Left ventricular pressure-volume relations and myocardial dysfunction in pressure or volume overload

Walter J. Paulus
Cardiovascular Center, O.L.V. Hospital, Aalst, Belgium
Correspondence: Dr Walter J. Paulus, Cardiovascular Center, O.L.V. Ziekenhuis, Moorselbaan 164, 9300 Aalst, Belgium. Tel: +32 53 724433, fax: +32 53 724587, e-mail: walter.paulus@pi.be

The left ventricular (LV) end-systolic pressure-volume relation in clinical practice
The slope of the left ventricular (LV) end-systolic pressure-volume relation was first proposed as an index of LV contractility by Suga and Sagawa.[1] The slope of the LV end-systolic pressure-volume relation is called maximal LV elastance (Emax) and is determined in the clinical setting by connecting, during titrated intravenous infusion of sodium nitroprusside, different LV end-systolic pressure-volume points (ie, the outer left-hand corners of the LV pressure-volume loops). LV end-systolic pressure-volume loops can be obtained clinically using invasive techniques[2] (ie, sequential LV contrast angiograms or sequential conductance catheter LV volume measurements and micromanometer LV pressure recordings) or noninvasive techniques[3] (ie, sequential two-dimensional and targeted M-mode echocardiograms and indirect oscillometric brachial artery pressures).
Determination of the slope of an LV pressure-volume relation is cumbersome because it requires construction of at least two LV pressure-volume loops, one at rest and one after a pharmacological intervention such as an intravenous infusion of sodium nitroprusside. Numerous investigators have therefore tried to obtain similar information on LV performance from a single measurement of LV end-systolic performance. These measurements include (Figure 1):

Figure 1. Overview of indices of LV end-systolic performance derived from the LV end-systolic wall stress/ejection fraction ratio.

 (1) LV end-systolic short-axis internal dimension and LV end-systolic volume; (2) LV end-systolic pressure/end-systolic volume ratio and LV peak-systolic pressure/end-systolic volume ratio; (3) LV end-systolic wall stress/end-systolic volume ratio and LV end-systolic wall stress/ejection fraction ratio.

LV end-systolic short-axis internal dimension and LV end-systolic volume
LV dimensions and volume at end-systole are independent of preload1 and vary only with afterload. End-systolic LV dimensions and volume have therefore been proposed as an index of LV myocardial contractility in patients with LV volume overload of chronic aortic or mitral regurgitation and as a predictor of surgical outcome.[4,5] Use of LV end-systolic dimensions or volume as an index of contractility assumes no derangement of LV afterload. This assumption is open to critique because LV afterload measured as LV end-systolic myocardial wall stress is higher in patients with chronic aortic regurgitation than in healthy subjects or patients with chronic mitral regurgitation.[6] This higher than normal LV end-systolic wall stress in patients with chronic aortic regurgitation suggests replication of sarcomeres unable to increase LV wall thickness sufficiently to normalize the LV end-diastolic radius/thickness ratio[7] and to normalize LV wall stress. This LV “afterload mismatch”[8] should be taken into account when using LV end-systolic dimensions or volume as a guide to postoperative prognosis because correction of the afterload mismatch by valve replacement could induce a larger improvement in LV end-systolic dimensions or volume than predicted by preoperative measurements.

LV end-systolic pressure/end-systolic volume ratio and LV peak-systolic pressure/end-systolic volume ratio
To correct for afterload variability, investigators used the LV end-systolic pressure/end-systolic volume ratio or the LV peak-systolic pressure/end-systolic volume ratio as a surrogate measure of Emax.[9] In order for a ratio generated by a single point measurement to reflect the slope of a linear relation, the linear relation has to pass through the origin of the plot. This condition is not satisfied for LV pressure-volume relations in clinical practice, where the intercept of the LV end-systolic pressure-volume relation with the volume axis is variable certainly in dilated left ventricles.[10] Moreover, substitution of LV end-systolic pressure by LV peak-systolic pressure is open to critique, particularly when the arterial pulse pressure is wide, as in chronic aortic regurgitation.

LV end-systolic wall stress/end-systolic volume ratio and LV end-systolic wall stress/ejection fraction ratio
To include the degree of compensatory LV hypertrophy, LV end-systolic pressure was substituted by LV end-systolic wall stress in several studies. LV end-systolic wall stress is indeed directly related to LV end-systolic pressure and LV end-systolic volume and inversely related to LV end-systolic wall thickness. The ratio between LV end-systolic stress and LV end-systolic volume was the only independent predictor of surgical outcome in patients with LV volume overload due to chronic mitral regurgitation;[11] in patients with chronic aortic regurgitation the ratio between LV ejection fraction and LV end-systolic stress was a predictor of unfavorable outcome.[12]
When invasive techniques are used, other relations can be obtained simultaneously to corroborate conclusions on changes in contractility drawn from the calculation of Emax. These relations include the LV dP/dtmax–end-diastolic volume relation or the LV stroke volume–end-diastolic volume relation.[13] When noninvasive techniques are used, simultaneous determination of the mean rate-corrected velocity of fiber shortening (vcfc) vs LV circumferential end-systolic wall stress provides another way to assess LV contractility in humans.[14] This latter index corrects both for the inappropriate use of LV pressure as a measurement of LV wall force and for the unequal LV sizes and wall masses.

The LV diastolic pressure-volume relation in clinical practice
When discussing diastolic LV properties in clinical practice, a distinction needs to be made between diastolic LV distensibility, diastolic LV compliance, and diastolic LV stiffness (Figure 2).

