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Restoration of Regional Wall Motion by Nitroglycerin Therapy in Patients with Left Ventricular Asynergy* Allan D. Sniderman, M.D.;"' Peter Herscooitch, B.Eng.; Derek Marpole, M.D.;t and Ernest L. Fallen, M . D S Abnormalities in regional wall motion are not uniformly improved following aortocoronary bypass operation. This study demonstrates that regional wan motion abnormalities may be reversed with nitroglycerin therapy. Eighteen asynergic regions in seven patients with coronary artery &ease were studied before and after sublingually administered nitroglycerin. Although none of the normal areas became abnormal after nitroglycerin therapy, there were marked changes in the asynergic regions. Of the seven hypokinetic areas, three became normal. Of the 11 dyskinelic areas, 4 showed a normal reduction in area after nitroglycerin treatment. The stndy illustrates that because ereas of regional dysfunction may not exist as fixed lesions, their recoverability can be realized by changing the loading conditions of the ventricle. Identification of such potentially viable areas of asynergy may prove helpful in the selection of cases for aortocoronary bypasa o p eration. ortocoronary bypass operation has a variable e£€ect on the function of the left ventric1e,l4 This may be due, in part, to inability to predict the behavior of regional wall abnormalities following revascularization. Areas of asynergy may have pronounced influence on left ventricular fun~tion,4.~ and yet traditional hemodynamic techniques measure the integrated response of the left ventricle as though all segments made a uniform contribution to total function. Previous investigations show that abnormal wall motion occurs in zones supplied by those arteries with critical stenosi~.~,' It is pertinent therefore to inquire whether these regional areas of malfunction are due to irreversibly damaged tissue or to viable but ischemic myocardial fibers, which under different loading conditions may be recruited in the contractile process. A demonstration that an asynergic segment supplied by an obstructed artery may be recoverable would help in case selection for bypass operation. This study examines the question by quantitating regional wall motion before and after the administration of nitroglycerin (NTG) in patients with coronary artery disease. years. Selective coronary arteriograms revealed occlusive disease in all cases. Each patient received premeditation of 10 mg of diazepam orally. Through the right antecubital vein, a 7 F Goodale-Lubin or Zucker bipolar pacing catheter was directed into the coronary sinus and advanced to the obtuse margin of the left ventricle. In this position, the catheter outlined the msterior arc of the atrioventricular groove. By continuous monitoring of phasic undamped coronary sinus pressure, care was taken to avoid wedging of the catheter. A transfernoral approach was used to pass a 100-cm multiple-hole catheter retrograde across the aortic valve and position it in the midleft ventricular cavity. After recording the heart rate and left ventricular pressures, a resting left ventricular angiogram was performed at 30' right anterior oblique, using 45 to 60 ml of meglumine diatrizoate (Renograb 76 percent) over 4 sec at 80 frames per sec. At least 15 min were allowed to elapse before the left ventricular enddiastolic pressure ( LVEDP ) either returned to levels before angiogram was performed or stabilized for another 5 min. At this juncture, 0.6 mg of nitroglycerin was administered sublingually. Five minutes following complete absorption of the pill (the time at which maximum decrease in left ventricular volume occurs)f+lo the heart rate and pressure were once again recorded, and a left ventricular an&ogram repeated in a manner identical to that previously described. A Data Reduction and Analysh The method for quantifying regional contraction patterns has been detailed in a previous report.6 The ventriculographic images selected for analysis were among the first four sinusconducted beats following contrast injection. No postextraSeven patients undergoing diagnostic cardiac cathetersystolic beats were analyzed. The left ventricle was visualization for anterior chest pain were selected for this study on ized as a truncated ellipsoid of revolution subtended by the the basis of their abnormal ventriculograms. They included atrioventricular ring, which in turn (outlined by the coronary six