Early Diastolic Pressure Research Articles

The early diastolic pressure-flow relationship is dependent on pressure sampling sites and timing factors

Background Peak early diastolic flow velocity (E) across the mitral valve has been shown to be directly related to the magnitude of the early diastolic transmitral pressure difference (TPD). Although this relationship has been verified by a number of investigators, the statistical strengths of the reported relationships have varied. This variation may be attributable, at least in part, to the lack of standardization of 1) the site of measurement of left ventricular pressure, and 2) the method for determination of the atrioventricular pressure difference. Methods To assess the degree to which the E-TPD relation is affected by early diastolic left ventricular intraventricular pressure gradients, or by the timing of the measurement (ie. instantaneous versus noninstantaneous) of the TPD, we recorded left atrial and two regional (mid and apical) left ventricular pressures with micromanometers, and E by transesophageal Doppler in 16 closed-chest anesthetized dogs. Two noninstantaneous TPDs were measured: pressure at the first crossover of left atrial and left ventricular pressures (X1) minus minimum left ventricular-apical pressure [X1LVPapex]; and X1 minus minimum mid-left ventricular pressure [X1LVPmid]. Two TPDs were also measured at a single point in time (instantaneous): the maximum left atrial to left ventricular-apical early diastolic TPD [MAXapex]; and the maximum left atrial to mid-left ventricular TPD [MAXmid]. Results Correlations with E were as follows: X1 apex, γ=0.805, P<0.001; X1mid, γ= 0.735, P<0.001; MAXapex, r=0.716, P<0.002; MAXmid, r= 0.369, Pis not significant. Conclusions: In this study, a wide range of correlations were observed between E and the four early diastolic TPDs measured as described above. Clearly, transmitral pressure gradients measured in different left ventricular regions and at different points in time are not proportional. Thus, the recorded partem of the transmitral pressure difference is so critically dependent on the intraventricular site and method of timing employed in its measurement, it is doubtful that any physiologically valid, simple relation can be proven.

Doppler assessment of pulmonary artery flow patterns and ventricular function after the Fontan operation

To assess the relation between ventricular systolic and diastolic function and pulmonary artery (PA) flow patterns after the Fontan operation, 15 postoperative patients were prospectively evaluated with echocardiography. Blood flow velocities in the PA were recorded with pulsed Doppler echocardiography. Ejection fraction was measured by 2-dimensional echocardiography using Simpson's rule. Indexes of diastolic function were measured from the systemic atrioventricular valve inflow Doppler and included peak E and A velocities, peak filling rate normalized for stroke volume, the fractions of filling in early and late diastole (E and A area fractions), and the E/A velocity and area ratios. Compared with 15 age-matched control subjects, the 15 patients who had undergone the Fontan procedure had decreased peak E velocity (0.65 ± 0.20 vs 0.87 ± 0.10 m/s), decreased E A velocity ratio (1.29 ± 0.23 vs 1.98 ± 0.46), decreased normalized peak filling rate (6.09 ± 0.90 vs 6.81 ± 0.83 s −1), decreased E area fraction (0.63 ± 0.09 vs 0.72 ± 0.07), increased A area fraction (0.37 ± 0.07 vs 0.24 ± 0.06), and decreased E A area ratio (1.77 ± 0.45 vs 3.33 ± 1.15) (p < 0.05). These diastolic filling abnormalities are consistent with impaired ventricular relaxation and decreased early diastolic transvalvular pressure gradient. PA Doppler recordings showed 2 distinct patterns of flow. Pattern I, observed in 9 patients, showed biphasic forward flow with peak velocities in mid to late systole and middiastole. Pattern II, observed in the remaining 6 patients, showed decreased systolic forward flow, a late systolic to early diastolic flow reversal, and delayed onset of diastolic forward flow. Compared with pattern I patients, pattern II patients had no significant differences in any of the Doppler indexes of diastolic function; however, pattern II patients had a significantly tower ejection fraction (43 ± 9 vs 57 ± 5%). Thus, many patients undergoing the Fontan procedure have impaired ventricular relaxation, but, in the presence of a normal ejection fraction, biphasic forward PA flow is maintained. With the development of decreased ejection fraction, atrial systolic filling pressures are likely increased, the ventricular suction effect is decreased, and PA flow is diminished or absent in systole and early diastole.

Pericardial influences on right and left ventricular filling dynamics.

