Relationship of pulmonary artery diastolic and pulmonary artery wedge pressures in mitral stenosis

Resting and exercise hemodynamic studies were performed in 33 patients with mitral stenosis (14 men and 19 women; average age, 25 years) in normal sinus rhythm with normal pulmonary vascular resistances. A normal pulmonary vascular resistance was assumed when the resting pressure gradient between the pulmonary artery diastolic and mean pulmonary artery wedge pressures was 5 mm. Hg or less. A satisfactory correlation existed between the pulmonary artery wedge and pulmonary artery diastolic pressures at rest (r = 0.9017) and during exercise (r = 0.8670). A method of predicting pulmonary artery wedge pressure from pulmonary artery diastolic pressure during exercise was formulated. The correlation between the predicted and measured exercise pulmonary artery wedge pressures was very close (r = 0.9561). It is suggested that during exercise the pulmonary artery diastolic pressure can be modified as above and substituted for mean pulmonary artery wedge pressure if the resting gradient between pulmonary artery wedge and pulmonary artery diastolic pressure is known.     

Continuous-wave Doppler echocardiographic detection of pulmonary regurgitation and its application to noninvasive estimation of pulmonary artery pressure

Continuous-wave Doppler echocardiography was used to estimate pulmonary artery pressures by measuring pulmonary regurgitant flow velocity in 21 patients with pulmonary hypertension (mean pulmonary artery pressure greater than or equal to 20 mm Hg) and 24 patients without pulmonary hypertension. The pulmonary regurgitant flow velocity patterns, characterized by a rapid rise in flow velocity immediately after closure of the pulmonary valve and a gradual deceleration until the next pulmonary valve opening, were successfully obtained in 18 of the 21 patients with pulmonary hypertension and in 13 of the 24 patients without pulmonary hypertension. As pulmonary artery pressure increased, pulmonary regurgitant flow velocity became higher; the pulmonary artery-to-right ventricular pressure gradient in diastole (PG) was estimated from the pulmonary regurgitant flow velocity (V) by means of the simplified Bernoulli equation (PG = 4V2). The Doppler-determined pressure gradient at end-diastole correlated well with the catheter measurement of the pressure gradient at end-diastole (r = .94, SEE = 3 mm Hg) and with pulmonary artery end-diastolic pressure (r = .92, SEE = 4 mm Hg). The peak of Doppler-determined pressure gradient during diastole correlated well with mean pulmonary artery pressure (r = .92, SEE = 5 mm Hg). Thus continuous-wave Doppler echocardiography was useful for noninvasive estimation of pulmonary artery pressures.     

Comparison of three Doppler ultrasound methods in the prediction of pulmonary artery pressure

Pulmonary artery pressure was noninvasively estimated by three Doppler echocardiographic methods in 50 consecutive patients undergoing cardiac catheterization. First, a systolic transtricuspid gradient was calculated from Doppler-detected tricuspid regurgitation; clinical jugular venous pressure or a fixed value of 14 mm Hg was added to yield systolic pulmonary artery pressure. Second, acceleration time from pulmonary flow analysis was used in a regression equation to derive mean pulmonary artery pressure. Third, right ventricular isovolumic relaxation time was calculated from Doppler-determined pulmonary valve closure and tricuspid valve opening; systolic pulmonary artery pressure was then derived from a nomogram. In 48 patients (96%) at least one of the methods could be employed. A tricuspid pressure gradient, obtained in 36 patients (72%), provided reliable prediction of systolic pulmonary artery pressure. The prediction was superior when 14 mm Hg rather than estimated jugular venous pressure was used to account for right atrial pressure. In 44 patients (88%), pulmonary flow was analyzed. Prediction of mean pulmonary artery pressure was unsatisfactory (r = 0.65) but improved (r = 0.85) when only patients with a heart rate between 60 and 100 beats/min were considered. The effect of correcting pulmonary flow indexes for heart rate was examined by correlating different flow indexes before and after correction for heart rate. There was a good correlation between corrected acceleration time and either systolic (r = -0.85) or mean (r = -0.83) pulmonary artery pressure. Because of a high incidence of arrhythmia, right ventricular relaxation time could be determined in only 11 patients (22%). Noninvasive prediction of pulmonary artery pressure is feasible in most patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of pulmonary arterial pressure by Doppler colour flow mapping in patients with a ductus arteriosus.

