Adv. Cardiol., vol. 24, pp. 37-46 (Karger, Basel 1978)
Ventricular Function in Coronary Heart Disease J.M.DETRY, P.MENGEOT,
L.A. BRASSEUR,
J.COSYNS
and
M. F. ROUSSEAU
Our knowledge of the ventricular function is derived from data obtained on the papillary muscle [2]. It has been known for long time that the tension developed by a muscle depends on its initial length: when the latter increases, the active tension increases up to a maximum over which any further lengthening of the muscle is attended by a decrease in the active tension. These changes in the developed tension are observed without any concomitant change in the contractile state of the left ventricle. The contractility of the muscle can be modified and the velocity of shortening is increased by inotropic stimuli as norepinephrine and decreased by P-blocking agents. A comprehensive study of the left ventricular function requires, therefore, to consider three parameters, namely the length, the tension and the velocity of shortening of the muscle. The study of the left ventricle as a muscle and the calculation of all indices of muscle function are based on several assumptions: one of those is that the left ventricular contraction is homogeneous and the concepts of cardiac mechanics are no longer valid when a significant portion (15-20%) of the left ventricle is hypokinetic or akinetic [1]. This is a very frequent situation in coronary heart disease (CHD) which is by definition a regional disease: some regions of the left ventricle are normal while others are affected by a decreased or totally abolished coronary blood flow. Also, the left ventricular contraction pattern is not constant in CHD and it can change drastically during stresses as atrial pacing or exercise [5, 12]. The 'muscle' aspect of the left ventricular function will therefore not be considered and the pumping function of the left ventricle will be briefly reviewed; its adaptation during exercise is emphasized.
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Division of Cardiology of the University Clinic St.Luc, University of Louvain, Bruxelles
38
DETRY/MENGECIT/BRASSEUR/CoSYNS/ROUSSEAU
';':' 1>:
~
~ g
~..0
.3
J!
e
be;
~c;
o
'Iii
III
:'j
:'j
LVEDP
LVEDP
Fig. 1. Left ventricular function (left panel) and compliance (right panel).
In clinical cardiology, the pumping function of the left ventricle is best expressed by the ventricular function curve which is an indirect estimation of the tension-length relationship (fig. I); the stroke work (product of stroke volume and systolic pressure) represents the tension developed while the length or the volume of the left ventricle is expressed by the left ventricular end-diastolic pressure (LVEDP). This function curve is displaced to the left when the ventricular contractility increases and is shifted to the right when the ventricular contractility is diminished (flattened curve). In normal conditions, the LVEDP is closely correlated to the left ventricular volume; this pressure-volume relationship is curvilinear and corresponds to the compliance of the left ventricle (fig. I). The assumption that the changes in LVEDP adequately reflect changes in left ventricular volume is no longer valid if the ventricular compliance changes, which probably occurs during myocardial ischemia [5,7]. In these circumstances, an increase in LVEDP can either reflect an increase in volume or a decrease in compliance: the only way to identify the basic mechanism is then to measure simultaneously the left ventricular volume.
In normal subjects, the contractility of the left ventricle increases during exercise (fig. 2); these changes in contractility which are due to the increased sympathetic activity are closely correlated to the changes in heart rate during exercise [2]. The achievement of a normal maximal exercise performance requires this adjustment [6].
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Left Ventricular Function during Exercise
Ventricular Function in CHD
39
Exercise
f'~' -'"
-'" ~
~
~
~
o
~
e
e
iii
iii LVEDP
LVEDP
When the contractility of the heart is decreased (fig. 2), the function curve is progressively shifted to the right and, simultaneously, the heart looses its capacity to respond adequately to exercise so that both resting and exercise curves are practically similar [2]. Initially, all clinical and hemodynamic data will be abnormal only during exertion of sufficient intensity; progressively, the signs of ventricular dysfunction will appear during exercise oflesser intensity. Finally, heart failure will be manifest at rest and, at this stage of the disease, exercise is very poorly tolerated. In the progressive deterioration of the left ventricular function, one can therefore describe three stages [9]. At the first stage, the ventricular function is normal at rest and the decrease in contractility will be manifest only during exercise. At the second stage, the contractility is slightly reduced at rest and these abnormalities will be exaggerated during exercise. At the third stage, the heart has completely lost its contractility reserve resulting in pump failure with its classical signs. From these simple considerations, it is clear that the study of the left ventricular function should not be limited at measurements made at rest but should also include measurements during exercise and ideally at several exercise levels of increasing severity up to the maximal exercise level. In coronary heart disease, the clinical signs of heart failure are not frequent at rest but the resting LVEDP can be elevated in the absence of any clinical signs or symptoms (table I); when the left ventricle is stressed, either by atrial pacing or mainly by exercise, the majority of the patients present transient signs of ventricular dysfunction [4]. In some instances, the abnormal left ventricular function is detectable only during exercise of maximal intensity (fig. 3).