The influence of the pericardium on right and left ventricular filling was studied using two-dimensional and Doppler echocardiography in 14 open-chest dogs. Doppler echo parameters of filling included early (E) and late (A) velocities and their ratio (E/A) for the mitral and tricuspid valves. Right and left ventricular volumes were calculated from orthogonal two-dimensional echocardiographic images. Data were compared at three levels of left ventricular end-diastolic pressure (6 +/- 2, 13 +/- 3, and 21 +/- 4 mm Hg) at matched heart rates before and after pericardiectomy. The instantaneous diastolic pressure gradient was measured in 12 of the dogs. Pericardiectomy resulted in an increase in early mitral velocity, peak early diastolic pressure gradient, and E/A but not early mitral velocity normalized for end-diastolic volume. In contrast, for the tricuspid valve flow, pericardiectomy did not change E but caused a marked increase in A and a decrease in E/A. Right ventricular end-diastolic volumes at matched left ventricular end-diastolic volumes were similar before and after the pericardium was removed. However, removal of the pericardium caused a significant decrease of the slope for the right (86.0 +/- 27.0 x 10(-4) versus 50.0 +/- 19.5 x 10(-4) mm Hg/ml, p less than 0.01), but not left, ventricular ln end-diastolic pressure-volume relation (21.2 +/- 9.2 x 10(-3) versus 21.4 +/- 5.3 x 10(-3) mm Hg/ml, p = NS), and a decrease of the pressure intercept for the left (3.0 +/- 2.0 versus 1.6 +/- 0.9 mm Hg, p less than 0.05), but not right, ventricular ln end-diastolic pressure-volume relation (2.8 +/- 1.4 versus 1.4 +/- 0.8 mm Hg, p = NS). In conclusion, filling of the two ventricles is affected by the pericardium over a wide range of physiological ventricular volumes and pressures. At matched left ventricular end-diastolic volume, pericardiectomy causes a fundamental alteration in right, but not left, ventricular filling.

Characterization of regional diastolic pressure gradients in the right ventricle.

Regional intraventricular pressure gradients exist in the left ventricle (LV) during both the early and late filling phases of diastole. These regional pressure gradients comprise a fundamental component of the mechanism of normal LV filling. To determine whether similar diastolic pressure gradients also occur in the right ventricle (RV), we measured right atrial (RA) and RV regional pressures with use of micromanometers in six anesthetized, closed-chest dogs. Tricuspid flow velocity was recorded with use of transesophageal Doppler echocardiography, and right ventriculograms were obtained with contrast angiography. As in the LV, the maximum RA-RV pressure gradient during early diastole was consistently greater if RV pressure was measured near the apex than in the inflow tract (1.6 +/- 0.5 versus 0.8 +/- 0.4 mm Hg). The area of reversed pressure was also found to be significantly greater in the apex than in the inflow tract (72 +/- 43 versus 8 +/- 6 mm Hg.msec). However, unlike the LV, the lowest minimum pressure was usually recorded in the RV outflow tract, resulting in a significantly increased RA-RV outflow tract pressure gradient compared with the RA-RV apex pressure gradient (2.5 +/- 0.8 versus 1.6 +/- 0.5 mm Hg). Analysis of right ventriculograms indicates marked narrowing of the RV outflow tract at end systole in all six animals, suggesting that an end-systolic deformation in this region is the likely mechanism for production of low early diastolic pressure in this region. During atrial contraction the RV regional pressure gradient pattern was similar to the LV pattern: the RV a-wave ascent occurred earlier in the inflow tract and later in the apex. A-wave ascent appeared to occur almost simultaneously in the apex and outflow tract. In the six animals, Doppler-derived peak tricuspid flow velocity during early diastole was 35 +/- 6 cm/sec. Early tricuspid flow acceleration (393 +/- 101 cm/sec2) was found to be significantly greater than deceleration of flow (182 +/- 59 cm/sec2). Comparison of tricuspid pressure-flow data with mitral pressure-flow data previously obtained in our laboratory indicates that the driving pressure gradient across the tricuspid valve is significantly less than across the mitral. This pressure difference corresponds to differences in acceleration and peak flow found across the two valves. Consideration of these physiological patterns of RV diastolic intraventricular pressure and their relation to filling has important implications with regard to the development of indexes that characterize diastolic pressure-flow relations and provides physiological insight relating to the location of ventricular restoring forces.

