| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Service de Cardiologie, Hôpital Antoine-Béclère, 92141 Clamart; Inserm U451-Loa-Ensta-Ecole Polytechnique, 91125 Palaiseau; Service de Cardiologie, Hôpital Tenon, 75970 Paris; and Service de Physiologie Cardio-Respiratoire, Hôpital de Bicêtre, 94275 Le Kremlin-Bicêtre, France
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Colin, Patrice, Michel Slama, Alec Vahanian, Yves
Lecarpentier, Gilbert Motté, and Denis Chemla. Hemodynamic
correlates of effective arterial elastance in mitral stenosis before
and after balloon valvotomy. J. Appl.
Physiol. 83(4): 1083-1089, 1997.
This study had
the purpose of documenting the hemodynamic correlates of effective
arterial elastance (Ea; i.e., an accurate estimate of hydraulic load)
in mitral stenosis (MS) patients. The main hypothesis tested was that
Ea relates to the total vascular resistance (R)-to-pulse interval
duration (T) ratio
(R/T) in MS patients both before and
after successful balloon mitral valvotomy (BMV). High-fidelity aortic
pressure recordings were obtained in 10 patients (40 ± 12 yr)
before and 15 min after BMV. Ea value was calculated as the ratio of
the steady-state end-systolic aortic pressure (ESAP) to stroke volume
(thermodilution). Ea increased after BMV (from 1.55 ± 0.63 to 1.83 ± 0.71 mmHg/ml; P < 0.05). Throughout the procedure, there was a strong linear
relationship between Ea and R/T: Ea = 1.09R/T 
0.01 mmHg/ml,
r = 0.99, P = 0.0001. This ultimately depended
on the powerful link between ESAP and mean aortic pressure [MAP;
r = 0.99, 95% confidence interval for the difference (MAP ESAP) from 18.5 to +4.5 mmHg].
Ea was also related to total arterial compliance (area method) and to
wave reflections (augmentation index), although to a lesser extent. After BMV, enhanced and anticipated wave reflections were observed, and
this was likely to be explained by decreased arterial compliance. The
present study indicated that Ea depended mainly on the steady component
of hydraulic load (i.e., R) and on heart period (i.e., T) in MS patients.
aorta; arterial load; arterial wave reflections; arterial
compliance
INTRODUCTION INCREASED AFTERLOAD has been proposed as one of the
causal factors of left ventricular (LV) systolic dysfunction observed in ~30% of patients with pure mitral stenosis (MS) (5). In this
subgroup of patients, both the relatively thin-walled LV chamber and
the presence of high systemic vascular resistance result in abnormally
high end-systolic wall stress (5, 29). Given impaired LV filling, some
researchers have reported that this elevation in afterload was not
offset by the Frank-Starling mechanism, thus leading to low ejection
performance (5); others have suggested that decreased intrinsic
contractility may also be involved (18). Given the potential role of
increased arterial load in the development of systolic dysfunction in
MS patients, it is important to improve the way in which arterial load
is estimated in such patients.
A precise and complete description of LV afterload (i.e., hydraulic
load) is provided by the input impedance of systemic circulation (17,
20, 21), but this complex approach is not always feasible in clinical
practice. Sunagawa et al. (25, 26) have proposed an alternative
assessment of hydraulic load, namely, effective arterial elastance
(Ea). In both healthy subjects and hypertensive patients, Ea has been
shown to mainly depend on 1) the
R-to-T ratio
(R/T) (12, 25, 26), where R is the
peripheral resistance and T is heart
period, and 2) the magnitude of wave
reflections (4, 23). Conversely, Ea poorly depends on total arterial compliance (25, 26). The above-mentioned studies were performed under
baseline conditions, and it remains to be established whether acute
load manipulations modify the hemodynamic correlates of Ea. The loading
conditions of the heart are dramatically modified in MS patients at
both baseline and after balloon valvotomy (27, 28), and this may well
modify the hemodynamic correlates of Ea. To the best of our knowledge,
only one study has documented Ea values in MS patients (14), and none
has examined the effects of percutaneous balloon mitral valvotomy (BMV)
on arterial load, as reflected in Ea values.
