Biphasic changes in left ventricular end-diastolic pressure during dynamic exercise in patients with nonobstructive hypertrophic cardiomyopathy

OBJECTIVES: The aim of this study was to clarify the serial changes in left ventricular (LV) end-diastolic pressure (LVEDP) during dynamic exercise in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: Although HCM is characterized by impaired resting LV diastolic function, serial changes in LVEDP during exercise have not been characterized. METHODS: We simultaneously measured LV pressure and LV dimensions during symptom-limited supine bicycle exercise in 5 healthy individuals and 20 patients with HCM. Exercise thallium-201 scintigraphic studies were also performed. RESULTS: The LVEDP (baseline: 12 +/- 5 mm Hg) progressively increased to a maximum value at peak exercise (28 +/- 8 mm Hg) in 11 patients with HCM (group I). In the remaining nine patients with HCM (group II), changes in LVEDP during exercise were biphasic, with an initial progressive increase and a subsequent gradual decline up to peak exercise (14 +/- 4 mm Hg at baseline, 27 +/- 5 mm Hg at the critical heart rate, 16 +/- 3 mm Hg at peak exercise). Exercise-induced changes in LV dimensions and LV peak systolic pressures were similar in both groups. However, the maximum first derivative of LV pressure was greater and the LV pressure half-time was shorter in group II than in group I at a similar peak exercise heart rate. The biphasic changes in LVEDP disappeared by pretreatment with propranolol. The LV hypertrophy scores were higher in group I than in group II. Exercise thallium-201 images showed more severe perfusion defects in group I than in group II patients. CONCLUSIONS: The biphasic changes in LVEDP seen during exercise may be related to improved coronary microcirculation in response to beta-adrenergic stimulation in patients with mild to moderate HCM.     

Accuracy of left atrial and pulmonary artery wedge pressure in pure mitral regurgitation in predicting left ventricular end-diastolic pressure

In most clinical conditions pulmonary artery (PA) wedge pressure accurately reflects left ventricular (LV) end-diastolic pressure. In the presence of mitral regurgitation (MR), large V waves can distort PA wedge pressure and result in incorrect estimation of LV end-diastolic pressure. In 52 patients with MR simultaneous measurement of PA wedge pressure or left atrial pressure and LV end-diastolic pressure was recorded. Twenty-one (40%) patients had large V waves (V wave greater than A wave by greater than 10 mm Hg, group 1), and 31 (60%) patients had small V waves (group 2). Group 1 had significantly higher V waves than group 2 (46 +/- 3 vs 21 +/- 2 mm Hg, p less than 0.001). The LV end-diastolic pressure was similar in both groups (21 +/- 2 vs 19 +/- 2 mm Hg, difference not significant). The mean PA wedge or left atrial pressure in group 1 (26 +/- 2 mm Hg) overestimated LV end-diastolic pressure (21 +/- 2 mm Hg) by 30% (p less than 0.01), but the trough of the X descent (20 +/- 2 mm Hg) was similar to the LV end-diastolic pressure. In group 2 patients with small V waves the mean PA wedge pressure was not significantly different from the LV end-diastolic pressure (16 +/- 2 vs 19 +/- 2 mm Hg, p = 0.06), but the trough of the X descent (13 +/- 2 mm Hg) underestimated LV end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left atrial function in acute transient left ventricular ischemia produced during percutaneous transluminal coronary angioplasty of the left anterior descending coronary artery

