Surgical intervention for preinfarction angina.

Integrated Medical-Surgical Care in Acute Coronary Artery Disease Adv. Cardio!., vo!. 15, pp. 59-69 (Karger, Basel 1975)

Surgical Intervention for Preinfarction Angina 1 E. D. MUNDTH, M. J. BUCKLEY, W. M. DAGGETT, M. T. McENANY, H. K. GOLD, R. C. LEINBACH and W. G. AUSTEN Massachusetts General Hospital, and Departments of Surgery and Medicine, Harvard Medical School, Boston, Mass.

1 Supported in part by MIRU Grant Contract No. 43-67-1443 and Program Project No. USPHS HE-06664. 2 MIRU: Myocardial Infarction Research Units. This study includes the Massachusetts General Hospital, the John Hopkins University Hospital, the University of Alabama Hospital, the University of Chicago Hospital, Cornell Medical Center, Duke University Hospital, University of Rochester Hospital and Stanford Medical Center

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Although 'preinfarction angina' is a term which can be applied accurately only in retrospect, numerous clinical studies have indicated that there is a potentially identifiable intermediate syndrome of unstable angina associated with an increased incidence of subsequent acute myocardial infarction and death [2,15,18,22,25,27,30]. The preinfarction syndrome has been defined in various terms, but the most exacting criteria are those outlined by the ongoing multi-institutional MIRV 2 study and include: (1) anginal pain lasting longer than 30 min within 7 days of the current hospitalization; (2) documented electrocardiographic ST and T wave changes of myocardial ischemia associated with at least one episode of ischemic pain during the period of hospitalization, and (3) no evidence of progression to actual myocardial infarction by electrocardiographic or serum enzyme changes. The incidence of myocardial infarction within 6 months following an episode of preinfarction angina has been reported from various series to be in the range of 10-870/0, associated with a mortality of 10-460/0 (table I) [2, 6, 13, 15, 21, 22, 27, 30, 32]. The considerable variance in the apparent natural history of this syndrome reflects the relative lack of objective criteria for definition of the syndrome [9]. The relatively low

MUNDTH/BuCKLEY/DAGGETT/McENANY/GOLD/LEINBACH/AUSTEN

60

Table I. Preinfarction syndrome: incidence of myocardial infarction (MI) and mortality rate with medical therapy

Author

Number of patients

Average followup

Incidence MI No. Ofo

VAKIL [30] WOOD [32] BEAMISH and STORRIE [2] KRAuss et al. [15] CONTI et at. [6] SCANLON et al. [22, 23] ROBINSON et al. [21] SUSTAITA et al. [26,27] GOODIN et at. [13]

360 150 100 100 15 22 38 15 7

3 mo. 4mo. 6 mo. 12mo. 10mo. Imo. 6mo. Imo. 3mo.

148 33 29 14 1 13 12 13 5

Total

807

(41) (22) (29) (14) (8) (59) (32) (87) (71)

264 (33)

Mortality rate No. Ofo 58 10 13 15 2 6 7 7 3

(16) (7) (13) (15) (13) (27) (18) (46) (43)

121 (15)

incidence of myocardial infarction and death reported by KRAuss et al. [15] may in part be due to the fact that all patients in this study were observed for a 48-hour period after hospitalization. If a myocardial infarction ensued during this time, it was considered as 'an evolving myocardial infarction' and the patient was not included in the category of preinfarction syndrome even though the patient may have had a prodromal crescendo angina pattern prior to hospitalization. The much higher incidence of myocardial infarction and death in the series reported by VAKIL [30], WOOD [32] and BEAMISH and STORRIE [2] (table I) reflects the fact that these were retrospective studies and included some patients whose prodromal unstable angina was not treated intensively in the hospital. One can also expect considerable variance in the results of clinical studies where coronary angiography has not been done. SCANLON et at. [22] reported 15 of 79 (190/0) patients with clinically diagnosed accelerated (preinfarction) angina had normal coronary arteries and a benign subsequent course. The authors concluded that studies that did not include coronary arteriography might provide resultant false-low morbidity and mortality rates. However, this study did not insist on the criterion of documented transient ischemic ST- T wave changes for inclusion in the preinfarction syndrome. Only 31 % of the patients studied had ischemic electrocardiographic changes,


Percentage in brackets.