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Fig. 2. Left ventricular function in normal subjects (left panel) and in patients with pump failure (right panel).
DETRY/MENGEOT/BRASSEUR/COSYNs/RoUSSEAU
Table I. Ventricular function in coronary heart disease (n and PARKER, 41
40 =
266) [from BURGGRAF
% Congestive heart failure
11
Elevated L VEDP At rest During pacing During exercise
80
Abnormal left ventriculogram
50
27 60
+.
'.
1100 E
No pain
01
x
~ .S .x
(; ~
o
~
e
iii 50 10
20
30
LVEDP, mmHg
Fig. 3. Ventricular function in a patient (K. F., d', 45 years) with a previous inferior myocardial infarction but no exertional angina pectoris; the ventriculogram was normal at rest and the ejection fraction was 75 %. 0 = Rest (HR = 74; ST = -0.5); + = submaximal exercise (HR = 121; ST = -3.0); • = maximal exercise (HR = 163; ST =
The study of the left ventricular function in CHD is more complex than in other diseases like cardiomyopathies for two reasons: the first one is the regional character of the disease which has already been mentioned, and the second one is the transient myocardial ischemia which often appears during stress. This myocardial ischemia depresses by itself the myocardial function but the hemodynamic abnormalities are eminently transient and they progres-
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
-5.0).
Ventricular Function in CHD
41
sively disappear when the stress is interrupted [8]. It is often impossible to separate what is due to chronic myocardial damage from what is directly caused by transient myocardial ischemia. Myocardial ischemia is usually attended by an increase in the LVEDP; the latter reflects either a transient heart failure or a decreased compliance of the left ventricle: both mechanisms probably playa role and their respective roles are difficult to evaluate [5,7,8]. It should also be noted that the geometry of the left ventricular cavity can be drastically changed during ischemia since transient ventricular dyskinetic zones have been observed during exercise-induced angina pectoris [12].
Although the most accurate information is provided by direct measurement of the LVEDP, it is possible to obtain a reliable information from technically easier measurements such as the mean pulmonary capillary wedge pressure [10] or from the mean pulmonary artery pressure; the advantage of these parameters is that they are easily obtained during exercise of all intensities and that the procedures are well accepted by most patients. Hemodynamic data (Fick cardiac output and pressure measurements) have been obtained in 74 patients studied in upright posture at rest, during submaximal exercise and during maximal exercise limited either by angina pectoris or by exhaustion without any pain; the detailed methods have been previously reported [11]. All patients had an arteriographically documented CHD and 48 had a history of previous myocardial infarction. None of these patients had clinical signs of heart failure at rest. The data have been compared with those obtained at rest and during several exercise levels up to the maximum in 15 young healthy subjects. In patients not limited by angina pectoris during exercise, the hemodynamic response to exercise is determined by the presence of a previous myocardial infarction (fig. 4, table II); the importance of the observed abnormalities is not closely related to the number of involved vessels but mainly depends on the aspect of the left ventriculogram at rest (presence of ventricular asynergy and ejection fraction). The patients limited by angina pectoris exhibit more severe signs ofventricular dysfunction, and these signs occur at a lower level of exercise and at a lower heart rate (fig. 4, table 11); again, the patients with a previous myocardial infarction have a poorer response to exercise. In these patients with
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Indirect Invasive Assessment of Left Ventricular Function
DETRyjMENGEOT/BRASSEURjCOSYNsjRouSSEAU
42
angina pectoris, the severity of angina and the hemodynamic signs of ventricular dysfunction are not closely correlated nor with the number of involved vessels nor with the left ventriculogram. Interestingly (fig. 5), the hemodynamic signs of ventricular dysfunction observed during angina pectoris are reversible when sublingual nitroglycerin is given to the patients [8] of after successful coronary bypass surgery [10]. This indicates that transient myocardial ischemia plays a determinant role in these hemodynamic abnormalities. One can speculate that both in angina and non-angina patients, myocardial ischemia is responsible for the left ventricular dysfunction and that this transient myocardial ischemia is less well tolerated in presence of chronic myocardial damage as after an acute myocardial infarction. More studies on larger groups of patients are needed to determine the prognostic value of these transient abnormalities.
