Significance of reduced regional myocardial blood flow in asynergic areas evaluated with intervention ventriculography

Significance of Reduced Regional Myocardial Blood Flow in Asynergic Areas Evaluated With Intervention Ventriculography Results of Studies Combining Washout of Xenon-133 and Postextrasystolic Potentiation

JACKIE R. SEE, MD PETER F. COHN, MD, FACC B. LEONARD HOLMAN, ME), FACC* DOUGLASS F. ADAMS, MD DENIS E. MADDOX, MD

Boston, Massachusetts

From the Departmentsof Medicine and Radiology, Peter Bent Brigham Hospital and Harvard Medical School, Boston, Massachusetts. Manuscript received August 30, 1978, accepted September 6, 1978. This study was supported by Grants HL7049, GM-18674 and HL-20895 from the U. S. Public Health Service, Bethesda, Maryland. * Established Investigator, American Heart Association, Dallas, Texas. Address for reprints: Peter F. Cohn, MD, Cardiovascular Division, Peter Bent Brigham Hospital, 721 Huntington Avenue, Boston, Massachusetts 02115.

Nineteen patients with coronary artery disease were studied to determine the significance of reduced regional myocardial blood flow (50 ml/min per 100 g or less) in areas of abnormal wall motion. Regional myocardial blood flow was measured in four regions of the left ventricle with an Anger camera after the injection of xenon-133 into the left main coronary artery. Abnormal wall motion was evaluated with biplane left ventriculography at rest and during postextrasystolic potentiation, a potent inotropic stimulus. Abnormal wall motion was defined as hemiaxis shortening of less than 20 percent. Four hemiaxes were designated as corresponding to the four regions of myocardial blood flow. Of 76 hemiaxes evaluated in the 19 patients, 54 manifested normal wall motion and 22 abnormal wall motion; 8 of the 22 hemiaxes had reduced regional myocardial blood flow. In these 8, hemiaxis shortening increased 6 4- 2 percent (mean 4- standard error of the mean) above values at rest during postextrasystolic potentiation (with normalization of hemiaxis shortening in only 1 of the 8), compared with an increase of 19:1- 4 percent (P <0.001) in the 12 hemiaxes with borderline regional myocardial blood flow (with normalization of hemiaxis shortening in 9 of the 12, P <0.05). These results indicate that the presence of reduced regional myocardial blood flow in areas of abnormal wall motion usually predicts a poor response to postextrasystolic potenUaUon, whereas~abnormal .wall motion without reduced regional myocardial blood flow usually predicts a good response. The combination of reduced regional myocardial blood flow and abnormal wall motion suggests scarred and nonviable myocardium.

In patients with coronary artery disease, a reduction in regional myocardial blood flow in regions of left ventricuiar asynergy has been demonstrated using the xenon-133 techniqueJ -3 The reduction in myocardial perfusion in these regions can be attributed either to a "primary" reduction in flow caused by the ischemic effects of the coronary arterial stenosis or to a "secondary" reduction in flow caused by the decreased myocardial oxygen requirements of fibrotic scar tissue, or to both. To clarify further the basis for the reduced flow, we combined myocardial flow determinations with a proved technique for assessing contractile reserve in asynergic areas of myocardium: two state, or intervention, ventriculography using postextrasystolic potentiation. Although there is considerable overlap in values for myocardial blood flow in patients with and without coronary artery disease(attributable in part to variability in myocardial oxygen requirements at the time of study), Klocke,4 using a helium desaturation technique, suggested that m e a n leftventricular perfusion rates of less than 50 ml/min per 100 g are probably abnormal and values greater than 70 ml/min per 100 g are probably normal, whereas intermediate values of 50 to 70 ml/min per 100 g are of February 1979 The AmericanJournalof CARDIOLOGY Volume43

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REDUCED MYOCARDIAL BLOOD FLOW--SEE ET AL.