61

perhaps thus attributing for the number of patients without demonstrable coronary artery disease. The prospective study of unstable (preinfarction) angina by CONTI et al. [6], which included coronary arteriographic confirmation of coronary artery disease, included 15 patients treated medically with bed-rest, shortand long-acting nitrates and p-adrenergic blockade with an incidence of nonfatal myocardial infarction of only 8010 and fatal myocardial infarction of 13 % over a 10-month follow-up period. The results of intensive medical therapy for this group of patients tended to confirm the earlier study of KRAUSS et al. [15] in which the incidence of nonfatal myocardial infarction was 10010 at 6 months and the mortality at the end of 1 year only 15010. However, CONTI et al. [6] found that 47010 of surviving patients treated medically remained symptomatic. ROBINSON et al. [21] and SCANLON et al. [22] similarly have noted persistent intractable angina (47 and 62010, respectively) in patients treated medically. Further evidence as to the severity of disease and prognosis in patients with the preinfarction syndrome is gained from the report of KRAUSS et al. [15] who found a steady increase in morbidity and mortality as a function of time. At an average follow-up time of 20 months after the documented preinfarction syndrome, 36010 of the patients had developed myocardial infarction and 22010 had died of their disease. The risk was particularly greatest in those patients with a history of angina or previous myocardial infarction. Despite the difficulty of precisely defining the preinfarction syndrome, it is apparent that there are patients with unstable angina who can be identified and who have a much increased risk of myocardial infarction and death. It also has been shown that the majority of these patients remain incapacitated symptomatically even if they escape the substantial mortality associated with the syndrome. Coronary arterial revascularization has been successful in interrupting the preinfarction syndrome and in many centers is undertaken as an emergency procedure as the therapy of choice [1, 5, 13, 16, 22, 24, 27, 31]. There has been a significant operative mortality and morbidity which varies considerably due to the variable group of patients included in this clinical syndrome (table II) [1, 3, 6, 8, 13, 14, 16, 17, 19, 20, 22, 24, 31]. The operative mortality varies from 0 to 23'010 and the incidence of myocardial infarction occurring postoperatively has also varied considerably from 0 to 25010. The latter is an important factor to consider, particularly as one of the objectives of urgent revascularization is to prevent the evolution of myocardial infarction in the pre-


Surgical Intervention for Preinfarction Angina

M UNDTH/BuCKLEY /DAGGETT/McENANY /GOLD/LEINBACH/AUSTEN

62

Table II. Preinfarction syndrome: incidence of myocardial infarction and mortality rate with coronary bypass surgery

Author

HARRISON and SHUMWAY [14] LAMBERT et al. [16] AVER et al. [1] SUSTAITA et al. [26, 27] CONTI et al. [6] GOODIN et al. [13] MOTLAGH et al. [19] SCANLON et al. [22,23] WISOFF et al. [31] FAVALORO et al. [8] SEGAL et al. [24] BOLOOKI et al. [3] LINHART et al. [17] MUNDTH et al. [20] Total

Number of patients

Hospital mortality No. 0/0

67 76 41 36 40 30 43 39 26 18 17 11 5 25

7 5 0 3 9 4 0 4 2 2 3 0 0 1

474

40

(10) (7)

Incidence of new infarction No. 0/0

(4)

8 4 0 3 0 2 4 10 3 1 3 0 0 0

(8)

38

(8) (23) (13) (10) (8) (11) (18)

(14) (5) (9)

(8) (10) (25) (12) (6) (20)

