at end-expiration before, during and after cardiopulmonary bypass. RESULTS: ITCP measurements were different between groups during CPB at aortic cross-clamping (13.9 +/- 0.8 mmHg in the normothermic group versus 11.3 +/- 0.4 mmHg in the hypothermic group, P < 0.05), and respectively during CPB after aortic declamping (15.3 +/- 0.8 mmHg and 12.6 +/- 0.8 mmHg, P < 0.05) and after CPB at the end of surgery (16.8 +/- 0.7 mmHg and 18.6 +/- 0.3 mmHg, P < 0.05). CONCLUSION: We conclude that the ITCP is higher in normothermic CPB than in hypothermic CPB; however, the clinical significance of this observation needs further investigation.     

Deep hypothermic circulatory arrest and the femoral-to-radial arterial pressure gradient

OBJECTIVES: To determine the femoral-to-radial arterial pressure gradient, as well as the factors associated with them, in patients receiving cardiopulmonary bypass (CPB) with profound hypothermia and circulatory arrest. DESIGN: Retrospective automated hemodynamic record review. SETTING: University hospital. PARTICIPANTS: Patients undergoing pulmonary thromboendarterectomy with deep hypothermic circulatory arrest. MEASUREMENTS AND MAIN RESULTS: The automated hemodynamic records of 54 consecutive patients undergoing pulmonary thromboendarterectomy with deep hypothermic circulatory arrest were reviewed, comparing the femoral and radial arterial pressures throughout the intraoperative period. In 20 of the patients, the hemodynamic data from the first 16 postoperative hours were also studied. Forty-one of 54 (76%) of the patients exhibited a mean arterial gradient of at least 10 mmHg either during or after CPB, femoral being higher. Clinically significant gradients were noted throughout the CPB period and the post-CPB period in these patients. In the 54 patients studied, the systolic blood pressure (SBP) gradient was 32 +/- 19 mmHg after CPB (95% confidence limits 28.2 mmHg, 39.0 mmHg), and the mean arterial pressure (MAP) gradient was 6.3 +/- 4.9 mmHg (95% confidence limits 5.5 mmHg, 8.6 mmHg). The duration of clinically significant SBP (>10 mmHg) and MAP (>5 mmHg) gradients in the postoperative period were 5.2 +/- 5.7 hours and 5.8 +/- 7.2 hours, respectively. Advanced age correlated with high post-CPB pressure gradients in this population and was associated with prolonged postoperative resolution of the gradients. CONCLUSIONS: The femoral-to-radial arterial pressure gradients, particularly systolic, after CPB, were greater and of longer duration in these patients undergoing deep hypothermic circulatory arrest than gradients previously reported for routine CPB. Central arterial pressure monitoring is recommended for patients undergoing deep hypothermic circulatory arrest, being valuable both for intraoperative and postoperative care.     

Inhaled iloprost in patients with chronic thromboembolic pulmonary hypertension: effects before and after pulmonary thromboendarterectomy

BACKGROUND: In primary pulmonary hypertension, aerosolized prostanoids selectively reduce pulmonary vascular resistance and improve right ventricular function. In this study, hemodynamic effects of inhaled iloprost, a stable prostacyclin analogue, were evaluated in patients with chronic thromboembolic pulmonary hypertension (CTEPH) before and early after pulmonary thromboendarterctomy (PTE). METHODS: Ten patients (mean age 49 years old [32 to 70 years old], New York Heart Association functional class III and IV) received a dose of 33 micro g aerosolized iloprost immediately before surgery (T1), after intensive care unit admission (T2), and 12-hours postoperatively (T3). Effects on pulmonary and systemic hemodynamics and gas exchange were recorded and compared with preinhalation baseline values. RESULTS: Preoperatively, inhaled iloprost did not significantly change mean pulmonary artery pressure (mPAP), cardiac index (CI), or pulmonary vascular resistance (PVR). Postoperatively, inhaled iloprost induced a significant reduction of mPAP and PVR and a significant increase of CI at T2 and T3. Preinhalation versus postinhalation PVR was as follows: at T1, 847 versus 729 dynes. s. cm(-5), p = 0.45; at T2, 502 versus 316 dynes. s. cm(-5), p = 0.008; and at T3, 299 versus 227 dynes. s. cm(-5), p = 0.004. CONCLUSIONS: In patients with CTEPH, inhalation of iloprost elicits no significant pulmonary vasodilation before surgery, and may have detrimental effects on systemic hemodynamics. Postoperatively, it significantly reduces mPAP and PVR, and enhances CI. Following PTE, inhalation of iloprost is useful to improve early postoperative hemodynamics.     