Blood flow in the pulmonary artery was studied by Doppler colour flow mapping and cardiac catheterisation in 19 patients with a ductus arteriosus and different pulmonary artery pressures. In the four patients with normal pulmonary artery pressures colour Doppler flow mapping showed multicoloured wide and long systolic and diastolic jets in the pulmonary artery. In the 15 patients with raised pulmonary arterial pressure the systolic jets varied from multicoloured to red and were thinner: in patients with considerably raised pulmonary arterial pressure the jets became redder during diastole. The Doppler velocity tracings showed that in patients with normal pulmonary artery pressures the mean peak systolic velocity was higher than the mean end diastolic velocity--so that in all four the ratio of peak systolic velocity to end diastolic velocity was less than 2. The mean peak systolic velocity was much higher than the mean end diastolic velocity in 13 of the 15 patients with raised pulmonary artery pressure; this meant that the ratio of peak systolic velocity to end diastolic velocity was greater than 2 in 10 of 11 patients. The end diastolic velocity was significantly lower in those patients with raised pulmonary artery pressure than in those with normal artery pressure. There was an inverse linear correlation between the mean pulmonary artery pressure and end diastolic ductal jet velocity in 17 of the 19 patients. Colour flow mapping and this quantitative Doppler technique can detect pulmonary artery hypertension in patients with a ductus arteriosus.     

Evaluation of pulmonary arterial pressure by Doppler colour flow mapping in patients with a ductus arteriosus

Blood flow in the pulmonary artery was studied by Doppler colour flow mapping and cardiac catheterisation in 19 patients with a ductus arteriosus and different pulmonary artery pressures. In the four patients with normal pulmonary artery pressures colour Doppler flow mapping showed multicoloured wide and long systolic and diastolic jets in the pulmonary artery. In the 15 patients with raised pulmonary arterial pressure the systolic jets varied from multicoloured to red and were thinner: in patients with considerably raised pulmonary arterial pressure the jets became redder during diastole. The Doppler velocity tracings showed that in patients with normal pulmonary artery pressures the mean peak systolic velocity was higher than the mean end diastolic velocity--so that in all four the ratio of peak systolic velocity to end diastolic velocity was less than 2. The mean peak systolic velocity was much higher than the mean end diastolic velocity in 13 of the 15 patients with raised pulmonary artery pressure; this meant that the ratio of peak systolic velocity to end diastolic velocity was greater than 2 in 10 of 11 patients. The end diastolic velocity was significantly lower in those patients with raised pulmonary artery pressure than in those with normal artery pressure. There was an inverse linear correlation between the mean pulmonary artery pressure and end diastolic ductal jet velocity in 17 of the 19 patients. Colour flow mapping and this quantitative Doppler technique can detect pulmonary artery hypertension in patients with a ductus arteriosus.     

肺血栓栓塞症患者高敏C反应蛋白水平与肺动脉压相关性的研究

目的探讨急、慢性肺血栓栓塞症患者血清高敏C反应蛋白（high-sensitive C-reactive protein,hs-CRP）的差异及其与肺动脉压之间的相关性。方法选择肺血栓栓塞症患者102例,其中急性44例,慢性58例。所有患者均经多普勒超声心动图检查,将两组患者各自分为肺动脉压正常组与高压组,采用颗粒增强免疫透射比浊法检测hs-CRP水平。结果急性组hs-CRP（24.0±13.4 mg/L）明显高于慢性组（5.2±4.6 mg/L）（P〈0.01）。急性患者中肺动脉压正常组与高压组hs-CRP无明显差异（P=0.338）。慢性患者肺动脉压正常组hs-CRP（3.3±3.0）明显低于高压组（9.5±4.7 mg/L）（P〈0.05）。慢性肺血栓栓塞症肺动脉高压组患者hs-CRP水平和肺动脉压呈正相关（P〈0.05）。结论急性肺血栓栓塞症患者血清hs-CRP水平明显升高,慢性肺血栓栓塞症肺动脉高压组患者血清hs-CRP水平和肺动脉压显著相关。血清hs-CRP水平可用于PTE的危险分层及判断预后。     

Pulmonary artery diastolic pressure: a simultaneous Doppler echocardiography and catheterization study

