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Prevalence of Mural Thrombi and Systemic Embolization with Left Ventricular Aneurysm
CLINICAL INVESTIGATIONS
Prevalence of Mural Thrombi and Systemic Embolization with Left Ventricular Aneurysm· Effect of Anticoagulation Therapy M iehaeZ T. Simpson, M.D .;t Albert Oberman, M.D .;t Nicho1o.sT. Kouchoukos, M.D.;§andWilliam/. Rogers, M.D., F.C.C.P.II Fifty-eigbt coosec:utive post-myocardial iDfan:tion (MI) patients undergoing Slll'gery for left ventricular (LV) anenrysm were studied retrospectively to assess the frequency, characteristics, and complications of mural thrombi found at surgery, and to determine wbat effect chronic anticoagulation might have bad upon the cUnical course of these patients. Mural thrombi at surgery were found In 66 percent (38/58). Of these, only 10 (26 percent) were prospectively identified by LV angiography; conversely, LV angiography misidentified the presence of mural thrombi In 10 percent (2/20) who bad no thrombus at surgery. Patients with mural thrombi were not different from those without thrombi In terms of time elapsed since their MI (28 ± 7 vs 24 ± 10 mOl), LV end-diastoUc pressure (LVEDP) (18 ± 2 vs 18 ± 2 mm JIg), ejection fraction (22 ± 1 vs 25 ± 2 %), or angiograpbic scar size (33 ± 2 vs 29 ± 3%).
Of 17 patients receiving long-term thenpy with war-
farin sodium preopentively for anticoagu1ation, nine bad mural thrombi, whereas eight did not (NS). There were only two patients In the total group (2/58=3 percent) with a preopentive event compatible with systemic arterial embolization--one of these was anticoagulated. Thus, In postmyocardlal patients baving LV anenrysmectomy; (1) the prevalence of mural thrombus is high but CaDnot be reUably ideutified prospectively by LV angiography or predicted by time since their MI, angiograpbic scar size, ejection fraction, or LVEDP; (2) the occurrence of preoperative systemic arterial embolization is very low; and (3) chronic: anticoagulation bas no apparent effect on the frequency of preopentive systemic arterial embolization or the prevalence of LV mural thrombus at surgery.
-From the Division of Cardiology, Department of Medicine~ and the Division of Cardiovascular Surgery, Department or Surgery, University of Alabama Medical Center, Birmingham. This research was supported by the National Heart and Lung Institute (Specialized Center of Research for Ischemic Heart Disease) Contract Number IP17HL17667-04 by 'Program Project grant HL 11, 310, and by the Clinical Research Unit grant MO-RROOO-13 (General Clinical Research Centers Program, Division of Research Resources of the National Institutes of Health). Presented in part at the 27th Annual Scientific Session, American College of Cardiology, Anaheim, CA, March 6-9, 1978. tFeIlow in Cardiology. tAssociate Professor of Medicine. §Professor of Surgery. IIAssistant Professor of Medicine. . Manuscript received January 26; revision accepted June 21. Reprint requests: Dr. Rogers, 330 Lfiona-HlJf'riacm Building, University of Alabama Medical Cettter, Binnlngham 35294
frequency of systemic embolization as judged by evidence of peripheral organ infarcts, but clinical studies of patients with aneurysmsll,1'l1,13-21 suggest a much lower occurrence of clinically apparent systemic embolization. No study, however, has systematically investigated the influence of anticoagulation on the formation of mural thrombi or occurrence of systemic embolization. The diagnosis of left ventricular ( LV) mural thrombi prior to inspection of the ventricular chamber either at surgery or at autopsy is difficult and frequently involves intuitive clinical diagnosis following an episode of sudden arterial insufficiency in patients with a known LV aneurysm, Certain findings at LV angiography are suggestive of mural thrombus in the ventricle; however, several studies8.11.12.11 have demonstrated the limitations of the single plane angiogram in diagnosing mural thrombi. The purpose of this study was to determine, in a group of patients undergoing surgical resection of LV aneurysm the following: (1) the prevalence of mural thrombi at surgery; (2) the effectiveness of biplane LV angiography in detecting mural throm-
CHEST, 77: 4, APRIl, 1980
ANTICOAGULATION IN LEn VENTRICULAR ANEURYSM 483
patients known or suspected of having aneurysms of the left ventricle following myocardial infarction (MI) are frequently maintained on warfarin sodium because of the occasional occurrence of systemic embolization. Several autopsy studies1-li and surgical studies6-13 reveal that mural thrombi occur in the ventricles of approximately one-half of all patients with postinfarction ventricular aneurysms. The incidence of systemic embolic events, however, is not clear. Autopsy studies'" suggest a substantial
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t8~~:fc~~~~ SEGMENT
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AKINETIC OR OYSKINETIC LENGTH OF ENO DIASTOLIC CIRCUMFERENCE TOTAL END DIASTOLIC CIRCUMFERENCE
• x
100
FIGURE 1. Angiographic estimation of aneurysm size. 23 End-diastolic (solid lines) and endsystolic (do8hed lines) left ventricular silhouettes in AP and lateral projections were superimposed, using fixed x-ray beam markers (solid dots) as references. Portion of end-diastolic circumference which was akinetic or dyskinetic, shown as the region between the brackets, was expressed as a percentage of the total end-diastolic circumference, averaged for two projections, and designated "percent abnormally contracting segment." Hypokinesis was not quantitated by this model.
bi; (3) factors which may predict the presence of mural thrombi preoperatively; (4) the occurrence of clinically apparent systemic embolization; and (5) the effect of long-term anticoagulation therapy with warfarin sodium on the frequency of mural thrombi and systemic embolization. METHODS
Patient Population The study population consisted of 58 consecutive patients from September 1971 through December 1976 at the University of Alabama Medical Center undergoing (1) coronary angiography, (2) biplane LV angiography, and (3) resection of postinfarction LV aneurysm. Patients having cardiac catheterization at other hospitals and referred to this institution for surgery were not included in this analysis. Due to the referral nature of this institution, uniformity in clinical management prior to surgery could not be assured; therefore, some patients had received anticoagulants while others had not. Clinical Analysis
Clinical charts were reviewed to ascertain the past history of anticoagulation and systemic embolic events. Operative notes were examined to determine the presence or absence of mural thrombi in the left ventricle. Surgery In this study, aneurysm was defined as an abnormally thinned, scarred, or bulging segment of LV free wall noted at the time of surgery. Resection of myocardial scars not conforming to this definition were not included in this series. The surgical technique has been described previously.21 The
4&4 SIMPSON ET AL
primary indication for surgery was congestive heart failure in 35 patients, angina in 16 patients, and serious rhythm disturbances in 7 patients. Systemic arterial embolization was not the indication for surgery in any patient. Angiographic Studies
Subjects were classified as having single or multiple vessel coronary artery disease on the basis of preoperative selective coronary angiography; a coronary artery diameter stenosis of ~ 70 percent in any projection was considered significant. The angiographic studies of patients undergoing biplane left ventriculography at our institution were reviewed, and angiographic volumes were obtained by techniques previously described. 22 Calculations were made of LV ejection fraotion and percent abnormally contracting segments, the latter an angiographic estimation of scar size, obtained by first superimposing the end-diastolic and end-systolic LV silhouettes and then ascertaining the percentage of end-diastolic circumference which was either akinetic or dyskinetic18 (Fig 1). The original angiographic interpretations by both the cardiologists and radiologists were reviewed with respect to the preoperative diagnosis of LV mural thrombi. These anglograms had been reviewed simultaneously by both a cardiologist and a cardiac radiologist, and there was agreement between their interpretations in all but two of the 58 studies. However, a mural thrombus mentioned in either report rendered the angiogram "positive" for the purpose of this analysis. Statistical Analysis
Data are reported as mean ± standard error of the mean. The nonpaired t-test and Chi-square test were used to assess differences between groups of nonpaired data.