1

:2

3

: ::

4

XENON ,3:~ DISTRIBUTION IMAGE

1/ \

~3

R2

RAO L V G R A M

LAO L V G R A M

FIGURE 1. Regional mYocardial blood flow related to left ventricuiar wall motion. Four quadrants are depicted in the xenon-133 distribution image indicating regions subserved by the left anterior descending coronary artery (1 and 3) and the left circumflex artery (2 and 4). Quadrants 1 and 3 are designated as corresponding to hemia~xesR1 and R3 in the right anterior oblique ventriculogram (RAO LV GRAM), and quadrants 2 and 4 are designated as corresponding to hemiaxes R2 and R4 in the the left anterior oblique ventriculogram (LAO LV GRAM) (see text). The outer ventriculographic silhouettes represent end-diastole, the inner silhouettes end-systole.

uncertain significance. On the basis of our own experience with more than 100 patients studied from 1972 to 1977, these values also appear to be valid guidelines for regional m y o c a r d i a l flow determinations with the xenon-133 technique and were used in the present study. Material and Methods Patient Selection

The study group consisted of 19 patients with anglographically documented coronary artery disease--at least 50 percent stenosis of the proximal portion of one of the three major coronary arterial systems, as observed in our previous blood flow-angiographic study. 2 The mean age of the group was 45 years (range 35 to 61), and 18 were men. These patients were not selected in any systematic fashion except that all were in clinically stable condition and those with concomitant valvular, congenital or cardiomyopathic heart disease were excluded. All gave informed consent for the cardiac catheterization procedures to be described. C a r d i a c C a t h e t e r i z a t i o n Procedures

Each patient was in the fasting state and was premedicated with 50 mg of diphenhydramine and 10 mg of diazepam given orally. Standard right and left heart catheterization was performed, followed by biplane left cineventriculography, then selective coronary angiography and, finally, regional myocardial blood flow measurements with xenon-133. Left ventriculography: With the techniques described in detail in previous work from our laboratory, 5 simultaneous left cineventriculograms were obtained in both the right anterior oblique (60°) and left anterior oblique (30°) projections. The induction of ventricular premature beats during these studies will be described in the following section. Axis shortening at end-diastole and end-systole was determined from hand-drawn ventriculographic silhouettes (end-diastole being 180

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the largest silhouette, end-systole the smallest). The method of Leighton et al. 6 was used to superimpose silhouettes, and the long axis in each view was trisected (Fig. 1). In the right anterior oblique projection, hemiaxes R1 and R3 were designated as representing, respectively, proximal and distal regions of the left anterior descending coronary artery, and hemiaxes.R2 and Ra in the left anterior oblique projection were designated as representing, respectively, proximal and distal regions of the left circumflex coronary artery. These designations are discussed further in the subsequent section on myocardial blood flow techniques. Percent hemiaxis shortening was determined in the beat preceding and following the ventricular premature beat, using the formula: hemiaxis shortening equals end-diastolic length minus end-systolic length divided by end-diastolic length X 100 percent. As in our previous study, 2 less than 20 percent shortening in these transverse hemiaxes was considered abnormal. Postextrasystolic potentiation: The techniques used to induce ventricular premature beats in our laboratory during left cineventriculography were previously described in detail; 7 Briefly, in 11 patients, the ventricular premature beat was induced using a bipolar pacing catheter positioned in the right ventricle and attached to an R wave coupled stimulator. The R-stimulus interval averaged 400 msec with a range of 320 to 460 msec as measured with simultaneous electrocardiographic recordings. When the stimulator was not available, ventricular premature beats were obtained by pullback of a catheter from the pulmonary artery to the right ventricle, or by a power injection of angiographic contrast medium into the left ventricle during left ventriculography. These latter ventricular premature beats were used in this study if they satisfied the same criteria 7,s used for the electrically induced beats, that is, single ventricular premature beats occurring within 320 to 460 msec of the R wave of the preceding sinus beat. No difference in response to ventricular premature beats induced by any of these techniques has been noted if these criteria are adhered to. In addition, previous studies from our hospital demonstrated no significant differences in postextrasystolic potentiation (when measured using the ejection fraction) when coupling intervals within this range were compared in the same patients. 9 Coronary arteriography: Selective coronary angiograms were performed using the femoral approach in all patients and interpreted by a consensus of three of us. At least 10 minutes was allowed to elapse between the last injection of contrast medium for diagnostic coronary angiography and the selective intracoronary injection of xenon- 133.