200
No AP] No previous MJ
'+Z~AP
150
,T :..L.
/
:i----- ___ •
No AP]
/+----------. AP
Previous MI
//
E
//
//
'"
//
//
xc'100
//
// ';,
~ xc 'e"
o
ih 50
.--
m
I
W
--r-----T--
~
~
I
~
Fig. 4. Mean hemodynamic data collected in 4 groups of patients with arteriographically documented CHD. The rectangle represents the normal limits for these measurements and has been drawn from 80 measurements obtained in 15 normal young subjects. The number of patients in each group, the resting ejection fraction and the hemodynamic data at the maximal exercise level are presented in table II. 0 = Rest; + = submaximal exercise; • = maximal exercise or angina pectoris (AP); MI = myocardial infarction.
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Mean pulmonary artery pressure, mm Hg
Ventricular Function in CHD
43
Table II. Hemodynamic data at the maximal exercise level in CHD patients V02 HR SV CO (A-V)02 AP SW l/min beats/min ml/beat l/min diff. mmHg g'm ml/100ml
EF
No angina pectoris during exercise No previous MI 9 Previous MI 17
2.13 1.96
163 171
91 77
14.8 13.2
14.4 14.8
31 40
167 142
73 61
Angina pee/oris during exercise No previous MI Previous MI
1.41 1.31
137 137
84 69
11.5 9.4
12.3 14.0
34 41
146 117
53
n
30 18
%
69
HR = Heart rate; SV = stroke volume; CO = cardiac output; (A-V)02 diff. = arterio-mixed venous oxygen difference; AP = mean pulmonary artery pressure; SW = stroke work (product of heart rate and mean arterial pressure); EF = ejection fraction; MI = myocardial infarction.
200
150 E 01
t.- 100 ~
~
e
iii
50
I
I
t
10
20
30
---
----r-
40
r
50
Fig. 5. Effects of nitroglycerin in CHD patients limited by exertional angina pectoris. Mean hemodynamic data collected during exertional angina pectoris in 19 patients subdivided according to the existence or not of a prior myocardial infarction (MI); after the completion of the measurements during angina pectoris, the patients received 1 mg of sublingual nitroglycerin and continued to exercise at the same work load. The pain progressively disappeared in all patients and the measurements were repeated at the same level of exercise, 2 min after the disappearance of angina pectoris. • = Exertional angina pectoris; + = same level of exercise after nitroglycerin (no pain).
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Mean puLmonary artery pressure, mmHg
DETRy/MENGEOT/BRASSEUR/COSYNS/RoUSSEAU
44
Information Provided by Maximal Exercise Testing
As already mentioned, in the absence of clinical signs of heart failure at rest, the severity of angina pectoris (maximal work load or V02 at the occurrence of symptoms) does not give a reliable information on the severity of the disease nor in terms of number of involved vessels nor in terms of left ventricular function.
100 o :
90
I •
80 •
j E
o
70
(J,
60
>
50
E .3 o
•
.
:.1
••
00
..
~
e
ill 40 I
-T
1.0
1.5
1--
-- I
2.0
2.5
,",°2 max, l/min
Fig. 6. Relationship between the maximal oxygen intake and the stroke volume during maximal exercise in 37 coronary patients not limited by angina pectoris. r = 0.89.
Patients
Vaamax l/min
HR
x
SV mI
X
(A-V)02 diff. ml/l00mI
CO l/min
PAP mmHg
1-12 13-25 26-37
1.55 2.08 2.41
168 167 174
X
64 86 95
X
14.5 14.5 14.7
10.7 14.3 16.6
34 36 37
X X
X X
The patients have been numbered from the lowest to the highest V02 max and arbitrarily subdivided in 3 groups of equal size. For abbreviations, see table II.