CHEST, 77: 4, APRIL, 1980
Table I--Clinic:al and Angiographic: Charac:teri.tiu of PaeieR" wieh and wiehoue Mural Thrombi * Total Group
With Thrombi
Without Thrombi
58
38
20
50M,8F
33M,5F
17M,3F
Age (yr)
55±1
57±1
52±!
Time since infarction (mos)
26±6
28±7
24±5
No. of patients Sex
Multivessel CAD
28 18 10 (48 percent) (47 percent) (50 percent)
LVEDP (mm Hg)
17±1
18±2
18±1
Ejection fraction (percent)
23±1
22±1
25±1
ABN contracting segment (percent)
32±1
33±1
29±1
*All values are mean ± standard error of the mean. Multivessel CAD was defined as double or triple vessel coronary artery disease. LVEDP indicates left ventricular enddiastolic pressure. REsULTS
Clinical and Angiographic Data Fifty eight patients satisfied the study criteria (Table 1). The group was composed of 50 men and 8 women with an average age of 55 + 1 years. The mean elapsed time since MI was 26 ± 6
months. Twenty-eight patients, representing 48 percent, had multivessel coronary artery disease representing either two or three-vessel disease. The mean LV end-diastolic pressure was 17 ± 1 mm Hg, while the average ejection fraction was 23 ± 1 percent. The mean size of the abnormally contracting segment was 32 ± 1 percent. All patients demonstrated sinus rhythm, and no episodes of supraventricular arrhythmias were documented or suggested in any patient. Seven patients underwent left ventricular aneurysmectomy primarily due to serious ventricular arrhythmias. The prevalence of mural thrombi was not different in the groups operated upon for arrhythmias and those operated upon for other indications. Incidence of Mural Thrombi and Effect of Anticoagulation The operative notes of the 58 patients were reviewed with respect to the presence or absence of thrombi in the ventricle. There were 38 patients with mural thrombi; this represents a 66 percent prevalence of mural thrombi in this group. When compared with patients without mural thrombi, the group with mural thrombi were no different with respect to age, elapsed time since infarction, prevalence of multivessel coronary artery disease, LV end-diastolic pressure, ejection fraction, or size of the abnormally contracting segment (Table 1).
FIGURE 2. Angiographic detection of left ventricular mural thrombi; AP and lateral projections of left ventricular angiogram. This angiogram was reported as revealing an apical thrombus due to persistent filling defect in apex inside thin line of calcification indicated by the am)ws. At surgery, the aneurysm was lined with calcium, and adherent to its endocardial surface was a moderate amount of thrombus. This represents a "true positive" angiogram with respect to mural thrombus detection.
CHEST, 77: 4, APRIl, 1980
ANTICOAGULATION IN LEn VENTRICULAR ANEURYSM 465
Therefore, these factors were not helpful in predicting the patient with a mural thrombus. Seventeen patients had been maintained on anticoagulants, most since their initial hospitalization for MI. Nine patients receiving anticoagulants had mural thrombi, whereas eight patients had no mural thrombi (p = NS). Of those 41 patients not receiving anticoagulants, 29 had mural thrombi and 12 had no mural thrombi. Angiographic Detection of Mural Thrombi
Of the 38 patients with mural thrombi at surgery, only 10 thrombi (26 percent) were diagnosed angiographically while 28 thrombi (74 percent) were not detected. Of the 20 patients without mural thrombi at surgery, 18 patients (90 percent) had no angiographic evidence of thrombi; however, two patients (10 percent) were incorrectly suspected of having mural thrombi on the basis of left ventriculography. Thus, 30 out of 58 angiograms (52 percent) were misleading with respect to predicting the presence or absence of mural thrombi (Fig 2 and 3). Effect of Rhythm Disorders on Prevalence of Mural Thrombi and Incidence of Systemic Embolization
All patients demonstrated sinus rhythm at the time of surgery. Seven patients, however, had had previous supraventricular arrhythmias. All seven patients with supraventricular arrhythmias had mural thrombi, whereas only 31 of the 51 patients without supraventricular arrhythmias had mural thrombi (p < .05). None of these seven patients with supraventricular arrhythmias had a history of systemic embolization. Seven patients underwent surgery due to serious ventricular arrhythmias. The prevalence of mural thrombi and incidence of systemic embolization was not different in groups with and without serious ventricular arrhythmias. Incidence of Systemic Embolization and Effect of Anticoagulation
Only two of the 58 patients had previous events which were clinically thought to be systemic arterial embolization. One was a 34-year-old man who had an embolus to his left femoral artery two months following an anterior MI. This patient had not been maintained on anticoagulants. The other was a 56year-old man with an apparent embolic cerebrovascular accident two years following an anterior MI even though he had taken warfarin sodium since the infarction. Of the 17 patients maintained on anticoagulants, only the one patient had an embolic 46& SIMPSON ET AL
FIGURE 3. Angiographic detection of left ventricular mural thrombi; AP and lateral projections of left ventricular angiogram. This angiogram was not reported to reveal evidence of left ventricular mural thrombus; however, at surgery there was a moderate amount of clot underlying thin-walled aneurysm. This represents a "false negative" angiogram with respect to mural thrombus detection.
event-an incidence of 6 percent. Of the 41 patients not on anticoagulants, the one patient with an embolic event represents a 2 percent incidence. DISCUSSION
The results of this study suggest the following: CHEST, 77: 4, APRIL, 1980
T.ble ~eeurrenee 01 Mural Thrombi and Sy*mie Emboli.lion in LV ~neury.nu: ~ulD,.,. S. . . .