Accordingly, the purpose of our preliminary study was to document the
hemodynamic correlates of Ea in MS patients studied both before and
after valvotomy. In our patients, we tested the hypothesis that Ea
could relate to R, T,
R/T, total arterial compliance, and
the indexes of wave reflection.
METHODS Patients
2+)
aortic valve insufficiency, or any degree of aortic stenosis,
significant calcification of the mitral valve, evidence of left atrial
thrombus on transesophageal echography, or a previous
history of coronary artery disease. Seven patients had normal sinus
rhythm. Three patients were in atrial fibrillation and were given oral
anticoagulant therapy (n = 3),
digitalis (n = 3), furosemide
(n = 1), and amiodarone (n = 1). Six patients were undergoing
diuretic therapy.
Table 1.
Characteristics of study population
Subject No.
Age, yr
Gender
Body Surface Area, m2
NYHA
Therapy
MVA, cm2
Before
After
1
32
M
2.07
II
F-D-AC
1.0
2.3
2
22
F
2.25
II
AC
1.0
2.2
3
42
F
1.48
III
F-A-AC-N
0.8
1.9
4
35
F
1.55
II
F-A-AC-N
0.8
1.5
5
51
M
2.01
III
D-AC
1.0
1.7
6
40
F
1.93
II
F
1.0
2.2
7
37
F
1.58
II
F-D-AC
0.7
2.2
8
42
F
1.37
II
AC-FL
0.9
1.8
9
31
F
1.71
II
F
1.0
2.0
10
68
F
1.82
II
A-D-AC
1.0
2.0
Mean ± SD
40 ± 12
1.78 ± 0.29
0.92 ± 0.11
1.97 ± 0.26*
M, male; F, female; NYHA, New York Heart Association
classification; MVA, mitral valve area; Before, before mitral
valvotomy; After, after mitral valvotomy; F, furosemide; D, digitalis;
AC, anticoagulant therapy; A, amiodarone; FL, flecainide; N, nitrates.
*
P < 0.01.
Catheterization Technique and BMV Procedure
Patients were studied at baseline, at least 12 h after previous intake of their usual medication according to our routine protocol (27, 28). Patients were sedated by using clorazepate (10 mg). Aortic pressure was measured by using an 8-Fr single-lumen catheter equipped with a high-fidelity transducer (Sentron/Cordis, Roden, The Netherlands) (8). The catheter was advanced from the left femoral artery to the aortic root. Routine right-heart catheterization was performed by using the Seldinger technique through the left femoral vein. Before BMV, right heart pressures were obtained and cardiac output was measured in triplicate in all patients by using the thermodilution technique. Stroke volume (SV) was calculated as the cardiac output-to-heart rate ratio. Left ventriculography was performed in the 30° right anterior oblique projection. LV volumes were calculated by using the area-length method, taking care not to include either ventricular premature beats or postextrasystolic beats. Transseptal catheterization was then performed from the right femoral vein by using the Brockenbrough technique, and patients were then given heparin (4,000 IU iv). Balloon dilatation of the mitral valve was performed on all patients with the Inoue balloon catheter system (Toray Industries, Tokyo, Japan) (9) by using a stepwise technique and transthoracic echographic monitoring. Optimal results were defined as a final mitral valve area >1.5 cm2 without appearance or worsening of mitral valve regurgitation of >1+. Final hemodynamic variables and cardiac output were obtained with the balloon catheter across the transseptal puncture site so as to reduce the error caused by atrial septal defect blood flow. Fifteen minutes after BMV, hemodynamic pressures and flow measurements were repeated. Left ventriculography was then repeated in the right anterior oblique projection to evaluate the severity of mitral regurgitation. Oxymetry was performed after BMV to evaluate left-to-right shunting. Before BMV, three patients had no mitral regurgitation, and seven patients had 1+ mitral regurgitation. Immediately after BMV, seven patients showed no change in the degree of mitral regurgitation, and three patients had 1+ increase (from 1+ to 2+). No left-to-right shunt was detected after BMV.High-Fidelity Pressure Recordings