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Table III. Hemodynamic significance ofVaa max in CHD patients without angina
Ventricular Function in CHD
45
In patients not limited by angina pectoris, the physical working capacity (maximal work load or VOl! max) is determined by the stroke volume during maximal exercise and, therefore, by the left ventricular function (fig. 6, table III). In these patients not limited by angina pectoris, the data collected during noninvasive maximal exercise testing furnish an important information on the left ventricular function. The most limited patients have the lowest maximal stroke volume and they also have the most impaired left ventriculograms; this relationship is largely independent of the number of involved vessels. It can be concluded that coronary heart disease affects the left ventricular function in a double way. Firstly, the loss of cardiac tissue decreases the contractile force of the left ventricle proportionally to the extent of the infarcted area. When clinical, hemodynamic or ventriculographic signs of ventricular dysfunction are present at rest, the prognosis is significantly worsened [3,4]. Secondly, myocardial ischemia induced by stress transiently depresses the myocardial function and induces the appearance of hemodynamic signs of pump failure and/or altered compliance; these abnormalities are more marked in patients with a previous myocardial infarction but their prognostic significance remains to be established.
1
2 3
4 5
6
7
BESSE, P.; CHOUSSAT, A.; DAUBEZE, J. et BRICAUD, H.: Validite et limites d'utilisation chez l'homme, des indices de contractilite bases sur l'application du concept de la mecamque myocardique a la phase isovolumetrique de la contraction ventriculaire. Archs Mal. Camr 67: 381-391 (1974). BRAUNWALD, E.; Ross, J., and SONNENBUCK, E. H.: Mechanisms of circulation of the normal and failing heart, p.205 (Little, Brown, Boston 1967). BRUSCHKE, A. V. G.; PROUDFIT, W. L., and SONES, F. M.: Progress study of 590 consecutive nonsurgical cases of coronary disease followed 5-9 years. II. Ventriculographic and other correlations. Circulation 47: 1154-1163 (1973). BURGGRAF, G. W. and PARKER, J. 0.: Prognosis in coronary artery disease. Angiographic, hemodynamic and clinical factors. Circulation 51: 146-156 (1975). DWYER, E. M.: Left ventricular pressure-volume alterations and regional disorders of contraction during myocardial ischemia induced by atrial pacing. Circulation 42: 1111-1122 (1970). EpSTEIN, S. E.; ROBINSON, B. F.; KAHLER, R. L., and BRAUNWALD, E.: Effects of beta-adrenergic blockade on the cardiac response to maximal and submaximal exercise in man. J. clin. Invest. 44: 1745-1753 (1965). MCCANS, J. L. and PARKER, J. 0.: Left ventricular pressure volume relationship during myocardial ischemia in man. Circulation 48: 775-785 (1973).
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References
DETRY/MENGEOT/BRASSEUR/CosYNS/RoUSSEAU
9
10
11
12
PARKER, J. 0.; WEST, R. 0., and DI GIORGI, S.: The hemodynamic response to exercise in patients with healed myocardial infarction without angina. With observations on the effects of nitroglycerin. Circulation 36: 734-751 (1967). ROSKAMM, H.: Ventricular function at rest and during exercise; in ROSKAMM and HANN, pp. 17-19 (Springer, Berlin 1976). RosKAMM,H.; WEISSWANGE,A.; HANN, C.; JAUCH,K. W.; SCHMUZIGER, M.; PETERSEN, J.; RENTROP, P., and SCHNELLBACHER, K.: Hemodynamics at rest and during exercise in 222 patients with coronary heart disease before and after aorta-coronary bypass surgery. Cardiology 62: 247-260 (1977). ROUSSEAU, M. F.; BRASSEUR, L. A., 'and DETRY, J. M. R.: Hemodynamic determinants of maximal oxygen intake in patients with healed myocardial infarction: influence of physical training. Circulation 48: 943-949 (1973). SHARMA, B. and TAYLOR, S. H.: Localization of left ventricular ischemia in angina pectoris by cineangiography during exercise. Br. Heart J. 37: 963-970 (1975).