Effects of ischemia, bypass surgery and past infarction on myocardial contraction, relaxation and compliance during exercise

Abnormalities of left ventricular function during ischemia have been described in animal models and in humans. Exercise, while a physiologic means of inducing ischemia, has a complex effect on left ventricular function by itself. In addition, patients with coronary artery disease have a diversity of chronic changes in myocardial structure and function. Therefore, with use of micromanometer left ventricular pressure measurements and ventricular volumes, calculated from biplane cineangiograms, left ventricular function at rest and during exercise was studied in 57 patients. Exercise-induced ischemia produced a decrease in ejection fraction, an increase in end-systolic volume, dramatic increases in diastolic pressures and an upward shift in the diastolic pressure-volume relation. Central to these changes was abnormal myocardial contraction and relaxation, with reduced regional shortening and impaired left ventricular pressure decay. However, nonischemic areas were capable of augmented shortening, and global pressure decay did accelerate slightly. These findings demonstrate that exercise-induced adjustments in contraction and relaxation are intertwined with ischemia-related abnormalities. Exercise studies in patients after bypass surgery and in patients with scars from distant myocardial infarction were useful in clarifying confounding factors. For example, asynchrony of contraction and relaxation, and chronic changes in passive chamber properties, also compromise systolic and diastolic function during exercise. In patients with coronary artery disease without ischemia during exercise, left ventricular end-diastolic pressure, but not early diastolic pressure, increased during exercise. The increase in pressure was appropriate for a slight increase in end-diastolic volume in a ventricle with a steep pressure-volume relation. Furthermore, end-systolic volume, while maintained during exercise, was not reduced, as occurs normally. Intraoperative myocardial biopsy specimens showed myocardial hypertrophy and increased interstitial fibrosis in many patients. Thus, the acute abnormalities of exercise-induced ischemia are superimposed on the hemodynamics of exercise and occur in the setting of chronic structural and functional abnormalities frequently seen in coronary artery disease.

Abnormalities in jugular venous flow velocity in pulmonary hypertension

Doppler recordings of jugular venous flow velocity previously performed in this laboratory in patients with pulmonary hypertension had shown variations from the normal dominant systolic flow (SF) greater than diastolic flow (DF), to SF = DF, SF < DF or DF alone. The mechanisms underlying these flow alterations were studied in 25 patients and correlated with hemodynamics. The patients with abnormal flow patterns had increased right atrial V-wave pressures. This was associated with an increased right ventricular early diastolic pressure. The incidence of clinical heart failure was higher in patients with SF < DF or DF alone (8 of 11) compared with 5 of 10 patients with SF = DF. Thus, in patients with pulmonary hypertension, the abnormal jugular venous flow patterns appear to be caused by both an increased DF velocity and a decrease in SF velocity. Because the right atrial V-wave pressures were similar in patients with both SF = DF and SF < DF or DF alone and the incidence of heart failure was higher in the latter, the decrease in SF must be a later phenomenon. Serial observations confirmed this temporal sequence. The applicability of these observations to bedside evaluation of patients with pulmonary hypertension is emphasized.

Mid-cavity obstruction in apical hypertrophy: Doppler evidence of diastolic intraventricular gradient with higher apical pressure

Three cases of apical left ventricular hypertrophy demonstrating a sequestered small left ventricular apical cavity with complete systolic and partial diastolic intraventricular obstruction are described. Doppler studies revealed that flow from the apical chamber is aborted during early systole with further emptying during diastole through a narrow intraventricular channel, where a diastolic high-velocity jet (≥2.5 m/sec) directed from apex to base was localized. This indicated a significantly higher pressure in early diastole in the sequestered apical cavity. Filling of the apical chamber occurred late in diastole and during isovolumic ventricular contraction. The observations by Doppler of complete intraventricular systolic and partial diastolic obstruction in apical hypertrophy are new and may have significant clinical implications.

Postextrasystolic potentiation worsens fast filling of the hypertrophied left ventricle in aortic stenosis and hypertrophic cardiomyopathy.