High-fidelity pressure data were computed throughout the procedures on a Toshiba 6400-SX portable computer with customized software (sampling rate = 1,000 Hz) as previously described (3, 8). Pressure recordings were obtained at the aortic root level. Mean aortic pressure (MAP) was defined as the area under the pressure curve divided by pulse interval duration (T). T (in ms) was defined as the time between two consecutive aortic pressure upstrokes. Aortic dicrotic notch pressure (ESAP), i.e., aortic end-systolic pressure, was defined as the trough of the incisura (dicrotic notch). We measured systolic aortic pressure (SAP), initial diastolic aortic pressure (DAP), end-diastolic aortic pressure (EDAP), and pulse aortic pressure (PAP = SAP DAP). MAP and PAP reflect the steady and pulsed components
of aortic pressure, respectively (21). We also calculated two
previously proposed estimates of ESAP, namely, 0.9 SAP and 2/3 SAP + 1/3 DAP (12). Total vascular resistance (R;
mmHg · ms · ml
1)
was calculated according to the following formula
|
(1) |
Effective Ea
Theoretical background. In the Ea model, the proximal aorta is considered as an elastic chamber, the effective volume elastance Ea (mmHg/ml) of which is the slope of the relationship between ESAP and SV. This model has markedly improved the evaluation of the systemic circulation for two reasons. First, in humans, Ea provides a reasonable characterization of arterial load in the time domain (12). Second, the LV can also be considered as an elastic chamber, the end-systolic elastance (Ees; i.e., the slope of the LV end-systolic pressure-volume relationship) of which is of similar dimension to Ea (24). The operating point of the coupled equilibrium between LV and the arterial system is located at the intersection of LV end-systolic pressure-volume and ESAP-SV relationships in the pressure-volume plane (24-26). Coordinated changes in the Ees-to-Ea ratio, stroke work, and mechanical efficiency have been reported (1, 11, 25, 26). The concept of Ea is based on the Windkessel model of arterial circulation (25). Theoretical Ea values are obtained by means of a mathematical formula taking into account the intrinsic properties of circulation, namely, total peripheral resistance (R), total arterial compliance (C), and systolic and diastolic time intervals. Because the mathematical model fits with experimental (25) and clinical (12) data, Ea is currently obtained by calculating the steady-state ratio of ESAP to SV (4, 11, 12). The hemodynamic correlates of Ea have been documented in experimental studies and in studies performed on normotensive and hypertensive subjects without valve disease. In this population, Ea depends mainly on both R and heart period (i.e., T) (12, 25, 26), in such a way that R/T is a reasonable approximation of Ea (12). Although experimental studies have shown that Ea is poorly influenced by C (25, 26), recent studies have demonstrated a relationship between Ea and the extent of pressure-wave reflection from periphery to the heart (4, 23). Calculation of Ea. Ea (mmHg/ml) was calculated according to the following steady-state formula
|
(2) |
|
(3) |
|
(4) |
|
(5) |
2+) aortic insufficiency
were excluded from the study.
Wave reflection and augmentation index.
The human aortic pressure waveform exhibits an inflection point (Pi),
indicating the end of the forward (or incident) wave and resulting from
peak flow input into the vasculature previous to the effects of wave
reflection (20, 21). The relative increase in the height of the
mid-to-late systolic peak pressure above the Pi shoulder (
P) is
because of arterial wave reflection and the early return of pressure
wave from the lower body (13, 16, 20). The backward or reflected wave
cumulates with the incident wave, resulting in a mid-to-late increase
in SAP. The ratio of P to PAP defines a so-called "augmentation
index" (P/PAP). The time from the foot of the pressure wave to Pi
(tp) is thought to represent the
travel time of the pulse wave to peripheral reflecting sites and its
return. According to Murgo et al. (20),
tp is a reasonable estimate of 1/2
fmin, where
fmin corresponds to the frequency
of the minimum impedance spectra modulus. In three patients, Pi could
not be clearly individualized. Thus the values of Pi, P, P/PAP,
and tp were recorded and averaged
out over 10 consecutive cycles in 7 of 10 patients only.