Patients With LVA
Mural Thrombi (Percent)
Emboli (Percent)
40
27 (68)
6 (15)
102
55 (54)
53 (52)
65
9 (14)
9 (14)
Dubnow et a1
80
52 (65)
30 (38)
Davis and Ebert'
27
12 (44)
2 (5)
314
155 (49)
100 (32)
Phares et all Schlichter et a1
2
Abrams et al' 4
Total (Mean)
LVA =-left ventricular aneurysm.
( 1) the prevalence of mural thrombi is high in patients with LV aneurysm; (2 ) factors such as severity of coronary artery disease, LV function, and size of the abnormally contracting segment do not identify patients at risk to have mural thrombi; (3) biplane LV angiography is neither sensitive nor specific for the detection of mural thrombi; (4) clinically apparent systemic embolization is uncommon and does not appear to be affected by long-term anticoagulation therapy with warfarin sodium.
Incidence and Preoperative Identification of Mural Thrombi This study reaffirms the relatively common prevalence of mural thrombi in the ventricle of the patient with postinfarction LV aneurysm as reported in previous studies (Table 2 and 3). We were unable to identify unique characteristics of patients with mural thrombi by examining clinical or hemodynamic factors (Table 1). The angiographic detection of mural thrombi by single-plane left ventriculography has been shown in previous studies to be limited when the "confirmed" absence or presence of thrombus (by inspection at surgery or autopsy) is compared with the angiographic interpretation (Table 4). Our study utilized biplane left ventriculography, and likewise, failed to reliably detect the thrombi. Angiographic criteria for diagnosing mural thrombi have included (1) persistent chamber fllling defects, (2) venbicular wall calcification, and (3) "mackeral sky" appearance of the contrast medium-filled ventricle. Wall calcification is an infrequent· finding and- .may be seen in other cardiac disorders.P' The "maekeral sky" appearance refers to areas of uneven mixing or puddling of contrast media in the ventricle, and while suggestive of mural thrombus, is nonspecific and may be seen in the enlarged, relatively atonic aneurysmal ventricle with poor mixing without mural thrombus.F Most of the angiographically diagnosed thrombi in this series were on the basis of fllling defects within the
CHEST, 77: 4, APRIL, 1980
ventricular chamber during both systole and diastole ( Fig 2). Many mural thrombi, even those found to be quite large at the time of surgery, were not detected angiographically. Mural thrombi frequently are covered by endothelium which may produce a smooth contour to the venbicular cavity resulting in failure to suspect a thrombus when interpreting angiograms. Case reports have appeared of M-mode echocardiographic diagnosis of ventricular thrombi;2s,26 however, this would appear to lack sensitivity. Cross-sectional echocardiography may provide a realistic noninvasive approach to detection of mural thrombi in the ventricle/"
Frequency of Systemic EmboUzation The 3 percent frequency of clinically apparent systemic embolization in this study is consistent with most similar previous reports on LV aneurysms (Table 3 ). The occurrence of systemic embolization judged by autopsy data (Table 2) is almost uniformly higher than that reported in clinical studies (Table 3). Clinical studies probably overlook small or subclinical emboli and may underestimate the numTable 3--Oeeurrenee 01 Mural Thrombi and Sy.eemie Emboli.don in LV ~neury.m.: CUnieal-Surpeal Studi. *
Patients With LVA
Author
Thrombi (Percent)
Cooley et al'
6
3 (50)
7
Cooley et a1
37
37 (100)
Gorlin et al
14
Emboli (Percent)
2 (5)
24
0 (0)
16
41
0 (0)
Schattenberg et all'
37
4 (11)
Cheng"
35
(3)
Key et al
Kluge et a1
36
25 (69)
0 (0)
Graber et al t
23
18 (78)
3 (13)
Davis and Ebert'
40
8
Loop et al
Stoney et al Roo et al
400
lO
18
212 (53)
29 60
ll
2 (5) 19 (5) 2 (7) 19 (32)
0 (0)
Cooperman et alIt
55
5 (9)
Watson et al-
16
0 (0)
Marco et al
80
13 (16)
Mullen et alII
60
10 (17)
0 (0)
Simpson et al (1978)
58
38 (66)
2 (3)
Total
l2
1037
*Elipses indicate no information available. LVA ~ left ventricular aneurysm.
ANTICOASULAnON IN LEFT VENTRICULAR ANEURYSM 487
Table 4--Sin.le Plane Anpo.,.aplde Dea«lion 01 LV Mural Tlarombi in Palienla willa LV Aneu,.,..m.
No. of Patients
Confirmed Thrombus
True Positive Angiogram
False Negative Angiogram
ConfirmedNo Thrombus
Cheng 17
35
20
10
10
15
Kluge et a18
36
25
6
19
11
0
11
Rao et alII
60
19
6
13
41
0
41
Marco et a112
80
13
12
67
2
65
211
77 (36 percent)
54 (70 percent)
134 (64 percent)
3 (2 percent)
(98 percent)
Totals
23 (30 percent)
ber of emboli in part by their retrospective design. However, autopsy evidence of peripheral organ infarction may be seen in patients dying in other circumstances, such as following prolonged arterial hypotension, and is not felt to be entirely diagnostic of arterial embolization. The true frequency of systemic embolization is probably higher than that determined by clinical studies but lower than reported by autopsy studies.