Left atrial (LA) function was studied in 32 patients during percutaneous transluminal coronary angioplasty of the proximal left anterior descending artery with a dual micromanometer positioned transseptally in the left atrium and in the left ventricle. In 10 patients LA and left ventricular (LV) cineangiography was performed 30 minutes before percutaneous transluminal coronary angioplasty and 30 seconds after the occlusion of the left anterior descending coronary artery. Thirty seconds after left anterior descending occlusion, LV peak systolic pressure decreased from 135 +/- 12 to 106 +/- 9 mm Hg (p less than 0.05) and LV maximum dP/dt decreased from 1,634 +/- 136 to 1,137 +/- 127 mm Hg/s (p less than 0.01). Simultaneously, LA mean pressure increased from 11 +/- 2 to 29 +/- 1 mm Hg (p 177 +/- 13 to 381 +/- 21 mm Hg (p less than 0.001). There was a difference between LV end-diastolic pressure and LA mean pressure of 1.5 mm Hg at rest and 7.8 mm Hg during ischemia and LA pulse pressure increased from 16 +/- 3 to 26 +/- 3 mm Hg (p less than 0.05) together with increase of LA A and V waves peak pressure. LV stroke volume index decreased from 46 +/- 5 to 43 +/- 3 ml/m2 (difference not significant). The LA maximal volume increased from 18 +/- 2 to 29 +/- 3 ml/m2 (p less than 0.001). LA volume before LA contraction increased from 29 +/- 2 to 54 +/- 3 ml/m2 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute inotropic stimulation with dopamine in severe congestive heart failure: beneficial hemodynamic effect at rest but not during maximal exercise

Hemodynamic and metabolic effects of dopamine were studied at rest and during maximal exercise in 13 patients with severe chronic congestive heart failure (CHF). During exercise before the administration of dopamine, the stroke volume index increased from 17.1 +/- 5.2 ml/m2 at rest to 28.1 +/- 10.9 ml/m2 (p less than 0.001) at exhaustion, while pulmonary capillary wedge (PCW) pressure increased from 22.7 +/- 12.7 to 43.9 +/- 11.9 mm Hg (p less than 0.001). The arteriovenous oxygen difference increased from 8.9 +/- 2.3 ml/100 ml to 12.4 +/- 2.0 ml/100 ml (p less than 0.001) and oxygen uptake increased from 3.5 +/- 0.6 0.6 to 11.9 +/- 2.5 ml/kg/min (p less than 0.001). At rest, dopamine increased the stroke volume index to 23.3 +/- 8.1 ml/m2 (p less than 0.001) and reduced the PCW pressure to 20.5 +/- 1.1 mm Hg (p less than 0.05). However, during maximal exercise, the stroke volume index and PCW pressure were not changed by dopamine: 28.1 +/- 10.9 versus 28.6 +/- 10.2 ml/m2 (difference not significant [NS]) and 43.9 +/- 11.9 versus 42.5 +/- 11.2 mm Hg (NS), respectively. In contrast, the maximal heart rate achieved during exercise was significantly higher with dopamine, 140.3 +/- 29.3 versus 136.0 +/- 29.7 beats/min (p less than 0.05), which contributed to a slight augmentation in the maximal cardiac index, 3.82 +/- 1.13 versus 3.64 +/- 1.17 liters/min/m2 (p less than 0.05). Nonetheless, neither peak arteriovenous oxygen difference nor maximal oxygen uptake were significantly changed by dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlates and prognostic implication of exercise capacity in chronic congestive heart failure

Previous studies have shown poor correlations between exercise tolerance and measurements of left ventricular (LV) function during rest in patients with congestive heart failure (CHF). To further evaluate the determinants of exercise tolerance and their relation to prognosis, we performed rest and exercise hemodynamic measurements and blood pool scintigraphy in 27 patients with CHF. All patients were treated with digitalis and diuretic drugs, but not vasodilator drugs. Exercise capacity was assessed by maximal oxygen consumption (VO2max) during upright bicycle ergometry. Both right ventricular (RV) and LV ejection fractions were measured by radionuclide techniques, and arterial, right atrial and pulmonary artery pressures, cardiac output, and derived hemodynamic indexes were determined. As a group, patients with severely impaired exercise tolerance (group 1, VO2max less than 10 ml/min/kg) had significantly higher rest pulmonary capillary wedge and right atrial pressures (30 +/- 4 vs 23 +/- 6 and 12 +/- 4 vs 7 +/- 2 mm Hg, respectively) than those with a VO2max of 10 to 18 ml/min/kg (group 2). They also had lower LV and RV ejection fractions (16 +/- 4% vs 21 +/- 4% and 19 +/- 12% vs 27 +/- 7%, respectively). However, overlap among individual patients was considerable, and only pulmonary capillary wedge pressure at rest correlated significantly (r = 0.69, p less than 0.001) with VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of exercise on transmitral gradient and pulmonary artery pressure in patients with mitral stenosis or a prosthetic mitral valve: a Doppler echocardiographic study