Statistical Analysis
Data are expressed as means ± SD. Data were averaged out over 10 consecutive beats. Linear regression was obtained by using the least squares method. Comparisons between Ea and R/T were performed by using the Mann-Whitney U-test; we also calculated the 95% confidence intervals (CI) for the difference (2). The same was performed for comparisons between ESAP and each of three estimates of ESAP, namely, MAP, 0.9 SAP, and 2/3 SAP + 1/3 DAP. A P < 0.05 was considered statistically significant.RESULTS
Hemodynamic data before and after BMV are listed in Tables 2 and 3 and in Fig. 1.
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||||||||||
Hemodynamic Correlates of Ea in MS Patients at Baseline
Ea was 1.55 ± 0.63 mmHg/ml. There was no relationship between Ea and age, MAP, ESAP, or mitral valve area. There was a negative linear relationship between Ea and T (r =0.72,
P < 0.01). Ea was closely related to
R (r = 0.96, P = 0.0001). There was a strong linear
relationship between Ea and R/T (Ea = 1.09 R/T 0.01 mmHg/ml, r = 0.99, P = 0.0001) (Fig.
2). R/T
slightly but significantly underestimated Ea (Table 2, Fig. 2),
especially at high Ea values. There was also a negative linear
relationship between Ea and C (r = 0.85, P < 0.01). After the
influence of SV was taken into account, Ea and C were still
significantly related [partial correlation coefficient
(r
) = 0.66,
P < 0.05]. There was no
relationship between Ea and P/PAP
(r = 0.61, P = 0.15).
0.01 (mmHg/ml). B:
R/T as an estimate of Ea at baseline.
Solid line, mean difference (i.e,
R/T Ea); dashed
lines, ±2 SD; dotted line, zero axis. There was a positive linear
relationship (r = 0.64, P = 0.046) between
difference and Ea: R/T Ea = 0.09 Ea + 0.03.
Effects of BMV
After BMV, Ea increased in eight patients and decreased in two patients (Fig. 1). On average, Ea increased (P < 0.05), whereas C decreased (P = 0.02) (Table 2). MAP increased (from 87.0 to 96.7 mmHg, P = 0.0001), but changes in C were not related to increases in MAP [r =0.31, P = not significant
(NS)]. The decrease in C was not related to the increase in Ea
(r = 0.25, P = NS) nor to the increase in mitral
valve area as induced by BMV (r = 0.41, P = NS). P/PAP increased
(P < 0.001) (Table 3). This was
linked to an increase in P (from 13.5 ± 8.2 to 18.7 ± 12.7 mmHg, P < 0.001) that was
proportionally more marked than the increase in PAP (from 49.3 ± 11.8 to 53.7 ± 16.2 mmHg, P < 0.001).
Hemodynamic Correlates of Ea After BMV
Ea was related to R (r = 0.94, P = 0.0001) but not to heart period (r =0.30). There was a strong
linear relationship between Ea and R/T
(Fig. 3), and
R/T underestimated Ea (Table 2, Fig. 3). There was a negative linear relationship between Ea and C (r = 0.85,
P < 0.01). After the influence of SV
was taken into account, Ea and C were no longer related
(r = 0.56,
P = NS). Increases in Ea
were not related to increases in mitral valve area as induced by BMV
(r = 0.42,
P = NS). There was a positive relationship between Ea and P/PAP
(r = 0.82, P = 0.025).
0.13 (mmHg/ml).
B:
R/T as an estimate of Ea after BMV.
