Portopulmonary hypertension

Portopulmonary hypertension (PPHT) is a respiratory complication of portal hypertension, defined as an increase in mean pulmonary artery pressure (PAP) of > 25 mmHg with an increase in pulmonary vascular resistance of > 240 dyn.s/cm(-5) and a normal pulmonary capillary wedge pressure ( < 15 mmHg), which often occurs in subjects with liver cirrhosis. Histopathological features of PPHT are endothelial and smooth-muscle cell proliferation and fibrosis leading to luminal obstruction in the resistance arteries. The pathogenesis of PPHT may result from an imbalance between vasoconstrictor and vasodilating factors. The most common pulmonary symptom is exertional dyspnea; fatigue, chest pain and syncope occur more often at an advanced stage. Edema, ascites and prominent jugular veins are signs of both decompensated hepatic cirrhosis and right ventricular failure. Right heart catheterisation is the gold standard for the diagnosis and defines PPHT in mild disease with PAP less than 35 mmHg, moderate disease with PAP between 35 and 45 mmHg, and severe disease with PAP of 45 mmHg or higher. The medical treatment of portopulmonary hypertension is based on the treatment of other forms of pulmonary arterial hypertension, including vasomodulating pharmacologic agents. Liver transplantation is accompanied by high risk of mortality, generally due to acute right ventricular failure and cardiovascular collapse. The prognosis of PPHT is poor with mean survival of 15 months.     

终末期肝衰竭患者肝脏移植术后血流动力学变化

目的 :观察终末期肝衰竭患者肝脏移植术后的血流动力学变化。方法 :5例终末期肝衰竭患者行肝脏移植手术 ,监测其手术后 3日内中心静脉压 (CVP)、肺动脉压 (PAP)、肺小动脉楔压 (PAWP)、心排血量 (CO)和平均动脉压 (MAP)等参数的变化。结果 :患者术后进入 ICU当时的 MAP、肺毛细血管楔压 (PCWP)和 CVP均明显低于正常参考值 ,心率 (HR)显著增快 ;术后 3日内经过积极扩容 ,MAP、PCWP和 CVP显著升高(P均 <0 .0 1)。入 ICU后 8小时内的心脏指数 (CI)轻度降低 ,但与术后 2 4、4 8小时的 CI值比较均无显著性差异 (P均 >0 .0 5 )。入室后 8小时内的外周血管阻力指数 (SVRI)、肺血管阻力指数 (PVRI)轻度降低 ;术后 3日内上述指标逐渐恢复正常。结论 :终末期肝衰竭患者肝移植术后血流动力学不稳定 ,出现明显的血容量不足表现 ,如不及时纠正可能导致脏器灌注不足 ,乃至器官功能衰竭 ,因此 ,密切监测其血流动力学的变化 ,估计其血容量不足状态并予充分纠正 ,是肝移植患者安度围手术期的关键     

Cardiac-pulmonary edema and low pulmonary capillary wedge pressure

We describe a patient who presented with acute massive pulmonary edema, clinically and on chest roentgenogram. Two hours later the patient became hypotensive and was found to have a low pulmonary capillary wedge pressure (PCWP). The blood pressure returned to normal after administration of fluids. Acute pulmonary edema develops if PCWP rises higher than 25 to 30 mm Hg. In our patient, the elevated PCWP fell to low normal within two hours, when chest roentgenogram and clinical examination still suggested severe pulmonary edema. A phase lag existed between lowering of the pulmonary capillary wedge pressure and clearing of fluid from the alveolar and interstitial spaces in the lungs. At least three different pathogenetic mechanisms in patients with coronary artery disease can produce this phase lag. Transient global ischemia of the left ventricle was thought to be the responsible mechanism in our patient.     