Figure 2. Distinction between LV distensibility and LV stiffness

Diastolic LV distensibility is defined by the position of the diastolic portion of the LV pressure-volume relation in the LV pressure-volume plane. A reduction in diastolic LV distensibility implies an upward and leftward displacement of the diastolic portion of the LV pressure-volume relation and does not require a simultaneous increase in the slope of the diastolic portion of the LV pressure-volume relation.[15] The diastolic portion of the LV pressure-volume relation can be obtained from a single beat, but such an approach includes dynamic effects related to LV relaxation and LV filling especially in the early diastolic portion of the graph.[16–18] Using a caval balloon occlusion, several LV end-diastolic pressure-volume points can be obtained and a diastolic LV pressure-volume relation can be constructed, which is only composed of “static” LV end-diastolic pressure-volume points without “dynamic” interference related to LV relaxation or LV filling.[19,20] End-diastolic LV distensibility is considered to be decreased if, in the presence of a normal LV end-diastolic volume index (<102 mL/m2), LV end-diastolic pressure is higher than 16 mm Hg.[21]
LV diastolic stiffness is the ratio of the change in LV diastolic pressure divided by the change in LV diastolic volume and equals the slope of the diastolic LV pressure-volume relation (dP/dV). LV diastolic compliance is the inverse of LV diastolic stiffness and therefore equals the change in LV diastolic volume divided by the change in LV diastolic pressure. As the diastolic LV pressure-volume relation changes its slope over its entire course, LV diastolic stiffness values need to be compared at a common level of LV diastolic pressure[22] or the LV pressure-volume data points need to be logarithmically transformed to a linear relation, the unique slope of which equals the LV diastolic stiffness constant.[23] Recently, a relation was demonstrated between the deceleration time of the Doppler mitral flow velocity signal and the LV diastolic stiffness constant.[24] Myocardial diastolic stiffness has also been reported and equals the slope of the diastolic myocardial stress-myocardial strain relation and implies transformation of LV pressure to wall stress and of LV volume to myocardial strain.[23]
In LV pressure overload, concentric LV hypertrophy reduces LV diastolic distensibility and hinders LV filling at normal diastolic LV filling pressures. In order to maintain normal LV filling, left atrial filling pressures will rise and LV filling will become more dependent on left atrial contraction. Significant hemodynamic deterioration can result from the loss of atrial contraction because of the occurrence of atrial fibrillation. The reduction in LV diastolic distensibility in the hypertrophied left ventricle persists even after aortic valve replacement probably because of failure of regression of LV interstitial fibrosis.[25] In patients with aortic stenosis, the reduction in diastolic LV distensibility depends on both the sex and age of the patient, being most frequent in elderly men.[26]

Summary
Indices derived from LV end-systolic pressure-volume relations have important prognostic value in LV volume overload of chronic aortic or mitral regurgitation. Their sequential determination is useful for correct timing of valve replacement or valve repair. Indices derived from diastolic LV pressure-volume relations are especially useful in concentric LV hypertrophy of aortic stenosis. They can remain abnormal for a prolonged period following valve replacement despite regression of LV hypertrophy because of persistence of LV fibrosis.

REFERENCES
 

1: Circ Res 1974 Jul;35(1):117-26 Related Articles, Books, LinkOut

Instantaneous pressure-volume relationships and their ratio in the excised, supported canine left ventricle.

Suga H, Sagawa K.

PMID: 4841253 [PubMed - indexed for MEDLINE]
 
2: Circulation 1982 May;65(5):988-97 Related Articles, Books, LinkOut

Sensitivity of end-systolic pressure-dimension and pressure-volume relations to the inotropic state in humans.

Borow KM, Neumann A, Wynne J.

The value for the slope of the left ventricular (LV) end-systolic pressure-dimension and pressure-volume relations has been proposed as a quantitative measure of the LV inotropic state. This measure of LV inotropic state is attractive because it is independent of preload and incorporates afterload. To investigate the sensitivity of the slope of these relations to alterations in contractile state, 10 normal subjects were studied using M-mode echocardiographic, phonocardiographic and indirect carotid pulse recordings during infusion of methoxamine to alter end-systolic pressure and during infusion of dobutamine (5 micrograms/kg/min) to increase LV inotropic state. Heart rate was maintained within a narrow range for each subject. End-systolic volume was calculated from end-systolic echocardiographic dimension by standard methods. End-systolic pressure was estimated from the dicrotic notch pressure determined from a calibrated carotid pulse recording; peak systolic pressure was also measured. Regardless of the method of approximating end-systolic pressure, the positive inotropic intervention caused a leftward shift in the end-systolic pressure-dimension and pressure-volume lines. With the dobutamine infusion, the value for the slope of the end-systolic pressure-dimension relation increased by 25% (range 16-46%, p less than 0.001), while the slope of the end-systolic pressure-volume relation increased by 55% (range 37-85%, p less than 0.001). In all cases, the curves were linear and became steeper with the positive inotropic intervention. In contrast, the value of the slope of the peak systolic pressure-end-systolic dimension relation showed a variable response to the dobutamine infusion (mean change 13%, range -77% to 73%; NS). Although the position of the peak systolic pressure-end-systolic dimension curve is consistently shifted with an alteration in inotropic state, the values of the slope of these curves are not reliable indicators of change in LV contractility. The values for the slope of the line relating end-systolic pressure (estimated by dicrotic notch pressure) to end-systolic dimension or volume, however, are highly sensitive to a change in inotropic state in human subjects.

PMID: 7074764 [PubMed - indexed for MEDLINE]
 
3: J Am Coll Cardiol 1993 Mar 15;21(4):939-49 Related Articles, Books, LinkOut

Noninvasive assessment of the direct action of oral nifedipine and nicardipine on left ventricular contractile state in patients with systemic hypertension: importance of reflex sympathetic responses.

Borow KM, Neumann A, Lang RM, Ehler D, Valentine-Bates B, Wolff A, Friday K, Murphy M.