Impaired left ventricular (LV) filling in aortic stenosis (AS) and in hypertrophic cardiomyopathy (HCM) is caused by slow LV pressure decay, which could be explained by depressed inactivation of hypertrophied myocardium. Postextrasystolic potentiation (PESP), which increases activator calcium, could lead to further deterioration of LV relaxation. The influence of PESP on LV filling dynamics was, therefore, investigated in normal controls and in patients with LV hypertrophy caused by AS or by HCM. LV hemodynamics and LV hemodynamic relaxation indexes were determined during normal sinus rhythm (NSR) and after PESP. LV pressures were recorded by micromanometer tip catheters (controls, n = 10; AS, n = 17; HCM, n = 11). Simultaneous mitral flow Doppler echocardiograms were obtained in patients with LV hypertrophy (AS, n = 8, HCM, n = 5). Despite significant increases of LV dP/dtmax after PESP in all three study groups, PESP affected LV hemodynamic relaxation indexes differently. The time constant of LV pressure decay (TPB) derived from exponential curve fits with nonzero asymptote pressure remained unaltered after PESP in normal controls, rose from 62 +/- 17 to 74 +/- 21 msec (p less than 0.02) in patients with AS, and rose from 74 +/- 18 to 84 +/- 19 msec (p less than 0.02) in patients with HCM. Early diastolic LV pressure decay was measured by phi (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves) and by t (time interval from LV dP/dtmin to LV minimum diastolic pressure). After PESP, phi remained unaltered in normal controls but decreased in AS from 42.8 +/- 19.1 degrees to 24.0 +/- 28.8 degrees (p less than 0.001) and in HCM from 39.7 +/- 15.4 degrees to 26.9 +/- 15.7 degrees (p less than 0.001). Similarly, t was unchanged after PESP in normal controls but prolonged in AS from 146 +/- 48 to 205 +/- 86 msec (p less than 0.001) and in HCM from 168 +/- 40 to 208 +/- 53 msec (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)

Diastolic properties of the normal left ventricle during supine exercise.

Diastolic function in response to dynamic exercise was studied by biplane left ventriculography and by measuring left ventricular pressure with a high fidelity micromanometer tipped catheter at rest and during supine bicycle exercise in nine normal subjects. During exercise there was a fall in end systolic volume, in the time constant of left ventricular isovolumic pressure decay, and in the lowest diastolic pressure. Stroke volume, peak filling rate, mean passive filling rate, and the volume at the lowest diastolic pressure increased. There was an increase in the number of time constants that had elapsed before the lowest diastolic pressure was reached and the slope of the pressure-volume curves during passive filling (delta P/delta V) increased without changes in end diastolic pressure and volume. These results show that during exercise elastic recoil is enhanced and left ventricular relaxation is faster and more complete. Both phenomena reduce the lowest diastolic filling pressure. The observed increase in chamber stiffness from rest to exercise is probably related to increased resistance of the left ventricular wall caused by higher passive filling rates. The enhanced early diastolic pressure decay during exercise allows stroke volume to increase despite an increase in diastolic viscoelastic resistance and chamber stiffness.

Impaired relaxation of the hypertrophied left ventricle in aortic stenosis: effects of aortic valvuloplasty and of postextrasystolic potentiation

Impaired left ventricular (LV) filling in aortic stenosis (AS) is explained by slow LV pressure decay, which impedes LV inflow. This slow LV pressure decay could be explained by the altered myocardial wall stress pattern of AS or by a failure of inactivation of hypertrophied myocardium. To evaluate whether altered LV loading or impaired myocardial inactivation is the predominant control of LV relaxation and filling in AS, we studied the effects of aortic valvuloplasty (PTAV) and of postextrasystolic potentiation (PESP). LV micromanometer tip pressure recordings and simultaneous LV angiograms were obtained before and after PTAV in 10 patients with AS. PTAV reduced peak-to-peak aortic valve gradient from 101 +/- 7 to 40 +/- 5 mmHg (P less than 0.01), peak LV systolic pressure from 211 +/- 8 to 169 +/- 4 mmHg (P less than 0.01) and LV end-diastolic pressure from 22 +/- 3 to 13 +/- 2 mmHg (P less than 0.01). Despite these large drops of LV loading after PTAV, the time constant, T, of LV pressure decay decreased only slightly from 47 +/- 4 to 44 +/- 4 ms (P less than 0.05) and the LV peak filling rate remained unaltered. The influence of PESP on LV relaxation and filling was investigated in patients with AS using LV micromanometer tip pressures (n = 22) and simultaneous mitral valve Doppler echocardiograms (n = 9). After PESP the time constant, T, of isovolumic LV pressure decay increased from 43 +/- 4 to 54 +/- 4 ms (P less than 0.01).2+ 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular systolic and diastolic function in coronary artery disease: effects of revascularization on exercise-induced ischemia.