非心源性休克患者脑钠肽与血流动力学参数的相关性分析及两者预测预后的价值探讨

目的 探讨非心源性休克患者血浆脑钠肽(BNP)水平与肺动脉漂浮导管(Swan-Ganz导管)所测得数据的相关性,以及与患者预后的关系.方法 采用前瞻性对照研究方法,选择本院重症监护病房(ICU)21例非心源性休克患者,置入Swan-Ganz导管,连续3d测定中心静脉压(CVP)、肺动脉压(PAP)、肺毛细血管楔压(PCWP)、心排血量(CO),同时进行血浆BNP定量检测;分析存活患者(8例)和死亡患者(13例)BNP及CVP、PAP、PCWP、CO的差异.采用多元回归分析法分析BNP与CVP、PAP、PCWP、CO的相关性.结果 死亡患者入院时血浆BNP浓度(ng/L)显著高于存活患者(708.06±242.58比317.05±140.21,P＜0.05);而两组患者血流动力学参数无明显差异.治疗3d后,死亡患者CVP (mm Hg,1 mm Hg=0.133 kPa)显著高于存活患者(13.64±4.00比9.92±1.26,P＜0.05),而CO( L/min)显著低于存活患者(4.61±2.06比6.95±1.28,P＜0.05),死亡患者和存活患者PAP( mm Hg)、PCWP( mm Hg)无明显差异(PAP:20.84±8.48比16.82±4.97,PCWP:13.60±5.71比12.72±4.98,均P＞0.05).多元回归分析显示,BNP与CVP、PAP、PCWP、CO均无明显相关性(r值分别为0.157、0.306、0.229、-0.269,P值分别为0.16、0.25、0.09、0.12).结论 血浆BNP和Swan-Ganz导管监测血流动力学参数对休克患者病情和预后的评估均有一定价值;但在非心源性休克患者中,BNP增高不能作为反映心功能的指标,不能替代Swan-Ganz导管用于指导治疗.     

Pulmonary hypertension complicating portal hypertension: portopulmonary hypertension]

Portopulmonary hypertension is a condition with a poor prognosis, which is defined as precapillary pulmonary hypertension complicating portal hypertension mainly due to cirrhosis of various etiologies. A mean pulmonary arterial pressure greater than 25 mmHg at rest with a pulmonary capillary wedge pressure less than 15 mmHg and a pulmonary vascular resistance greater than 120 dynes.sec.cm-5, in the setting of the presence of portosystemic shunting has been proposed as hemodynamic criteria for portopulmonary hypertension. Prevalence of pulmonary hypertension ascertained by right cardiac catheterization was 2% among patients with cirrhosis, and reached to 4% particularly among candidates for liver transplantation. Hyperdynamic systemic circulation seen commonly in patients with cirrhosis appeared to be normalized by complication of pulmonary hypertension with a contraction of circulating plasma volume. Long term treatment by epoprostenol administration or nitric oxide inhalation could induce a gradual decline in pulmonary arterial pressure in patients with poor response to acute vasodilator administration.     

右心室流出道多普勒血流频谱和肺毛嵌压对老年肺心病的临床诊断价值

为了评价脉冲多普勒记录右心室流出道（ＲＶＯＴ）及左室流入道（ＬＶＩＴ）血流频谱以检测肺动脉压（ＰＡＰ）和肺毛嵌压（ＰＣＷＰ）对老年肺心病的临床意义。研究老年肺心病（ＣＰ）２１例、老年慢性支气管炎（ＣＢ）２２例、健康老人（Ｈ）１５名。结果和结论：１）在ＲＶＯＴ比在肺动脉主干内记录血流图容易成功，在ＬＶＩＴ测定左室等容舒张时间比心机图容易；２）ＲＶＯＴ血流频谱可将ＣＰ与ＣＢ及Ｈ区别开来（Ｐ＜０．０１）。ＣＰ的ＲＶＯＴ血流图的特点是，加速时间缩短，＜１００ｍｓ；右心室收缩时间间期异常，ＲＰＥＰ／ＲＶＥＴ＞０．４；由血流曲线计算的肺动脉压及即血管总阻力增高；３）有气短和肺湿性罗音，如ＰＣＷＰ不高，则不支持左心功能不全或舒张型心力衰竭；４）ＣＰ患者的血浆心钠素（ＡＮＰ）显著升高。这反映肺动脉压和右心房压力升高；５）本文ＲＶＯＴ血流图诊断ＣＰ的敏感性为９０．５％，特异性９４．６％。     

Factors associated with increased extravascular lung water in cardiac tamponade and myocardial ischemia.