Department of Medicine, University of Chicago Medical Center, Illinois.

OBJECTIVES. This study was designed to noninvasively assess the direct action of calcium channel blockers on left ventricular contractility in humans and to establish a framework for determining the importance of reflex sympathetic responses to any pharmacologic intervention. BACKGROUND. Assessment of left ventricular contractility in patients taking calcium channel blockers by using traditional indexes of systolic performance is difficult because of the after-load-reducing and reflex sympathetic effects of the drugs. METHODS. Fifteen hypertensive patients (mean blood pressure 127 +/- 15 mm Hg) were studied with Doppler echocardiography and calibrated subclavian pulse tracings while receiving placebo and 1 week after randomization to treatment with oral nifedipine (20 mg three times daily; n = 7) or nicardipine (30 mg three times daily; n = 8). Left ventricular circumferential end-systolic wall stress versus rate-corrected velocity of shortening (Vcfc) relations were generated over a range of loads using nitroprusside. Data were acquired before and during esmolol infusion, thereby allowing assessment of hemodynamic responses with the sympathetic nervous system functionally intact as well as ablated. The adequacy of sympathetic blockade was confirmed with isoproterenol challenges. In each case, left ventricular contractile state was measured relative to placebo and esmolol data as delta Vcfc at a common end-systolic wall stress. Increased and decreased contractility were defined as delta Vcfc > 0 and delta Vcfc < 0, respectively. RESULTS. Nifedipine and nicardipine equally decreased blood pressure and end-systolic wall stress and increased left ventricular percent fractional shortening and stroke volume. Neither drug alone consistently altered ventricular contractility compared with placebo. Ablation of reflex sympathetic tone with esmolol unmasked a negative inotropic effect for nifedipine (p = 0.03 vs. esmolol alone) but not nicardipine (p = 0.68 vs. esmolol alone). The difference between the contractility effects of nifedipine plus esmolol versus those of nicardipine plus esmolol approached statistical significance (p = 0.07). CONCLUSIONS. Totally noninvasive techniques showed a differential effect on left ventricular contractility between nifedipine and nicardipine when alterations in afterload and reflex sympathetic responses were eliminated as confounding variables. This diagnostic approach, based on the use of pharmacologic probes, should have wide applicability for assessing the direct inotropic effect of any agent, even in the presence of complex primary and secondary physiologic modes of action.

Publication Types:
  • Clinical Trial
  • Randomized Controlled Trial


PMID: 8095507 [PubMed - indexed for MEDLINE]

 
4: Circulation 1980 Mar;61(3):484-92 Related Articles, Books, LinkOut

Observations on the optimum time for operative intervention for aortic regurgitation. II. Serial echocardiographic evaluation of asymptomatic patients.

Henry WL, Bonow RO, Rosing DR, Epstein SE.

PMID: 7353237 [PubMed - indexed for MEDLINE]
 
5: Am J Med 1980 May;68(5):655-63 Related Articles, Books, LinkOut

End-systolic volume as a predictor of postoperative left ventricular performance in volume overload from valvular regurgitation.

Borow KM, Green LH, Mann T, Sloss LJ, Braunwald E, Collins JJ, Cohn L, Grossman W.

PMID: 7377221 [PubMed - indexed for MEDLINE]
 
6: J Am Coll Cardiol 1984 Apr;3(4):916-23 Related Articles, Books, LinkOut

Differences in myocardial performance and load between patients with similar amounts of chronic aortic versus chronic mitral regurgitation.

Wisenbaugh T, Spann JF, Carabello BA.

It is not known if the favorable changes in preload and afterload that augment ejection performance in acute experimental aortic and mitral regurgitation are also present in patients with chronic regurgitation. Additionally, observations that patients with mitral versus aortic regurgitation respond differently to valve replacement suggest that differences exist preoperatively between these two types of volume overload. Therefore, ventricular mechanics were compared in nine patients with severe aortic regurgitation, eight patients with severe mitral regurgitation and seven normal subjects. The amount of volume overload was similar in both groups with regurgitation. In both aortic and mitral regurgitation, ejection performance was reduced compared with findings in normal subjects. Preload estimated as enddiastolic stress was comparably elevated above normal in both groups with regurgitation: 69 +/- 24 dynes X 10(3)/cm2 in mitral regurgitation compared with 81 +/- 34 dynes X 10(3)/cm2 in aortic regurgitation and 36 +/- 11 dynes X 10(3)/cm2 in normal subjects. However, afterload estimated as mean systolic stress was normal in mitral regurgitation (186 +/- 34 dynes X 10(3)/cm2) but markedly elevated in aortic regurgitation (260 +/- 41 dynes X 10(3)/cm2) (p less than 0.01). Contractile depression tended to be more severe in mitral regurgitation despite similar ejection performance in mitral and aortic regurgitation. Thus, in mitral regurgitation favorable loading conditions may mask contractile dysfunction, and in aortic regurgitation excessive afterload contributes to poor pump performance, possibly accounting for previously observed differences in the response to valve replacement.

PMID: 6707357 [PubMed - indexed for MEDLINE]
 
7: J Am Coll Cardiol 1983 Mar;1(3):775-82 Related Articles, Books, LinkOut

Chronic aortic regurgitation: prognostic value of left ventricular end-systolic dimension and end-diastolic radius/thickness ratio.

Gaasch WH, Carroll JD, Levine HJ, Criscitiello MG.