J. M. DETRY, MD, Division of Cardiology of the University Clinic St. Luc, University of Louvain, B-1200 Bruxelles (Belgium)
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
8
46
Ventricular Function in Coronary Heart Disease J.M.DETRY, P.MENGEOT,
L.A. BRASSEUR,
J.COSYNS
and
M. F. ROUSSEAU
Our knowledge of the ventricular function is derived from data obtained on the papillary muscle [2]. It has been known for long time that the tension developed by a muscle depends on its initial length: when the latter increases, the active tension increases up to a maximum over which any further lengthening of the muscle is attended by a decrease in the active tension. These changes in the developed tension are observed without any concomitant change in the contractile state of the left ventricle. The contractility of the muscle can be modified and the velocity of shortening is increased by inotropic stimuli as norepinephrine and decreased by P-blocking agents. A comprehensive study of the left ventricular function requires, therefore, to consider three parameters, namely the length, the tension and the velocity of shortening of the muscle. The study of the left ventricle as a muscle and the calculation of all indices of muscle function are based on several assumptions: one of those is that the left ventricular contraction is homogeneous and the concepts of cardiac mechanics are no longer valid when a significant portion (15-20%) of the left ventricle is hypokinetic or akinetic [1]. This is a very frequent situation in coronary heart disease (CHD) which is by definition a regional disease: some regions of the left ventricle are normal while others are affected by a decreased or totally abolished coronary blood flow. Also, the left ventricular contraction pattern is not constant in CHD and it can change drastically during stresses as atrial pacing or exercise [5, 12]. The 'muscle' aspect of the left ventricular function will therefore not be considered and the pumping function of the left ventricle will be briefly reviewed; its adaptation during exercise is emphasized.
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Division of Cardiology of the University Clinic St.Luc, University of Louvain, Bruxelles
38
DETRY/MENGECIT/BRASSEUR/CoSYNS/ROUSSEAU
';':' 1>:
~
~ g
~..0
.3
J!
e
be;
~c;
o
'Iii
III
:'j
:'j
LVEDP
LVEDP
Fig. 1. Left ventricular function (left panel) and compliance (right panel).
In clinical cardiology, the pumping function of the left ventricle is best expressed by the ventricular function curve which is an indirect estimation of the tension-length relationship (fig. I); the stroke work (product of stroke volume and systolic pressure) represents the tension developed while the length or the volume of the left ventricle is expressed by the left ventricular end-diastolic pressure (LVEDP). This function curve is displaced to the left when the ventricular contractility increases and is shifted to the right when the ventricular contractility is diminished (flattened curve). In normal conditions, the LVEDP is closely correlated to the left ventricular volume; this pressure-volume relationship is curvilinear and corresponds to the compliance of the left ventricle (fig. I). The assumption that the changes in LVEDP adequately reflect changes in left ventricular volume is no longer valid if the ventricular compliance changes, which probably occurs during myocardial ischemia [5,7]. In these circumstances, an increase in LVEDP can either reflect an increase in volume or a decrease in compliance: the only way to identify the basic mechanism is then to measure simultaneously the left ventricular volume.
In normal subjects, the contractility of the left ventricle increases during exercise (fig. 2); these changes in contractility which are due to the increased sympathetic activity are closely correlated to the changes in heart rate during exercise [2]. The achievement of a normal maximal exercise performance requires this adjustment [6].
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Left Ventricular Function during Exercise
Ventricular Function in CHD
39
Exercise
f'~' -'"
-'" ~
~
~
~
o
~
e
e
iii
iii LVEDP
LVEDP
When the contractility of the heart is decreased (fig. 2), the function curve is progressively shifted to the right and, simultaneously, the heart looses its capacity to respond adequately to exercise so that both resting and exercise curves are practically similar [2]. Initially, all clinical and hemodynamic data will be abnormal only during exertion of sufficient intensity; progressively, the signs of ventricular dysfunction will appear during exercise oflesser intensity. Finally, heart failure will be manifest at rest and, at this stage of the disease, exercise is very poorly tolerated. In the progressive deterioration of the left ventricular function, one can therefore describe three stages [9]. At the first stage, the ventricular function is normal at rest and the decrease in contractility will be manifest only during exercise. At the second stage, the contractility is slightly reduced at rest and these abnormalities will be exaggerated during exercise. At the third stage, the heart has completely lost its contractility reserve resulting in pump failure with its classical signs. From these simple considerations, it is clear that the study of the left ventricular function should not be limited at measurements made at rest but should also include measurements during exercise and ideally at several exercise levels of increasing severity up to the maximal exercise level. In coronary heart disease, the clinical signs of heart failure are not frequent at rest but the resting LVEDP can be elevated in the absence of any clinical signs or symptoms (table I); when the left ventricle is stressed, either by atrial pacing or mainly by exercise, the majority of the patients present transient signs of ventricular dysfunction [4]. In some instances, the abnormal left ventricular function is detectable only during exercise of maximal intensity (fig. 3).