Pulmonary hypertension is an important determinant of the clinical presentation of and surgical approach to patients with heart disease. To confirm the utility of continuous wave Doppler echocardiography in assessing the pulmonary artery diastolic pressure in patients with pulmonary regurgitation, 51 patients representing the wide hemodynamic spectrum of pulmonary artery pressure underwent simultaneous determination of pulmonary artery diastolic pressure by continuous wave Doppler echocardiography and cardiac catheterization. Pulmonary artery diastolic pressure was estimated from the Doppler recordings by the end-diastolic pressure gradient obtained by the modified Bernoulli equation plus the estimated right atrial pressure. A correlation was observed (r = 0.935, SEE = 7.4 mmHg) between Doppler and catheterization pulmonary artery diastolic pressure. In addition, comparison between the mean diastolic pressure gradient across the pulmonary valve by Doppler and pulmonary artery diastolic pressure at catheterization yielded a high correlation (r = 0.947, SEE = 5.1 mmHg). These data demonstrate that continuous wave Doppler echocardiography is a useful noninvasive technique for evaluating the pulmonary artery diastolic pressure in patients with pulmonary regurgitation.     

Echocardiographic assessment of pulmonary hypertension in patients with advanced lung disease

Doppler echocardiography is commonly used to estimate systolic pulmonary artery pressure and to diagnose pulmonary hypertension, but data relating to its utility in patients with advanced lung disease are limited. In a cohort study of 374 lung transplant candidates, the performance characteristics of echocardiography compared with right heart catheterization in the determination of systolic pulmonary artery pressure and diagnosis of pulmonary hypertension were investigated. The prevalence of pulmonary hypertension was 25% in the study population. Estimation of systolic pulmonary artery pressure by echocardiography was possible in 166 patients (44%). The correlation between systolic pulmonary artery pressure estimated by echocardiography and measured by cardiac catheterization was good (r = 0.69, p < 0.0001). However, 52% of pressure estimations were found to be inaccurate (more than 10 mm Hg difference compared with measured pressure), and 48% of patients were misclassified as having pulmonary hypertension by echocardiography. Sensitivity, specificity, and positive and negative predictive values of systolic pulmonary artery pressure estimation for diagnosis of pulmonary hypertension were 85%, 55%, 52%, and 87%, respectively. In conclusion, despite a statistically significant correlation with directly measured values, estimation of systolic pulmonary artery pressure by echocardiography is frequently inaccurate in patients with advanced lung disease and leads to considerable overdiagnosis of pulmonary hypertension.     

Pulmonary "capillary" wedge pressure not the pressure in the pulmonary capillaries

In 1949, Hellems, Haynes, and Dexter proposed that the pressure in a catheter wedged so as to occlude a pulmonary artery was an "estimate" of the pressure in the pulmonary capillaries. Their report led to the designation of this pulmonary artery wedge pressure as the pulmonary "capillary" wedge pressure. In fact, the pulmonary artery wedge pressure is a distorted measure of the pressure in the pulmonary veins. Usually this pressure differs only slightly from the capillary pressure, and the misconception fostered by the inaccurate name is inconsequential; however, sometimes this misconception leads to errors in diagnosis. This report briefly reviews the early history of pulmonary vascular catheterization, offers an explanation of pulmonary artery wedge pressure, and discusses a disease in which pulmonary artery wedge pressure is normal, even though capillary pressure is elevated.     

Diurnal variation of pulmonary artery pressure in chronic heart failure.

Variation in pulmonary artery pressure has important consequences for the interpretation of isolated pressure measurements in patients with chronic heart failure. To investigate the nature of diurnal variation in pulmonary artery pressure in chronic heart failure, eight angina-free men (aged 50-72 years) with treated chronic heart failure caused by ischaemic heart disease underwent continuous ambulatory pulmonary artery pressure recording by a transducer tipped catheter. The mean (1 SD) daytime pulmonary artery pressure was 29.6 (5.0) mm Hg systolic and 13.7 (5.6) mm Hg diastolic. The mean change in pressure from day to night was +5.1 (3.2) mm Hg systolic and +3.8 (1.7) mm Hg diastolic; and the mean change from standing to lying +9.3 (2.3) mm Hg systolic and +6.4 (2.1) mm Hg diastolic. In six of the eight patients there was considerable rise in pulmonary artery pressure at night, but in the two patients with the most severe symptoms there was no nocturnal rise. In patients with chronic heart failure, nocturnal pulmonary artery pressure is not determined by postural change alone. But interpretation of isolated pulmonary artery pressure measurements must take the posture of the patient into account.     