EDect of Rhythm Disorders on Prevalence of Mural Thrombi An apparently increased prevalence of ventricular mural thrombi in patients with prior supraventricular arrhythmias was observed in our study, and to our knowledge, has not been previously reported. The history of serious ventricular arrhythmias did not appear to inHuence either the prevalence of mural thrombi or incidence of systemic embolization. I nfluence of Anticoagulation on Mural Thrombi and
Systemic Embolization
The prevalence of mural thrombi was not signicantly different in the patients receiving anticoagulants as compared to the patients not taking them. In this study, only two of the 58 patients had events suggestive of systemic embolization, and one of these patients had been maintained on warfarin sodium. This low frequency of embolization would render it difficult to demonstrate a protective effect due to any intervention, including anticoagulation. The degree and consistency of anticoagulation could not be evaluated in this retrospective study; however, the commonly obtained history was that the patient had taken anticoagulants, and therefore, visited his personal physician regularly for prothrombin time determinations. The problems of anticoagulant monitoring, patient compliance, and interfering drugs are always difficult to assess, even in prospective controlled trials. Some authors'' have suggested a decline in the
488 SIMPSON ET AL
False Positive Angiogram
True Negative Angiogram
14
131
frequency of systemic embolization in patients with LV aneurysm which may be due to the increased use of anticoagulants. This change in embolization frequency may, however, represent the comparison of earlier, predominantly autopsy studies with more recent clinical studies. The problems with this comparison were delineated above. The failure to note an obvious therapeutic benefit of administering anticoagulants to patients with left ventricular aneurysms may in part relate to the pathogenesis of mural thrombosis in LV aneurysms. Thrombi may be classified into three general types: 28 platelet, coagulation, and intermediate or mixed. Thrombi forming in areas of high pressure and How, such as arterial intimal lesions, tend to be composed primarily of platelets, and prevention of such platelet thrombi might result from use of specific anti-platelet pharmacologic agents. Thrombi, such as venous thrombi or mural thrombi, in the atonic atria of patients with rheumatic mitral valve disease form in areas of low pressure and slow flow and would appear to be most effectively prevented by antithrombin agents such as heparin or warfarin sodium. Mural thrombi in left ventricular aneurysms may represent the intermediate or mixed thrombi in which rapid How, turbulence, and static zones are present together." their prevention may require a dual approach of combined drugs such as warfarin sodium together with platelet inhibitors such as aspirin, sulfinpyrazone, and dipyridamole. Such a combination would be expected to be more hazardous in terms of bleeding complications and would probably not be warranted in this condition of relatively infrequent embolic complications. Results from this study, as well as from previous studies cited here, fail to support the long-term administration of warfarin sodium to patients with known LV aneurysms for prevention of systemic embolization. The current recommendation in our institution advises anticoagulation for six months for the early postinfarction patient shown to have a LV aneurysm whether or not the angiogram is "positive" for mural thrombus. Even though there is no docu-
CHEST, 77: 4, APRIL, 1980
1 Phares WS, Edwards JE, Burchell HB: Cardiac aneurysms: clinicopathologic studies. Mayo Coo Proc 195~; 28:264-271 2 Schlichter J, Hellerstein HK, Katz LN: Aneurysms of the heart: a correlative study of one hundred and two proven cases. Medicine 1954; 33:43-86 3 Abrams DL, Edelist A, Luria MH, Miller AJ: Ventricular aneurysm: a reappraisal based on a study of sixty-five consecutive autopsied cases. Circulation 1965; 27: 164169 4 Dubnow MH, Burchell HB, Titus JL: Post-infarction ventricular aneurysm: a clinicopathologic and electrocardiographic study of 80 cases. Am Heart J 1965; 70:753760 5 Davis RW, Ebert PA: Ventricular aneurysm: a clinicalpathologic correlation. Am J Cardiol 1972; 29: 1-6 6 Cooley DA, Henly WS, Amad KH, Chapman DW: Ventricular aneurysm following myocardial infarction: results of surgical treatment. Ann Surg 1959; 150:595-612 7 Cooley DA, Hallman GL, Henly WS: Left ventricular aneurysm due to myocardial infarction. Arch Surg 1964; 88:114-121 8 Kluge TH, UDal SR, Hill JD, Kerth WJ, Gerbode F: Dyskinesis and aneurysm of the left ventricle: surgical experience in 36 patients. J Cardiovasc Surg 1971; 12:273280 9 Graber JD, Oakley CM, Pickering BN, Goodwin ]F, Raphael MJ, Steiner RE: Ventricular aneurysm: an appraisal of diagnosis and surgical treatment. Br Heart J 1972; 34:830-838 10 Loop FD, EfBer DB, Navia JA, Sheldon WC, Groves LK: Aneurysms of the left ventricle: survival and results of a ten-year surgical experience. Ann Surg 1973; 178:399405
11 Rao G, Zikria EA, Miller WH, Samadani sa, Ford WB: Experience with sixty consecutive ventricular aneurysm resections. Circulation 1974; 50( suppl 2) :149-153 12 Marco JD, Kaiser GC, Barner HE, Codd JE, Willman VL: Left ventricular aneurysmectomy. Arch Surg 1976; 3:419-422 1~ Mullen DC, Posey L, Grabriel R, Singh HM, Flemma RJ, Lepley D: Prognostic considerations in the management of left ventricular aneurysms. Ann Thorac Surg 1977; 23:455-460 14 Gorlin R, Klein MD, Sullivan JM: Prospective correlative study of ventricular aneurysm. Am J Med 1967; 42:512531 15 Key JA, Aldridge HE, MacGregor DC: The selection of patients for resection of left ventricular aneurysm. J Thorac Cardiovasc Surg 1968; 56:477-483 16 Schattenberg TT, Giuliani ER, Campion BC, Danielson GK: Post-infarction ventricular aneurysm. Mayo Clin Proc 1970; 45:13-19 17 Cheng TO: Incidence of ventricular aneurysm in coronary artery disease: an angiographical appraisal. Am J Med 1971; 50:340-355 18 Stoney WS, Alford WC, Burrus GR, Thomas CS: Repair of anteroseptal ventricular aneurysm. Ann Thorac Surg 1973; 15:394-404 19 Cooperman M, Stinson EB, Griepp RB, Shumway NE: Survival and function after left venbicular aneurysmectomy. J Thorac Cardiovas Surg 1975; 69:321-328 20 Watson LE, Diekhaus DW, Martin RH: Left ventricular aneurysm: preoperative hemodynamics, chamber volume, and results of aneurysmectomy. Circulation 1975; 52-868873 21 Kouehoukos NT, Doty DB, Buettner LE, Kirklin JW: Treatment of postinfarction cardiac failure by myocardial excision and revascularization. Circulation 1972; 45 ( suppl 1) :172-178 22 Rackley CE, Hood WP: Measurements of ventricular volume, mass, and ejection fraction. In: Grossman W, 00. Cardiac catheterization and angiography. Philadelphia: Lea and Febiger, 1974, 176 23 Feild BJ, Russell RO, Dowling JT, Rackley CE: Regional left ventricular performance in the year following myocardial infarction. Circulation 1972; 46:679-689 24 Hurst JW: The heart, 4th 00. New York: McGraw-Hill, 1978, 318-322 25 Levisman JA, MacAlpin RN, Abbasi AS, Ellis N, Eber LM: Echocardiographic diagnosis of a mobile, pedunculated tumor in the left ventricular cavity. Am J Cardiol 1975; ~:957-959 26 Dejoseph RL, ShiroH RA, Levenson LW, Martin CE, Zelis RF: Echocardiographic diagnosis of intraventricular clot. Chest 1977; 71:417-419 27 DeMaria AN, Bommer W, Neumann A, et al: Left ventricular thrombi identified by cross-sectional echocardiography, Ann Intern Med 1979; 90:14-18 28 Rogers PH, Sherry S: Current status of antithrombotic therapy in cardiovascular disease. Prog Cardiovasc Dis 1976; 19:235-253
CHEST, 77: 4, APRIl, 1980
ANTICOAGULATION IN LEFT VENTRICULAR ANEURYSM 488
mented basis for this, the short-term anticoagulation is advised to promote endothelialization of the thrombus known to be present in over one half of the aneurysms. Anticoagulation therapy is not routinely advised for the patient undergoing angiography and found to have a ventricular aneurysm as a result of a remote infarction even if a thrombus is suspected at angiography. The present study is subject to the limitations inherent in retrospective studies, and results should be carefully considered when formulating clinical policies and decisions. Further studies of a prospective nature are needed to further define the problem of management of patients with LV aneurysms. ACKNOWLEDGMENTS: The authors gratefully acknowledge the secretarial assistance of Ms. Dana Murray. Gratitude is expressed to cardiovascular surgeons John W. Kirklin, M.D., Robert B. Karp, M.D., and Albert D. Pacifico, M.D., for the opportunity to include their patients in this study.