The prognostic value of preoperative echocardiographic data was assessed in 32 patients who underwent aortic valve replacement for chronic aortic regurgitation. All patients had preoperative studies and were followed up prospectively for 1 to 6 years after surgery. Postoperatively, 25 patients (Group A) achieved a normal left ventricular end-diastolic dimension and a significant regression of myocardial hypertrophy; 7 patients (Group B) had persistent left ventricular enlargement. During the follow-up period, the patients in Group A had fewer symptoms and used fewer medications than those in Group B. Moreover, survival at 4 years appeared to be better in Group A (96%) than in Group B (71%); two patients in Group B died with congestive heart failure; there were no such deaths in Group A. Preoperatively, a left ventricular dimension at end-diastole (DED) larger than 3.8 cm/m2 body surface area, a dimension at end-systole (DES) greater than 2.6 cm/m2 body surface area, an end-diastolic radius/wall thickness ratio (R/Th) greater than 3.8 or a product of R/Th and left ventricular systolic pressure (P X R/Th) exceeding 600 are predictive of a Group B result. If end-systolic dimension is greater than 2.6 and P X R/Th is greater than 600, all Group B patients can be identified; all but one patient in Group A had an end-systolic dimension less than 2.6 and P X R/Th less than 600. It is concluded that patients with chronic aortic regurgitation who are at risk of persistent postoperative left ventricular enlargement (with associated cardiac symptoms and reduced survival) can be identified by preoperative echocardiography.

PMID: 6219153 [PubMed - indexed for MEDLINE]
 
8: J Am Coll Cardiol 1985 Apr;5(4):811-26 Related Articles, Books, LinkOut

Afterload mismatch in aortic and mitral valve disease: implications for surgical therapy.

Ross J Jr.

In the management of patients with valvular heart disease, an understanding of the effects of altered loading conditions on the left ventricle is important in reaching a proper decision concerning the timing of corrective operation. In acquired valvular aortic stenosis, concentric hypertrophy generally maintains left ventricular chamber size and ejection fraction within normal limits, but in late stage disease function can deteriorate as preload reserve is lost and aortic stenosis progresses. In this setting, even when the ejection fraction is markedly reduced (less than 25%), it can improve to normal after aortic valve replacement, suggesting that afterload mismatch rather than irreversibly depressed myocardial contractility was responsible for left ventricular failure. Therefore, patients with severe aortic stenosis and symptoms should not be denied operation because of impaired cardiac function. In chronic severe aortic and mitral regurgitation, operation is generally recommended when symptoms are present, but whether to recommend operation to prevent irreversible myocardial damage in patients with few or no symptoms has remained controversial. In aortic regurgitation, left ventricular function generally improves postoperatively, even if it is moderately impaired preoperatively, indicating correction of afterload mismatch. Most such patients can be carefully followed by echocardiography. However, in some patients, severe left ventricular dysfunction fails to improve postoperatively. Therefore, when echocardiographic studies in the patient with severe aortic regurgitation show an ejection fraction of less than 40% (fractional shortening less than 25%) plus enlarging left ventricular end-diastolic diameter (approaching 38 mm/m2 body surface area) and end-systolic diameter (approaching 50 mm or 26 mm/m2), confirmation of these findings by cardiac catheterization and consideration of operation are advisable even in patients with minimal symptoms. In chronic mitral regurgitation, maintenance of a normal ejection fraction can mask depressed myocardial contractility. Pre- and postoperative studies in such patients have shown a poor clinical result after mitral valve replacement, associated with a sharp decrease in the ejection fraction after operation. This response appears to reflect unmasking of decreased myocardial contractility by mitral valve replacement, with ejection of the total stroke volume into the high impedance of the aorta (afterload mismatch produced by operation).(ABSTRACT TRUNCATED AT 400 WORDS)

Publication Types:
  • Review


PMID: 3882814 [PubMed - indexed for MEDLINE]

 
9: J Am Coll Cardiol 1994 Dec;24(7):1672-7 Related Articles, Books, LinkOut

Use of the left ventricular peak systolic pressure/end-systolic volume ratio to predict symptomatic improvement with valve replacement in patients with aortic regurgitation and enlarged end-systolic volume.

Pirwitz MJ, Lange RA, Willard JE, Landau C, Glamann DB, Hillis LD.

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9047.

OBJECTIVES. This study was designed to assess the left ventricular peak systolic pressure/end-systolic volume (PSP/ESV) ratio in predicting symptomatic improvement with valve replacement in patients with aortic regurgitation and enlarged left ventricular volume. BACKGROUND. Patients with aortic regurgitation and a left ventricular end-systolic volume < or = 60 ml/m2 show symptomatic improvement with valve replacement, whereas the response of those with an enlarged end-systolic volume > 60 ml/m2 is mixed. Most benefit, but some do not. Valve replacement appears to help those whose end-systolic volume is enlarged because of excessive left ventricular afterload but appears to have little or no effect in those whose end-systolic volume is enlarged because of depressed left ventricular contractility. METHODS. We studied 27 patients (21 men and 6 women aged 18 to 72 years) with moderate or severe aortic regurgitation, no other cardiovascular abnormalities and left ventricular end-systolic volume > 60 ml/m2. In this group we assessed the ability of preoperative variables routinely measured at cardiac catheterization to predict symptomatic improvement with valve replacement. RESULTS. Of the 27 subjects, 1 (4%) died 51 days postoperatively. Six months postoperatively, symptoms had lessened in 17 patients (63%), were unchanged in 8 (29%) and had worsened in 1 (4%). By multivariate analysis, the PSP/ESV ratio was the strongest predictor of both functional class 6 months postoperatively (p = 0.026) and change in functional class from before operation to 6 months postoperatively (p = 0.033). By 6 months after valve replacement, all patients with a ratio > or = 1.72 mm Hg/ml per m2 were in functional class I or II; in contrast, of those with a ratio < 1.72 mm Hg/ml per m2, 31% were in functional class III, and 1 (8%) had died. CONCLUSIONS. The PSP/ESV ratio may help to predict which patients with aortic regurgitation and enlarged left ventricular end-systolic volume will have symptomatic improvement with valve replacement.