OBJECTIVE: To evaluate and compare the factors associated with pulmonary edema in cardiac tamponade and myocardial ischemia. DESIGN: Prospective, controlled laboratory study. SETTING: Animal research laboratory of a university hospital. SUBJECTS: Fourteen anesthetized dogs. INTERVENTION: Extravascular lung water (EVLW) was measured with thermal indocyanine green dye double-indicator dilution method and hemodynamic indices were determined by the pulmonary artery flotation catheter. Seven dogs were used in the tamponade model, and seven other dogs were used in the myocardial ischemia model. Furthermore, ten dogs were dedicated to measure plasma colloid osmotic pressure (COP) and blood gas analysis during cardiac tamponade and myocardial ischemia. MEASUREMENTS AND MAIN RESULTS: Mean right atrial pressure (MRAP) (7-->10 mm Hg), pulmonary capillary wedge pressure (PCWP) (10-->13 mm Hg), and EVLW (5.4-->10.1 mL/kg) increased during tamponade, but all of these indices returned to the control level after release of tamponade (MRAP, 7 mm Hg; mean PCWP, 11 mm Hg; mean EVLW, 5.2 mL/kg). Myocardial ischemia caused increases in PCWP (10-->14 mm Hg) and EVLW (5.6-->9.6 mL/kg). Although PCWP returned to the control level, EVLW remained elevated (9.2 mL/kg) after reperfusion. EVLW had good correlations with MRAP (r2 = .64, p < .05) and PCWP (r2 = .62, p < .05) during cardiac tamponade. Despite a fair correlation between EVLW and PCWP during ischemia (r2 = .73, p < .05), EVLW was not related to PCWP after reperfusion. COP decreased during myocardial ischemia and at the reperfusion period, but there was no significant change in COP in the cardiac tamponade model. CONCLUSIONS: In contrast to a close relation between hydrostatic pressure and EVLW in cardiac tamponade, hydrostatic pressure was not a determinant of pulmonary edema during the reperfusion period after myocardial ischemia.     

Contrast-enhanced Doppler hemodynamics for noninvasive assessment of patients with chronic heart failure and left ventricular systolic dysfunction.

We sought to evaluate whether contrast-enhanced Doppler echocardiography can improve the noninvasive estimation of hemodynamic variables in left ventricular (LV) dysfunction. Right-heart catheterization and Doppler echocardiography were simultaneously performed in 45 patients with LV dysfunction (ejection fraction: 29 +/- 7%) in sinus rhythm. Noninvasive variables were estimated as follows: cardiac output by pulsed Doppler of LV outflow tract; pulmonary capillary wedge pressure by a regression equation including mitral and pulmonary venous flow variables; pulmonary artery mean pressure from the calculated systolic and diastolic pulmonary artery pressures; and pulmonary vascular resistance from the previous measurements according to hemodynamic definition. Contrast enhancement increased the feasibility of pulmonary capillary wedge pressure estimation from 60% to 100%; of pulmonary artery mean pressure from 42% to 91%; and of pulmonary vascular resistance from 42% to 91%. Strong correlations between invasive and noninvasive hemodynamic variables were found: r = 0.90, standard error of the estimate (SEE) 0.45 L/min for cardiac output; r = 0.90, SEE 3.1 mm Hg for pulmonary capillary wedge pressure; r = 0.93, SEE 3.7 mm Hg for pulmonary artery mean pressure; and r = 0.85 SEE 1.0 Wood units for pulmonary vascular resistance. Weaker correlations for PAMP (r = 0.82, SEE 5.6 mm Hg) and PVR (r = 0.66, SEE 1.7 Wood units) were apparent prior to contrast enhancement. When patients were separated according to PVR threshold values, the contrast allowed the correct placement of 88% of patients, whereas only 57% were correctly assigned without it. The contrast increased accuracy and reduced interobserver variability in the evaluation of hemodynamic variables. The contrast-enhanced study is capable of increasing the value of noninvasive hemodynamic assessment in LV dysfunction.     

重组人脑利钠肽治疗顽固性心力衰竭临床研究

目的 研究重组人脑利钠肽(rhBNP)治疗顽固性心力衰竭(RHF)患者血液动力学效应及安全性.方法 选择住院期间经常规抗心力衰竭药物强化治疗无明显改善的RHF患者16例,给予rhBNP 1.5 μg/kg静脉冲击后,以0.007 5μg/(kg·min)连续静脉滴注24h.在给药后24h内监测有创血液动力学参数、血压、心率及血清生化指标,应用rhBND 3 d后,行超声心动图检测心脏指数(CI)、左心室舒张末期容积(LEVDD)、左心室射血分数(LVEF).结果 在注射rhBNP 15 min时肺毛细血管楔压[PCWP(22.7±4.0)mm Hg与(25.3±3.9)mm Hg]、平均肺动脉压[MPAP(31.9±3.6)mm Hg与(34.6±7.8)mm Hg]较基础值明显下降(P＜0.05);收缩压在给药后1h下降[(105.2±11.5)mm Hg与(119.0±17.2)mm Hg],差异有统计学意义(P均＜0.01),以后逐渐恢复至基线时水平;用药24h心率也明显改善[(109.0±10.8)次/min与(82.2±8.6)次/min](P ＜0.01);血钾、血钠、血肌酐无明显变化;用药3d后CI[(3.7±0.6)L/m2与(1.8±0.4)L/m2]和EF[(43.1±8.3)％与(31.2±6.4)％]均有明显改善,LVEDD明显缩小[(63.6±5.7)mm与(67.3±6.2)mm](P均＜0.01).未发生与rhBNP相关的症状性低血压及其他严重不良反应.结论 静脉应用rhBNP能迅速改善RHF患者血液动力学状况,且安全可行.     