Prevalence of Mural Thrombi and Systemic Embolization with Left Ventricular Aneurysm· Effect of Anticoagulation Therapy M iehaeZ T. Simpson, M.D .;t Albert Oberman, M.D .;t Nicho1o.sT. Kouchoukos, M.D.;§andWilliam/. Rogers, M.D., F.C.C.P.II Fifty-eigbt coosec:utive post-myocardial iDfan:tion (MI) patients undergoing Slll'gery for left ventricular (LV) anenrysm were studied retrospectively to assess the frequency, characteristics, and complications of mural thrombi found at surgery, and to determine wbat effect chronic anticoagulation might have bad upon the cUnical course of these patients. Mural thrombi at surgery were found In 66 percent (38/58). Of these, only 10 (26 percent) were prospectively identified by LV angiography; conversely, LV angiography misidentified the presence of mural thrombi In 10 percent (2/20) who bad no thrombus at surgery. Patients with mural thrombi were not different from those without thrombi In terms of time elapsed since their MI (28 ± 7 vs 24 ± 10 mOl), LV end-diastoUc pressure (LVEDP) (18 ± 2 vs 18 ± 2 mm JIg), ejection fraction (22 ± 1 vs 25 ± 2 %), or angiograpbic scar size (33 ± 2 vs 29 ± 3%).
Of 17 patients receiving long-term thenpy with war-
farin sodium preopentively for anticoagu1ation, nine bad mural thrombi, whereas eight did not (NS). There were only two patients In the total group (2/58=3 percent) with a preopentive event compatible with systemic arterial embolization--one of these was anticoagulated. Thus, In postmyocardlal patients baving LV anenrysmectomy; (1) the prevalence of mural thrombus is high but CaDnot be reUably ideutified prospectively by LV angiography or predicted by time since their MI, angiograpbic scar size, ejection fraction, or LVEDP; (2) the occurrence of preoperative systemic arterial embolization is very low; and (3) chronic: anticoagulation bas no apparent effect on the frequency of preopentive systemic arterial embolization or the prevalence of LV mural thrombus at surgery.
-From the Division of Cardiology, Department of Medicine~ and the Division of Cardiovascular Surgery, Department or Surgery, University of Alabama Medical Center, Birmingham. This research was supported by the National Heart and Lung Institute (Specialized Center of Research for Ischemic Heart Disease) Contract Number IP17HL17667-04 by 'Program Project grant HL 11, 310, and by the Clinical Research Unit grant MO-RROOO-13 (General Clinical Research Centers Program, Division of Research Resources of the National Institutes of Health). Presented in part at the 27th Annual Scientific Session, American College of Cardiology, Anaheim, CA, March 6-9, 1978. tFeIlow in Cardiology. tAssociate Professor of Medicine. §Professor of Surgery. IIAssistant Professor of Medicine. . Manuscript received January 26; revision accepted June 21. Reprint requests: Dr. Rogers, 330 Lfiona-HlJf'riacm Building, University of Alabama Medical Cettter, Binnlngham 35294
frequency of systemic embolization as judged by evidence of peripheral organ infarcts, but clinical studies of patients with aneurysmsll,1'l1,13-21 suggest a much lower occurrence of clinically apparent systemic embolization. No study, however, has systematically investigated the influence of anticoagulation on the formation of mural thrombi or occurrence of systemic embolization. The diagnosis of left ventricular ( LV) mural thrombi prior to inspection of the ventricular chamber either at surgery or at autopsy is difficult and frequently involves intuitive clinical diagnosis following an episode of sudden arterial insufficiency in patients with a known LV aneurysm, Certain findings at LV angiography are suggestive of mural thrombus in the ventricle; however, several studies8.11.12.11 have demonstrated the limitations of the single plane angiogram in diagnosing mural thrombi. The purpose of this study was to determine, in a group of patients undergoing surgical resection of LV aneurysm the following: (1) the prevalence of mural thrombi at surgery; (2) the effectiveness of biplane LV angiography in detecting mural throm-
CHEST, 77: 4, APRIl, 1980
ANTICOAGULATION IN LEn VENTRICULAR ANEURYSM 483
patients known or suspected of having aneurysms of the left ventricle following myocardial infarction (MI) are frequently maintained on warfarin sodium because of the occasional occurrence of systemic embolization. Several autopsy studies1-li and surgical studies6-13 reveal that mural thrombi occur in the ventricles of approximately one-half of all patients with postinfarction ventricular aneurysms. The incidence of systemic embolic events, however, is not clear. Autopsy studies'" suggest a substantial
AP VIEW
LATERAL VIEW
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I I
I
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AKINETIC OR OYSKINETIC LENGTH OF ENO DIASTOLIC CIRCUMFERENCE TOTAL END DIASTOLIC CIRCUMFERENCE
• x
100
FIGURE 1. Angiographic estimation of aneurysm size. 23 End-diastolic (solid lines) and endsystolic (do8hed lines) left ventricular silhouettes in AP and lateral projections were superimposed, using fixed x-ray beam markers (solid dots) as references. Portion of end-diastolic circumference which was akinetic or dyskinetic, shown as the region between the brackets, was expressed as a percentage of the total end-diastolic circumference, averaged for two projections, and designated "percent abnormally contracting segment." Hypokinesis was not quantitated by this model.