Left ventricular systolic and diastolic function were studied before and after surgical revascularization in a group of 24 patients with stable angina who all had an excellent clinical response to surgery. With use of micromanometer left ventricular pressure measurements and ventricular volumes, calculated from biplane cineangiograms, left ventricular function at rest and during exercise before and after surgery was compared. Before surgery all patients had exercise-induced ischemia with new asynergy, a fall in ejection fraction from 57% to 49% (p less than .001), and a rise in left ventricular end-diastolic pressure from 23 to 37 mm Hg (p less than .001). Postoperative exercise resulted in no new asynergy and ejection fraction rose from 59% to 61% (p less than .05). Left ventricular end-diastolic pressure still rose from 17 to 25 mm Hg (p less than .01). Left ventricular pressure decay during exercise was greatly improved after revascularization and allowed maintenance of reduced early diastolic pressures. The early diastolic pressure nadir before surgery rose from 9 to 21 mm Hg (p less than .001); the postoperative nadir was 5 mm Hg at rest and 6 mm Hg during exercise. All patients had an upward shift in the diastolic pressure-volume relationship during preoperative exercise. After revascularization there was no upward shift in some patients and a much smaller shift in others. The postoperative increase in left ventricular end-diastolic pressure was due to increased end-diastolic volume, not altered compliance. There was an increase in mean right atrial pressure during exercise either before (6 to 11 mm Hg) or after surgery (4 to 10 mm Hg). These increases were quite variable, suggesting no consistent role of pericardial restraint during exercise. Early diastolic peak filling rate during exercise was greater after surgery (1260 vs 950 ml/sec, p less than .001). In fact, during postoperative exercise early diastolic filling rates were greater than normal, reflecting the persistence of abnormally high atrial pressures for filling. As at preoperative study, late diastolic filling during exercise was restricted after revascularization when compared with that in a control group. Postoperatively patients undergoing bypass procedures with a good clinical result showed significantly improved left ventricular diastolic and systolic function. Persistent elevation of end-diastolic and atrial pressures and other abnormalities of diastolic function may reflect chronic structural changes and need to be taken into account when evaluating patients after bypass surgery.

Mitral valve alternans

An echogram showing mitral valve alternans was recorded in a patient with advanced cardiomyopathy and pulsus alternans induced by premature ventricular depolarizations. Decreased left ventricular emptying by the weak beat was followed by blunting of the subsequent mitral valve E point, a finding compatible with a significant elevation of left ventricular pressure in early diastole. Both alternating systolic (contractile state) and diastolic (pressure and dimension) variables seemed to participate in the alternans phenomenon in this patient.

Does post-exercise ST depression reflect local ischemia or some global effect in the left ventricle?

As exercise-induced ST depressions are most frequent and marked in lead V5 independent of which single coronary artery is obstructed, some other mechanisms of ST depressions than local ischemia should be searched for. Left ventricular hemodynamics during exercise was studied in two groups of patients with severe effort angina, 19 with and 12 without ST depression after exercise (STAE). During supine exercise until angina, stroke index became significantly lower (37 vs. 52 ml/m2) and left ventricular end-diastolic pressure (LVEDP) significantly higher (40 vs. 30 mmHg) in the STAE group. The best discriminator was the early diastolic pressure (LVeDP) (22 vs. 11 mmHg), which is interpreted as a sign of a more ischemic ventricle in the STAE group. The sum of STAE in all leads is correlated to LVeDP but not to LVEDP during exercise. The link between the significant ischemia in various locations and STAE appearing most frequently and markedly in V5 seems to be some global mechanism as the occurrence of STAE and the height of the R wave were positively correlated in the various leads. As STAE in coronary heart disease shows similar configuration and distribution as in aortic valvular stenosis and digoxin medication of healthy subjects, a possible link could be the compensatory increase in contractility in non-ischemic parts of the ventricle.

The hemodynamic derangement associated with right ventricular diastolic collapse in cardiac tamponade: an experimental echocardiographic study.