Measurement of regional myocardial specific blood flow: This method has also been described in detail previouslyJ, 3J°,u To summarize, patients were placed in the left anterior oblique position under the fluoroscopy unit, and the center and borders of the heart were marked on the chest wall. A catheter was placed in the left main coronary artery and its position confirmed by injection of 0.25 ml of contrast material. After the catheter was cleared with I ml of saline solution, the table with the patient on it was moved under an Anger scintillation camera (Nuclear Chicago Pho Gamma HP). Injection of 20 to 25 mCi of xenon-133 in 2 ml of saline solution was followed by a 3 ml saline flush. The catheter was then removed from the coronary artery. Washout was monitored with the scintillation camera for 1 minute after the injection of xenon-133. Data were acquired and processed on a PDP 11/20 digital computer. Regional washout curves were obtained by placing electronic cursors over the proximal and distal portions of the left anterior descending and left circumflex coronary arteries (four quadrants). The position of these vessels was determined from the initial frames of the gamma camera image during the arterial phase of the study (Fig. 1). v^, . . . . Je

REDUCED M Y O C A R D I A L BLOOD F L O W - - S E E ET AL.

Regional washout curves were constructed using 2 second time franies from the peak counting rate (0 time) to 40 seconds afterward. To minimize possible effects of fat or other nonmuscular components of the myocardium on the blood flow calculations, only the slope of the curve representing the first 40 seconds of washout data was computed, using a nonweighted monoexponential computer program, and the standard deviation of the slope was calculated. From the initial slope, an index of specific flow (flow per weight of myocardium expressed as ml/min per 100 g of tissue) was determined using the equation F/W = (100k~)/p, where k is the mean slope calculated from 0 to 40 seconds as defined, },is the blood/tissue partition coefficient (assumed to be 0.72), and p is the specific gravity of myocardial tissue (assumed to be

],5

~

NL HAS wqth PESP ABNL HAS with PESP

p<,05

~ 10

"~

I

5

t.05).

Relating regional myocardial specific blood flow to areas of left ventricular myocardium on the ventriculogram: The left anterior oblique projection is utilized for regional myocardial blood flow determinations because it best separates regions of the left anterior descending and left circumflex coronary arteries (Fig. 1). The left anterior oblique projection was also used for ventriculographic analysis of regions supplied by the left circumflexartery, and we designated posterolateral hemiaxes R2 and R4 as corresponding to proximal and distal left circumflex regional myocardial blood flow quadrants 2 and 4, respectively. However, the left anterior oblique view is not optimal for evaluating asynergy, in the left anterior descending coronary artery. In this view, all or part of the septum may be obscured by "overhanging" anteroapical asynergic segments and, even when well visualized, anterior septal motion may appear normal with complete occlusion of the left anterior descending artery if the large first septal branch is spared, and posterior septai motion may likewise appear normal when this area is supplied by the right coronary artery, whose flow is not evaluated with our regional myocardial blood flow technique. For these reasons, we again'used the right anterior oblique projection for evaluating left anterior descending asynergy (as we did in our initial study relating regional myocardial blood flow to wall motion1) and designated anterior hemiaxes Rt and R3 as corresponding to proximal and distal left anterior descending regional myocardial blood flow quadrants 1 and 3, respectively. Evaluation of the ventricuIograms and coronary arteriograms was performed without prior knowledge of the quadrantal flow measurements, and vice versa. Results

All data concerning age, sex, site of prior myocardial infarction on electrocardiography, coronary arterial anatomy, presence or absence of collateral vessels, hemiaxis shortening and regional myocardial blood flow (both at rest and after postextrasystolic potentiation) are noted in Table I. Eleven patients had evidence of prior transmural infarction. Ten patients had triple vessel coronary disease, five double vessel disease and four single vessel disease. Collateralization to the left coronary system was present in 11 patients. As in our previous studies,7, s augmentation of hemiaxis shortening with postextrasystolic potentiation occurred in most regions (56 of 76); no change was found in 11 regions and a decrease occurred in 9. Relating the presence of anterior wall infarction or collateral vessels (to the left anterior descending system) to the degree of augmentation of proximal and distal left anterior descending hemiaxes induced by postextrasystolic potentiation indicated that the percent shortening with

RMBF

RMBF

~-50,.¢.,/./loo 51-eg,.//,.,dloo~ FIGURE 2. Normalization (NL) of hemiaxial shortening (HAS) in asynergic regions with postextrasystolic potentiation (PESP). Seven of 8 asynergic regions with regional myocardial-specific blood flow (RMBF) of 50 ml/min per 100 g or less did not demonstrate normalization of hemiaxial shortening compared with 3 of 12 regions with blood flow of 51 to 69 ml/min per 100 g (P [probability] <0.05). ABNL = abnormal.