bi; (3) factors which may predict the presence of mural thrombi preoperatively; (4) the occurrence of clinically apparent systemic embolization; and (5) the effect of long-term anticoagulation therapy with warfarin sodium on the frequency of mural thrombi and systemic embolization. METHODS
Patient Population The study population consisted of 58 consecutive patients from September 1971 through December 1976 at the University of Alabama Medical Center undergoing (1) coronary angiography, (2) biplane LV angiography, and (3) resection of postinfarction LV aneurysm. Patients having cardiac catheterization at other hospitals and referred to this institution for surgery were not included in this analysis. Due to the referral nature of this institution, uniformity in clinical management prior to surgery could not be assured; therefore, some patients had received anticoagulants while others had not. Clinical Analysis
Clinical charts were reviewed to ascertain the past history of anticoagulation and systemic embolic events. Operative notes were examined to determine the presence or absence of mural thrombi in the left ventricle. Surgery In this study, aneurysm was defined as an abnormally thinned, scarred, or bulging segment of LV free wall noted at the time of surgery. Resection of myocardial scars not conforming to this definition were not included in this series. The surgical technique has been described previously.21 The
4&4 SIMPSON ET AL
primary indication for surgery was congestive heart failure in 35 patients, angina in 16 patients, and serious rhythm disturbances in 7 patients. Systemic arterial embolization was not the indication for surgery in any patient. Angiographic Studies
Subjects were classified as having single or multiple vessel coronary artery disease on the basis of preoperative selective coronary angiography; a coronary artery diameter stenosis of ~ 70 percent in any projection was considered significant. The angiographic studies of patients undergoing biplane left ventriculography at our institution were reviewed, and angiographic volumes were obtained by techniques previously described. 22 Calculations were made of LV ejection fraotion and percent abnormally contracting segments, the latter an angiographic estimation of scar size, obtained by first superimposing the end-diastolic and end-systolic LV silhouettes and then ascertaining the percentage of end-diastolic circumference which was either akinetic or dyskinetic18 (Fig 1). The original angiographic interpretations by both the cardiologists and radiologists were reviewed with respect to the preoperative diagnosis of LV mural thrombi. These anglograms had been reviewed simultaneously by both a cardiologist and a cardiac radiologist, and there was agreement between their interpretations in all but two of the 58 studies. However, a mural thrombus mentioned in either report rendered the angiogram "positive" for the purpose of this analysis. Statistical Analysis
Data are reported as mean ± standard error of the mean. The nonpaired t-test and Chi-square test were used to assess differences between groups of nonpaired data.
CHEST, 77: 4, APRIL, 1980
Table I--Clinic:al and Angiographic: Charac:teri.tiu of PaeieR" wieh and wiehoue Mural Thrombi * Total Group
With Thrombi
Without Thrombi
58
38
20
50M,8F
33M,5F
17M,3F
Age (yr)
55±1
57±1
52±!
Time since infarction (mos)
26±6
28±7
24±5
No. of patients Sex
Multivessel CAD
28 18 10 (48 percent) (47 percent) (50 percent)
LVEDP (mm Hg)
17±1
18±2
18±1
Ejection fraction (percent)
23±1
22±1
25±1
ABN contracting segment (percent)
32±1
33±1
29±1
*All values are mean ± standard error of the mean. Multivessel CAD was defined as double or triple vessel coronary artery disease. LVEDP indicates left ventricular enddiastolic pressure. REsULTS
Clinical and Angiographic Data Fifty eight patients satisfied the study criteria (Table 1). The group was composed of 50 men and 8 women with an average age of 55 + 1 years. The mean elapsed time since MI was 26 ± 6
months. Twenty-eight patients, representing 48 percent, had multivessel coronary artery disease representing either two or three-vessel disease. The mean LV end-diastolic pressure was 17 ± 1 mm Hg, while the average ejection fraction was 23 ± 1 percent. The mean size of the abnormally contracting segment was 32 ± 1 percent. All patients demonstrated sinus rhythm, and no episodes of supraventricular arrhythmias were documented or suggested in any patient. Seven patients underwent left ventricular aneurysmectomy primarily due to serious ventricular arrhythmias. The prevalence of mural thrombi was not different in the groups operated upon for arrhythmias and those operated upon for other indications. Incidence of Mural Thrombi and Effect of Anticoagulation The operative notes of the 58 patients were reviewed with respect to the presence or absence of thrombi in the ventricle. There were 38 patients with mural thrombi; this represents a 66 percent prevalence of mural thrombi in this group. When compared with patients without mural thrombi, the group with mural thrombi were no different with respect to age, elapsed time since infarction, prevalence of multivessel coronary artery disease, LV end-diastolic pressure, ejection fraction, or size of the abnormally contracting segment (Table 1).
FIGURE 2. Angiographic detection of left ventricular mural thrombi; AP and lateral projections of left ventricular angiogram. This angiogram was reported as revealing an apical thrombus due to persistent filling defect in apex inside thin line of calcification indicated by the am)ws. At surgery, the aneurysm was lined with calcium, and adherent to its endocardial surface was a moderate amount of thrombus. This represents a "true positive" angiogram with respect to mural thrombus detection.
CHEST, 77: 4, APRIl, 1980
ANTICOAGULATION IN LEn VENTRICULAR ANEURYSM 465
Therefore, these factors were not helpful in predicting the patient with a mural thrombus. Seventeen patients had been maintained on anticoagulants, most since their initial hospitalization for MI. Nine patients receiving anticoagulants had mural thrombi, whereas eight patients had no mural thrombi (p = NS). Of those 41 patients not receiving anticoagulants, 29 had mural thrombi and 12 had no mural thrombi. Angiographic Detection of Mural Thrombi
Of the 38 patients with mural thrombi at surgery, only 10 thrombi (26 percent) were diagnosed angiographically while 28 thrombi (74 percent) were not detected. Of the 20 patients without mural thrombi at surgery, 18 patients (90 percent) had no angiographic evidence of thrombi; however, two patients (10 percent) were incorrectly suspected of having mural thrombi on the basis of left ventriculography. Thus, 30 out of 58 angiograms (52 percent) were misleading with respect to predicting the presence or absence of mural thrombi (Fig 2 and 3). Effect of Rhythm Disorders on Prevalence of Mural Thrombi and Incidence of Systemic Embolization
All patients demonstrated sinus rhythm at the time of surgery. Seven patients, however, had had previous supraventricular arrhythmias. All seven patients with supraventricular arrhythmias had mural thrombi, whereas only 31 of the 51 patients without supraventricular arrhythmias had mural thrombi (p < .05). None of these seven patients with supraventricular arrhythmias had a history of systemic embolization. Seven patients underwent surgery due to serious ventricular arrhythmias. The prevalence of mural thrombi and incidence of systemic embolization was not different in groups with and without serious ventricular arrhythmias. Incidence of Systemic Embolization and Effect of Anticoagulation
Only two of the 58 patients had previous events which were clinically thought to be systemic arterial embolization. One was a 34-year-old man who had an embolus to his left femoral artery two months following an anterior MI. This patient had not been maintained on anticoagulants. The other was a 56year-old man with an apparent embolic cerebrovascular accident two years following an anterior MI even though he had taken warfarin sodium since the infarction. Of the 17 patients maintained on anticoagulants, only the one patient had an embolic 46& SIMPSON ET AL
FIGURE 3. Angiographic detection of left ventricular mural thrombi; AP and lateral projections of left ventricular angiogram. This angiogram was not reported to reveal evidence of left ventricular mural thrombus; however, at surgery there was a moderate amount of clot underlying thin-walled aneurysm. This represents a "false negative" angiogram with respect to mural thrombus detection.