Pulmonary hypertension: a review of pathophysiology and anesthetic management

Pulmonary hypertension is a condition that can result in serious complications in patients undergoing any type of anesthesia during the perioperative period. By definition, pulmonary artery hypertension is caused by a persistent rise in mean pulmonary artery pressure ≥25 mm Hg with Pulmonary capillary wedge pressure ≤ 15 mm Hg or exercise mean pulmonary artery pressure ≥35 mm Hg and pulmonary vascular resistance ≥ 3 wood unit's. The severity of the complications depends on the severity of the underlying condition, other comorbidities, and type of procedure, anesthetic technique, and anesthetic drugs. In this article, we briefly review the pulmonary vascular physiology, pathophysiology of the disease, clinical assessment and diagnosis, treatment options, and the anesthetic management of these patients.     

Effect of the 30 degree lateral recumbent position on pulmonary artery and pulmonary artery wedge pressures in critically ill adult cardiac surgery patients.

BACKGROUND: Despite demonstrated benefits of lateral positioning, critically ill patients may require prolonged supine positioning to obtain reproducible hemodynamic measurements. OBJECTIVES: TO determine the effect of 30 degree right and left lateral positions on pulmonary artery and pulmonary artery wedge pressures after cardiac surgery in critically ill adult patients. METHODS: An experimental repeated-measures design was used to study 35 patients with stable hemodynamics after cardiac surgery. Subjects were randomly assigned to 1 of 2 position sequences. Pulmonary artery and pulmonary artery wedge pressures were measured in each position. RESULTS: Measurements obtained from patients in the 30 degree left lateral position differed significantly (all Ps < .05) from measurements obtained from patients in the supine position for pulmonary artery systolic, end-diastolic, and mean pressures. Pulmonary artery wedge pressures did not differ significantly; however, data were available from only 17 subjects. The largest mean difference in pressures between the 2 positions was 2.0 +/- 2.1 mm Hg for pulmonary artery systolic pressures, whereas maximum differences for end-diastolic and pulmonary artery wedge pressures were 1.4 +/- 2.7 mm Hg and 1.6 +/- 2.4 mm Hg, respectively. Clinically significant position-related changes in pressure occurred in 12 (2.1%) of 581 pressure pairs. Clinically significant changes occurred in end-diastolic pressure in 2 subjects and in pulmonary artery wedge pressure in 1 subject. CONCLUSiONS: In patients with stable hemodynamics during the first 12 to 24 hours after cardiac surgery, measurements of pulmonary artery and pulmonary artery wedge pressures obtained in the 30 degree lateral and supine positions are clinically interchangeable.     

A case of respiratory distress syndrome complicated by the development of interstitial emphysema and pneumomediastinum

A 15-year-old patient has been admitted to the intensive care unit for severe respiratory distress syndrome that developed as a result of pneumonia. Interstitial lung edema was confirmed by computer-aided tomography. It was successfully treated by positive pressure ventilation (PPV). Although PEEP did not exceed 7 cm H2O, PPV was complicated by interstitial emphysema, pneumomediastinum, and bilateral pneumothorax as a result of barotrauma. Pulmonary artery pressure (PAP) and pulmonary capillary wedge pressure (PCWP) were monitored. High PCWP values were inconsistent with the diagnosis of acute respiratory distress syndrome. The authors suggest that high PCWP was caused by high intraalveolar pressure, pneumomediastinum, and venule constriction in the hypoxic sites of the lung.     