postextrasystolic potentiation in regions without infarction was 12 4- 3 percent (mean 4- standard error of the mean) versus 9 + 6 percent in regions with infarction, and that shortening in regions without collateral vessels was 12 ± 3 percent compared with 15 ~: 6 percent in regions with collateral vessels. However, neither comparison was statistically significant using unpaired t tests. Relation B e t w e e n Regional Myocardial Specific Blood F l o w and W a l l Motion

Table II summarizes the effect of postextrasystolic potentiation on hemiaxis shortening in normal (greater than 20 percent shortening) and asynergic (less than 20 percent shortening) regions in relation to regional myocardial blood flow. The regions with regional myocardial blood flow of 50 ml/min per 100 g or less were considered to have reduced flow, those with regional myocardial blood flow of 51 to 69 ml/min per 100 g to have borderline flow (that is, of uncertain significance) and those with flow of 70 ml/min per 100 g or greater to have normal flow, similar to the values described by Klocke4 for mean left ventricular flow. In the control state, there was no significant difference in hemiaxis shortenin_g between regions with" reduced, borderline or normal regional myocardial blood flow within the subgroups with asynergy or normal wall motion. R e d u c e d f l o w regions: in eight regions with both reduced myocardial blood flow and asynergy, the mean hemiaxis shortening was 7 + 1 percent with normally conducted beats and 13 4- 2 percent with postextrasystolic potentiation (P <0.05)*, but only one of these eight regions h a d greater than 20 percent shortening after postextrasystolic potentiation. In nine regions with reduced flow but normal contraction, the * All statistical comparisons between control beats and those after ventricular extrasystoles were performed using the paired t test.

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TABLE I Clinical, Angiographic and Myocardial Blood Flow Data in 19 Patients Hemiaxis Shortening (%)

RMBF (ml/min per 100 g)

Case no.