Diurnal variation of pulmonary artery pressure in chronic heart failure

Variation in pulmonary artery pressure has important consequences for the interpretation of isolated pressure measurements in patients with chronic heart failure. To investigate the nature of diurnal variation in pulmonary artery pressure in chronic heart failure, eight angina-free men (aged 50-72 years) with treated chronic heart failure caused by ischaemic heart disease underwent continuous ambulatory pulmonary artery pressure recording by a transducer tipped catheter. The mean (1 SD) daytime pulmonary artery pressure was 29.6 (5.0) mm Hg systolic and 13.7 (5.6) mm Hg diastolic. The mean change in pressure from day to night was +5.1 (3.2) mm Hg systolic and +3.8 (1.7) mm Hg diastolic; and the mean change from standing to lying +9.3 (2.3) mm Hg systolic and +6.4 (2.1) mm Hg diastolic. In six of the eight patients there was considerable rise in pulmonary artery pressure at night, but in the two patients with the most severe symptoms there was no nocturnal rise. In patients with chronic heart failure, nocturnal pulmonary artery pressure is not determined by postural change alone. But interpretation of isolated pulmonary artery pressure measurements must take the posture of the patient into account.     

Estimation of pulmonary artery pressure from pulmonary vein wedge pressure

Correlations between pulmonary artery and pulmonary vein wedge pressures were investigated in 13 patients with atrial septal defect and 1 patient with Tetralogy of Fallot. Pulmonary vein wedge pressure wave form resembled that of pulmonary artery pressure, and the former lagged behind the latter by 70 to 110 msec (mean 88 ± 14) as observed by the fluid-filled catheter system. Diastolic pulmonary artery and diastolic pulmonary vein wedge pressures were nearly identical. Although systolic and mean pulmonary artery pressures correlated well with respective pulmonary vein wedge pressures, there were discrepancies when systolic and mean pulmonary artery pressure exceeded 35 and 20 mm Hg, respectively. However, systolic and mean pulmonary artery pressures could be estimated by adding the difference between the diastolic pulmonary vein wedge pressure and the mean left atrial pressure to corresponding systolic or mean pulmonary artery pressure. In conclusion, pulmonary artery pressures can be estimated by measuring pulmonary vein wedge pressures and the mean left atrial pressure.     

The haemodynamic significance of asymptomatic ST segment depression assessed by ambulatory pulmonary artery pressure monitoring

A transducer-tipped catheter with simultaneous frequency modulated electrocardiograms and a miniaturised tape recorder was used to record ambulatory pulmonary artery pressure for 24-48 hours in 19 men (mean age 57.7) with clinical and angiographic evidence of coronary artery disease. Sixty seven episodes of ST segment depression (greater than 1 mm) were recorded. Thirty five were accompanied by pain of which six occurred at night; in 34 pulmonary artery diastolic pressure rose significantly. In all but two of the 32 episodes of painless ST segment depression (four of which were at night) there was a significant rise in pulmonary artery diastolic pressure. No such rise was found in six normal subjects during exertion. ST segment changes tended to occur before (24 episodes) or at the same time (27 episodes) as changes in pulmonary artery diastolic pressure. ST segment depression followed an increase in pulmonary artery diastolic pressure in only 13 episodes. The times to maximum ST depression and maximum pulmonary artery diastolic pressure rise were similar. Painful and painless ST segment depression could not be distinguished on the basis of the configuration of the ST segment or in terms of the changes in the pulmonary artery diastolic pressure.     

Echocardiographic estimation of pulmonary artery pressure in transposition of the great arteries

To determine their usefulness in estimating pulmonary artery pressure, left ventricular systolic time intervals (STI) were determined by echocardiography in 65 patients with dextro-transposition of the great arteries (TGA). The STI were measured from recordings of pulmonary valve motion at 100 mm/sec paper speed. The pre-ejection period (PEP) and the ratio of PEP to left ventricular ejection time (PEP/LVET) were directly related to pulmonary artery pressure. The strongest correlations were that between PEP/LVET and pulmonary artery diastolic pressure (r = 0.70) and that between PEP/LVET and the ratio of mean pulmonary pressure to mean systemic pressure (r = 0.71). A value of PEP/LVET of less than 0.26 was consistently associated with pulmonary artery diastolic pressures of less than 20 mm Hg and, in 28 of 31 patients, pulmonary artery pressure less than one-third of mean systemic arterial pressure. Pulmonary hypertension was present in 18 of 22 patients with PEP/LVET of 0.30 or greater; elevated PEP/LVET was also present in four patients with abnormalities of cardiac rhythm or conduction, two of whom also had angiographic evidence of myocardial dysfunction.     