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Fig. 2. Left ventricular function in normal subjects (left panel) and in patients with pump failure (right panel).
DETRY/MENGEOT/BRASSEUR/COSYNs/RoUSSEAU
Table I. Ventricular function in coronary heart disease (n and PARKER, 41
40 =
266) [from BURGGRAF
% Congestive heart failure
11
Elevated L VEDP At rest During pacing During exercise
80
Abnormal left ventriculogram
50
27 60
+.
'.
1100 E
No pain
01
x
~ .S .x
(; ~
o
~
e
iii 50 10
20
30
LVEDP, mmHg
Fig. 3. Ventricular function in a patient (K. F., d', 45 years) with a previous inferior myocardial infarction but no exertional angina pectoris; the ventriculogram was normal at rest and the ejection fraction was 75 %. 0 = Rest (HR = 74; ST = -0.5); + = submaximal exercise (HR = 121; ST = -3.0); • = maximal exercise (HR = 163; ST =
The study of the left ventricular function in CHD is more complex than in other diseases like cardiomyopathies for two reasons: the first one is the regional character of the disease which has already been mentioned, and the second one is the transient myocardial ischemia which often appears during stress. This myocardial ischemia depresses by itself the myocardial function but the hemodynamic abnormalities are eminently transient and they progres-
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
-5.0).
Ventricular Function in CHD
41
sively disappear when the stress is interrupted [8]. It is often impossible to separate what is due to chronic myocardial damage from what is directly caused by transient myocardial ischemia. Myocardial ischemia is usually attended by an increase in the LVEDP; the latter reflects either a transient heart failure or a decreased compliance of the left ventricle: both mechanisms probably playa role and their respective roles are difficult to evaluate [5,7,8]. It should also be noted that the geometry of the left ventricular cavity can be drastically changed during ischemia since transient ventricular dyskinetic zones have been observed during exercise-induced angina pectoris [12].
Although the most accurate information is provided by direct measurement of the LVEDP, it is possible to obtain a reliable information from technically easier measurements such as the mean pulmonary capillary wedge pressure [10] or from the mean pulmonary artery pressure; the advantage of these parameters is that they are easily obtained during exercise of all intensities and that the procedures are well accepted by most patients. Hemodynamic data (Fick cardiac output and pressure measurements) have been obtained in 74 patients studied in upright posture at rest, during submaximal exercise and during maximal exercise limited either by angina pectoris or by exhaustion without any pain; the detailed methods have been previously reported [11]. All patients had an arteriographically documented CHD and 48 had a history of previous myocardial infarction. None of these patients had clinical signs of heart failure at rest. The data have been compared with those obtained at rest and during several exercise levels up to the maximum in 15 young healthy subjects. In patients not limited by angina pectoris during exercise, the hemodynamic response to exercise is determined by the presence of a previous myocardial infarction (fig. 4, table II); the importance of the observed abnormalities is not closely related to the number of involved vessels but mainly depends on the aspect of the left ventriculogram at rest (presence of ventricular asynergy and ejection fraction). The patients limited by angina pectoris exhibit more severe signs ofventricular dysfunction, and these signs occur at a lower level of exercise and at a lower heart rate (fig. 4, table 11); again, the patients with a previous myocardial infarction have a poorer response to exercise. In these patients with
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Indirect Invasive Assessment of Left Ventricular Function
DETRyjMENGEOT/BRASSEURjCOSYNsjRouSSEAU
42
angina pectoris, the severity of angina and the hemodynamic signs of ventricular dysfunction are not closely correlated nor with the number of involved vessels nor with the left ventriculogram. Interestingly (fig. 5), the hemodynamic signs of ventricular dysfunction observed during angina pectoris are reversible when sublingual nitroglycerin is given to the patients [8] of after successful coronary bypass surgery [10]. This indicates that transient myocardial ischemia plays a determinant role in these hemodynamic abnormalities. One can speculate that both in angina and non-angina patients, myocardial ischemia is responsible for the left ventricular dysfunction and that this transient myocardial ischemia is less well tolerated in presence of chronic myocardial damage as after an acute myocardial infarction. More studies on larger groups of patients are needed to determine the prognostic value of these transient abnormalities.