Doppler echocardiography was used to determine changes in transmitral gradient and pulmonary artery pressure after exercise in 12 patients with mitral stenosis and 11 patients with a prosthetic mitral valve. The mean transmitral gradient in the mitral stenosis group was 9 +/- 7 mm Hg at rest and increased to 17 +/- 8 mm Hg after exercise. In patients with a prosthetic mitral valve, exercise resulted in an increase in mean transmitral gradient from 5 +/- 2 to 8 +/- 3 mm Hg. Calculated pulmonary artery systolic pressure increased with exercise from 41 +/- 19 to 70 +/- 32 mm Hg in the mitral stenosis group and from 28 +/- 8 to 39 +/- 15 mm Hg in patients with a prosthetic valve. Exercise Doppler echocardiographic evaluation of changes in transmitral gradient and pulmonary artery systolic pressure was found to be technically simple and an important addition to the noninvasive evaluation of patients with mitral valve disease.     

Assessing left ventricular filling pressure with flow-directed (Swan-Ganz) catheters. Detection of sudden changes in patients with left ventricular dysfunction.

The accuracy with which pulmonary pressures reflect sudden changes in left ventricular (LV) pressures was studied in 15 patients without mitral disease. Mean pulmonary artery (PA), pulmonary artery end-diastolic (PAd), mean pulmonary capillary (PC), and pulmonary capillary "a" wave (PCa) pressures were compared with simultaneous LV diastolic pressures measured before (LV pre "a") and after atrial systole (LVEDP). Recordings were made at rest and after angiography. There were significant correlations (r greater than 0.75, P less than 0.01) between LV diastolic pressures and each of the pulmonary pressures. The LVEDP and PCa related most closely (r = 0.98). Differences of 5 mm Hg or more between LVEDP and either PAd or PC occurred in more than 50 percent of the observations and were due to large LV "a" waves. The PC, and to a lesser degree the PAd, were more closely related to LV pre "a" than to LVEDP. Changes (delta) in PCa after LV angiography approximated deltaLVEDP, whild deltaPAD and deltaPC reflected deltaLV pre "a" more closely than deltaLVEDP. In conclusion, PCa reflects the LV "a" wave and, thus, is the most accurate index for LVEDP and deltaLVEDP in patients with LV dysfunction. The PC reflects LV pre "a" (mean LV filling pressure) but is an unreliable index of LVEDP. The PC is more easily measured than PCa and, with proper interpretation, should remain the most useful measurement for patient monitoring.     

Pulmonary artery pressure changes during exercise and daily activities in chronic heart failure

Long-term continuous pulmonary artery pressure monitoring was used to investigate pressure changes during different types of exercise and normal daily activities in patients with chronic heart failure. Nine men (mean age 55 years) with treated chronic heart failure underwent continuous pulmonary artery pressure measurement with use of a micromanometer-tipped catheter with in vivo calibration and frequency-modulated recording. The mean (+/- SD) maximal systolic pulmonary artery pressure (in mm Hg) was 59.4 +/- 26.1 on treadmill exercise, 54.9 +/- 30.6 on bicycle exercise, 52.5 +/- 26.1 walking up and down stairs and 43.5 +/- 23.9 walking on a flat surface. The mean maximal diastolic pressure (in mm Hg) was 27.8 +/- 14.6 on treadmill exercise, 25.5 +/- 14.9 on bicycle exercise, 24.9 +/- 14.8 walking up and down stairs and 20.4 +/- 12.5 walking on a flat surface. The increase in pulmonary artery pressure did not correlate with the severity of the limiting symptoms except during walking on a flat surface. All patients had marked postural changes in pressure, with the systolic pressure difference from lying to standing ranging from 8 to 25 mm Hg and the diastolic pressure difference ranging from 3 to 13 mm Hg. Eating meals caused an increase in pressure in three patients, but less than that when lying flat. There was an increase in pressure during urination in four patients equal to that when walking on a flat surface. None of these activities was associated with symptoms. Neither symptoms nor pulmonary artery pressure during maximal exercise is the same as during daily activities. This may restrict the value of maximal exercise tests in assessing patients with chronic heart failure.     