Lines are defined as in Fig. 2. There was a positive linear
relationship (r = 0.76, P = 0.01) between difference and Ea:
R/T Ea = 0.15 Ea + 0.15.
Evaluation of MAP as an Estimate of ESAP
There was a powerful linear relationship between ESAP and MAP both before and after BMV in patients either in sinus rhythm or in atrial fibrillation (Fig. 4). When MAP was taken as an estimate of ESAP, MAP underestimated ESAP (P < 0.001) (Fig. 4). There was a negative linear relationship between the MAP-ESAP difference and ESAP, such that the higher the ESAP, the more negative the difference. Table 4 indicates the accuracy of the two empirical formulas (ESAP = 2/3 SAP + 1/3 DAP; and ESAP = 0.9 SAP), both of which significantly overestimated ESAP.
)
and after (
) BMV, repectively, in accordance with following equations: ESAP = 1.06 MAP + 1.1 (r = 0.98, P = 0.0001); ESAP = 1.16 MAP 9.0 (r = 0.98, P = 0.0001).
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
DISCUSSION
The present study indicated that Ea depended mainly on R and T in patients with MS studied at baseline. We also observed that R/T was a reasonable estimate of Ea in the study population. These results extended to MS patients the primary results obtained by Sunagawa et al. in animals (25, 26) and by Kelly et al. (12) in human subjects without valve disease. The short-term effects of BMV were also studied. Ea increased after BMV and remained closely dependent on both R and T. Ea also related to C and wave reflections, although to a lesser extent.
Comparison with Previous Studies
Before BMV, Ea (1.55 ± 0.63 mmHg/ml) was lower than the value previously reported (3.1 ± 1.1 mmHg/ml) (14), and this may be explained by the lower ESAP and the higher SV in our study. The higher SV in our study (67 vs. 38 ml in Ref. 14) could be explained by differences in body surface area (1.8 ± 0.3 vs. 1.5 ± 0.12 m2). In our study, the 67-ml SV value was consistent with the 58-ml value previously reported (29, 30). SV did not significantly change after BVM, as reported in some studies (7, 19). Others have reported that SV increased after BMV (14, 29). These disparities may be related to differences in the incidence and severity of mitral regurgitation and atrial shunts after BMV. Alternatively, LV end-diastolic pressure increases after BMV, and Yasuda et al. (30) reported that SV was either increased or unchanged, depending on the capacity of the LV to increase end-diastolic volume.Relationship Between Ea and R/T in MS Patients at Baseline and After BMV
Importantly, we documented a powerful link between Ea and R/T at baseline
|
(6) |
On the assumption that 0.01 mmHg/ml is so small as to be
negligible, the following equation is obtained
|
(7) |
To the best of our knowledge, no study has so far documented the effects of BMV on arterial load, as reflected in Ea, C, and the indexes of wave reflection. In our study, Ea significantly increased after BMV, although BMV did not modify the hemodynamic correlates of Ea. We found that
|
(8) |
On the assumption that 0.13 mmHg/ml is so small as to be
negligible, the following equation is obtained
|
(9) |
Although the Ea concept is based on the Windkessel model, which also takes C into account, experimental studies have shown that Ea is poorly influenced by C (25, 26). In our MS patients studied at baseline, there was a negative linear relationship between Ea and C both before and after BMV. After the effects of SV were taken into account, this relationship was no longer observed after BMV. Furthermore, the increase in Ea induced by BMV and the decrease in C were not related.
A positive relationship between Ea and P/PAP has been previously
reported in normotensive and hypertensive patients (23), a finding also
observed in our MS patients after but not before BMV.
Effects of BMV on C and Wave Reflections
Estimated C significantly decreased after BMV. Even though MAP significantly increased, relative changes in C were not related to relative increases in MAP. The decrease in C was not related to the increase in mitral valve area induced by BMV. After BMV, PAP significantly increased, and this was consistent with the observed decrease in C (21). The values of PAP, Pi, SAP Pi, and (SAP Pi)/PAP significantly increased, thus
attesting to enhanced wave reflection, whereas the decreased
tPi suggested anticipated timing of
wave reflection. A similar hemodynamic pattern has been attributed to
decreased C in aged and hypertensive subjects (12, 16, 20, 21). Thus
increased and anticipated wave reflection are probably explained by
decreased C.
