Use of atrial pacing and exercise in studying ventricular function during angina

Autor: David F. Cross
Rok vydání: 1970
Předmět:
Zdroj: The American journal of cardiology. 26(2)
ISSN: 0002-9149
Popis: Until recently, little was known about the hemodynamic and physiologic rvents associated with angina.’ Investigations were limited to angina occurring spontaneously or provoked by drugs or exertion until Sowton et al.2 demonstrated that angina can be easily and repeatably produced in most susceptible patients by atria1 pacing at increasing rates. This method is partirularly advantageous since inrreasing the rntc in the range of 60 to 150 beats/min causes no change in the cardiac output. With pacing the investigator is afforded greater control over events than in exercise-or drug-induced angina. Pain can be produced and trrminuted rapidly by manipulating the cardiac rate. On the other hand, rxrrcise and drugs alter physiologic conditions so that assurance of a return after angina to the preexisting status is not possible for a lengthy period, even if hemodynnmic values return to normal. In an article elsewhere in this Journal, Khaja et al.” report their investigations of the hemodynamic changes associated with angina produced by both exercise and atria1 pacing. Their findings may bc compared with similar work by others.415 These investigators believe that exercise is a “superior” stress test , and if the object of study is the hemodynamic effect of stress rather than angina, no doubt this is true. During escrcisc, the cardiac output increases many times. The hcmodynamic and, particularly, geometric changes inducrd by txcrcise cause uncontrollable, diverse and not rntirely mrnsur:ible changes questionably related to angina. Reflex and humerally mediated alterations in myocardial contractility, coronary flow, venous return and peripheral rcsistnncr occur independent of the occurrence of angina. How products of striated muscle metabolism and increasing osygcn delit affcrt the myorardium is poorly understood. In a prrvious study Parkrr et al.” concluded that angina produced by atria1 pacing is preferable to that produced by exercise in the study of mgocnrdial metabolism. They noted tt1nt “:~bsrnrc~ of important hemodynamic and metabolic effects of csrrcist provides a stable arterial lactate concentration during angina.” Psychic factors play a profomld role in experiments relying on the subject to announce his own endpoint. In exercise-induced angina the patient is asked to bring on his own pain. This demands remarkably objective and stoic subjects. Angina produced by atria1 pacing to some extent frees the experiment of this psychic component brcause the patient is at rest and does not know when angina will commence. Angina releases caterholamines, and it is surprising if this does not occur in a patient actively striving to bring on his own angina. Sowton et al. have shown that there is a threshold defined by the tension-time index which is constant for most patients in angina produced by atria1 pacing. Parker’s patients appear to show this same threshold when exercire and atria1 pacing are compared. This observation is at variance with the findings of others4,” and is surprising since the geometry of the left ventricle must be quite different using these 2 methods. With greater flow the Laplace relation suggests that wall tension and, hence, myocardial oxygen consumption should be greater in exercise. Using electrocardiograph-triggered chest films during pacing is a crude means of assessing volume changes during angina.2 More refined methods of measuring ventricular volume changes are a logical next step since end-diastolic pressure, systolic pressure and stroke vohtme provide only indirect information concerning the ventricular end-diastolic volume, wall tension and the extent and rate of shortening of the myocardial fibers.7 It is evident that severe inadequacies are inherent in the analysis of angina using exercise and, to a significantly lesser extent, with atria1 pacing. The observations of Khaja et al. represent a superb use of present catheterization techniques and must represent the near limit imposed by the “present state 1,:’ the art.” Their conclusion that “when ischemic sympton :ire induced by either exercise or pacing they are associat ! 1. with depression of left ventricular performance” is remir;.92ent of recent work along similar lines on left ventricular hgpertrophy. Ventricular hypertrophy alone has been shown to be associated with depressed contractility even when the other measures of performance are normal or even increased.8 The riddle that, remains to be answered is how are depressed contractility and angina related now that we know they are associated. From the Department of Medicine, Rutland Hospital, Rutland, Vt. Address for reprints: David F. Cross, MD, 23 Washington St., Rutland, Vt 05701.
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