Clinical and hemodynamic significance of left ventricular diastolic volume changes by exercise radionuclide ventriculography in coronary artery disease

Recent studies have suggested that left ventricular (LV) dilatation during exercise radionuclide ventriculography may identify coronary artery disease (CAD). Coronary anatomy and LV end-diastolic pressure at catheterization were compared with results of supine exercise radionuclide ventriculography in 66 patients evaluated for chest pain. Forty-six patients had significant CAD (greater than 75% diameter stenosis) and 20 patients were normal. Radionuclide ventriculography was performed within 18 hours of catheterization, at rest and at peak exercise. Relative LV end-diastolic volumes were extrapolated from end-diastolic counts. LV end-diastolic counts increased during exercise in 19 of 20 normal subjects. In patients with CAD, LV end-diastolic counts increased in 35 (group A) and decreased in 11 (group B). The percent change in LV end-diastolic counts from rest to exercise, rest ejection fraction, exercise ejection fraction and rest LV end-diastolic pressure for each group were 20 +/- 23%, 60 +/- 13%, 67 +/- 13% and 8 +/- 3 mm Hg in normal subjects; 20 +/- 20%, 50 +/- 12%, 47 +/- 13% and 12 +/- 4 mm Hg in group A; and -9 +/- 8%, 54 +/- 21%, 49 +/- 18% and 21 +/- 7 mm Hg in group B (mean +/- standard deviation). An increase in LV end-diastolic counts was unrelated to ejection fraction response or presence of underlying CAD but only correlated to rest LV end-diastolic pressure (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

The influence of left ventricular filling pressure on atrial contribution to cardiac output.

The influence of left ventricular filling pressure on the atrial contribution filling pressure and atrial contribution was seen in studies done at baseline (PCW (r=-.53, p less than .025), as well as in studies done after PCW was modified by volume expansion and/or nitrates (r=-.53, p less than .005). At baseline, atrial contribution averaged 9.3 +/- 1.3 c.c./M.2 in patients with PCW less than 20 mm. Hg, while it was only 2.4 +/- 1.2 c.c./M.2 in patients with PCW greater than or equal to 20 mm. Hg (p less than .005). Atrial contribution was significantly greater in patients who had no history of heart failure when they were volume loaded to a PCW above 20 mm. Hg than in patients with impaired ventricular function whose baseline PCW was above 20 mm. Hg. Thus, atrial contribution tends to be less effective in augmenting cardiac output when filling pressure is already elevated, particularly in patients with impaired left ventricular function.     

The role of atrial pressure in secreting atrial natriuretic polypeptides

The role of atrial pressure and catecholamines in secreting human atrial natriuretic polypeptides (hANP) were investigated in patients with acute or old myocardial infarction (AMI or OMI). No differences were observed in hANP levels obtained from brachial vein, right atrium, pulmonary artery and femoral artery, suggesting that hANP degradation in the pulmonary circulation has little clinical significance in hANP measurement. Plasma hANP levels in 10 patients with AMI were higher than those in controls and significantly correlated to both mean right atrial pressure (mRA) and pulmonary wedge pressure (PCW) (r = 0.76, p less than 0.05; r = 0.95; p less than 0.01, respectively). In 12 patients with OMI, plasma hANP levels were normal at rest and were significantly increased (p less than 0.01) with bicycle ergometer exercise associated with significant elevations of plasma catecholamine levels, mRA, and PCW. However, the increments of hANP correlated only to those of PCW. These results suggest that the elevation of atrial (principally left atrial) pressure rather than catecholamine stimulates hANP secretion.     