Inhaled nitric oxide does not alter pulmonary or cardiac effects of fat embolism in dogs after cemented arthroplasty

PURPOSE: We examined the effect of inhaled nitric oxide (NO) on the acute pulmonary hypertension and right ventricular (RV) dilation after fat embolism. METHODS: A bilateral cemented arthroplasty (BCA), created fat embolism in 20 dogs. In Part A, 12 dogs were randomized to an NO group (n=6, inhaled NO 40 ppm before BCA and throughout the study) or a control group (n=6). In Part B, a third group of dogs (n=8) were given NO 20-40 ppm 2-3 min after BCA when pulmonary artery pressure (PAP) increased. Transesophageal echocardiography (TEE) and invasive hemodynamic monitoring evaluated the hemodynamic response to BCA. Postmortem, quantitative morphometry was used to estimate the number of fat emboli and diameter of lung vessel occluded by fat. RESULTS: Part A: The increase in PAP in the NO group (16 +/- 1 to 34 +/- 9 mmHg) within three minutes of BCA was not different from that in the control group (14 +/- 4 to 35 +/- 9 mmHg). Within three minutes of BCA, TEE demonstrated RV dilation in all groups (P < 0.05) but there was no difference in the change in RV area in the NO and control groups. When NO was given after BCA, no difference in PAP or RV dilation was noted from that in the control group. There were no differences, at post mortem, between the groups in the diameter of lung vessel occluded by fat CONCLUSION: Whether given before the embolic insult or two to three minutes after the onset of pulmonary hypertension, inhaled NO did not attenuate the acute pulmonary hypertension or RV dilation after cemented arthroplasty.     

吸入伊洛前列素行急性肺血管扩张试验在先天性心脏病合并重度肺动脉高压术前评估中的作用

目的 评价吸入伊洛前列素的急性肺血管扩张试验在先天性心脏病(CHD)肺动脉高压(PH)患者心脏外科手术适应证选择中的作用.方法 对2006年6月至2008年12月46例CHD合并重度PH患者的临床资料进行回顾性分析.其中男性15例,女性31例,平均年龄(12±9)岁.所有患者术前均接受心导管检查和吸入伊洛前列索试验,患者平均肺动脉压(mPAP)(80±13)mm Hg(1 mill Hg=0.133 kPa),平均肺小动脉阻力指数(PVRI)(17±10)wood·m2.将吸入伊洛前列素试验肺血管阳性反应定义为在体循环压力不变或上升的情况下,PVRI下降≥20%,并作为选择手术适应证的重要条件.药物试验阳性患者在心脏外科修补术后均放置肺动脉漂浮导管,监测术后肺动脉压力、阻力以及心功能状况.结果 46例患者中,药物试验阳性29例(63.1%),吸药后PVRI由(15±6)wood·m2降至(9-4-4)wood·m2,肺循环体循环阻力比(Rp/Rs)由0.7±0.2降至0.4±0.2(P值均<0.05).药物试验反应阴性者17例(36.9%),吸药后PVRI由(21±10)wood·m2降至(19±9)wood·m2(P<0.05),Rp/Rs由1.0±0.5降至0.9±0.5(P>0.05).23例患者接受了心脏外科手术治疗,全部存活.其中药物试验阳性组21例,术后mPAP降至(27±10)mm Hg.药物试验阴性组仅2例接受外科修补术,术后mPAP均>45 mm Hg.结论 吸入伊洛前列素试验阳性患者术后肺动脉压力和PVRI明显降低,可作为评价合并PH的CHD手术适应证的一种蕈要手段.     

Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension.

Patients with mitral valve disease can develop pulmonary artery hypertension that persists after mitral valve replacement. In 1987, nitric oxide (NO) was reported to be an important factor accounting for the biologic activity of endothelium-derived relaxing factor. Inhaled NO was subsequently reported to be a selective pulmonary vasodilator in animals and patients. Therefore we investigated the vasodilating effect of inhaled NO in patients with mild pulmonary artery hypertension after mitral valve replacement. Six patients who underwent mitral valve replacement for mitral stenosis presented with a mean pulmonary artery pressure greater than 25 mmHg within 24 h after surgery. During mechanical ventilation at FIO2 0.5, NO (36.8-38.4 ppm) was breathed for 10 min. Hemodynamic data were recorded before NO, after 10 min of NO inhalation, and 30 min after the end of NO inhalation. Statistically significant (P < 0.05) hemodynamic response to inhaled NO included a transient decrease in systolic (-10%), diastolic (-8%), and mean (-10%) pulmonary artery pressures; a decrease in pulmonary vascular resistance (-22%); an increase in mixed venous hemoglobin O2 saturation (+6%); and a decrease in arteriovenous O2 content difference (-7%). During NO inhalation, there was no change in systemic arterial or pulmonary wedge pressures. Methemoglobin levels remained < 1%. Inhalation of this concentration of NO for 10 min causes transient pulmonary artery vasodilation and hemodynamic improvement in patients with mild chronic pulmonary artery hypertension after mitral valve replacement.     