(8)

infarction patient. Also of importance is the functional result of the infarct, whether it occurs as a sequel to preinfarction angina or to coronary bypass surgery. The average hospital mortality taken from collected series for coronary bypass surgery in the treatment of the preinfarction syndrome was 8 Ofo, probably significantly less than the average mortality of 15 Ofo for medically treated patients followed from 1 to 6 months, although the groups are not truly comparable (table I, II). The average incidence of postoperative myocardial infarction was 8 0/ 0, considerably less than the figure of 33 Ofo as the average for medically treated patients followed from 1 to 6 months. There were few late deaths at 6 months to 1 year following surgery and the functional results have been similar to those obtained for coronary bypass surgery in the treatment of stable angina [14,25]. It is not surprising that the risk of coronary arteriography and revascularization surgery is significantly greater for patients with acute coronary insufficiency as compared to chronic stable angina. CONTI et al. [6] reported 2 deaths in 57 patients with the preinfarction syndrome resulting from coronary arteriography and SCANLON et al. [22] reported


Percentage in brackets.

Surgical Intervention for Preinfarction Angina MAP, mm Hg

HR, beats/min

Mean wedge pressure, mm Hg

160 140 120 100

0·

801- * .,/

::u 601-

Prior to pain

140

28

120

24

100

20

801-

During pain

~

63

I

If1

*

16

~*

601-*~

12 I *

40 4 21

Prior to pain

During pain

0

Prior to pain

During pain

Fig. 1. Hemodynamic changes associated with ischemic pain in 6 patients with the pre infarction syndrome. HR = heart rate; MAP = mean arterial pressure; p values: MAP = p < 0.01; HR not significant; wedge pressure = p < 0.01. [From et a/., 12.]

2 myocardial infarctions and one episode of ventricular fibrillation in 79 patients with accelerated angina pectoris undergoing angiography. In a separate report, SCANLON et al. [23] reported that of 8 patients undergoing emergency myocardial revascularization for an evolving myocardial infarction, 5 were in the preinfarction syndrome category prior to cardiac catheterization and sustained the infarction during the angiographic study. SUSTAITA et al. [26] reported that of 18 patients with the preinfarction syndrome undergoing urgent coronary arteriography, 3 patients developed myocardial ischemia during the study and one patient developed an acute myocardial infarction, ventricular fibrillation and cardiogenic shock. GOLD et al. [12] and CANNOM et al. [4] have documented the hemodynamic alterations that occur with acute coronary insufficiency. The former study reported carefully documented hemodynamic changes during acute coronary insufficiency in 6 patients. The mean aortic pressure increased from an average of 79 to 118 mm Hg, the heart rate from 62 to 70/min, and the pulmonary capillary wedge pressure from 9 to 23 mm Hg (fig. 1). Because of the marginal hemodynamic status of patients with the


GOLD

MUNDlH/BuCKLEY/DAGGElT/McENANy/GOLD/LEINBACH/AuSTEN

64

r-

18

r-

16

Hospital admission

14

1

r-

r-

r-r-

r-r-

12

c

2. 10 v

~

L

SUI 'gery

8

v

"'

.: 6

...-IASP

0

~ 4 0

"'0. w

I I

I

D

1 2 3 4- 5 6 7 8 9 10 11 12 Days

Fig.2. Illustration of ischemia pattern in a patient with pre infarction syndrome. Each square represents a prolonged episode of ischemia pain. On day 9, intra-aortic balloon pump (IABP) was initiated. The one subsequent mild episode of pain occurred during coronary arteriography. [From GOLD et al., 12.]

1 min

Arteria l pressure, mmHg

200r

-,

.;;-

...

.---~-,

pew pressure, mmHg

ECG (V 4 )

t

IABP ON

PAIN-FREE

Fig. 3. Effect of IABP on hemodynamics and electrocardiogram of patient with preinfarction angina. Within 3 min of IABP, the patient was pain free and associated with this was resolution of ST segment depression and reduction of the pulmonary capillary wedge pressure (peW). The arterial pressure tracing demonstrates a 35-mm Hg reduction in peak left ventricular pressure and excellent diastolic augmentation. [From GOLD et al., 12.]