Doppler-derived left ventricular end-diastolic pressure prediction model using the combined analysis of mitral and pulmonary A waves in patients with coronary artery disease and preserved left ventricular systolic function

The aim of this study was to analyze the components of mitral and pulmonary A waves and to construct a Doppler-derived left ventricular (LV) end-diastolic pressure (EDP) prediction model based on the combined analysis of transmitral and pulmonary venous flow velocity curves. Combined analysis of transmitral and pulmonary venous flow velocity curves at atrial contraction is a reliable predictor of increased LV filling pressure. The duration of pulmonary and mitral A waves is determined by the sum of respective acceleration and deceleration time. Mitral flow and left upper pulmonary vein flow velocity curves were recorded simultaneously with LVEDP in 40 consecutive patients (aged 59 +/- 8 years) with coronary artery disease and preserved LV systolic function. Differences in all parameters represent values of pulmonary minus those of mitral A wave curve. The difference in deceleration time was the strongest candidate, being included in all models. After redundancy evaluation, we reached the following model: LVEDP = 20.61 + 0.229 x difference in deceleration time (r(2) = 0.80, p <0.001). In the entire study group, the difference in duration and in deceleration time of the A wave was highly correlated with LVEDP (r = 0.79, p <0.001, and r = 0.88, p <0.001, respectively). The entire study group was further divided according to whether LVEDP was above (group I, 20 patients) or below (group II, 20 patients) the median value (15.5 mm Hg). In group I, the difference in duration and in deceleration time correlated well (r = 0.62, p = 0.01, and r = 0.75, p = 0.001, respectively) with LVEDP, whereas in group II only the difference in deceleration time correlated well (r = 0.68, p = 0.005). In patients with coronary artery disease and preserved LV systolic function, the combined analysis of mitral and pulmonary A waves can predict LVEDP. The difference in deceleration time between pulmonary and mitral A waves can reliably evaluate high and normal LVEDP.     

Acute changes in pulmonary artery pressures due to exercise and exposure to high altitude do not cause left ventricular diastolic dysfunction

BACKGROUND: Altitude-induced pulmonary hypertension has been suggested to cause left ventricular (LV) diastolic dysfunction due to ventricular interaction. In this study, we evaluate the effects of exercise- and altitude-induced increase in pulmonary artery pressures on LV diastolic function in an interventional setting investigating high-altitude pulmonary edema (HAPE) prophylaxis. METHODS: Among 39 subjects, 29 were HAPE susceptible (HAPE-S) and 10 served as control subjects. HAPE-S subjects were randomly assigned to prophylactic tadalafil (10 mg), dexamethasone (8 mg), or placebo bid, starting 1 day before ascent. Doppler echocardiography at rest and during submaximal exercise was performed at low altitude (490 m) and high altitude (4,559 m). The ratio of early transmitral inflow peak velocity (E) to atrial transmitral inflow peak velocity (A), pulmonary venous flow parameters, and tissue velocity within the septal mitral annulus during early diastole (E') were used to assess LV diastolic properties. LV filling pressures were estimated by E/E'. Systolic right ventricular to atrial pressure gradients (RVPGs) were measured in order to estimate pulmonary artery pressures. RESULTS: At 490 m, E/A decreased similarly with exercise in HAPE-S and control subjects (HAPE-S, 1.5 +/- 0.3 to 1.3 +/- 0.3; control, 1.7 +/- 0.4 to 1.3 +/- 0.3; p = 0.12 between groups) [mean +/- SD], whereas RVPG increased significantly more in HAPE-S subjects (20 +/- 5 to 43 +/- 9 mm Hg vs 18 +/- 3 to 28 +/- 3 mm Hg, p < 0.001). Changes in RVPG levels during exercise did not correlate with changes in E/A (p > 0.1). From 490 to 4,559 m, no correlations between changes in RVPG and changes in E/A or atrial reversal (both p > 0.1) were observed. Neither of the groups showed an increase in E/E' from 490 to 4,559 m. CONCLUSION: Increased pulmonary artery pressure associated with exercise and acute exposure to 4,559 m appears not to cause LV diastolic dysfunction in healthy subjects. Therefore, ventricular interaction seems not to be of hemodynamic relevance in this setting.     