Does a hyperoncotic cardiopulmonary bypass prime affect extravascular lung water and cardiopulmonary function in patients undergoing coronary artery bypass surgery?

OBJECTIVE: Different types of colloidal priming for cardiopulmonary bypass (CPB) have been used to reduce fluid load and to avoid the fall of plasma colloid osmotic pressure (COP) that leads to edema formation and consequently can cause organ dysfunction. The discussion about the optimal priming composition, however, is still controversial. We investigated the effect of a hyperoncotic CPB-prime with hydroxyethyl starch (HES) 10% (200;0.5) on extravascular lung water (EVLW) and post-pump cardiac and pulmonary functions. METHODS: In 20 randomized patients undergoing elective coronary artery bypass graft surgery (CABG), a colloid prime (COP: 48 mmHg, HES-group, n = 10) and a crystalloid prime (Ringer's lactate, crystalloid group, n = 10) of equal volume were compared with respect to the effects on cardiopulmonary function. Cardiac index (CI), mean arterial pressure (MAP), pulmonary capillary wedge pressure (PCWP), systemic vascular resistance index (SVRI), pulmonary artery pressure (PAP), pulmonary vascular resistance index (PVRI), alveolo-arterial oxygen difference (AaDO(2)), pulmonary shunt fraction (Q(s)/Q(T)), EVLW (double-indicator dilution technique with ice-cold indocyanine green), COP, fluid balance and body weight were evaluated peri-operatively. RESULTS: Pre-operative demographic and clinical data, CPB-time, cross-clamp time and the number of anastomoses were comparable for both groups. During CPB, COP was reduced by 20% in the HES-group (18.9 +/- 3.7 vs. 23.7 +/- 2.2 mmHg, P < 0.05) while it was reduced by more than 50% of the pre-CPB value (9.8 +/- 2.0 vs. 21.4 +/- 2.1 mmHg, P < 0.05) in the crystalloid group (P < 0.05 HES- vs. crystalloid group). Post-CPB EVLW was unchanged in the HES-group but it was elevated by 22% in the crystalloid group (P < 0.05 HES- vs. crystalloid group), CI was higher in the HES-group (3.4 +/- 0.3 vs. 2.7 +/- 0.5l/min, P < 0.05). Fluid balance was less in the HES-group (813 +/- 619 vs. 2143 +/- 538, P < 0.05). Post-operative weight gain could be prevented in the HES-group but not in the crystalloid group (1.5 +/- 1.2 vs. -0.3 +/- 1.5, P < 0.05). No significant differences were seen for MAP, PAP, PCWP, SVRI, PVRI, AaDO(2) and (Q(s)/Q(T)) between the two groups at any time. CONCLUSIONS: Hyperoncotic CPB-prime using HES 10% improves CI and prevents EVLW accumulation in the early post-pump period, while pulmonary function is unchanged. This effect can be of benefit especially in patients with congestive heart failure.     

Early replacement of pulmonary valve after repair of tetralogy: is it really beneficial?

OBJECTIVES: Debate on the proper timing of pulmonary valve replacement (PVR) after repair of tetralogy of Fallot (TOF) is still continuing. Significant pulmonary regurgitation (PR) could result in right ventricular (RV) dysfunction, exercise intolerance, arrhythmia, and sudden death. We analyzed clinical results of PVR after repair of TOF to investigate potential risk factor for late outcomes. METHODS: From January 1993 to July 2002, 58 patients (38 males and 20 females) received PVR after repair of TOF. More than moderate degree of PR was observed in these patients by echocardiography. Mean age at PVR was 13.5+/-9.6 years (1.2-44) and TOF repair was performed at 5.2+/-7.1 years of age (0.5-34). Therefore, PVR was performed at 8.3+/-5.2 years (4 months-28 years) after repair. Preoperative electrocardiogram showed complete right bundle branch block in 49 patients (84.5%). Mean duration of QRS complex was 142+/-30 ms. Major arrhythmia occurred in eight patients. Twenty-nine patients complained decreased physical activity and 10 patients showed clinical signs of right heart failure. RESULTS: Early death occurred in one patient (2.5%). Major complication occurred in three patients (complete heart block in two, aortic rupture in one). Follow-up was performed for 2.5+/-2.4 years (46 days-10.3 years). There was no late death. Postoperative cardiothoracic ratio was significantly decreased (0.61+/-0.07 to 0.55+/-0.06, P < 0.001). Marked symptomatic improvement was noted in all patients. Postoperative symptomatic group (n = 14) showed older age at repair of TOF (12.5+/-10.7 vs 2.6+/-2.3 years, P = 0.003), older age at PVR (23.2+/-12.8 vs 10.1+/-5.0 years, P = 0.001), longer interval between repair of TOF and PVR (10.6+/-7.0 vs 7.5+/-4.2 years, P < 0.05), higher degree of functional class (2.4+/-0.5 vs 1.4+/-0.8, P < 0.001), and longer duration of hospitalization (30.0+/-14.2 vs 18.9+/-11.4 days, P = 0.004) than postoperative asymptomatic group (n = 43). CONCLUSIONS: In patients with significant PR after repair of TOF, PVR had clinical benefits including symptomatic improvement with low mortality and morbidity. Proper timing must be carefully selected according to objective evaluation of RV function. In our study, earlier PVR prior to symptomatic manifestation showed beneficial effects.     