Clinical reports indicate that right ventricular diastolic collapse (RVDC) is associated with cardiac tamponade. To assess the hemodynamic abnormalities associated with RVDC, we studied six chronically instrumented conscious dogs (group A) with two-dimensional echocardiography during cardiac tamponade induced by continuous saline infusion into the pericardial space. We recorded cardiac output (electromagnetic flowmeter), heart rate, respiration, and aortic, intrapericardial, and right atrial pressures. In four additional animals (group B), we recorded right ventricular pressure and placed a hydraulic occluder around the pulmonary artery so that short-term reversible obstruction to right ventricular outflow could be produced. None of the dogs had RVDC when the pericardial space was empty, but all dogs showed RVDC during cardiac tamponade. The appearance of RVDC in group A was associated with a 21% reduction in cardiac output (p less than .01) and no change in mean aortic pressure. Short-term partial pulmonary artery obstruction led to increased right ventricular pressures and a striking reduction in RVDC in early tamponade, suggesting that RVDC is caused by pericardial pressure exceeding right ventricular pressure in early diastole. An additional animal had right ventricular hypertrophy caused by a severe "heart worm" infestation and did not show RVDC during cardiac tamponade. These observations suggest that in the absence of increased resistance to right ventricular outflow or right ventricular hypertrophy, RVDC occurs early in the course of cardiac tamponade and is associated with a hemodynamically important decrease in cardiac output.

Mechanisms of left ventricular filling during increased preload and inotropy.

To examine the factors contributing to left ventricular filling, experiments were performed in anesthetized, open-chest dogs with intact or mechanically constricted mitral ostium. Stroke volume was raised either by increasing left ventricular end-diastolic volume (preload) by blood volume expansion or by infusing isoproterenol, a beta-adrenergic agonist. In all experimental settings, stroke volume rose in proportion (r greater than 0.9) to the pressure time product (PTP = integral of the diastolic atrio-ventricular (A-V) pressure difference). During saline infusion atrial distention and contraction increased atrial pressure more than ventricular pressure whereas diastolic filling time (DFT) was not lengthened. Peak mitral and peak aortic flow rose almost equally. During isoproterenol infusion at constant heart rate (atrial pacing), the increase in PTP was mainly caused by a longer DFT. When heart rate was allowed to rise, DFT was reduced and the A-V pressure difference increased because of a greater reduction in ventricular than in atrial pressure in early diastole. Thus, the A-V pressure difference is generated in different ways by raising preload and inotropy with and without changes in heart rate.

Exercise-induced ischemia: the influence of altered relaxation on early diastolic pressures.

Left ventricular pressure (LVP) decay and early diastolic pressures were studied at rest and during exercise in three groups of patients. Patients in the ischemia group (n = 15) had coronary artery disease and developed new regional wall motion abnormalities documented by biplane LV cineangiography during exercise. Patients in the control group (n = 4) had a normal exercise response. Patients in the scar group (n = 5) had prior infarction, akinetic scars and no ischemia with exercise. Isovolumic pressure data were used to compute the time constant (T) of LVP decay (from the linear relation of LVP and negative dP/dt) and an extrapolated baseline pressure (PB) at dP/dt = 0. During exercise in the ischemia group, minimal LV diastolic pressure (PL) increased from 9 +/- 3 to 21 +/- 5 mm Hg (p less than 0.001), end-systolic volume increased from 38 +/- 7 to 55 +/- 8 ml/m2 (p less than 0.001) and PB rose from -10 +/- 7 to 11 +/- 8 mm Hg (p less than 0.001); T decreased (from 55 +/- 9 to 37 +/- 8 msec, p less than 0.001), although inadequately, compared with the decrease in the control group (from 49 +/- 15 to 22 +/- 2 msec, p less than 0.01). Relaxation at PL during exercise was incomplete in the ischemia group (2.2 +/- 0.4 T) and complete in the control group (3.8 +/- 0.7 T, p less than 0.05). The time course of LVP fall was extrapolated from the isovolumic period into the passive LV filling phase. The extrapolated pressure at the time PL occurred (PE) rose from 0 +/- 4 to 20 +/- 7 mm Hg with ischemia (p less than 0.001). Thus, the characteristics of LVP decay can account for the elevated early diastolic pressures during ischemia. In contrast, the scar group maintained a low PL during exercise (11 +/- 3 to 8 +/- 3 mm Hg), even though T decreased inadequately (from 66 +/- 10 to 36 +/- 5 msec, p less than 0.01), because PB did not shift upward. Ischemia-related pressure elevations involve both delayed relaxation and a pressure baseline shift. During exercise, LVP decay is normally adjusted to maintain low diastolic pressures; with exercise-induced ischemia, LVP decay is abnormal and early diastolic pressures are severely elevated.