Effects of nifedipine on arterial oxygenation at rest and during exercise in patients with stable angina

The effects of nifedipine on arterial oxygenation and hemodynamics were studied at rest and during bicycle exercise in 12 men (mean age 55 years, range 41 to 67) with stable exertional angina. The study was conducted double-blind on 2 days, 1 week apart, using a placebo-controlled crossover design. On each day, measurements at rest were made before and 20 minutes after 20 mg sublingual nifedipine or placebo and were followed by measurements made during exercise. Compared with placebo, nifedipine reduced mean arterial pressure, systemic vascular resistance and pulmonary vascular resistance, and increased heart rate and cardiac output at rest and during exercise. It did not alter mean pulmonary artery or pulmonary artery wedge pressures at rest, but decreased them during exercise. Nifedipine decreased arterial oxygen tension (PaO2) from 96 +/- 10 to 90 +/- 13 mm Hg (p less than 0.05) at rest and from 99 +/- 11 to 92 +/- 12 mm Hg (p less than 0.005) at submaximal exercise (33 +/- 21 W), but did not alter it (100 +/- 12 versus 100 +/- 16 mm Hg, p = NS) at maximal exercise (68 +/- 30 W). The reduction in PaO2 was not due to alveolar hypoventilation, because nifedipine did not alter arterial carbon dioxide tension, or to changes in mixed venous oxygen tension, which nifedipine increased at rest (39 +/- 2 versus 43 +/- 3 mm Hg, p less than 0.001) and during submaximal exercise (31 +/- 4 versus 33 +/- 4 mm Hg, p less than 0.03) and maximal exercise (27 +/- 3 versus 31 +/- 3 mm Hg, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of the distribution of intramyocardial pressure across the canine left ventricular wall in the beating heart during diastole and in the arrested heart. Evidence of epicardial muscle tone during diastole

Computations of compliance of the left ventricle (LV) during diastole assume passive tissue characteristics. To evaluate this assumption, we measured diastolic LV intramyocardial pressure simultaneously in the subepicardium and subendocardium in 18 open-chest dogs, using 1-mm in diameter micromanometers. Subepicardial pressure, 26 +/- 1 mm Hg (mean +/- SEM) exceeded subendocardial pressure, 14 +/- 1 mm Hg (P less than 0.001), and it exceeded left ventricular end-diastolic pressure (LVEDP) (9 +/- 1 mm Hg) (P less than 0.001). After an infusion of dextran-40 (10 dogs), subepicardial diastolic pressure increased to 42 +/- 4 mm Hg which was higher than diastolic subendocardial pressure, 26 +/- 2 mm Hg (P less than 0.001) and LVEDP, 24 +/- 2 mm Hg (P less than 0.001). Following cardiac arrest (12 dogs) with the intramyocardial probes unchanged in position, LV intracavitary pressure, 9 +/- 1 mm Hg, and subendocardial pressure, 13 +/- 3 mm Hg, did not differ significantly from the pressures in the beating heart. Subepicardial pressure, 9 +/- 1 mm Hg, was lower than in the beating heart (P less than 0.001). Following distention of the arrested LV (12 dogs), subepicardial pressure, 31 +/- 7 mm Hg, was lower than both subendocardial pressure, 58 +/- 12 mm Hg (P less than 0.001) and LV intracavitary pressure, 54 +/- 11 mm Hg (P less than 0.001). These observations indicate that tone is maintained by the subepicardium during diastole. Furthermore, the LV wall does not appear to behave as a passive shell during ventricular filling.     

Function and interaction of the right and left ventricle in patients with mitral valve stenosis