men and one woman and ranged in age from 46 to 60 sinus catheter) served as an intracardiac plane of reference. The enddiastolic and end-systolic silhouettes were aligned 'From McCill University Clinic, Division of Cardiology, and the junction of the aortic and mitral valves superimposed. Royal Victoria Hospital, Montreal, Canada The longitudinal axis, which was drawn only for end-diastole '*Assistant Professor. ExDerimental Medicine: Fellow. Canadian Heart ~ssociatio;. from apex to midpoint of the aortic valve, was quadrisected ?Assistant Professor, Medicine. by six transverse chords, producing eight regional areas each *Associate Professor, Experimental Medicine. (Fig 1 ) at end-diastole ( D ) and end-systole (S). Each M ~ ~ received ~ ~ january ~ , 15;+revision ~ ~accepted 8, Reprint requests; Dr. Sniderman,~~~~l victoria ~ ~ ~ ~ 687 i t a l , regional area was integrated by an electronic planimeter in Pine Avenue West, Montreal, Quebec, Canada which output was plotted by a PDP 11/20 computer as the CHEST, 66: 5, NOVEMBER, 1974 RESTORATION OF REGIONAL WALL MOTION 545 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20958/ on 05/03/2017 Table M f f e c t of Nitro#lycerin on Regional Areor Before NTG 38 38 - Hypohetic 7 3 2 2 Dyakinetic 11 4 3 4 Normal FIGURE1. Left-hand &tion shows end-diastolic ventricular silhouette divided into eight regions, as described in text. Right-hand section shows end-systolic silhouette, divided into ameqnmding areas, werlaid on enddiastolic outline. After NTG Normal Hypokinetic Dyakinetic Regional Dynamics Of the 56 regions examined, 38 had a normal systolic decrease in area prior to treatment with nitroglycerin (Table 2); that is, the fractional change in systolic dimensions was greater than 20 percent. None of these areas became abnormal following use of the nitrate. Of the seven hypokinetic areas, three contracted normally after NTG, two remained hypokinetic, and two became frankly dyskinetic. Of the 11 dyskinetic areas, 4 showed a normal reduction in area after therapy with the drug, 3 became hypokinetic, and 4 were unchanged. Therefore, 3 of 7 hypokinetic areas and 7 of 11 W o x i c segments improved in their contraction pattern with administration of nitroglycerin. Eight of 18 abnormal segments either did not change or worsened with nitroglycerin treatment. Figure 2 (A, B ) illustrates one example of the effect of nitroglycerin therapy on regional wall motion in a patient with dyskinesis of the posterior wall. This does not represent the most dramatic amelioration of ventricular asynergy in the study, but it does demonstrate the reversibility of systolic expansion of a ventricular segment with use of nitroglycerin. The m i d valve prolapse indicated by the shaded area in Figure 2A was completely corrected in association with improvement in posterior wall motion. fractional change for each area during systole. A total of 56 regional areas in seven patients were analyzed before and after administration of nitroglycerin. Two types of abnormalities were distinguished. Dyskinesis was dehed as "a net systolic expausion of a regional area" and hypokinesis as "less than a Wpercent reduction of a regional area during systole." A comparison was then made of identical regions before and after treatment with nitroglycerin. Left ventricular volumes were calculated by the area-length method of Dodge et 4 1 1 and ejection fraction was derived from the ratio of angiographic stroke volume to end-diastolic volume. The effect of nitroglycerin therapy on hemodynamics is presented in Table 1. At the time that measurements were made, that is, 5 min following administration of nitroglycerin, there was a slight, insignificant increase in the average heart rate (77 to 82lmin) and a small, insignificant decrease in the average left ventricular peak systolic pressure (142135 mm Hg ). The mean resting LVEDP and ejection fractions were also unchanged. There was, however, a significant reduction in the end-diastolic volume, from 101 to 81 ml Ma( p < .01). A change in loading conditions was therefore produced with the nitrate, and since no appreciable effect in heart rate, peak systolic pressure, or ejection fraction was noted, the reduction in volume was presumably mediated by a preload mechanism. This study shows that the contraction pattern of asynergic wall segments was m&ed by altering Table 1--Effect of Nitroglycerin on E d Patient, NO. LVSP* Hg) Heart Rate LVEDP** (= Hg) (= CO NTGl C *Peak left ventricular systolic preeeure. **Left ventriculsr end-diaatolic pmmm. tEnd-dhtolic volume. NTG C NTG EDVt (ml/ms) C NTG EFtt C NTG ttEjection fraction. §Control &ate. INitroglyceriu. 