Effects of heart rate and pulmonary artery pressure on Doppler pulmonary artery acceleration time in experimental acute pulmonary hypertension

Chronic pulmonary hypertension in humans is characterized by shortening of the pulmonary artery acceleration time as measured by Doppler echocardiography, such that the higher the pulmonary artery pressure, the shorter the pulmonary acceleration time. Increases in heart rate are also known to produce decreases in the pulmonary artery acceleration time. To explore the relationship between mean pulmonary artery pressure, heart rate, and Doppler pulmonary artery acceleration time, experimental acute pulmonary hypertension was created in nine Duroc swine, either by infusion of Sephadex beads with embolization of the pulmonary arterial circulation or by partially occluding the main pulmonary artery 8 to 10 cm distal to the pulmonic valve. Pulmonary artery Doppler flow velocity recordings and invasive pressure measurements were made at baseline and at paced atrial rates ranging from 60 to 160 beats per minute, in 20-beat increments. The results in this acute animal model reveal that increases in heart rate produced significant decreases in Doppler pulmonary artery acceleration time at mean pressures below 25 mm Hg. However, with mean pulmonary artery pressures greater than 25 mm Hg, both heart rate and increases in pulmonary artery pressure had no significant effect on acceleration time.     

Noninvasive estimation of pulmonary artery diastolic pressure in patients with tricuspid regurgitation by Doppler echocardiography.

OBJECTIVES: The purpose of this study was to determine whether Doppler echocardiographic assessment of right ventricular pressure at the time of pulmonary valve opening could predict pulmonary artery diastolic pressure. BACKGROUND: Doppler echocardiography has been used to estimate right ventricular systolic pressure noninvasively. Because right ventricular and pulmonary artery diastolic pressure are equal at the time of pulmonary valve opening, Doppler echocardiographic estimation of right ventricular pressure at this point might provide an estimate of pulmonary artery diastolic pressure. METHODS: We studied 31 patients who underwent right heart catheterization and had tricuspid regurgitation. Pulmonary flow velocity was recorded by pulsed wave Doppler echocardiography, and tricuspid regurgitant velocity was recorded by continuous wave Doppler echocardiography. The time of pulmonary valve opening was determined as the onset of systolic flow in the pulmonary artery. Tricuspid velocity at the time of pulmonary valve opening was measured by superimposing the interval between the onset of the QRS complex on the ECG and the onset of pulmonary flow on the tricuspid regurgitant envelope. The tricuspid gradient at this instant was calculated from the measured tricuspid velocity using the Bernoulli equation. This gradient was compared to the pulmonary artery diastolic pressure obtained by right heart catheterization. MEASUREMENTS AND RESULTS: The pressure gradient between the right atrium and right ventricle obtained at the time of pulmonary valve opening ranged from 9 to 31 mm Hg (mean, 19+/-5) and correlated closely with invasively measured pulmonary artery diastolic pressure (range, 9 to 36 mm Hg; mean, 21+/-7 mm Hg; r = 0.92; SEE, 1.9 mm Hg). CONCLUSION: Doppler echocardiographic measurement of right ventricular pressure at the time of pulmonary valve opening is a reliable noninvasive method for estimating pulmonary diastolic pressure.     

Effects of terlipressin on systolic pulmonary artery pressure of patients with liver cirrhosis： An echocardiographic assessment

AIM: Portopulmonary hypertension is a serious complication of chronic liver disease. Our aim was to search into the effect of terlipressin on systolic pulmonary artery pressure among cirrhotic patients. METHODS: Twelve patients (6 males and 6 females) with liver cirrhosis were recruited in the study. Arterial blood gas samples were obtained in sitting position at rest. Contrast enhanced echocardiography and measurements of systolic pulmonary artery pressure were performed before and after the intravenous injection of 2 mg terlipressin. RESULTS: Of 12 patients studied, the contrast enhanced echocardiography was positive in 5, and the positive findings in contrast enhanced echocardiography were reversed to normal in two after terlipressin injection. The mean systolic pulmonary artery pressure was 25.5+/-3.6 mmHg before terlipressin injection, and was 22.5+/-2.5 mmHg after terlipressin (P=0.003). The systolic pulmonary artery pressure was above 25 mmHg in seven of these 12 patients. After the terlipressin injection, systolic pulmonary artery pressure was <25 mmHg in four of these cases (58.3% vs 25%, P=0.04). CONCLUSION: Terlipressin can decrease the systolic pulmonary artery pressure in patients with liver cirrhosis.     