I_ ..._... tp~·~


65

Table Ill. Results of intra-aortic balloon pump (IABP) and coronary bypass surgery in 25 patients with pre infarction syndrome 24

20 12 58 1 (4010)

o

12 months 19 (79010)

preinfarction syndrome, it has been our policy to institute circulatory assistance with the intra-aortic balloon pump (IABP) when the patient developed recurrent myocardial ischemia despite an intensive medical program including bed-rest, oxygen, heparin anticoagulation, short- and long-acting nitrates and p-blockade [12,20]. IABP was introduced in 24 of 25 patients with medically refractory preinfarction angina and effectively abolished pain, reversed electrocardiographic ST-T wave changes of ischemia and improved the altered hemodynamics in 20 of the 24 patients (fig. 2, 3). In the remaining 4 patients, IABP significantly reduced pain and the electrocardiographic ischemic changes, but did not abolish them. Pain and electrocardiographic changes of ischemia reappeared with temporary discontinuation of IABP in 12 patients. Complete angiographic study was carried out safely in all patients and revascularization was performed within 24-96 h from the episode of prolonged pain, but was not considered a true emergency. In one patient, IABP was not instituted prior to study because of failure to recognize impending myocardial infarction. Anesthesia was complicated by hypotension and ventricular arrhythmias necessitating early institution of cardiopulmonary bypass. IABP was required to hemodynamically stabilize the patient coming off cardiopulmonary bypass. There was one operative mortality and postoperative electrocardiograms indicated no progression of ischemic changes to infarction. At follow-up study 6 months to 2 years postoperatively, 19 patients (79 %) were completely free of angina with recurrence of very mild angina in 2 patients and moderately severe in one (table III). Postoperative angiographic study in the latter patient demonstrated an occluded (LAD) graft and a patent (RCA) graft. Reoperation was performed with the insertion


IABP preoperatively Resolution ischemia Recurrence of ischemia with temporary cessation IABP Number of vein grafts Hospital mortality Incidence of new infarction Average period of follow-up Asymptomatic

66

of a new LAD graft. This patient remains free of angina 1 year following the second procedure. The use of IABP has clearly facilitated management of this critically ill group of patients in terms of safe angiographic study and induction of anesthesia. Coronary bypass surgery in this group of patients has proven to be functionally effective and associated with an acceptable operative risk. When compared to the morbidity and mortality of continued medical therapy, the results of carefully managed coronary bypass surgery indicate that it is the therapy of choice in the treatment of the preinfarction (unstable angina) syndrome. The question of the urgency of surgery in this group remains somewhat controversial. The excellent results [6, 15] of intensive in-hospital medical therapy in resolving an episode of pre infarction angina cannot be quickly dismissed. If the patient's episode of acute coronary insufficiency is resolved with effective medical therapy, one could expect the operative risk of surgery to be substantially less compared to emergency surgery in the presence of acute coronary insufficiency and significant left ventricular dysfunction. THEROUX et at. [29] found that the operative mortality was significantly higher when surgery was undertaken during or soon after an episode of crescendo angina. The mortality rate in 25 patients undergoing coronary bypass surgery less than 3 weeks after remission of unstable angina was 28 %, whereas the operative mortality was 5 % for 39 patients operated upon 3-12 weeks after remission of the unstable angina syndrome. In view of these reports, it has been our recommendation that all patients with the preinfarction syndrome should be initially treated intensively medically with close monitoring in a coronary care unit. If the episode of unstable angina promptly resolves, coronary arteriography and elective surgery is advised at an interval, usually during the same hospital admission. If medical therapy fails to control promptly the episode of unstable angina, IABP assistance, coronary arteriography and semielective coronary bypass surgery are advised (fig. 4). The fact that coronary bypass graft surgery is associated with a significant incidence of myocardial infarction as determined by the appearance of new and persistent Q waves may not be as large a source for concern when the functional significance is considered. ESPINOZA et at. [7] found a 30-percent incidence of new persistent Q waves following coronary bypass surgery but found there was no correlation between postoperative new Q waves and left ventricular end-diastolic pressure, indicating that the apparent myocardial infarction resulted in no significant alteration in left ventricular function. Using the vectorcardiograph as a more specific