PMID: 7963114 [PubMed - indexed for MEDLINE]
 
10: Circulation 1977 Nov;56(5):845-52 Related Articles, Books, LinkOut

Contractile state of the left ventricle in man as evaluated from end-systolic pressure-volume relations.

Grossman W, Braunwald E, Mann T, McLaurin LP, Green LH.

End-systolic pressure (PES), volume (VES), wall tension (TES) and circumference (CES) of the human left ventricle were studied at cardiac catheterization in 24 subjects with varying degrees of left ventricular dysfunction. Acute alterations in systolic load consistently resulted in changes in VES and CES, with a smaller volume and circumference characterizing the lower systolic load in each subject. End systolic pressure-volume lines were constructed by plotting PES against VES at the higher and lower systolic load in each subject. The slope of the resultant lines was considerably steeper for normal than for poorly contractile left ventricles. Vo, the volume axis intercept of the line (i.e., the theoretical VES at PES = O) was significantly smaller for normal than for poorly contractile ventricles. Similar findings were noted for Co, the theoretic end-systolic circumference at zero end-systolic ventricular wall tension. Post-extrasystolic potentiation resulted in decreased VES and CES with no change in PES and only a slight fall in TES. In conclusion, end-systolic pressure-volume and tension-circumference relations reflect the contractile state of left ventricular myocardium. Quantitation of these relationships may provide a useful new approach to the assessment of myocardial function in man.

PMID: 71960 [PubMed - indexed for MEDLINE]
 
11: Circulation 1986 Dec;74(6):1309-16 Related Articles, Books, LinkOut

Erratum in:
  • Circulation 1987 Mar;75(3):650


Hemodynamic predictors of outcome in patients undergoing valve replacement.

Carabello BA, Williams H, Gash AK, Kent R, Belber D, Maurer A, Siegel J, Blasius K, Spann JF.

The afterload-corrected end-systolic volume index (ratio of end-systolic stress to end-systolic volume index [ESS/ESVI]) was previously useful in predicting outcome in patients with mitral regurgitation undergoing valve replacement. Therefore we tested ESS/ESVI together with standard hemodynamic variables as possible predictors of outcome in 39 patients with various valvular lesions who underwent valve replacement. Thirteen patients had preoperative mitral regurgitation, 16 had aortic stenosis, nine had aortic regurgitation, and one had mitral stenosis. Twenty-seven patients (group S) had a satisfactory outcome as defined by a return to NYHA class I or II together with a normal postoperative ejection fraction. Twelve patients who died, remained in class III or IV, or had a subnormal postoperative ejection fraction were deemed to have an unsatisfactory result (group U). Mean right atrial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, end-diastolic volume index, end-systolic volume index (ESVI), and end-systolic wall stress were all greater in group U, whereas ESS/ESVI and ejection fraction were lower in group U. When these and other factors were submitted to stepwise discriminant multivariate analysis, ESS/ESVI and ESVI were the only independent predictors of outcome. However, when patients with mitral regurgitation (who might have biased the study) were excluded, discriminant analysis showed ESVI as the only independent predictive variable. We conclude that end-systolic indicators of ventricular function are superior to other standard hemodynamic variables in predicting outcome of valve replacement.

PMID: 3779916 [PubMed - indexed for MEDLINE]

 
12: Circulation 1998 Feb 17;97(6):525-34 Related Articles, Books, LinkOut

Comment in:

Click here to read
Prediction of indications for valve replacement among asymptomatic or minimally symptomatic patients with chronic aortic regurgitation and normal left ventricular performance.

Borer JS, Hochreiter C, Herrold EM, Supino P, Aschermann M, Wencker D, Devereux RB, Roman MJ, Szulc M, Kligfield P, Isom OW.

The New York Hospital-Cornell Medical Center, New York 10021, USA.

BACKGROUND: Optimal criteria for valve replacement are unclear in asymptomatic/minimally symptomatic patients with aortic regurgitation (AR) and normal left ventricular (LV) performance at rest. Moreover, previous studies have not assessed the prognostic capacity of load-adjusted LV performance ("contractility") variables, which may be fundamentally related to clinical state. Therefore, 18 years ago, we set out to test prospectively the hypothesis that objective noninvasive measures of LV size and performance and, specifically, of load-adjusted variables, assessed at rest and during exercise (ex), could predict the development of currently accepted indications for operation for AR. METHODS AND RESULTS: Clinical variables and measures of LV size, performance, and end-systolic wall stress (ESS) were assessed annually in 104 patients by radionuclide cineangiography at rest and maximal ex and by echocardiography at rest; ESS was derived during ex. During an average 7.3-year follow-up among patients who had not been operated on, 39 of 104 patients either died suddenly (n = 4) or developed operable symptoms only (n = 22) or subnormal LV performance with or without symptoms (n = 13) (progression rate=6.2%/y). By multivariate Cox model analysis, change (delta) in LV ejection fraction (EF) from rest to ex, normalized for deltaESS from rest to ex (deltaLVEF-deltaESS index), was the strongest predictor of progression to any end point or to sudden cardiac death alone. Unadjusted deltaLVEF was almost as efficient. Symptom status modified prediction on the basis of the deltaLVEF-deltaESS index. The population tercile at highest risk by deltaLVEF-deltaESS progressed to end points at a rate of 13.3%/y, and the lowest-risk tercile progressed at 1.8%/y. CONCLUSIONS: Currently accepted symptom and LV performance indications for valve replacement, as well as sudden cardiac death, can be predicted in asymptomatic/minimally symptomatic patients with AR by load-adjusted deltaLVEF-deltaESS index, which includes data obtained during exercise.