Clinical Implications: End-Systolic Pressure Estimated From Peripheral Arterial Pressure Recordings in MS Patients
Systolic arterial pressure increases from aorta to periphery, according to the so-called "pulse wave amplification" phenomenon. The magnitude of the pulse wave amplification phenomenon varies markedly from one individual to another, depending on body size, sex, age, arterial pressure, and arterial compliance (13, 16, 20). Thus the two formulas previously proposed (12) as estimates of ESAP, namely, 0.9 SAP and 2/3 SAP + 1/3 DAP, are more relevant to central pressure recordings than to noninvasive peripheral pressure recordings. Furthermore, these formulas significantly overestimated ESAP in MS patients (Table 4).Effective Ea has also been estimated indirectly after having replaced end-systolic pressure by 1) intrabrachial dicrotic notch pressure recorded invasively (1); 2) carotid dicrotic notch pressure measured by using external tonometry (23); and 3) cuff-determined systolic blood pressure (10). The cannulation of the brachial artery is an invasive procedure and therefore not routinely repeatable. The external tonometry technique is not available in all research laboratories, and the accuracy of carotid dicrotic notch pressure as an estimate of central end-systolic pressure, although probable, remains to be validated (23).
Numerous studies and physiological textbooks have reported that one key property of systemic circulation is that mean arterial pressure remains almost constant along the arterial tree, the drop in mean pressure between the ascending aorta and a large peripheral artery being <3 mmHg (21). We have found a powerful relationship between ESAP and MAP in MS patients, as also recently observed in children (22) and in adults without valve diseases (8). Thus, in patients with MS at baseline, one implication of our study is that ESAP could be reasonably estimated by using cuff-determined mean arterial pressure, rather than systolic arterial pressure, according to the following formula: ESAP = 1.09 mean peripheral arterial pressure. Further studies are needed to confirm this.
Limitations of the Study
The limitations of our study need to be discussed. First, given our invasive study design, clinical implications are limited by its short-term aspect. We judged it unethical to perform a left-sided catheterization in MS patients 1 mo after BMV, such that the long-term effects of valvotomy on Ea were not documented in our study. Further studies are needed to document the chronic effects of BMV on Ea. Second, we studied a limited sample size of MS patients. Despite this, we found an unusually powerful relationship both between Ea and R/T, and between ESAP and MAP, and this tends to strengthen the relevance of our results.Conclusions
Ea depends mainly on R and T in patients with MS studied at baseline or after BMV. The powerful relationship between Ea and R/T observed in our study extends to MS patients the primary results of Sunagawa et al. (25, 26) and Kelly et al. (12). The Ea vs. R/T relationship ultimately depends on the powerful link between MAP and ESAP in MS patients. Given that mean arterial pressure remains constant along the arterial tree, this result may have clinical implications for the noninvasive assessment of Ea in populations similar to ours. Last, in patients with MS, and for a given T, our study indicates that Ea depends mainly on the steady rather than the pulsatile component of arterial load (R), whether before or after BMV.ACKNOWLEDGEMENTS
The authors thank John Kenneth Hylton for helpful discussions.
FOOTNOTES
Address for reprint requests: P. Colin, Service de Cardiologie, 157 rue de la porte de Trivaux, Hôpital Antoine-Béclère, 92141 Clamart, France (E-mail: chemla{at}enstay.ensta.fr).
Received 14 January 1997; accepted in final form 16 May 1997.
REFERENCES
| 1. |
Asanoi, H.,
S. Sasayama,
and
T. Kameyama.
Ventriculo-arterial coupling in normal and failing heart in humans.
Circ. Res.