Age (yr) & Sex

Prior MI

1

45F

IMI

LAD, LCx, RCA; collateral to LAD

15 22 8 14

23 22 17 14

Proximal LAD Distal LAD Proximal LCx Distal LCx

54 60 44 5O

2

57M

0

LAD, LCx, RCA; collateral to LAD

43 42 23 15

50 60 22 18

Proximal LAD Distal LAD Proximal LCx Distal LCx

43 57 41 61

3

52M

PMI

LAD, LCx, RCA

29 0 25 16

49 14 25 29

Proximal LAD Distal LAD Proximal LCx Distal LCx

66 57 59 57

4

41M

AMI

LAD, LCx; collateral to LCx

21 11 18 21

25 15 45 21

Proximal LAD Distal LAD Proximal LCx Distal LCx

52 92 63 117

5

44M

AMI

LAD, LCx; collateral to LCx

9 33 30 32

47 43 30 32

Proximal LAD Distal LAD Proximal LCx Distal LCx

6O 67 56 60

6

45M

IMI

LAD, LCx, RCA; collateral to LAD, LCx

29 7 46 42

39 22 46 32

Proximal LAD Distal LAD Proximal LCx Distal LCx

84 68 68 64

7

38M

IMI

LAD, LCx, RCA

6 6 5 2

16 16 5 2

Proximal LAD Distal LAD Proximal LCx Distal LCx

4O 41 34 39

8

39M

0

LAD, RCA; collateral to LAD

9 11 25 25

20 14 25 30

Proximal LAD Distal LAD Proximal LCx Distal LCx

68 45 58 58

9

39M

IMI

LAD, LCx, RCA; collateral to LAD

44 28 25 25

53 37 34 33

Proximal LAD Distal LAD Proximal LCx Distal LCx

66 55 54 6O

10

37M

0

LAD

25 36 36 36

34 43 56 58

Proximal LAD Distal LAD Proximal LCx Distal LCx

108 103 120 94

11

47M

AMI

LAD, LCx, RCA; collateral to LAD

15 45 43 36

52 54 45 43

Proximal LAD Distal LAD Proximal LCx Distal LCx

77 71 82 9O

12

61M

IMI

LAD, LCx, RCA

32 42 33 33

39 43 45 27

Proximal LAD Distal LAD Proximal LCx Distal LCx

48 85 42 64

13

50M

AMI

LAD, LCx, RCA; collateral to LAD

65 29 28 70

62 31 17 74

Proximal LAD Distal LAD Proximal LCx Distal LCx

91 90 87 94

14

49M

IMI

LAD, LCx, RCA; collateral to LAD, LCx

36 42

Proximal LAD Distal LAD Proximal LCx Distal LCx

50 59 67 62

CAD

C

PESP

Regions

17

47 34 24 60

15

52M

0

LCx, RCA

35 37 51 30

46 45 60 53

Proximal LAD Distal LAD Proximal LCx Distal LCx

54 56 47 47

16

36M

O

LAD; collateral to LAD

40 42 24 32

64 51 43 40

Proximal LAD Distal LAD Proximal LCx Distal LCx

56 60 58 69

17

35M

0

LAD, RCA

31 60 26 61

37 57 42 53

Proximal LAD Distal LAD Proximal LCx Distal LCx

94 93 102 108

16

182

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TABLE I (continued)

no.

Age (yr) & Sex

Prior MI

CAD

18

53M

0

LAD

19

42M

0

LAD

Case

Hemiaxis Shortening (%) C PESP 7 3 49 25 31 50 20 26

20 27 54 36 56 60 27 26

Regions

RMBF (ml/min per 100 g)

Proximal LAD Distal LAD Proximal LCx Distal LCx Proximal LAD Distal LAD Proximal LCx Distal LCx

30 54 39 54 56 44 57 51

C = control beat; CAD = coronary artery disease; LAD = left anterior descending coronary artery; LCx = left circumflex artery; MI = transmural myocardial infarction on electrocardiography (A = anterior, I = inferior, P = posterior); PESP = during postextrasystolic potentiation; RCA = right coronary artery; RMBE = regional myocardial-specific blood flow.

mean hem±axis shortening was 37 ± 5 percent after a normal beat, and after postextrasystolic potentiation it increased to 45 ~- 4 percent (P <0.05). Borderline flow regions: Among the 12 regions with regional myocardial blood flow of 51 to 69 ml/min per 100 g and asynergy, 9 achieved greater than 20 percent hem±axis shortening with postextrasystolic potentiation. This is in contrast to the one of eight asynergic regions with reduced regional myocardial blood flow noted earlier (P <0.05, chi square testing) (Fig. 2). In these 12 borderline regions, hem±axis shortening after normal beats averaged 12 ± 4 percent and increased to 31 ± 5 percent (P <0.01) after postextrasystolic potentiation. In this subset the augmentation due to postextrasystolic potentiation was significant and was of a greater magnitude than that in the subset of patients with reduced flows and asynergy (6 ± 2 percent versus 19 ± 4 percent, P <0.001; by unpaired t test) (Fig. 3). In the 27 regions with borderline regional myocardial blood flow and normal hem±axis shortening after a normal beat, postextrasystolic potentiation also resulted in a significant increase in hem±axis shortening (33 ± 2 percent to 39 ± 2 percent, P <0.01). Normal flow regions: In the 22 regions with regional myocardial blood flow of 70 ml/min per I00 g or greater, there were only two regions of abnormal hem±axis shortening after normal beats and with postextrasys-

tolic potentiation augmentation, shortening increased from 13 ± 2 percent to 34 + 2 percent (P <0.05). In the 20 regions with normal regional myocardial blood flow and wall motion, hem±axis shortening after normally conducted beats was 39 + 3 percent and increased to 45

25

p %001

©

20

XF,-

5

m RMBF

RMBF

5o,@.,~/1OOgx-69mCm,n/lo@ FIGURE 3. Effect of postextrasystolic potentiation (PESP) on hemiaxis shortening in asynergic regions. Eight asynergic regions with regional myocardial-specific blood flow (RMBF) of 50 ml/min per 100 or less demonstrated significantly less of an increase in hemiaxis shortening compared with 12 asynergic regions with blood flow of 51 to 69 ml/min per 100 g (6 4- 2 percent versus 19 4- 4 percent, P [probability]

<0.001).

TABLE II Effect of Postextrasystolic Potentiation (PESP) on Hemiaxis Shortening in Normal and Asynergic Regions in Relation to Regional Myocardial-Specific Blood Flow (RMBF) RMBF* (ml/min per 100 g)

C

LOW (17) Borderline (39) Normal (20)

7 -4- 1% 12 4- 4% 13 4- 2%

Hemixais Shortening (mean 4- standard error of the mean) Asynergic Regions (22) Normal Regions (54) PESP C (P <0.05) (P <0.01) (P <0.05)

13 4- 2% (8) 31 4- 5% (12) 34 4- 7% (2)

37 4- 5% 33 4- 2% 39 4- 3%

(P <0.05) (P <0.01) (P <0.05)

PESP 45 4- 4 % (9) 39 4- 2 % (27) 45 4- 3% (18)

* Low ~< 50; borderline (uncertain significance) 51-69;,pormal >/70. Numbers in parentheses = number of regions studied. C = sinus beat; P = probability.