546 SNIDERMAN ET A 1 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20958/ on 05/03/2017 CHEST, 66: 5, NOVEMBER, 1974 coronary sim/ PRE NITROGLYCERIN POST NITROGLYCERIN FIGURE 2A ( Before nitroglycerin therapy). Superimposed enddiastolic and end-systolic ventricular silhouettes. Dyskinesis of inferior wall is evident, and stippled area represents prolapsed cusp of posterior mitral valve. FIGURE 2B (After nitroglycerin therapy). Prolapse of mitral cusp is no longer present, and inferior wall no longer expands paradoxically. the loading conditions of the ventricle. Distinct worsening of wall motion has been demonstrated following interventions such as atrial pacing and intravenously administered pr~pranolol.'~"In both cases, the mechanism was said to be due to an imbalance of the myocardial oxygen demand-tosupply ratio, which immobilized potentially viable ischemic tissue. In our investigation, most of the abnormal regions were improved with treatment with nitroglycerin, suggesting that an abnormal segment may be recoverable with a more favorable energy balance. This could imply that such an abnormal but potentially viable area may respond to the introduction of new blood supply by revascularization. There are a variety of mechanisms by which nitroglycerin or a reduction in ventricular volume could affect regional wall motion. First, restoration of a normal contraction pattern in an asynergic area may occur by virtue of a reduction in wall tension. According to Laplace's law, a decrease in ventricular volume without a corresponding change in intracavity pressure would decrease wall tension or wall stress, assuming no significant change in mural thickness. Such a decrease in tension on ischemic but viable muscle fibers would allow a greater capacity for fiber shortening. Second, nitroglycerin therapy may improve the contraction pattern of ischemic tissue by enhancing collateral blood supply with redistribution of blood flow through asynergic but viable zones of muscle.15 If this mechanism were operative, then improvement in contractile function and cardiac performance by revascularization would be all the more likely. Finally, improvement in contraction could occur because of the reflex catecholamine release, which may follow nitroglycerin administration.16 Thare is evidence, albeit sparse, to suggest that catechols can reverse segmental wall abn~rmalities.~ In our series, 44 percent of the abnormal segments either remained the same or became frankly paradoxic following volume reduction with administration of nitroglycerin. One explanation for this occurrence is that a thin akinetic scar, although not possessing contractile properties, does have certain compliance characteristics. When studied experimentally, ischemic wall segments show significantly reduced compliance. After reduction of the total endocardial surface area of the ventricle, a shift in the passive length tension curve of the segment may take place, so that systolic expansion of a segment could appear during early force development. Another possible explanation for worsening of segmental kinetics is that nitroglycerin could influence the distribution of coronary flow in such a way that the ischemic one would be sacrificed in favor of perischemic and other contractile zones (the socalled coronary steal effect)." Such an imbalance could result in more dyskinesis of the noncontractible segment. The cases in which no change in segmental motion occurred may indicate either a balance of opposing mechanisms or no discernible effect of the bg. We d e h e d hypokinesis as less than a U)-percent reduction in a regional systolic area. This is based on studies on normal rentriculograms in our laboratory, where there was greater than a 30-percent reduction in all regional areas in each of 12 patients. We presumed that single-plane angiograms were capable of tracking an abnormal segment through systole. Although several recent studies argue for biplane angiography to detect otherwise hidden areas of abnonnal m~tion,'~.lOit is generally held that those aneurysms, which are already identified in the RAO projection, show little or no rotational movement from the single-planeview.20 \ CHEST, 66: 5, NOVEMBER, 1974 RESTORATION OF REGIONAL WALL MOTION 547 