65:
483-493,
1989 |
| 2. | Bland, J. M., and D. G. Altman. Statistical methods for assessing agreement between two methods of clinical measurements. Lancet 1: 307-310, 1986[Medline]. |
| 3. |
Chemla, D.,
J. L. Hébert,
C. Coirault,
S. Salmeron,
K. Zamani,
and
Y. Lecarpentier.
Matching dicrotic notch and mean pulmonary artery pressures: implications for effective arterial elastance.
Am. J. Physiol.
271 (Heart Circ. Physiol. 40):
H1287-H1295,
1996 |
| 4. | Cohen-Solal, A., B. Caviezel, D. Himbert, and R. Gourgon. Left ventricular-arterial coupling in systemic hypertension: analysis by means of arterial effective and left ventricular elastances. J. Hypertens. 12: 591-600, 1994[Medline]. |
| 5. |
Gash, A. K.,
B. A. Carabello,
D. Cepin,
and
J. F. Spann.
Left ventricular ejection performance and systolic muscle function in patients with mitral stenosis.
Circulation
67:
148-154,
1983 |
| 6. | Goto, S., S. Handa, M. Akaishi, S. Abe, and S. Ogawa. Left ventricular ejection performance in mitral stenosis, and effects of successful percutaneous transvenous mitral commissurotomy. Am. J. Cardiol. 69: 233-237, 1992[Medline]. |
| 7. | Harisson, J. K., C. J. Davidson, J. B. Hermiller, M. B. Harding, J. D. Hanemann, J. T. Cusma, K. B. Kisslo, and T. M. Bashore. Left ventricular filling and ventricular diastolic performance after percutaneous balloon mitral valvotomy. Am. J. Cardiol. 69: 108-112, 1992. [Medline] |
| 8. | Hébert, J. L., Y. Lecarpentier, K. Zamani, C. Coirault, G. Daccache, and D. Chemla. Relation between aortic dicrotic notch pressure and mean aortic pressure in adults. Am. J. Cardiol. 76: 301-306, 1995[Medline]. |
| 9. | Inoue, K., T. Owaki, T. Nakamura, F. Kitamura, and M. Miyamoto. Clinical application of transvenous mitral commissurotomy by a new balloon catheter. J. Thorac. Cardiovasc. Surg. 87: 394-402, 1984[Abstract]. |
| 10. | Iwasaka, T., Y. Takayama, T. Izuoka, K. Takehana, T. Sugiura, Y. Matsui, K. Tamura, Y. Kimura, N. Tarumi, and M. Inada. Effect of ventriculo-arterial coupling on residual left ventricular pump function in diabetic patients with myocardial infarction. Cardiology 85: 1-7, 1994[Medline]. |
| 11. |
Kameyama, T.,
H. Asanoi,
S. Ishizaka,
K. Yamanishi,
M. Fujita,
and
S. Sasayama.
Energy conversion efficiency in human left ventricle.
Circulation
85:
988-996,
1992 |
| 12. |
Kelly, R. P.,
C. T. Ting,
T. M. Yang,
C. P. Liu,
W. L. Maughan,
M. S. Chang,
and
D. A. Kass.
Effective arterial elastance as index of arterial vascular load in humans.
Circulation
86:
513-521,
1992 |
| 13. | Kroeker, E. J., and E. H. Wood. Beat-to-beat alteration in relationship of simultaneously recorded central and peripheral arterial pressure pulses during Valsalva maneuver and prolonged expiration in man. J. Appl. Physiol. 5: 483-494, 1956. |
| 14. |
Liu, C. P.,
C. T. Ting,
T. M. Yang,
J. W. Chen,
M. S. Chang,
L. Maughan,
W. Lawrence,
and
D. A. Kass.
Reduced left ventricular compliance in human mitral stenosis. Role of reversible internal constraint.
Circulation
85:
1447-1456,
1992 |
| 15. |
Liu, Z.,
K. P. Brin,
and
F. C. P. Yin.
Estimation of total arterial compliance: an improved method and evaluation of current methods.