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4- 3 percent (P <0.05) after postextrasystolic potentiation. Discussion Inotropic stimulation has proved useful in identifying viable but ischemic myocardium in both animal 12 and human studies.7,13 Areas that do not augment significantly after inotropic stimulation often show fibrosis rather than muscle when examined histologically. 13 Postextrasystolic potentiation is now the preferred inotropic stimulus for identifying viable but poorly perfused myocardium, s Popio et al. 14 and Hamby et al. !5 reported that angiographic and ventriculographic studies performed before and after myocardial revascularization surgery demonstrated excellent correlation between improvement in contractile pattern after postextrasystolic potentiation and after subsequent revascularization. They noted t h a t postextrasystolic potentiation was effective both in regions of hypokinesia and akinesia, including areas of old transmural myocardial infarction. In our study, we used this method of intervention ventriculography to determine if reduced regional myocardial blood flow measurements in regions of asynergy in patients with coronary artery disease reflect myocardial nonviability (that is, fibrous scar). The guidelines for reduced, borderline and normal regional myocardial blood flow that we used are modified from those of Klocke4 for the entire ventricle. Their usefulness appears to be confirmed by our observation that only 2 of 22 regions (9 percent) with abnormal wall motion had normal flow (that is, 70 ml/min per 100 g or greater). Similarly, reduced flow (50 ml/min per 100 g or less) was found in only 9 of the 54 regions (16 percent) with normal wall motion, and Some of these latter instances may simply represent an appropriate response to reduced myocardial oxygen requirements in individual patients. These findings confirm our earlier impression 1,3 that combining ventriculographic analysis with regional myocardial blood flow measurements is helpful in evaluating the significance of the flow data because there are not always clear-cut differences in flow values in some patients with coronary artery disease when only the degree of coronary aterial stenosis is considered. E f f e c t of postextrasystolic potentiation on asynergic regions with reduced or borderline blood flow: Because the postextrasystolic potentiation technique is only of limited clinical value in regions that are already moving normally at rest, we were most interested in comparing the effect of postextrasystolic potentiation on asynergic regions with either low or borderline regional myocardial blood flow. As noted, only two regions with asynergy had normal flow, a number too small for such comparisons. Although ab-

normal hemiaxis shortening increased significantly in regions with both reduced flow and borderline flow after postextrasystolic potentiation (Table II), the absolute increase in hemiaxial shortening (an index of the degree of augmentation with postextrasystolic potentiation) was 6 + 2 percent for reduced flow regions after postextrasystolic potentiation versus 19 + 5 percent for the borderline flow regions (P <0.001) (Fig. 3). Before postextrasystolic potentiation, the difference between the degree of Shortening was not significantly different. In evaluating individual regions, only 1 of 8 regions with both reduced regional myocardial blood flow and abnormal hemiaxis shortening after normal beats achieved normal shortening during postextrasystolic potentiation, compared with 9 of 12 regions with borderline flow and abnormal resting hemiaxial shortening (P <0.05) (Fig. 2). Based on previous histopathologic correlates, 1~ nonresponding regions are mostly viable muscle that is probably only temporarily ischemic as a result of the coronary arterial stenosis alone or in combination with factors related to the cardiac catheterization procedure (such as premedication and contrast agent). In our patients, the presence of either previous anterior wall infarction or the lack of collateralization to the left anterior descending artery appeared to influence adversely augmentation of hemiaxis shortening in left anterior descending regions, but the differences were not statistically significant. Limitations and implications of study: Our results are qualified by the limitations inherent in any clinical study that attempts to relate regional myocardial blood flow to contrast ventriculography: There is no certainty that the regions of interest for flow analysis are the same regions evaluated in the ventriculogram. In addition, the xenon-133 method has its own limitations, especially because the technique may overrepresent high flow areas and underrepresent low flow areas, in addition to not separating subepicardial from subendocardial flow. ~6 Given these qualifications, our results do suggest that the finding of regional myocardial blood flow of 50 ml/min per 100 g or less with the xenon-133 technique in areas of ventricular asynergy is a valid indicator of probably irreversibly damaged myocardium. Furthermore, our conclusion that the combination of reduced regional myocardial perfusion and impaired regional wall motion suggests scar formation is in agreement with the conclusion reached by Zir et al. ~7 in a preliminary report using a different radionuclide technique (intravenously administered thallium-201). These investigators also reported a good correlation between reduced myocardial perfusion (as demonstrated in scintigrams) and irreversibility of asynergy (again demonstrated with postextrasystolic potentiation during contrast ventriculography).