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20958/ on 05/03/2017 Since the initial observation,2l data have already been presented which support the theory that if treatment with nitroglycerin improves the motion and function of regional areas of ischemia, then bypass of vessels supplying those ischemic zones results in some restoration of contractile function.22 Our study also suggests that noncontractile ischemic segments are potentially recoverable under different loading states, but in addition it demonstrates that there was an appreciable number of those segments which remained unchanged or worsened in association with nitroglycerin therapy. The identification of the contraction patterns in regional zones of ischemia and the mechanisms underlying their behavior in response to a change in loading state are important fields for further investigation. 1 Bourassa MG, L'Esperance J, Campeau L, et al: Fate of left ventricular contraction following aorto-coronary venous grafts: Early and late post-operative modifications. Circulation 46:724-730, 1972 2 Chatterjee K, Swan HJC, Parmley WW, et al: Influence of direct myocardial revascularisation on left ventricular asynergy and function in patients with coronary heart disease. Circulation 47:276-286, 1973 3 Rees G, Bristow JD, Kremkau EL, et al: Influence of aorto-coronary bypass surgery on left ventricular performance. N Engl J Med 284:1116-1121, 1971 4 Herman MV, Heinle RA, Klein MD, et al: Localized disorders in myocardial contraction: Asynergy and its role in congestive heart failure. N Engl J ~ed277:222-232, 1967 5 Baxley WA, Jones WD, Doslye HT: Left ventricular anatomical and functional abnormalities in chronic postinfarction heart failure. AM Intern Med 74:499-508, 1971 6 Sniderman AD, Marpole D, Fallen EL: Regional contraction patterns in the normal and ischemic left ventricle in man. Am J Cardiol31:484-489, 1973 7 Gorlin R, Klein MD, Sullivan JM: Prospective correlative study of ventricular aneurysm with special reference to mechanistic concept and clinical recognition. Am J Med 42:512-531, 1967 8 Lee SJK, Sung YK, Zaragosa AJ: Effects of nitroglycerin on left ventricular volumes and wall tension in patients with ischemic heart disease. Br Heart J 32:790-794, 1970 9 Williams Jr JF, Glick G, Braunwald E: Studies on cardiac dimensions in intact unanesthetized man. V. Effects of nitroglycerin. Circulation 32:767-771,1965 10 Burggraf GW, Parker JO: Left ventricular volume changes after arnyl nitrite and nitroglycerin in man as measured by ultrasound. Circulation 49: 136-143, 1974 11 Dodge HT, Sandler H, Bullew DW, et al: The use of biplane angiocardiography for measurement of left ventricular volume in man. Am Heart J 60:762-778, 1960 12 Pasternak A, Gorlin R, Sonnenblick EH, et al: Abnormalities of ventricular motion induced by atrial pacing in coronary artery disease. Circulation 45 :1195-1205, 1972 13 Dwyer EM: Left ventricular pressure-volume alterations and regional disorders of contraction during myocardial ischemia induced by atrial pacing. Circulation 42: 11111122,1970 14 Herman MV, Gorlin R: Implications of left ventricular asynergy. Am J Cardiol23:538-547,1969 15 Fam WM, McCregor M: Effects of coronary vasodilator drugs in areas of chronic myocardial ischemia. Circ Res 15:355-362, 1964 16 Mason DT, Zelis R, Amsterdam EA: Actions of the nitrites on the peripheral circulation and myocardial oxygen consumption: Significance in the relief of angina. Chest 59:296-305, 1971 17 Rowe GG: Inequalities of myocardial perfusion in coronary artery disease ("coronary steal"). Circulation 42: 193-194, 1970 18 Field BJ, Russel RO, Dawling JT, et al: Regional left ventricular performance in the year following myocardial infarction. Circulation 46:679689, 1972 19 McDonald IG: The shape and movements of the human left ventricle during systole. Am J Cardiol 26:221-230, 1970 20 Harrison DC, Goldblatt A, Braunwald E: Studies on cardiac dimensions in intact unanaesthetised man: Description of techniques and their validation. Circ Res 13:448-455, 1963 21 Sniderman AD, Marpole DGF, Palmer WH, et al: Observations on reversible left ventricular asynergy. Circulation (Suppl2) 44:869, 1971 22 Pine R, Meister SG, Banka VS: Detection of reversible ventricular contraction abnormalities with nitroglycerin: Correlation with post-coronary bypass ventriculography. Circulation ( Suppl4) 48: 104, 1973 CHEST, 66: 5, NOVEMBER, 1974 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20958/ on 05/03/2017