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Cardiac Function and Myocardial Contractility: a Perspective 52 J AM CaLL CARDIOL 1983;1:52-62 Cardiac Function and Myocardial Contractility: A Perspective JOHN ROSS, Jr., MD, FACC La Jolla, California Improved understanding of cardiac muscle and whole studying chronic cardiac adaptations. The clinical im• heart function has substantially benefited clinical diag• portance of systolicloading conditions and venous return nosis and therapy. Knowledge of the influence of systolic is illustrated within these frameworks by a description loading conditions has been of key importance in these of responses to a vasopressor stress test to produce an advances, and the role of peripheral circulatory re• apparent descending limb of left ventricular function, sponses is beginning to be appreciated. Dissociations be• the concept of steady state afterload mismatch in chronic tween myocardial contractility and cardiac function are and acute heart failure and the responses to vasodilator described, including acute heart failure due to afterload therapy in the normal and failing heart. The importance mismatch associated with normal myocardial contrac• of changes in venous return in determining the cardiac tility, and normal ventricular function associated with output response to a vasodilator, in addition to the effects depressed contractility in chronic mitral regurgitation. of reduced afterload on the ventricles, is emphasized. Frameworks for assessing cardiac and myocardial func• Finally, the problem of assessingleft ventricular function tion are examined. Standard invasive and noninvasive in patients with chronic mitral regurgitation is examined approaches can now be usefully supplemented by end• and, for the patient with severe mitral regurgitation and systolic pressure-volume and end-systolic wall stress-vol• few symptoms, tentative guidelines for recommending ume frameworks, the former being particularly useful operation to avoid irreversible left ventricular dysfunc• for analyzing the concept of "afterload mismatch with tion postoperatively are presented. limited preload reserve" and the latter being useful for Increased knowledge concerning the function of cardiac instances, favorable loading conditions or compensatory muscle and the whole heart has greatly enhanced our ability events can mask the presence of depressed myocardial con• to detect and quantify clinical disorders of myocardial con• tractility. In addition, impaired cardiac filling can produce traction. Perhaps most important has been improved un• changes in overall cardiac performance without impaired derstanding of the effects of normal and abnormal loading myocardial contraction. Thus, cardiac pump function and conditions, in particular the critical role of systolic loading myocardial contractility can be dissociated (I). Severe re• or afterload. The effects of preload and instantaneous myo• gional disorders may also exist in association with normal cardial fiber length and various abnormalities of cardiac overall cardiac function, but these are beyond the scope of filling also have become better appreciated. The result has this discussion. been both improved diagnostic ability and more logical ther• apy, based on knowledge of myocardial contractility and associated loading conditions. Such improvements are ev• Dissociations Between Myocardial and ident, for example, in the use of different types of vaso• Pump Function dilators or positive inotropic agents in heart failure, and the more accurate selection of patients with valvular heart dis• Heart Failure Without Myocardial Depression ease for operative treatment. Mechanicaloverload. The level of inotropic state (con• Under certain circumstances altered cardiac loading con• tractility) of the myocardium obviously affects the behavior ditions can produce failure of the heart as a pump. even of the heart, but cardiac performance (as distinguished from though myocardial contractility is not depressed. In other myocardial contractility) is also influenced by the interplay between preload and afterload. For example, sudden aortic From the Division of Cardiology. Department of Medicine. University or mitral regurgitation can rapidly lead to left ventricular of California. San Diego. School of Medicine. La Jolla. California. pump failure without significant myocardial depression; this Address for reprints: John Ross, Jr., MD. Division of Cardiology, Department of Medicine. M-013, University of California. San Diego, situation can be described within a framework of "afterload School of Medicine, La Jolla. California 92093. mismatch with limited preload reserve" (2). Thus when the © 1983 by the American College of Cardiology 0735-1097/83/010052-11$03.00 CARDIAC FUNCTION AND MYOCARDIAL CONTRACTILITY J AM COLL CARDIOL 53 1983;1:52-62 heart is pushed