Cardiac Function in Patients with Angina

It is a great honour and pleasure for me to be invited to this meeting, commemorating the introduction by your former member, T. Lauder Brunton, of amyl nitrite as a potent remedy for anginal pain, one hundred years ago. For some years, I have been interested in the haemodynamic consequences of coronary heart disease, the most common cause of anginal pain. That this symptom is due to an improper balance between the myocardial demand for energy and the supply available from the coronary circulation has been more or less generally accepted for a long time. This view seems, for instance, to have been held by Allan Burns in his book on cardiology printed in this city in 1809. The exact cause of the pain is still uncertain. It seems, however, to be linked to inadequate delivery of oxygen to the myocardium, either generally or locally. And metabolic studies (Cohen el al. 1965) have indicated changes probably due to hypoxia in patients with coronary heart disease not only during but also in the intervals between attacks of angina pectoris. If reduction of the coronary circulation and abnormal metabolism are common in these patients, it is reasonable to expect a reduction in ventricular function as well. However, one of the main symptoms of impaired left heart function, namely dyspnoea, has not been generally regarded as a feature of this condition (P. Wood 1953). Copyright Royal Medical Society. All rights reserved. The copyright is retained by the author and the Royal Medical Society, except where explicitly otherwise stated. Scans have been produced by the Digital Imaging Unit at Edinburgh University Library. Res Medica is supported by the University of Edinburgh’s Journal Hosting Service: http://journals.ed.ac.uk ISSN: 2051-7580 (Online) ISSN: 0482-3206 (Print) Res Medica is published by the Royal Medical Society, 5/5 Bristo Square, Edinburgh, EH8 9AL Res Medica, April 1967, Special Issue – Lauder Brunton Centenary Symposium on Angina Pectoris: 32-36 doi: 10.2218/resmedica.v5i3-4.483 CARDIAC FUNCTION IN PATIENTS WITH ANGINA O ttar M uller, Ulleva l H o sp ital, University o f Oslo It is a great honour and pleasure for me to be invited to this meeting, commemorating the introduction by your former member, T. Lauder Brunton, of amyl nitrite as a potent remedy for anginal pain, one hundred years ago. For some years, I have been interested in the haemodynamic consequences of coronary heart disease, the most common cause of anginal pain. That this symptom is due to an improper balance between the myocardial demand for energy and the supply available from the coronary circula­ tion has been more or less generally accepted for a long time. This view seems, for instance, to have been held by Allan Burns in his book on cardi­ ology printed in this city in 180g. The exact cause of the pain is still uncertain. It seems, however, to be linked to inadequate delivery of oxygen to the myocardium, either generally or locally. And metabolic studies (Cohen el al. 1965) have in­ dicated changes probably due to hypoxia in pa­ tients with coronary heart disease not only during but also in the intervals between attacks of angina pectoris. I f reduction of the coronary circulation and abnormal metabolism are common in these patients, it is reasonable to expect a reduction in ventricular function as well. However, one of the main symptoms of impaired left heart function, namely dyspnoea, has not been generally regard­ ed as a feature of this condition (P. Wood 1953)A number of investigations have been pub­ lished in the last 10 years concerning the cardiac function in patients with coronary heart disease, but in my presentation today, I will concentrate mainly on my own investigations which have been carried out by means of right heart catheter­ ization and include measurements of the pulmonary capillary venous pressures. Theseobservations will also be discussed in the light of two other published studies, of R. Malmborg, 1964 and of Cohen et al., 1965. My investigations involved patients in whom the diagnosis of coronary heart disease had been established clinically with reasonable certainty, and in whom complicating factors such as valvu­ lar disease, hypertension, anaemia, and thyro­ toxicosis have been excluded. The investigations comprised studies both at rest and during light recumbent leg exercise (approximately 140 kgm/min for 5 min). Figure 1 shows mean values of the main ob­ served and calculated parameters in a resting state, for a control group with the same average age as two groups of patients, one consisting of 18 patients without recognised previous infarction and one of 61 patients with a history of infarction. The only parameter listed which deviated signifi­ cantly from the controls was pulmonary capillary venous pressure.