Haemodynamic response to myocardial ischaemia during unrestricted activity, exercise testing, and atrial pacing assessed by ambulatory pulmonary artery pressure monitoring

Ambulatory pulmonary artery pressure monitoring by means of a transducer tipped catheter with a simultaneous frequency modulated electrocardiogram and a miniaturised tape recorder was used to study the haemodynamic implications of ST segment depression in patients with coronary artery disease. Nineteen male patients (mean (SD) age 58 (11) years) with clinical and angiographic evidence of coronary artery disease were studied together with six controls. Changes in the ST segment and pulmonary artery diastolic pressure during treadmill exercise, atrial pacing, and unrestricted ambulant activity were analysed. During exercise, pulmonary artery diastolic pressure rose significantly in patients with coronary artery disease but not in the controls. One patient with ST depression greater than 1 mm did not have a rise in pulmonary artery diastolic pressure on exercise; two had a rise in pulmonary artery diastolic pressure with no ST segment change despite severe angina. The pulmonary artery diastolic pressure tended to rise before or simultaneously with the onset of ST segment depression. The haemodynamic response to atrial pacing was similar in normal controls and patients with coronary artery disease. During ambulatory monitoring there were 29 episodes of ST segment depression all of which were associated with a rise in pulmonary artery diastolic pressure and chest pain. The onset of ST segment depression occurred before a rise in pulmonary artery diastolic pressure in 11 episodes, was simultaneous with it in 11, and followed it in seven episodes. During exercise and ambulatory monitoring there was a correlation between the magnitude of ST segment depression and the rise in pulmonary artery diastolic pressure. Pain was a late feature during exercise, atrial pacing, and anginal episodes. This technique for the first time allows the relation between ST segment changes and haemodynamic alterations in left ventricular function to be assessed in ambulant patients with coronary artery disease.     

Contrast echocardiography of the left ventricle an independent predictor of pulmonary artery pressure?

To test the hypothesis that left heart opacification is dependent on pulmonary artery pressure, we analyzed consecutively 12 patients with normal and 8 patients with abnormal pulmonary artery pressure with a new lung capillary stable echo contrast agent. Patients underwent contrast echocardiographic examination within 6 hours before right and left heart catheterization with 200 mg/ml and 400 mg/ml SHU 508A intravenously. The mean pulmonary artery pressure was 15.4 mmHg in the patients with normal pulmonary artery pressures and 46.4 mmHg in the patients with pulmonary hypertension (p< 0.000). Echocardiograms were video-intensitometrically analyzed for intensity maximum (MAX), half-time of video-intensity decay (T1/2), area under the intensity curve (AUC) in the right and left ventricle and transit time from left to right heart (TT). Patients with normal pulmonary artery pressure showed sufficient left heart opacification, in the left ventricle MAX was 37±15 IU, AUC measured 653±463 IUxs and Tl/2 was 4.4±2.6 s, while patients with elevated pulmonary artery pressure showed no significant left heart opacification. In the left ventricle MAX was 8±10 IU (p=0.006), AUC measured 66±108 (p=0.003) and T1/2 was 2.0±2.0 s (p=0.041). TT was significantly increased in patients with elevated pulmonary artery pressure (11.8±4.6 s versus 6.5±2.8 s in patients with normal pulmonary artery pressure, p=0.005). Thus, elevated pulmonary pressure has a significant impact on left heart opacification, which may be used for diagnostic purposes.Presented in part at the 64th session of the American Heart Association     

The haemodynamic significance of asymptomatic ST segment depression assessed by ambulatory pulmonary artery pressure monitoring.

A transducer-tipped catheter with simultaneous frequency modulated electrocardiograms and a miniaturised tape recorder was used to record ambulatory pulmonary artery pressure for 24-48 hours in 19 men (mean age 57.7) with clinical and angiographic evidence of coronary artery disease. Sixty seven episodes of ST segment depression (greater than 1 mm) were recorded. Thirty five were accompanied by pain of which six occurred at night; in 34 pulmonary artery diastolic pressure rose significantly. In all but two of the 32 episodes of painless ST segment depression (four of which were at night) there was a significant rise in pulmonary artery diastolic pressure. No such rise was found in six normal subjects during exertion. ST segment changes tended to occur before (24 episodes) or at the same time (27 episodes) as changes in pulmonary artery diastolic pressure. ST segment depression followed an increase in pulmonary artery diastolic pressure in only 13 episodes. The times to maximum ST depression and maximum pulmonary artery diastolic pressure rise were similar. Painful and painless ST segment depression could not be distinguished on the basis of the configuration of the ST segment or in terms of the changes in the pulmonary artery diastolic pressure.