200
No AP] No previous MJ
'+Z~AP
150
,T :..L.
/
:i----- ___ •
No AP]
/+----------. AP
Previous MI
//
E
//
//
'"
//
//
xc'100
//
// ';,
~ xc 'e"
o
ih 50
.--
m
I
W
--r-----T--
~
~
I
~
Fig. 4. Mean hemodynamic data collected in 4 groups of patients with arteriographically documented CHD. The rectangle represents the normal limits for these measurements and has been drawn from 80 measurements obtained in 15 normal young subjects. The number of patients in each group, the resting ejection fraction and the hemodynamic data at the maximal exercise level are presented in table II. 0 = Rest; + = submaximal exercise; • = maximal exercise or angina pectoris (AP); MI = myocardial infarction.
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Mean pulmonary artery pressure, mm Hg
Ventricular Function in CHD
43
Table II. Hemodynamic data at the maximal exercise level in CHD patients V02 HR SV CO (A-V)02 AP SW l/min beats/min ml/beat l/min diff. mmHg g'm ml/100ml
EF
No angina pectoris during exercise No previous MI 9 Previous MI 17
2.13 1.96
163 171
91 77
14.8 13.2
14.4 14.8
31 40
167 142
73 61
Angina pee/oris during exercise No previous MI Previous MI
1.41 1.31
137 137
84 69
11.5 9.4
12.3 14.0
34 41
146 117
53
n
30 18
%
69
HR = Heart rate; SV = stroke volume; CO = cardiac output; (A-V)02 diff. = arterio-mixed venous oxygen difference; AP = mean pulmonary artery pressure; SW = stroke work (product of heart rate and mean arterial pressure); EF = ejection fraction; MI = myocardial infarction.
200
150 E 01
t.- 100 ~
~
e
iii
50
I
I
t
10
20
30
---
----r-
40
r
50
Fig. 5. Effects of nitroglycerin in CHD patients limited by exertional angina pectoris. Mean hemodynamic data collected during exertional angina pectoris in 19 patients subdivided according to the existence or not of a prior myocardial infarction (MI); after the completion of the measurements during angina pectoris, the patients received 1 mg of sublingual nitroglycerin and continued to exercise at the same work load. The pain progressively disappeared in all patients and the measurements were repeated at the same level of exercise, 2 min after the disappearance of angina pectoris. • = Exertional angina pectoris; + = same level of exercise after nitroglycerin (no pain).
Downloaded by: University of Cambridge 131.111.164.128 - 3/18/2019 9:31:41 AM
Mean puLmonary artery pressure, mmHg
DETRy/MENGEOT/BRASSEUR/COSYNS/RoUSSEAU
44
Information Provided by Maximal Exercise Testing
As already mentioned, in the absence of clinical signs of heart failure at rest, the severity of angina pectoris (maximal work load or V02 at the occurrence of symptoms) does not give a reliable information on the severity of the disease nor in terms of number of involved vessels nor in terms of left ventricular function.
100 o :
90
I •
80 •
j E
o
70
(J,
60
>
50
E .3 o
•
.
:.1
••
00
..
~
e
ill 40 I
-T
1.0
1.5
1--
-- I
2.0
2.5
,",°2 max, l/min
Fig. 6. Relationship between the maximal oxygen intake and the stroke volume during maximal exercise in 37 coronary patients not limited by angina pectoris. r = 0.89.
Patients
Vaamax l/min
HR
x
SV mI
X
(A-V)02 diff. ml/l00mI
CO l/min
PAP mmHg
1-12 13-25 26-37
1.55 2.08 2.41
168 167 174
X
64 86 95
X
14.5 14.5 14.7
10.7 14.3 16.6
34 36 37
X X
X X
The patients have been numbered from the lowest to the highest V02 max and arbitrarily subdivided in 3 groups of equal size. For abbreviations, see table II.