PMID: 9494022 [PubMed - indexed for MEDLINE]

 
13: Circ Res 1985 Jun;56(6):808-15 Related Articles, Books, LinkOut

The left ventricular dP/dtmax-end-diastolic volume relation in closed-chest dogs.

Little WC.

I investigated the relation of the maximum rate of left ventricular pressure rise to the end-diastolic volume and the comparison of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to the end-systolic pressure-volume relation, using the time-varying elastance model. These studies were performed in 11 dogs chronically instrumented to measure left ventricular pressure and determine left ventricular volume from three orthogonal dimensions. During vena caval occlusions, the relations between the maximum rate of left ventricular pressure rise and end-diastolic volume were described by straight lines (r = 0.97 +/- 0.01, mean +/- SD). Dobutamine increased the slope of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to 358 +/- 94% of control. This increase was greater than the 244 +/- 61% increase in the slope of the end-systolic pressure-volume relation (P less than 0.005). The volume intercepts of the maximum rate of left ventricular pressure rise-end-diastolic volume relation and end-systolic pressure-volume relation were similar and were not significantly altered by dobutamine. The ratio of the slope of the maximum rate of left ventricular pressure rise-end-diastolic volume relation to the slope of the end-systolic pressure-volume relation divided by the time from end-diastole to end-systole was similar before (2.2 +/- 0.7) and after dobutamine (2.3 +/- 0.7, P = NS). Angiotensin II did not significantly alter the maximum rate of left ventricular pressure rise-end-diastolic volume relation generated by caval occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 4006092 [PubMed - indexed for MEDLINE]
 
14: J Am Coll Cardiol 1992 Oct;20(4):787-95 Related Articles, Books, LinkOut

Effects of simultaneous alterations in preload and afterload on measurements of left ventricular contractility in patients with dilated cardiomyopathy: comparisons of ejection phase, isovolumetric and end-systolic force-velocity indexes.

Borow KM, Neumann A, Marcus RH, Sareli P, Lang RM.

Department of Medicine, University of Chicago, Illinois.

OBJECTIVES. The study was designed to critically evaluate the clinical utility of ejection phase and nonejection phase indexes of contractile state in patients with severe left ventricular dysfunction. BACKGROUND. Ejection phase indexes of left ventricular systolic performance are unable to differentiate contractility changes from alterations in loading conditions. Isovolumetric and end-systolic force-velocity indexes have been proposed as alternative measurements of contractile state that are load independent. METHODS. Seventeen patients with nonischemic dilated cardiomyopathy were studied during cardiac catheterization. High fidelity central aortic and left ventricular pressure measurements were made with simultaneous echocardiographic recordings of chamber minor- and long-axis dimensions and wall thickness. Data were acquired under control conditions, during nitroprusside infusion and with dopamine (6 micrograms/kg per min). RESULTS. Patients were classified into those without (group 1, n = 10) and those with (group 2, n = 7) a decrease in end-diastolic circumferential wall stress in response to dopamine. There were no baseline differences between the groups in functional class, left ventricular chamber geometry or cardiovascular hemodynamics. Ejection phase indexes were variably altered by changes in preload, afterload and heart rate, thereby complicating physiologic interpretation of data. Dopamine increased the commonly used isovolumetric index, maximal rate of rise in left ventricular pressure (dP/dtmax), by 64% for group 1 but by only 16% for group 2 (p less than 0.001), resulting in an underestimation of contractile state change in 41% of patients. In contrast, the left ventricular end-systolic circumferential wall stress-rate-corrected velocity of fiber shortening relation, which incorporates afterload, ventricular wall mass and heart rate in its analysis, was a sensitive contractility measurement that was preload independent and equally augmented by dopamine for both groups. CONCLUSIONS. Of the left ventricular contractility indexes evaluated, the end-systolic circumferential wall stress-rate-corrected velocity of fiber shortening relation was the most physiologically appropriate for assessing pharmacologically induced changes in inotropic state that were accompanied by complex alterations in loading conditions in patients with dilated cardiomyopathy.

PMID: 1527288 [PubMed - indexed for MEDLINE]

15. Grossman W. Relaxation and diastolic distensibility of the regionally ischemic left ventricle. In: Grossman W, Lorell BH, eds. Diastolic Relaxation of the Heart. Boston, Mass: Martinus Nijhoff; 1987:193–203.
16. Pak PH, Maughan WL, Baughman KL, Kass DA. Marked discordance between dynamic and passive diastolic pressure-volume relations in idiopathic hypertrophic cardiomyopathy. Circulation. 1996;94:52–60.
 

17: Circulation 1986 Nov;74(5):991-1001 Related Articles, Books, LinkOut

Myocardial relaxation and passive diastolic properties in man.

Pasipoularides A, Mirsky I, Hess OM, Grimm J, Krayenbuehl HP.

We have developed a model for assessing the influence of the decaying contractile systolic tension on diastolic wall dynamics and the passive properties of left ventricular muscle. Total measured left ventricular diastolic pressure and stress (sigma T) are determined by two overlapping processes: the decay of actively developed pressure and stress (sigma A) and the buildup of passive filling pressure and stress (sigma*). The decaying contractile stress sigma A is formulated in terms of a relaxation pressure with a time constant (T) assessed during the isovolumic relaxation interval. By subtracting the contribution of sigma A from sigma T we obtain sigma*. With micromanometry, echocardiography, and cineangiography, total and passive stress-strain relations and strain rates were evaluated over the entire filling period in six normal control subjects and in seven patients with aortic stenosis. Elastic stiffness constants (k), the slopes of the linear passive stiffness vs sigma* relations, did not differ in the two groups over a common lower stress range (6/6 normal, k = 9.37 +/- 1.23; 7/7 aortic stenosis, k = 9.34 +/- 1.08). Over a higher sigma* range, transition into a much steeper linear region occurred, and k values were much larger (4/7 aortic stenosis, k = 28.76 +/- 2.02). When diastolic stress levels are elevated, passive stiffness-stress relations can be better described as bilinear, with a much greater wall stiffness constant in the higher than in the lower stress range. Dynamic effects of decaying systolic contractile wall stress components are important in the rapid filling phase in normal hearts as well as in those with aortic stenosis.