event-an incidence of 6 percent. Of the 41 patients not on anticoagulants, the one patient with an embolic event represents a 2 percent incidence. DISCUSSION
The results of this study suggest the following: CHEST, 77: 4, APRIL, 1980
T.ble ~eeurrenee 01 Mural Thrombi and Sy*mie Emboli.lion in LV ~neury.nu: ~ulD,.,. S. . . .
Patients With LVA
Mural Thrombi (Percent)
Emboli (Percent)
40
27 (68)
6 (15)
102
55 (54)
53 (52)
65
9 (14)
9 (14)
Dubnow et a1
80
52 (65)
30 (38)
Davis and Ebert'
27
12 (44)
2 (5)
314
155 (49)
100 (32)
Phares et all Schlichter et a1
2
Abrams et al' 4
Total (Mean)
LVA =-left ventricular aneurysm.
( 1) the prevalence of mural thrombi is high in patients with LV aneurysm; (2 ) factors such as severity of coronary artery disease, LV function, and size of the abnormally contracting segment do not identify patients at risk to have mural thrombi; (3) biplane LV angiography is neither sensitive nor specific for the detection of mural thrombi; (4) clinically apparent systemic embolization is uncommon and does not appear to be affected by long-term anticoagulation therapy with warfarin sodium.
Incidence and Preoperative Identification of Mural Thrombi This study reaffirms the relatively common prevalence of mural thrombi in the ventricle of the patient with postinfarction LV aneurysm as reported in previous studies (Table 2 and 3). We were unable to identify unique characteristics of patients with mural thrombi by examining clinical or hemodynamic factors (Table 1). The angiographic detection of mural thrombi by single-plane left ventriculography has been shown in previous studies to be limited when the "confirmed" absence or presence of thrombus (by inspection at surgery or autopsy) is compared with the angiographic interpretation (Table 4). Our study utilized biplane left ventriculography, and likewise, failed to reliably detect the thrombi. Angiographic criteria for diagnosing mural thrombi have included (1) persistent chamber fllling defects, (2) venbicular wall calcification, and (3) "mackeral sky" appearance of the contrast medium-filled ventricle. Wall calcification is an infrequent· finding and- .may be seen in other cardiac disorders.P' The "maekeral sky" appearance refers to areas of uneven mixing or puddling of contrast media in the ventricle, and while suggestive of mural thrombus, is nonspecific and may be seen in the enlarged, relatively atonic aneurysmal ventricle with poor mixing without mural thrombus.F Most of the angiographically diagnosed thrombi in this series were on the basis of fllling defects within the
CHEST, 77: 4, APRIL, 1980
ventricular chamber during both systole and diastole ( Fig 2). Many mural thrombi, even those found to be quite large at the time of surgery, were not detected angiographically. Mural thrombi frequently are covered by endothelium which may produce a smooth contour to the venbicular cavity resulting in failure to suspect a thrombus when interpreting angiograms. Case reports have appeared of M-mode echocardiographic diagnosis of ventricular thrombi;2s,26 however, this would appear to lack sensitivity. Cross-sectional echocardiography may provide a realistic noninvasive approach to detection of mural thrombi in the ventricle/"
Frequency of Systemic EmboUzation The 3 percent frequency of clinically apparent systemic embolization in this study is consistent with most similar previous reports on LV aneurysms (Table 3 ). The occurrence of systemic embolization judged by autopsy data (Table 2) is almost uniformly higher than that reported in clinical studies (Table 3). Clinical studies probably overlook small or subclinical emboli and may underestimate the numTable 3--Oeeurrenee 01 Mural Thrombi and Sy.eemie Emboli.don in LV ~neury.m.: CUnieal-Surpeal Studi. *
Patients With LVA
Author
Thrombi (Percent)
Cooley et al'
6
3 (50)
7
Cooley et a1
37
37 (100)
Gorlin et al
14
Emboli (Percent)
2 (5)
24
0 (0)
16
41
0 (0)
Schattenberg et all'
37
4 (11)
Cheng"
35
(3)
Key et al
Kluge et a1
36
25 (69)
0 (0)
Graber et al t
23
18 (78)
3 (13)
Davis and Ebert'
40
8
Loop et al
Stoney et al Roo et al
400
lO
18
212 (53)
29 60
ll
2 (5) 19 (5) 2 (7) 19 (32)
0 (0)
Cooperman et alIt
55
5 (9)
Watson et al-
16
0 (0)
Marco et al
80
13 (16)
Mullen et alII
60
10 (17)
0 (0)
Simpson et al (1978)
58
38 (66)
2 (3)
Total
l2
1037
*Elipses indicate no information available. LVA ~ left ventricular aneurysm.
ANTICOASULAnON IN LEFT VENTRICULAR ANEURYSM 487
Table 4--Sin.le Plane Anpo.,.aplde Dea«lion 01 LV Mural Tlarombi in Palienla willa LV Aneu,.,..m.
No. of Patients
Confirmed Thrombus
True Positive Angiogram
False Negative Angiogram
ConfirmedNo Thrombus
Cheng 17
35
20
10
10
15
Kluge et a18
36
25
6
19
11
0
11
Rao et alII
60
19
6
13
41
0
41
Marco et a112
80
13
12
67
2
65
211
77 (36 percent)
54 (70 percent)
134 (64 percent)
3 (2 percent)
(98 percent)
Totals
23 (30 percent)
ber of emboli in part by their retrospective design. However, autopsy evidence of peripheral organ infarction may be seen in patients dying in other circumstances, such as following prolonged arterial hypotension, and is not felt to be entirely diagnostic of arterial embolization. The true frequency of systemic embolization is probably higher than that determined by clinical studies but lower than reported by autopsy studies.