Am. J. Physiol.
251(HeartCirc.Physiol.20):
H588-H600,
1986.
|
| 16. |
London, G.,
A. Guerin,
B. Pannier,
S. Marchais,
A. Benetos,
and
M. Safar.
Increased systolic pressure in chronic uremia. Role of arterial wave reflections.
Hypertension
20:
10-19,
1992 |
| 17. | Milnor, W. R. Hemodynamics. Baltimore, MD: Williams & Wilkins, 1982. |
| 18. | Mohan, J. C., M. Khalilullah, and R. Arora. Left ventricular intrinsic contractility in pure rheumatic mitral stenosis. Am. J. Cardiol. 64: 240-242, 1989[Medline]. |
| 19. | Mohan, J. C., M. Nair, and R. Arora. Left ventricular volumes and function immediately after balloon mitral valvuloplasty. Int. J. Cardiol. 33: 275-280, 1991[Medline]. |
| 20. |
Murgo, J. P.,
N. Westerhof,
J. P. Giolma,
and
S. A. Altobelli.
Aortic input impedance in man: relationship to pressure wave shape.
Circulation
62:
105-116,
1980 |
| 21. |
O'Rourke, M.
Mechanical principles in arterial disease.
Hypertension
26:
2-9,
1995 |
| 22. | Rowland, D. G., and H. P. Gutgesell. Use of mean arterial pressure for noninvasive determination of left ventricular wall stress in infants and children. Am. J. Cardiol. 74: 98-99, 1994[Medline]. |
| 23. | Saba, P. S., M. J. Roman, A. Ganau, R. Pini, E. C. Jones, T. G. Pickering, and R. B. Devereux. Relationship of effective arterial elastance to demographic and arterial characteristics in normotensive and hypertensive adults. J. Hypertens. 13: 971-977, 1995[Medline]. |
| 24. |
Suga, H.
Ventricular energetics.
Physiol. Rev.
70:
247-277,
1990 |
| 25. | Sunagawa, K., W. L. Maughan, D. Burkhoff, and K. Sagawa. Left ventricular interaction with arterial load studied in isolated canine left ventricle. Am. J. Physiol (Heart Circ. Physiol. 14): H773-H780, 1983. |
| 26. |
Sunagawa, K.,
W. L. Maughan,
and
K. Sagawa.
Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle.
Circ. Res.
56:
586-595,
1985 |
| 27. | Vahanian, A., and J. Acar. Mitral valvuloplasty: the French experience. In: Textbook of Interventional Cardiology, edited by E. J. Topol. Philadelphia, PA: Saunders, 1992, p. 1206-1225. |
| 28. | Vahanian, A., P. L. Michel, B. Cormier, B. Vitoux, X. Michel, M. L. Enriquez-Sarano, M. Slama, S. Travelsi, M. B. Ismaïl, and J. Acar. Results of percutaneous mitral commissurotomy in 200 patients. Am. J. Cardiol. 63: 847-852, 1989[Medline]. |
| 29. | Wisenbaugh, T., R. Essop, S. Middlemost, J. Skoularigis, and P. Sarelli. Excessive vasoconstriction in rheumatic mitral stenosis with modestly reduced ejection fraction. J. Am. Coll. Cardiol. 20: 1339-1344, 1992[Abstract]. |
| 30. | Yasuda, S., S. Nagata, J. Tamai, F. Ishikura, T. Yamabe, K. Kimura, and K. Miyatake. Left ventricular diastolic pressure-volume response immediately after successful percutaneous transvenous mitral commissurotomy. Am. J. Cardiol. 71: 932-937, 1993[Medline]. |
This article has been cited by other articles:
|
|
 |
|
  D. Chemla, I. Antony, Y. Lecarpentier, and A. Nitenberg Contribution of systemic vascular resistance and total arterial compliance to effective arterial elastance in humans Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H614 - H620. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