In 17 patients with mitral stenosis functional class III (NYHA) and chronic pulmonary hypertension, volumes and function of the right (RV) and left ventricle (LV) were analysed. Biplane cineventriculography of the right and left ventricle was performed subsequently and repeated 3 min after application of 1.6 mg nitroglycerin (NTG), which was given sublingually to decrease pre- and afterload. Pulmonary artery (PAP) and wedge pressures (PCW) were measured continuously. RV ejection fraction (EF) was 62.8 +/- 7.2% before and did not change significantly after NTG. RV enddiastolic volume index (EDVI) and endsystolic volume index (ESVI) was 80.7 +/- 27.2 ml/m2 and 31.7 +/- 11.9 ml/m2, respectively, and did not change significantly after NTG. Volumes and function of the LV were normal (LVEDVI: 66.5 +/- 13.5 ml/m2, LVESVI: 23.0 +/- 7.1 ml/m2, LVEF: 62.4 +/- 9.5%). Systolic PAP decreased significantly from 43.4 +/- 11.1 mm Hg before to 37.8 +/- 9.1 mm Hg after NTG (p less than 0.025) as well as total pulmonary resistance from 243 +/- 51 to 209 +/- 50.8 dynes . sec . cm-5 (p less than 0.05). No significant correlation was found between function and volumes of both ventricles. In 4 patients, however, the decrease in LV ejection fraction was associated with a considerable increase of right ventricular enddiastolic volume. Thus, the right ventricle compensates moderate pulmonary hypertension completely maintaining normal right ventricular function. If, however, septal dysfunction occurs, right ventricular insufficiency will develop in a shorter period of time.     

Noninvasive evaluation of pulmonary artery pressure during exercise by saline-enhanced Doppler echocardiography in chronic pulmonary disease

To determine the feasibility of noninvasive determination of right ventricular systolic pressure (RVSP) during a graded-exercise protocol, saline contrast-enhanced Doppler echocardiography of tricuspid insufficiency was performed in 36 patients with chronic lung disease and 12 normal controls. In the patients with chronic pulmonary disease, symptom-limited, incremental supine bicycle exercise and pulse oximetry were performed on and off high-flow oxygen. Technically adequate Doppler studies were initially obtained in 20 patients (56%) at rest and 14 (39%) on exercise; these numbers increased to 33 (92%) and 32 (89%), respectively, after enhancement with agitated saline (both p less than 0.001). In 10 patients with chronic lung disease who had simultaneous hemodynamic monitoring during exercise, the correlation between Doppler and catheter measurements of pulmonary artery systolic pressure was close (r = 0.98). Among controls, RVSP increased from 22 +/- 4 at rest (mean +/- SD) to 31 +/- 7 mm Hg at peak exercise. In patients with chronic lung disease, RVSP increased from 46 +/- 20 to 83 +/- 30 mm Hg (both p less than 0.001 vs. controls). Despite normal resting values for RVSP in 28% of study patients, nearly all showed abnormal increases in RVSP during supine bicycle exercise. Increases in RVSP during exercise were greatest in patients who showed oxyhemoglobin desaturation. The short-term administration of oxygen significantly blunted the increase in RVSP during exercise. Saline contrast-enhanced Doppler evaluation of tricuspid insufficiency seems a potentially valuable noninvasive method of determining the exercise response of RVSP in patients with chronic pulmonary disease.     

Relation of left ventricular end diastolic pressure to right ventricular end diastolic volume after operative treatment of tetralogy of fallot

Left ventricular (LV) diastolic dysfunction is associated with poor outcomes after tetralogy of Fallot (TOF) repair, although its cause is not known, and its relation to right ventricular (RV) performance has never been examined. The aim of this study was to test the hypothesis that RV dilation leads to LV diastolic dysfunction after TOF repair. Patients with repaired TOF who underwent cardiac catheterization and cardiac magnetic resonance imaging within 6 months from January 2003 and April 2011 were reviewed to assess the relation of LV end-diastolic pressure (LVEDP) and indexed RV end-diastolic volume (RVEDVi). Thirty-eight patients were included at a median age of 10.1 years (range 0.6 to 54.7). There was a significant linear association between RVEDVi and LVEDP (p = 0.05). RV end-diastolic pressure (p <0.001), right pulmonary artery systolic pressure (p = 0.009), left pulmonary artery systolic pressure (p = 0.02), and total cardiopulmonary support time (p = 0.04) during TOF repair were also significantly associated with LVEDP. Compared to patients with LVEDP <12 mm Hg, those with LVEDP ≥12 mm Hg had significantly higher mean RVEDVi (135.2 ± 47.8 vs 98.6 ± 28 ml/m(2), p = 0.007) and mean RV end-diastolic pressure (11.7 ± 1.6 vs 8.5 ± 2.8 mm Hg, p = 0.0003). In conclusion, after TOF repair, LVEDP is significantly associated with RVEDVi. Furthermore, mean RVEDVi is significantly higher in patients with LVEDP ≥12 mm Hg. These findings support the theory that RV dilation may impair LV diastolic function and that LV parameters may also be important to consider in determining timing of pulmonary valve replacement.     