CARDIAC FUNCTION IN PATIENTS WITH ANGINA O ttar M u ller, Ulle v a l H o s p ita l, U niversity o f O slo
It is a great honour and pleasure for me to be invited to this meeting, commemorating the introduction by your former member, T. Lauder Brunton, of amyl nitrite as a potent remedy for anginal pain, one hundred years ago.
For some years, I have been interested in the haemodynamic consequences of coronary heart disease, the most common cause of anginal pain.That this symptom is due to an improper balance between the myocardial demand for energy and the supply available from the coronary circula tion has been more or less generally accepted for a long time.This view seems, for instance, to have been held by Allan Burns in his book on cardi ology printed in this city in 180g.The exact cause o f the pain is still uncertain.It seems, however, to be linked to inadequate delivery of oxygen to the myocardium, either generally or locally.And metabolic studies (Cohen el al. 1965) have in dicated changes probably due to hypoxia in pa tients with coronary heart disease not only during but also in the intervals between attacks of angina pectoris.I f reduction of the coronary circulation and abnormal metabolism are common in these patients, it is reasonable to expect a reduction in ventricular function as well.However, one of the main symptoms of impaired left heart function, namely dyspnoea, has not been generally regard ed as a feature of this condition (P.Wood 1953)-A number of investigations have been pub lished in the last 10 years concerning the cardiac function in patients with coronary heart disease, but in my presentation today, I will concentrate mainly on my own investigations which have been carried out by means of right heart catheter ization and include measurements of the pulmonary capillary venous pressures.Theseobservations will also be discussed in the light of two other published studies, of R. Malmborg, 1964 andof Cohen et al., 1965.M y investigations involved patients in whom the diagnosis of coronary heart disease had been established clinically with reasonable certainty, and in whom complicating factors such as valvu lar disease, hypertension, anaemia, and thyro toxicosis have been excluded.
The investigations comprised studies both at rest and during light recumbent leg exercise (approximately 140 kgm/min for 5 min).
Figure 1 shows mean values of the main ob served and calculated parameters in a resting state, for a control group with the same average age as two groups of patients, one consisting of 18 patients without recognised previous infarction and one o f 61 patients with a history of infarction.The only parameter listed which deviated signifi cantly from the controls was pulmonary capillary venous pressure.previous myocardial infarcation exceeded the normal upper limit of 14 mm Hg, although the group average was elevated.In the group of patients with a history of infarction, pulmonary capillary venous pressure varied with heart size, and one patient was in pulmonary oedema during the investigation.On the other hand, with de creasing heart size, pulmonary capillary venous pressure approached normal levels.Thus, in vestigated in this way, only a small proportion of patients with coronary heart disease will, as individuals, display distinctly abnormal cardiac functions and these will mainly be found among those with enlarged hearts.

R E ST Mean
Figure 3 illustrates the mean values obtained during the exercise test.The higher oxygen up take in the infarct group reflects reduced effi ciency and not a heavier load.Increase in cardiac output is here expressed as relative to increase in   oxygen uptake.Marked deviations from the con trols were demonstrated, not only for pulmonary capillary venous pressure in both groups of pa tients but also for increase in cardiac output and stroke index in the group of patients with previous infarction.This was at least partly due to the patients with increased heart size.During the exercise test mean pulmonary capillary venous  Stroke volume seems to vary remarkably from one investigation to the other.

PCVP HEART SIZE-REST
Figure 6 illustrates mean stroke volume, peri pheral systolic blood pressure, heart rate and pulmonary capillary venous pressure in my patients with markedly elevated pulmonary capillary venous pressure, arranged according to whether or not they developed anginal pain dur ing the exercise test.There was a higher average peripheral blood pressure in the group o f patients with angina during the test.On the other hand, patients without angina had a greater average stroke volume.The differences were, however, very slight -and systolic blood pressure in both groups moderate as exercise-pressures.In M alm borg's series, patients with compar able pulmonary capillary venous pressure had an average stroke index o f under 40 m l.; while in Cohen's study the group o f patients who developed anginal pain during the exercise test had an average stroke index as low as 32 ml.In the group without anginal pain the figure was 38 ml., com pared to 49 ml. in the control group.
These variations in stroke index from group to group o f patients seem to me to offer a probable explanation o f the differences in observed pul monary capillary venous pressure and left ventri cular diastolic pressure.Nevertheless, I agree with the view that systolic blood pressure may be of some importance as well.