Left ventricular isovolumic pressure decay and diastolic mechanics after postextrasystolic potentiation and during exercise

Left ventricular contraction, relaxation, and diastolic mechanics were examined in subjects after postextrasystolic potentiation and compared with results during supine bicycle exercise. Twelve patients had ventricular extrasystoles induced during biplane left ventricular cineangiography (PES Group). Six patients with no or minimal cardiovascular disease underwent exercise (Exercise Group). From simultaneous high-fidelity pressure curves the time constant of relaxation (T), a theoretical baseline for isovolumic pressure decay (PB), and the lowest diastolic pressure (PL) were determined. Frame-by-frame volume analysis was completed in 6 patients from the PES Group and 4 in the Exercise Group to quantitate filling rates and to construct diastolic pressure-volume relations. In the PES Group, the ejection fraction increased from 65 to 74% (p In the Exercise Group, the ejection fraction increased from 65 to 75% (p Postextrasystolic potentiation, like dynamic exercise, enhances shortening and augments restoring forces by producing a smaller end-systolic chamber. Yet, postextrasystolic potentiation delays inactivation and prolongs relaxation. Diastolic mechanics (early diastolic pressure, filling, pressure-volume relation) are not subsequently altered, suggesting that enhanced restoring forces counterbalance the delayed inactivation. With exercise, diastolic filling is enhanced both by more rapid pressure decay and by increased restoring forces. Thus, diastolic mechanics can be dissociated from systolic and are determined by the nature of the inotropic stimulus.

Ventricular diastolic pressure-volume relations after the intra-atrial baffle operation for transposition of the great arteries.

Right and left ventricular diastolic pressure-volume (P-V) relations were assessed in 30 patients approximately 2 years after the Mustard operation. The overall distensibility index (delta V/ delta P), the compliance index at end-diastole (dv/dp), and the modulus of ventricular stiffness (Kp) were calculated in all, as well as the half-time of early diastolic pressure fall (T) in 10 cases. Transducer-tipped catheters were used in 15 patients and biplane cineangiography was employed in all. Values for the above indices equal to 2 standard deviations below the mean, obtained from five postoperative Mustard patients with no residual defects, were used as "normals." Seven patients with pulmonary hypertension (PH) and six with pulmonic stenosis (PS) were found to have impaired P-V relations. The impairment was more profound in the PH group. Delta v/delta p and dv/dp were abnormal in six of seven patients for both ventricles and T was abnormal in two of five. Kp was abnormal for the LV, and the RV ejection fraction was diminished. In the PS group (nine patients) the impairment was milder, affecting more than LV and end-diastole (dv/dp). Compliance studies might be useful in patients with LV afterload problems following the Mustard operation.

Role of Echocardiography in Detecting the Anatomic and Physiologic Abnormalities of Constrictive Pericarditis

Constrictive pericarditis (CP) is associated with thickening of the pericardium (P), rapid filling of the ventricles, and a steep rise of early diastolic pressure in the right and left ventricles. We investigated the frequency with which echocardiography detects the characteristic anatomic and physiologic abnormalities of CP. M-mode echocardiography was performed in 10 patients with CP. All patients had evidence of pericardial thickening. Eight patients had motion of the P parallel to the epicardium with an echo-free space between the two structures. Two patients had a small pericardial and left pleural effusion sandwiching the P which measured 8mm, and 14mm respectively. Premature pulmonic valve opening indicating a high right ventricular early diastolic pressure which exceeded the pulmonary artery diastolic pressure was present in all 5 patients in whom the pulmonic valve was recordable. A notch on the septum in early diastole was seen in 6 patients. Sharp posterior motion of the left ventricular posterior wall in early diastole followed by a flat segment was noted in 7 patients. Motion of the posterior wall of the aortic root (PWAo) in diastole has been shown to indicate left atrial volume changes or reflect left ventricular filling. An index of early diastolic left ventricular filling derived from the motion of the posterior wall of the aortic root, indicated abnormally rapid early diastolic filling in all 8 patients in whom this was measured. We conclude: 1) The anatomic and physiologic abnormalities in CP are commonly reflected on the echocardiogram, and 2) echocardiography should be useful in evaluation of patients suspected of having CP.

Exercise-induced ischemia: Does pressure decay influence early diastolic pressures?

Exercise-induced ischemia: Does pressure decay influence early diastolic pressures?