M UNDTH/BUCKLEY IDAGGETT IMCENANYIGOLD/LEINBACHIAUSTEN

PS


67

.--Improved -

Interval Elective coronary angiogram-.. bypass surgery

-+-

CCU medical therapy Bed-rest

-I

O2 Nitrates /i-blockade

Failure medical therapy- IABP __Angiography

l

Semielective coronary bypass surgery Fig. 4. Flow diagram of recommended method of stepwise management of patient with preinfarction syndrome (PS). CCU = cardiac care unit.

diagnostic means to detect new infarction in coronary bypass surgery, FRIEDBERG et at. [10] and FRIEDEWALD et at. [11] found that the incidence of myocardial infarction postoperatively in series with substantial numbers of patients was 8 and 6 0/0, respectively. Similar to this experience has been the experience with coronary bypass surgery for the preinfarction syndrome. The early and late postoperative morbidity and mortality usually has not paralleled the incidence of new infarction and has been significantly less than for preinfarction patients treated exclusively medically.

1

2 3

4 5

AVER, J.; JOHNSON, D.; FLEMMA, R.; TECTOR, A., and LEPLEY, D.: Direct coronary artery surgery for impending myocardial infarction. Circulation 44: supp!. II, p. 102 (1971). BEAMISH, R. and STORRIE, V.: Impending myocardial infarction. Circulation 21: 1107-1115 (1960). BOLOOKI, H.; VARGAS, A.; GHAHRAMANI, A.; SOMMER, L. S.; ORVALD, T., and JUDE, J. R.: Aortocoronary bypass graft for pre infarction angina. Chest 61: 247-252 (1972). CANNOM, D. S.; SCHROEDER, J. S., and HARRISON, D. C.: Hemodynamic observations during impending myocardial infarction. Amer. J. Cardio!. 31: 125 (1973). CHEANVECHAI, c.; EFFLER, D. B.; Loop, F. D.; GROVES, L. K.; SHELDON, W. C.; RAZAVI, M., and SONES, F. M., jr.: Emergency myocardial revascularization. Amer. J. Cardio!. 31: 125 (1973).


References

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7 8

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14 15 16

17 18 19

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30 31

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and PIFARRE, R.: Myocardial revascularization during acute phase of myocardial infarction. J. amer. med. Ass. 218: 207-212 (1971). SEGAL, B. L.; LIKOFF, W.; BROCK, H. VAN DEN; KUIMBIRIS, D.; NAJMI, M., and LINHART, J. W.: Saphenous vein bypass surgery for impending myocardial infarction. Critical evaluation and current concepts. J. amer. med. Ass. 223: 767-772 (1973). SPENCER, F. c.: Bypass grafting for preinfarction angina. Circulation 45: 274-278 (1972). SUSTAITA, H.; CHATTERJEE, K.; MATLOFF, J. M.; MARTY, A. T.; SWAN, H. J. c., and FIELDS, J.: Emergency bypass surgery in impending and complicated acute myocardial infarction. Arch. Surg., Chicago 105: 30-35 (1972). SUSTAITA, H.; CHATTERJEE, K.; MATLOFF, J. M., and SWAN, H. J. C.: The rationale for surgery in pre infarction angina. Amer. J. Cardiol. 31: 160 (1973). THEODOSIOU, G.; FLESSAS, A.; KLEIN, M.; BERGER, R., and RYAN, T. J.: Lethal characteristics of the pre-infarction syndrome. Circulation 48: suppl. IV, pp. IV224 (1973). THEROUX, P. and CAMPEAU, L.: The influence of timing of surgery on mortality and incidence of myocardial infarction following aortocoronary vein graft surgery in crescendo angina. Amer. J. Cardiol. 31: 162 (1973). VAKIL, R.: Preinfarction syndrome. Management and follow-up. Amer. J. Cardiol. 14: 55-63 (1964). WISOFF, B. G.; KOLKER, P.; HARTSTEIN, M. L., and HAMBY, R. I.: Surgical approach to impending myocardial infarction. J. thorac. cardiovasc. Surg. 65: 534-537 (1973). WOOD, P.: Acute and subacute coronary insufficiency. Brit. med. J. i: 17791782 (1961).

Author's address: Dr. E. D. MUNDTH, M.D., Department of Surgery, Massachusetts General Hospital, Boston, MA 02114 (USA)


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