Conclusion
Signs of impaired left ventricular function are obtainable from coronary heart disease patients under stress, and especially during attacks o f an ginal pain.T he manner in which this left ventri cular impairment manifests itself seems, however, to vary with several haemodynamic parameters of which systolic ventricular pressure andespecially -stroke volume may be the most important.

R E F
Figure I M ean values for the three g ro u p s: Controls, patients w ith coronary heart disease without previous m yo cardial infarction and patient w ith previous m yo cardial infarction.

Figure 2 (
Figure 2 (on page 33) demonstrates individual pulmonary capillary venous pressure readings in the two groups of patients related to heart size assessed by x-ray.None of the patients without Figure 2 P u lm o n ary capillary-venous p ressu re at rest related to heart size (m l/M 2).Patients w ith (Inf.) and w ith out (A.P.) previous m yo card ial infarction.
Figure 3 M ean values fo r the three groups during light exer cise.
showed a m ore m arked difference be tween patients and controls than at rest.F igu re 4 dem onstrates in dividual pulm on ary ca p illa ry venous pressure in the tw o groups o f patients related to heart size.O n ly a sm all p ro portion o f the patients' p u lm o n ary cap illary venous pressure valves rem ained close to the nor m al lim it o f 15 m m H g. A w ide scatter w as found and cases w ith grea tly increased pressure w ere distributed regardless o f heart size in both groups.W ith enlarged hearts, how ever, near-norm al o b servations w ere lacking.It seems therefore that under the conditions o f our exercise test, im paired left ven tricu lar function m a y be revealed in v a ry in g degree by increased left ven tricu lar diastolic, left a trial and p ulm o n ary venous pressures in most patients in w hom the diagnosis o f coronary h eart disease can be established b y o rd in ary cri teria.T h e exercise load used p roduced anginal pain in only a m in ority o f the patients.F ig u r e 4 P u lm o n a r y c a p illa r y -v e n o u s p r e s s u r e d u r in g e x e r c is e r e la t e d to h e a r t s iz e .F igure 5 (on p age 35) illustrates the p ulm on ary capillary-ven ous pressure values recorded during the exercise test in patients w ith anginal p ain as the p ain com p lain t and heart sizes o f 500 m l/M 2 or below .T h e grea t m ajority o f patients w ho developed typ ical anginal p ain had m arkedly elevated pulm on ary ca p illa ry venous pressure, w hile most o f the patients w ith atyp ical sensations in the chest h ad o n ly slightly o r m oderately elevated pressures.O n the other hand, a num ber o f patients developed m arkedly increased p u l m onary ca p illa ry venous pressure b u t denied any discom fort.A further group , not marked in the figure, h a d neither unpleasant sensations nor m arkedly increased p ulm o n ary ca p illa ry venous pressure.O bservation s in d icatin g im p aired left ven tricu lar function in patients w ith coron ary heart disease, especially d u rin g anginal p ain and w hen exposed to stress h ave been obtain ed b y several groups o f investigators.A b n o rm al in creases in p ulm o n ary ca p illa ry venous pressure on exertion and p articu larly w hen this precipitates anginal pain have been reported b y M a lm b o rg -R oss an d co-w orkers (1962) observed in creased left v e n tr ic u la r en d -d ia sto lic pressure d u rin g sp on tan eou s a n g in a , w h ile B en ch im o l an d D im o n d (1963) re co rd ed , tracin gs in d ica tiv e o f altered left h e a rt fu n ction b y a p e x c a rd io g ra p h y .
Figure 5 Pulm o nary capillary-venous pressures during exer cise in patients who developed anginal pain during the exercise test (A P -f) and who did not (AP-).H eart sizes ^ 500 m l/M 2. See also text.

Figure 6 M
Figure 6M ean values fo r patients w ith m arked increases in pulm onary capillary-venous pressures during exer cise.The tw o groups com prise patients who did (A P + ) and did not (A P -) develop anginal pain dur ing the test.