to the limit of its preload reserve, even in the presence of normal systolic contractile function of normal myocardium responds to a further increase in after• the myocardium (15). Several other conditions (mitral ste• load by reduced wall shortening and stroke volume (3,4). nosis, for example) can also produce signs of overall heart Under these conditions, as discussed in more detail later, failure despite normal left ventricular function. the situation resembles that in the normal heart when the preload is held constant and the afterload is varied (3). The Myocardial Depression Without Heart Failure stroke volume becomes inversely related to the afterload Favorable loading conditions masking depressed and systolic wall stress increases, leading to decreased per• myocardial contractility. The reverse of "afterload mis• formance and vice versa. Increased loading can then lead match" can occur when the preload is adequate but the to an apparent .. descending limb" of ventricular function afterload (or wall stress) on the myocardial fibers is abnor• due to excessive afterload rather than to sarcomere over• mally low. In chronic mitral regurgitation, the low imped• stretch (2,4). ance leak into the left atrium may permit a normal ejection Conditions of severe mechanical overload can, of course, fraction to be maintained until late in the clinical course be altered by acute changes in the inotropic state due to when irreversible depression of myocardial function has administration of positive inotropic agents. Also, in heart occurred (16). Favorable loading conditions, therefore, can failure due to acute afterload mismatch (as in acute valve mask depressed myocardial contractility that, under normal regurgitation), reduction of the overload by vasodilator ther• loading conditions, would produce a low ejection fraction. apy or replacement of a defective valve with a prosthesis Beneficial systolic loading conditions can also be produced will promptly reverse the pump failure because myocardial by treatment of the failing heart with a vasodilator (17, 18). contractility is basically intact (2). However, it may be However, recent experimental studies indicate that in acute postulated that subendocardial ischemia due to high diastolic heart failure improvement in cardiac output by a vasodilator intracardiac pressures can also contribute to heart failure such as nitroprusside, which has mixed arteriolar and ven• (5). odilator properties, results both from decreased afterload In chronic mechanical overload, such as that due to val• and from increased venous return (19,20), as will be dis• vular heart disease or to a large left to right shunt, slow cussed further. adaptations occur primarily through the development of con• Compensatory mechanisms to maintain normal pump centric or eccentric hypertrophy to prevent overall cardiac function. Normal cardiac pump function can often be main• failure (6,7). During such chronic overload, heart failure tained by compensatory mechanisms in mild forms of myo• generally does not occur until the myocardial inotropic state cardial depression. A slight increase in heart size with a becomes depressed (8). mild encroachment on the preload reserve that is also ac• Impaired cardiac filling. In chronic constrictive peri• companied by some reflex increase in heart rate and sym• carditis and acute cardiac tamponade, decreased forward pathetic stimulation of the myocardium can produce normal cardiac output and elevation of cardiac filling pressures are cardiac output and filling pressures despite modest intrinsic usually associated with normal myocardial function (9). There myocardial dysfunction. Under these conditions, it may be is also experimental evidence that in acute volume overload, possible to demonstrate limitations of the preload reserve such as that caused by overtransfusion, elevated cardiac by stressing the heart, perhaps by increasing blood pressure filling pressures and impaired filling of the heart are partly with a vasoconstrictor agent (2,21). Even patients with se• a result of limited pericardial expansion, and are accom• verely impaired myocardial function and low ejection frac• panied by elevation of the intrapericardial pressure with an tion can exhibit surprisingly good exercise capability (22), apparent depression of the ventricular function curve (10• partly because the dilated heart has the ability to produce a 12). Such a response can cause the entire diastolic pres• substantial stroke volume (23). sure-volume relation of the left ventricle to shift upward (11,12) as a result of increased intrapericardial pressure; this shift can be corrected by bleeding or the use of a vasodilator such as nitroprusside (II). Such responses may playa role Useful Frameworks for Assessing in acute downward shifts
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