Doppler echocardiographic-determined changes in left ventricular diastolic filling flow velocity during the lower body positive and negative pressure method

Changes in parameters of left ventricular (LV) diastolic filling flow obtained with Doppler echocardiography during the lower body positive and negative pressure method were analyzed in 15 patients (12 with coronary artery disease and 3 with dilated cardiomyopathy). Lower body pressure was altered at 5 steps (+20, +10, 0, -20 and -40 mm Hg vs atmospheric pressure). Pulmonary capillary wedge pressure measured with a balloon-tipped catheter was changed proportionally with lower body pressure during the procedures (p less than 0.01). Mean systemic arterial pressure was changed slightly during lower body positive pressure and negative pressure of -40 mm Hg. Heart rate was almost unchanged except at lower body pressure of -40 mm Hg. The peak velocity of LV early diastolic filling flow was changed with pulmonary capillary wedge pressure in an almost parallel fashion during the procedures (p less than 0.01). The peak velocity of LV late diastolic filling flow showed smaller changes than that of early diastolic filling flow. Changes in pulmonary capillary wedge pressure correlated positively with changes in the peak velocity of LV early diastolic filling flow (r = 0.759, p less than 0.01), but not with changes in the peak velocity of LV late diastolic filling flow (r = 0.039, not significant) during lower body negative pressure of -20 mm Hg. These data suggest that left atrial pressure is one of the important determinants of LV early diastolic filling flow in this acute clinical setting and that LV late diastolic filling flow is less sensitive to changes in left atrial pressure than LV early diastolic filling flow.     

Hemodynamic effects of aerosolized iloprost in pulmonary hypertension at rest and during exercise

STUDY OBJECTIVES: Aerosolized iloprost, a stable prostacyclin analog, improves functional capacity even in patients with pulmonary hypertension who did not show a vigorous hemodynamic response after iloprost inhalation at rest. We therefore speculated that aerosolized iloprost elicits more beneficial effects on pulmonary hemodynamics during exercise than at rest. DESIGN AND SETTING: A prospective, open, uncontrolled study at a university hospital. PATIENTS: Sixteen patients with primary or secondary pulmonary hypertension. INTERVENTIONS: Right-heart catheterization at rest and during exercise before and after the inhalation iloprost, 14 to 28 microg. RESULTS: Before iloprost treatment, exercise increased mean (+/- SD) pulmonary artery pressure (PAPm) from 45 +/- 8 to 70 +/- 13 mm Hg, cardiac output from 3.7 +/- 1.0 to 5.8 +/- 2.4 L/min, and pulmonary vascular resistance (PVR) from 904 +/- 322 to 1,013 +/- 432 dyne.s.cm(-5) (each p < 0.05). After recovery, iloprost reduced PAPm from 44 +/- 8 to 41 +/- 6 mm Hg, increased cardiac output from 3.7 +/- 1.0 to 4.9 +/- 1.4 L/min, and lowered PVR from 902 +/- 350 to 636 +/- 248 dyne x s x cm(-5) (each p < 0.05). During exercise after iloprost, PAPm increased to 57 +/- 8 mm Hg, cardiac output to 7.0 +/- 3.0 L/min, and PVR to 673 +/- 279 dyne x s x cm(-5) (each p < 0.05 vs first exercise test). Systemic BP was not altered significantly by iloprost treatment during exercise. CONCLUSIONS: Aerosolized iloprost treatment exerts more favorable effects on pulmonary hemodynamics during exercise than at rest. These findings explain the functional improvement observed in patients with pulmonary hypertension who show only a moderate pulmonary vasodilatory response during iloprost inhalation at rest. Whether these beneficial effects have prognostic significance needs to be elucidated by further study.