The additive pulmonary vasodilatory effects of inhaled prostacyclin and inhaled milrinone in postcardiac surgical patients with pulmonary hypertension.

Selective pulmonary vasodilation is an advantageous therapeutic strategy for cardiac surgical patients with increased pulmonary vascular resistance (PVR) and right ventricular failure. We hypothesized that milrinone, an adenosine-3',5'-cyclic monophosphate (cAMP)-selective phosphodiesterase enzyme (PDE) inhibitor may, when nebulized and inhaled, cause selective pulmonary vasodilation and potentiate the vasodilation by inhaled prostacyclin (iPGI(2)). Consequently, we investigated the hemodynamic effects of inhaled milrinone or the combination iPGI(2) + inhaled milrinone in cardiac surgical patients with postoperative mean pulmonary arterial pressure (MPAP) >25 mm Hg and PVR >200 dynes. s(-1). cm(-5). During mechanical ventilation and using a conventional nebulizing system, 9 patients inhaled incremental concentrations of milrinone (0.25, 0.5 and 1 mg/mL) in subsequent 10-min periods (Study Part 1). In the same manner, 11 patients received iPGI(2) (10 microg/mL) followed by the combination of iPGI(2) (10 microg/mL) and inhaled milrinone (1 mg/mL) (Study Part 2). Inhaled milrinone reduced PVR with a maximal effect (-20%, P < 0.001) at the largest concentration. As compared with iPGI(2) alone, iPGI(2) + inhaled milrinone caused a further and prolonged reduction of PVR (-8%, P < 0.05) and increased stroke volume (+5%, P < 0.05). Systemic vascular resistance or mean arterial pressure was not affected by inhalation of either drug(s). The authors conclude that inhalation of the cAMP-selective PDE-inhibitor milrinone selectively dilates the pulmonary vasculature without systemic effects in cardiac surgical patients with pulmonary hypertension. Furthermore, inhaled milrinone appears to potentiate and prolong the pulmonary selective vasodilatory effect of iPGI(2). Inhaled milrinone alone or combined with iPGI(2) may be an important therapeutic option in the treatment of patients with pulmonary hypertension and right ventricular failure. IMPLICATIONS: Pulmonary hypertension may cause or aggravate right heart failure. IV vasodilators reduce systemic blood pressure and might thereby further impair coronary perfusion and right heart performance. In the present study of cardiac surgical patients with pulmonary hypertension, selective pulmonary vasodilation without systemic effects was induced by nebulized, inhaled vasodilators.     

Arginine vasopressin is an ideal drug after cardiac surgery for the management of low systemic vascular resistant hypotension concomitant with pulmonary hypertension

Low systemic vascular resistance (SVR) hypotension concomitant with pulmonary hypertension (PH) is difficult to manage postoperatively because they are often catecholamine-resistant. So, we applied arginine vasopressin (AVP), which is a potent vasoconstrictor in a specific condition, for post-cardiotomy refractory low SVR hypotension concomitant with PH. We treated nine cases of postoperative refractory vasodilatory hypotension concomitant with PH even after conventional treatment that included nitric oxide inhalation and/or intraaortic balloon pump. AVP was administrated with 0.05 approximately 0.1 U/min intravenously. After AVP administration, the mean systemic arterial pressure increased from 47.3+/-9.5 to 76.5+/-12.2 mmHg (P<0.01) and SVR increased from 488.1+/-92.7 to 1188+/-87 dynes x s x cm(-5) (P<0.01). Fortunately, even though the cardiac index decreased, it remained in a normal range. Alteration in the PVR was not significant, but the Pp/Ps became somewhat lower (0.66+/-0.2 to 0.47+/-0.16, P<0.01). AVP increased the urine output and improved oxygenation. AVP improved systemic circulation (increased systemic blood pressure with maintaining cardiac output) without deterioration of pulmonary hypertension. AVP is an ideal drug for treating refractory low SVR hypotension concomitant with PH. But its indication must be limited.