Effects of Escherichia coli endotoxin on pulmonary vascular resistance in intact dogs

The effects of endotoxin on pulmonary hemodynamics were studied in seven intact dogs. The distribution of pulmonary vascular resistance was estimated by the effective pulmonary capillary pressure, which was derived from the pressure transient recorded while the pulmonary artery catheter was rapidly wedged. After the injection of endotoxin, cardiac output and aortic pressure consistently fell. Pulmonary artery occlusion (wedge) pressure also decreased, but not significantly. Although pulmonary artery pressure did not necessarily rise, total pulmonary vascular resistance increased in every dog. The absolute increase in pulmonary artery resistance was greater (142 mm Hg/L X min/kg); than in venous resistance (111 mm Hg/L X min/kg); however, the relative increase in venous resistance was higher (410% for venous resistance vs. 220% for pulmonary artery resistance). As a result of venoconstriction, there was a consistent increase in effective pulmonary capillary pressure (from 2.5 to 6.3 mm Hg). Our data indicate that the pulmonary vascular response to endotoxin injection is characterized by constriction of both pulmonary arteries and pulmonary veins. The capillary wedge pressure did not reflect the pulmonary microvascular pressure, since it varied in the opposite direction to the effective capillary pressure.     

单肺移植治疗伴有肺动脉高压的终末期肺病

目的观察单肺移植治疗对伴有肺动脉高压的终末期肺病患者的疗效。方法2002年9月—2005年11月我院22例单肺移植患者,其中肺气肿10例、肺纤维化10例、矽肺1例、肺淋巴管平滑肌瘤病1例。受体肺移植术前评估肺动脉压均显示有不同程度的升高。手术方式:左肺移植10例,右肺移植12例。术前常规心脏超声监测肺动脉收缩压,并通过动脉血气分析计算氧合指数(PaO2/FiO2)。结果术后1周用Swan-Ganz导管测定患者平均肺动脉收缩压,较术前有明显下降,从(50.00±13.00)mmHg(1mmHg=0.133kPa)降至(39.50±7.36)mmHg(P<0.05);PaO2/FiO2明显改善,从(241.26±79.54)mmHg升到(348.23±99.31)mmHg(P<0.05)。结论单肺移植是治疗伴肺动脉高压终末期肺病的有效和可选方法。     

Significance of diastolic pulmonary artery pressure peaks

We describe a patient undergoing elective surgery for treatment of an abdominal aortic aneurysm in whom an abrupt change in the contour of the pulmonary artery pressure (PAP) trace indicated the development of an intermediate (20 mm Hg) V wave in the pulmonary artery wedge pressure (PAWP) trace. As the PAP trace is displayed continuously, attention to its contour may allow for early detection of changes to the underlying PAWP trace.FC Anaesth     

Significance of diastolic pulmonary artery pressure peaks

We describe a patient undergoing elective surgery for treatment of an abdominal aortic aneurysm in whom an abrupt change in the contour of the pulmonary artery pressure (PAP) trace indicated the development of an intermediate (20 mm Hg) V wave in the pulmonary artery wedge pressure (PAWP) trace. As the PAP trace is displayed continuously, attention to its contour may allow for early detection of changes to the underlying PAWP trace.FC Anaesth     

Atrial Natriuretic Peptide During Different Pacing Modes in a Comparison with Hemodynamic Changes

The study investigates the response of atrial natriuretic peptide (ANP) to different cardiac pacing modes in comparison with hemodynamic changes. Ten patients underwent Swan-Ganz catheterization during pacemaker implant. Atrioventricular and ventricular pacing were performed consecutively at three pacing rate levels (80, 100, and 110 ppm). Blood samples were taken from the pulmonary artery for ANP determination, both basally and at the end of each pacing period. Concomitantly, mean pulmonary capillary wedge pressure (PCWP) and mean pulmonary artery pressure (PAP) were measured. Cardiac output (CO) was determined by thermodilution both basally and during the 110 ppm steps. During atrioventricular pacing, whereas no significant changes were observed for ANP, PCWP and PAP, CO increased significantly (P less than 0.0005). At the beginning of ventricular pacing hemodynamic parameters and ANP levels were comparable with those of baseline conditions. During subsequent ventricular pacing PCWP and ANP increased significantly at the 110 ppm rate step (P less than 0.05). PAP did not change significantly, whereas CO decreased in all cases (P less than 0.01). A positive correlation was observed between ANP and PCWP during ventricular (P less than 0.001), but not atrioventricular pacing. The results, while confirming the hemodynamic advantages of atrioventricular pacing, point to a major stimulation of ANP secretion during ventricular pacing. This fact, together with the observed drop in CO and the correlation between ANP and PCWP, suggest that the increase of ANP in ventricular pacing may be the expression of a compensatory mechanism to the hemodynamic disadvantages of atrioventricular asynchrony.     