PMID: 3769181 [PubMed - indexed for MEDLINE]

18. Rankin SJ, Arentzen CE, McHale PA, Ling D, Anderson RW. Viscoelastic properties of the diastolic left ventricle in the conscious dog. Circ Res. 1977;41:37–45.
 

19: Circulation 1990 Feb;81(2):447-60 Related Articles, Books, LinkOut

Influence of coronary occlusion during PTCA on end-systolic and end-diastolic pressure-volume relations in humans.

Kass DA, Midei M, Brinker J, Maughan WL.

Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.

The influence of acute coronary occlusion on systolic and diastolic left ventricular pressure-volume relations was studied in 10 patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Pressure-volume relations were obtained by conductance catheter and micromanometer techniques and with volume load altered by transient inferior vena caval occlusion. End-systolic and end-diastolic pressure-volume relations were obtained at baseline, during 60-90 seconds of ischemia, and at return to baseline after angioplasty balloon deflation. Coronary occlusion significantly altered systolic and diastolic chamber function. Systolic dysfunction was characterized by a reproducible rightward shift of the end-systolic pressure-volume relation (+25.4 +/- 18.4 ml) that was greater for proximal left anterior descending and circumflex coronary artery occlusions (+41 ml) than for distal or right coronary artery occlusions (+15.4 ml, p less than 0.05). Occlusion also lowered chamber systolic function indexes, such as the end-systolic pressure-volume relation slope (from 4.2 to 2.8 mm Hg/ml) and preload recruitable stroke work (from 97 to 78.6 mm Hg). All systolic (and diastolic) changes were resolved with successful angioplasty. Diastolic abnormalities during angioplasty were characterized by prolonged pressure relaxation and an upward shift of the resting diastolic pressure-volume data and by an apparent increase in chamber elastic stiffness. However, when end-diastolic data from multiple beats during inferior vena caval occlusion were compared, control and ischemic end-diastolic pressure-volume relations displayed little or no difference. Thus, elevations in resting diastolic pressure-volume relations and apparent increase in chamber elastic stiffness during coronary occlusion in humans appear dominated by altered right ventricular or pericardial loading. These data indicate that pressure-volume analysis is useful in assessing the functional significance of coronary lesions and reperfusion.

PMID: 2297855 [PubMed - indexed for MEDLINE]
 
20: Fed Proc 1980 Feb;39(2):141-7 Related Articles, Books, LinkOut

The diastolic mechanical properties of the intact left ventricle.

Rankin JS, Arentzen CE, Ring WS, Edwards CH 2nd, McHale PA, Anderson RW.

Recent studies have improved our understanding of the diastolic mechnical properties of intact myocardium. In order to obtain meaningful data, pressures external to the heart should be measured, forces and dimensions should be properly normalized, and measurements should be obtained over a wide range of ventricular volumes. Diastolic filling appears to be a passive phenomenon and is not affected significantly by systolic relaxation or mural inertia. Thus, the relationship between diastolic myocardial force and length is determined primarily by the elastic properties of the muscle and by viscous properties during dynamic filling. In the absence of ischemia, the diastolic mechanics of intact myocardium are not altered significantly by acute physiological interventions. Chronic changes in diastolic properties do occur, however, and are fundamentally important to the regulation of cardiac function. Myocardial creep induced by chronically elevated diastolic presssure produces ventricular dilatation, thereby altering chamber geometry, systolic loading, and overall global function. Thus, a detailed analysis of diastolic mechanical properties is essential to the assessment of the performance characteristics of the intact heart.

PMID: 6444387 [PubMed - indexed for MEDLINE]
 
21: Circulation 1997 Feb 18;95(4):917-23 Related Articles, Books, LinkOut
Click here to read
Effects of aging on left ventricular relaxation in humans. Analysis of left ventricular isovolumic pressure decay.

Yamakado T, Takagi E, Okubo S, Imanaka-Yoshida K, Tarumi T, Nakamura M, Nakano T.

First Department of Internal Medicine, Mie University, Tsu, Japan. yamakado@clin.medic.mie-u.ac.jp

BACKGROUND: Some experimental studies in animals have shown that myocardial relaxation is prolonged with aging. However, it is not known whether aging alters ventricular isovolumic relaxation in human subjects. METHODS AND RESULTS: We analyzed high-fidelity left ventricular pressures, measured by use of a catheter-tipped manometer, and biplane left ventriculograms in 55 normal subjects who underwent diagnostic cardiac catheterization but who were found to have normal cardiac anatomy and function. There were 38 men and 17 women, ranging in age from 20 to 77 years. Left ventricular isovolumic relaxation was assessed by the exponential time constants of isovolumic pressure decay with (Tb) and without (Tw) an asymptote pressure. Left ventricular volume, ejection fraction, and wall thickness or mass were calculated from left ventricular angiograms. Neither of the time constants of left ventricular relaxation correlated with age (Tb: r = .001 to .10, P = NS: Tw: r = .02 to .05, P = NS). Left ventricular systolic function (ie, ejection fraction and end-systolic volume index), heart rate, and left ventricular wall thickness or mass, which are major hemodynamic determinants of left ventricular relaxation, were not significantly affected by aging. The multivariate analysis of age and hemodynamic variables against the time constants of left ventricular relaxation also indicated that no significant relation was found between age and left ventricular relaxation. CONCLUSIONS: In the absence of coronary artery disease, systemic hypertension, left ventricular systolic dysfunction, or hypertrophy, left ventricular relaxation assessed by the time constant of isovolumic pressure decay remains essentially unchanged with normal adult aging, at least until the eighth decade.