References 1. See JR, Cohn PF, Holman BL, Roberts BH, Adams DE: Angiographic abnormalities associated with alterations in regional myocardial blood flow in coronary artery disease. Br Heart J 38: 1278-1285, 1976 2. Dwyer EM Jr, Dell RB, Cannon PJ: Regional myocardial blood flow

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in patients with residual anterior and inferior transmural infarction. Circulation 48:924-935, 1973 3. Holman BL, Cohn PF, Adams DF, See JR, Roberls BH, Idoine J, Godin R."Regional myocardial blood flow during hyperemia induced by contrast agent in patients with coronary artery disease. Am J

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Cardiol 38:416-421, 1976 4. Klocke FJ: Coronary blood flow in man. Prog Cardiovasc Dis 19:117-137, 1976 5. Cohn PF, Gorlln R, Adams OF, Chahine RA, Vokonas PS, Herman MV: Comparison of biplane and single-plane left ventriculograms in patients with coronary artery disease. Am J Cardiol 33:1-6, 1974 6. Leighton RF, Wilt SM, Lewis RP: Detection of hypokinesis by a quantitative analysis of left ventricular cineangiograms. Circulation .50:121-127, 1974 7. Dyke SH, Cohn PF, Gorlin R, Sonnenblick EH: Detection of residual myocardial function in coronary artery disease using postextrasystolic potentiation. Circulation 50:694-699, 1974 8. Cohn PF, Gorlln R, Herman MV, Sonnenblick EH, Horn HR, Cohn LH, Collins JJ Jr: Relation between contractile reserve and prognosis in patients with coronary artery disease anda depressed ejection fraction. Circulation 5t:414-420, 1975 9. Markis JE, Cohn PF, Roberts BH, Skelton CL, Sonnenblick EH: Effect of varying the coupling interval in postextrasystolic potentiation (abstr). Clin Res 23:567A, 1975 10. Holman BL, Adams DF, Cohn PF, Gorlin R, Adelstein SJ: Measuring regional myocardial blood flow with xenon-133 and the Anger camera. Radiology 112:99-107, 1974 11. Cohn PF, Maddox DE, Holman DL, Markis JE, Adams DF, See JR: Effect of sublingually administered nitroglycerin on regional myocardial blood flow in patients with coronary artery disease. Am

J Cardiol 39:672-678, 1977 12. Dyke SH, Urschel CW, Sonnenblick EH, Gorlin R, Cohn PF: Detection of latent function in acute ischemic myocardium in the dog. Comparison of pharmacologic inotropic stimulation and postextrasystolic potentiation. Circ Res 36:490-497, 1975 13. Horn HR, Teichholz LE, Cohn PF, Herman MV, Gorlln R: Augmentation of left ventricular contraction pattern in coronary artery disease by an inotropic catecholamine. The epinephrine ventriculogram. Circulation 49:1063-1071, 1974 14. Poplo KA, Gorlin R, Bechtel D, Levine JA: Postextrasystolic potentiation as a predictor of potential myocardial viability: preoperative analysis compared with studies after coronary bypass surgery. Am J Cardiol 39:944-953, 1977 15. Hamby RI, Aintablan A, Wisoff BG, Hartstein ML: Response of the left ventricle in coronary artery disease to postextrasystolic potentiation. Circulation 51:428-435, 1975 161 Cannon PJ, Sciacca RR, Fowler DC, Weiss MB, Schmidt DH, Casarella WJ: Measurement of regional myocardial blood flow in man: description and critique of the method using xenon-133 and a scintillation camera. Am J Cardiol 36:783-792, 1975 17. Zir LM, Pohost GM, Gold HK, Leinbach RC, Dinsmore RE: The significance of reversal of left ventricular asynergy by postextrasystolic potentiation. A comparison of left ventriculography and thallium-201 myocardial scans (abstr). Circulation 54:Supp111:11-5, 1976

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