第六届世界肺高血压会议:聚焦肺高血压定义与诊断分类更新

第六届世界肺高血压会议对肺高血压(pulmonary hypertension, PH)的定义和诊断分类进行了修订和更新。PH的血流动力学定义维持不变, 将毛细血管前性PH定义更新为:肺动脉平均压＞20 mm Hg、肺动脉楔压 < 15 mm Hg且肺血管阻力> 3 WU。诊断分类更新包括:增加急性肺血管扩张试验阳性肺动脉高压(pulmonary arterial hypertension, PAH)亚类, 将甲基苯丙胺(冰毒)和达沙替尼致PAH作用由可能升级为肯定, 将肺静脉闭塞病/肺毛细血管瘤病由特殊的1'更新为PAH的一个亚类, 将脾切除术后和甲状腺疾病从PH诊断分类中移除等。本次PH定义和诊断分类更新将为临床实践提供重要指导意义。     

Hemodynamic profiles of prostaglandin E1, isoproterenol, prostacyclin, and nifedipine in experimental porcine pulmonary hypertension

BACKGROUND AND METHODS: We compared the hemodynamic effects of four vasodilators in experimental embolic pulmonary hypertension in a randomized controlled trial, using nine pigs weighing 16 to 23 kg. After anesthesia induction and cannulation with arterial, central venous, and thermodilution output pulmonary artery catheters, animals were repetitively embolized with glass beads (60 to 160 mu) in order to establish pulmonary hypertension (pulmonary artery pressure [PAP] doubled from baseline). Prostaglandin E1 (PGE1), isoproterenol, prostacyclin (PGI2), and nifedipine were compared at doses producing equivalent reduction in systemic BP. RESULTS: Only PGE1 and PGI2 decreased both PAP and pulmonary vascular resistance (PVR). PGE1 decreased PAP from 39 +/- 1 to 33 +/- 1 mm Hg; prostacyclin decreased PAP from 38 +/- 1 to 31 +/- 1 mm Hg and produced the largest increase in cardiac output (Qt). Isoproterenol did not change PAP, markedly increased heart rate (162 +/- 8 to 216 +/- 11 beats/min), and resulted in significant arrhythmias. Nifedipine increased PVR from 1044 +/- 113 to 1125 +/- 100 dyne.sec.cm-5 and decreased Qt. CONCLUSIONS: Vasodilators demonstrate unique hemodynamic drug profiles. Isoproterenol infusion is characterized by tachycardia and arrhythmias. Both PGE1 and PGI2 effectively decrease PAP and PVR. Nifedipine depressed Qt significantly in this glass-bead embolization model of acute pulmonary hypertension.     

The spectrum of left ventricular filling in severe aortic stenosis

To assess left ventricular diastolic filling in valvular aortic stenosis, pulsed Doppler echocardiography was used prospectively in 35 patients with severe aortic stenosis (valve area < 1 cm²) and in 38 age-matched normal subjects. Twenty-seven patients had a normal left ventricular systolic function at rest (ejection fraction > 0.50) and a normal or only slightly increased mean pulmonary capillary wedge pressure (mean 11±4 mm Hg). Eight patients had a poor left ventricular systolic function (ejection fraction: 0.28±0.10) and an elevated mean pulmonary capillary wedge pressure (mean: 36±9 mm Hg). The Doppler derived filling parameters were correlated with hemodynamic data, left ventricular wall thickness derived from M-mode echocardiograms, heart rate and atrio-ventricular (A-V) conduction delay using stepwise multiple correlation. The data of this study suggest that left ventricular filling is significantly impaired in patients with severe aortic stenosis and left ventricular hypertrophy with an increase in late diastolic (A-wave) velocity, an increase in the A/E ratio, a decrease in the first one-half filling fraction and a prolongation of early diastolic deceleration time. These changes in filling hemodynamics are associated with alterations in mean pulmonary capillary wedge pressure, left ventricular wall thickness, heart rate and A-V conduction delay. When heart failure develops as a result of impaired left ventricular systolic function, an increase in left atrial filling pressure is associated with a shift of left ventricular filling towards early diastole with a ‘normalisation’ of the transmitral flow velocity curve. In extreme cases, a progression towards a ‘restrictive’ filling pattern is found with a marked shortening of the left ventricular early diastolic deceleration time. In the presence of high filling pressures, increased left atrial driving pressure (derived from the mean pulmonary capillary wedge pressure) is associated with changes in the left ventricular filling pattern irrespective of the presence and the degree of myocardial hypertrophy.