PMID: 9054751 [PubMed - indexed for MEDLINE]

22. Gaasch WH. Passive elastic properties of the left ventricle. In: Gaasch WH, LeWinter M, eds. Left Ventricular Diastolic Dysfunction and Heart Failure. Malvern, PA; Lea & Febiger; 1994:143–149.
23. Krayenbuehl HP, Hess OM, Ritter M, Schneider J, Monrad ES, Grimm J. Influence of pressure and volume overload on diastolic compliance. In: Grossman W, Lorell BH, eds. Diastolic Relaxation of the Heart. Boston, Mass: Martinus Nijhoff; 1987:143–150.
 

24: Circulation 1995 Oct 1;92(7):1933-9 Related Articles, Books, LinkOut
Click here to read
Determination of left ventricular chamber stiffness from the time for deceleration of early left ventricular filling.

Little WC, Ohno M, Kitzman DW, Thomas JD, Cheng CP.

Cardiology Section, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1045, USA.

BACKGROUND: A noninvasive measure of left ventricular (LV) chamber stiffness (KLV) would be clinically useful. Our theoretical analysis predicts that KLV can be calculated from the time for deceleration of LV early filling (tdec) by [formula: see text] where p = density of blood, L = effective mitral length, and A = mitral area. METHODS AND RESULTS: We tested this hypothesis in eight conscious dogs instrumented for measurement of LV pressure (P) with use of a micromanometer and volume (V) with use of sonomicrometers. KLV was determined as the slope of the late diastolic portion of the LV P-V loop. KLV was varied from 0.99 +/- 0.35 to 2.58 +/- 0.92 mm Hg/mL with use of three graded doses of phenylephrine. We assumed that p = 1.0 and that L/A = 3.4. Thus, we predicted that KLV = (0.08/tdec)2. The LV filling pattern was determined from the derivative of LV volume (dV/dt). tdec was measured from peak early filling to the end of early filling. Predicted KLV and actual KLV were closely correlated (r = .94, SEE = 0.06 mm Hg/mL, P < .05). The regression line was close to the line of identity (slope = 0.95, intercept = 0.13 mm Hg/mL). Dobutamine did not alter the relation between tdec and KLV.tdec determined from the mitral valve flow velocity measured with Doppler echocardiography correlated well with that measured by dV/dt (r = .89, P < .01) but was 0.02 seconds longer. KLV-calculated tdec from the corrected Doppler tdec provided a good estimate of measured KLV (r = .75, SEE = 0.5 mm Hg/mL, P < .01). CONCLUSIONS: LV chamber stiffness can be determined from the time for deceleration of LV early filling, which can be measured noninvasively.

PMID: 7671378 [PubMed - indexed for MEDLINE]
 
25: Circulation 1995 May 1;91(9):2353-8 Related Articles, Books, LinkOut
Click here to read
Normalization of diastolic dysfunction in aortic stenosis late after valve replacement.

Villari B, Vassalli G, Monrad ES, Chiariello M, Turina M, Hess OM.

Department of Internal Medicine, University Hospital, Zurich, Switzerland.

BACKGROUND: The remodeling of the left ventricle in patients with aortic stenosis after aortic valve replacement (AVR) is a complex process involving structural and functional changes. METHODS AND RESULTS: Twenty-two patients were included in the present analysis. Twelve patients with severe aortic stenosis were studied before surgery, early (22 +/- 8 months) and late (81 +/- 22 months) after AVR using left ventricular biplane angiograms, high-fidelity pressure measurements, and endomyocardial biopsies. Ten healthy subjects were used as controls. Left ventricular systolic function was assessed from biplane ejection fraction; and diastolic function from the time constant of relaxation, the peak filling rate, and the myocardial stiffness constant. Left ventricular structure was evaluated from interstitial fibrosis, fibrous content, and muscle fiber diameter. Left ventricular muscle mass was significantly increased before surgery in patients with aortic stenosis and remained increased early after surgery, although there was a 35% decrease. Late after AVR, muscle mass decreased significantly but remained slightly (P = NS) elevated. Left ventricular ejection fraction increased slightly after AVR. Left ventricular relaxation was significantly prolonged before surgery and returned toward normal early and late after AVR. Peak filling rates remained unchanged before and after surgery. Myocardial stiffness constant was increased before surgery in patients with aortic stenosis compared with controls and increased even further early after AVR but was normalized late after surgery. Muscle fiber diameter was elevated in patients with aortic stenosis before and after surgery compared with controls; however, it decreased significantly early and late after AVR with respect to preoperative data but remained hypertrophied even late after surgery. Interstitial fibrosis and fibrous contents were larger before surgery than in control subjects and increased even more early but decreased significantly late after AVR. CONCLUSIONS: Diastolic stiffness increases in aortic stenosis early after AVR parallel to the increase in interstitial fibrosis, whereas relaxation rate decreases with a reduction in left ventricular muscle mass. Late after AVR, both diastolic stiffness and relaxation are normalized due to the regression of both muscular and nonmuscular tissue. Thus, reversal of diastolic dysfunction in aortic stenosis takes years and is accompanied by a slow regression of interstitial fibrosis.

PMID: 7729021 [PubMed - indexed for MEDLINE]

Although great care has been taken in compiling the information given in this website,
the publisher or the sponsor is not responsible for the continued currency of the information,
for any errors or omissions, or for any consequence arising therefrom.
© 2010 Les Laboratoires Servier