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Table III. Hemodynamic significance ofVaa max in CHD patients without angina
Ventricular Function in CHD
45
In patients not limited by angina pectoris, the physical working capacity (maximal work load or VOl! max) is determined by the stroke volume during maximal exercise and, therefore, by the left ventricular function (fig. 6, table III). In these patients not limited by angina pectoris, the data collected during noninvasive maximal exercise testing furnish an important information on the left ventricular function. The most limited patients have the lowest maximal stroke volume and they also have the most impaired left ventriculograms; this relationship is largely independent of the number of involved vessels. It can be concluded that coronary heart disease affects the left ventricular function in a double way. Firstly, the loss of cardiac tissue decreases the contractile force of the left ventricle proportionally to the extent of the infarcted area. When clinical, hemodynamic or ventriculographic signs of ventricular dysfunction are present at rest, the prognosis is significantly worsened [3,4]. Secondly, myocardial ischemia induced by stress transiently depresses the myocardial function and induces the appearance of hemodynamic signs of pump failure and/or altered compliance; these abnormalities are more marked in patients with a previous myocardial infarction but their prognostic significance remains to be established.
1
2 3
4 5
6
7
BESSE, P.; CHOUSSAT, A.; DAUBEZE, J. et BRICAUD, H.: Validite et limites d'utilisation chez l'homme, des indices de contractilite bases sur l'application du concept de la mecamque myocardique a la phase isovolumetrique de la contraction ventriculaire. Archs Mal. Camr 67: 381-391 (1974). BRAUNWALD, E.; Ross, J., and SONNENBUCK, E. H.: Mechanisms of circulation of the normal and failing heart, p.205 (Little, Brown, Boston 1967). BRUSCHKE, A. V. G.; PROUDFIT, W. L., and SONES, F. M.: Progress study of 590 consecutive nonsurgical cases of coronary disease followed 5-9 years. II. Ventriculographic and other correlations. Circulation 47: 1154-1163 (1973). BURGGRAF, G. W. and PARKER, J. 0.: Prognosis in coronary artery disease. Angiographic, hemodynamic and clinical factors. Circulation 51: 146-156 (1975). DWYER, E. M.: Left ventricular pressure-volume alterations and regional disorders of contraction during myocardial ischemia induced by atrial pacing. Circulation 42: 1111-1122 (1970). EpSTEIN, S. E.; ROBINSON, B. F.; KAHLER, R. L., and BRAUNWALD, E.: Effects of beta-adrenergic blockade on the cardiac response to maximal and submaximal exercise in man. J. clin. Invest. 44: 1745-1753 (1965). MCCANS, J. L. and PARKER, J. 0.: Left ventricular pressure volume relationship during myocardial ischemia in man. Circulation 48: 775-785 (1973).
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References
DETRY/MENGEOT/BRASSEUR/CosYNS/RoUSSEAU
9
10
11
12
PARKER, J. 0.; WEST, R. 0., and DI GIORGI, S.: The hemodynamic response to exercise in patients with healed myocardial infarction without angina. With observations on the effects of nitroglycerin. Circulation 36: 734-751 (1967). ROSKAMM, H.: Ventricular function at rest and during exercise; in ROSKAMM and HANN, pp. 17-19 (Springer, Berlin 1976). RosKAMM,H.; WEISSWANGE,A.; HANN, C.; JAUCH,K. W.; SCHMUZIGER, M.; PETERSEN, J.; RENTROP, P., and SCHNELLBACHER, K.: Hemodynamics at rest and during exercise in 222 patients with coronary heart disease before and after aorta-coronary bypass surgery. Cardiology 62: 247-260 (1977). ROUSSEAU, M. F.; BRASSEUR, L. A., 'and DETRY, J. M. R.: Hemodynamic determinants of maximal oxygen intake in patients with healed myocardial infarction: influence of physical training. Circulation 48: 943-949 (1973). SHARMA, B. and TAYLOR, S. H.: Localization of left ventricular ischemia in angina pectoris by cineangiography during exercise. Br. Heart J. 37: 963-970 (1975).
J. M. DETRY, MD, Division of Cardiology of the University Clinic St. Luc, University of Louvain, B-1200 Bruxelles (Belgium)
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