EDect of Rhythm Disorders on Prevalence of Mural Thrombi An apparently increased prevalence of ventricular mural thrombi in patients with prior supraventricular arrhythmias was observed in our study, and to our knowledge, has not been previously reported. The history of serious ventricular arrhythmias did not appear to inHuence either the prevalence of mural thrombi or incidence of systemic embolization. I nfluence of Anticoagulation on Mural Thrombi and
Systemic Embolization
The prevalence of mural thrombi was not signicantly different in the patients receiving anticoagulants as compared to the patients not taking them. In this study, only two of the 58 patients had events suggestive of systemic embolization, and one of these patients had been maintained on warfarin sodium. This low frequency of embolization would render it difficult to demonstrate a protective effect due to any intervention, including anticoagulation. The degree and consistency of anticoagulation could not be evaluated in this retrospective study; however, the commonly obtained history was that the patient had taken anticoagulants, and therefore, visited his personal physician regularly for prothrombin time determinations. The problems of anticoagulant monitoring, patient compliance, and interfering drugs are always difficult to assess, even in prospective controlled trials. Some authors'' have suggested a decline in the
488 SIMPSON ET AL
False Positive Angiogram
True Negative Angiogram
14
131
frequency of systemic embolization in patients with LV aneurysm which may be due to the increased use of anticoagulants. This change in embolization frequency may, however, represent the comparison of earlier, predominantly autopsy studies with more recent clinical studies. The problems with this comparison were delineated above. The failure to note an obvious therapeutic benefit of administering anticoagulants to patients with left ventricular aneurysms may in part relate to the pathogenesis of mural thrombosis in LV aneurysms. Thrombi may be classified into three general types: 28 platelet, coagulation, and intermediate or mixed. Thrombi forming in areas of high pressure and How, such as arterial intimal lesions, tend to be composed primarily of platelets, and prevention of such platelet thrombi might result from use of specific anti-platelet pharmacologic agents. Thrombi, such as venous thrombi or mural thrombi, in the atonic atria of patients with rheumatic mitral valve disease form in areas of low pressure and slow flow and would appear to be most effectively prevented by antithrombin agents such as heparin or warfarin sodium. Mural thrombi in left ventricular aneurysms may represent the intermediate or mixed thrombi in which rapid How, turbulence, and static zones are present together." their prevention may require a dual approach of combined drugs such as warfarin sodium together with platelet inhibitors such as aspirin, sulfinpyrazone, and dipyridamole. Such a combination would be expected to be more hazardous in terms of bleeding complications and would probably not be warranted in this condition of relatively infrequent embolic complications. Results from this study, as well as from previous studies cited here, fail to support the long-term administration of warfarin sodium to patients with known LV aneurysms for prevention of systemic embolization. The current recommendation in our institution advises anticoagulation for six months for the early postinfarction patient shown to have a LV aneurysm whether or not the angiogram is "positive" for mural thrombus. Even though there is no docu-
CHEST, 77: 4, APRIL, 1980
1 Phares WS, Edwards JE, Burchell HB: Cardiac aneurysms: clinicopathologic studies. Mayo Coo Proc 195~; 28:264-271 2 Schlichter J, Hellerstein HK, Katz LN: Aneurysms of the heart: a correlative study of one hundred and two proven cases. Medicine 1954; 33:43-86 3 Abrams DL, Edelist A, Luria MH, Miller AJ: Ventricular aneurysm: a reappraisal based on a study of sixty-five consecutive autopsied cases. Circulation 1965; 27: 164169 4 Dubnow MH, Burchell HB, Titus JL: Post-infarction ventricular aneurysm: a clinicopathologic and electrocardiographic study of 80 cases. Am Heart J 1965; 70:753760 5 Davis RW, Ebert PA: Ventricular aneurysm: a clinicalpathologic correlation. Am J Cardiol 1972; 29: 1-6 6 Cooley DA, Henly WS, Amad KH, Chapman DW: Ventricular aneurysm following myocardial infarction: results of surgical treatment. Ann Surg 1959; 150:595-612 7 Cooley DA, Hallman GL, Henly WS: Left ventricular aneurysm due to myocardial infarction. Arch Surg 1964; 88:114-121 8 Kluge TH, UDal SR, Hill JD, Kerth WJ, Gerbode F: Dyskinesis and aneurysm of the left ventricle: surgical experience in 36 patients. J Cardiovasc Surg 1971; 12:273280 9 Graber JD, Oakley CM, Pickering BN, Goodwin ]F, Raphael MJ, Steiner RE: Ventricular aneurysm: an appraisal of diagnosis and surgical treatment. Br Heart J 1972; 34:830-838 10 Loop FD, EfBer DB, Navia JA, Sheldon WC, Groves LK: Aneurysms of the left ventricle: survival and results of a ten-year surgical experience. Ann Surg 1973; 178:399405
11 Rao G, Zikria EA, Miller WH, Samadani sa, Ford WB: Experience with sixty consecutive ventricular aneurysm resections. Circulation 1974; 50( suppl 2) :149-153 12 Marco JD, Kaiser GC, Barner HE, Codd JE, Willman VL: Left ventricular aneurysmectomy. Arch Surg 1976; 3:419-422 1~ Mullen DC, Posey L, Grabriel R, Singh HM, Flemma RJ, Lepley D: Prognostic considerations in the management of left ventricular aneurysms. Ann Thorac Surg 1977; 23:455-460 14 Gorlin R, Klein MD, Sullivan JM: Prospective correlative study of ventricular aneurysm. Am J Med 1967; 42:512531 15 Key JA, Aldridge HE, MacGregor DC: The selection of patients for resection of left ventricular aneurysm. J Thorac Cardiovasc Surg 1968; 56:477-483 16 Schattenberg TT, Giuliani ER, Campion BC, Danielson GK: Post-infarction ventricular aneurysm. Mayo Clin Proc 1970; 45:13-19 17 Cheng TO: Incidence of ventricular aneurysm in coronary artery disease: an angiographical appraisal. Am J Med 1971; 50:340-355 18 Stoney WS, Alford WC, Burrus GR, Thomas CS: Repair of anteroseptal ventricular aneurysm. Ann Thorac Surg 1973; 15:394-404 19 Cooperman M, Stinson EB, Griepp RB, Shumway NE: Survival and function after left venbicular aneurysmectomy. J Thorac Cardiovas Surg 1975; 69:321-328 20 Watson LE, Diekhaus DW, Martin RH: Left ventricular aneurysm: preoperative hemodynamics, chamber volume, and results of aneurysmectomy. Circulation 1975; 52-868873 21 Kouehoukos NT, Doty DB, Buettner LE, Kirklin JW: Treatment of postinfarction cardiac failure by myocardial excision and revascularization. Circulation 1972; 45 ( suppl 1) :172-178 22 Rackley CE, Hood WP: Measurements of ventricular volume, mass, and ejection fraction. In: Grossman W, 00. Cardiac catheterization and angiography. Philadelphia: Lea and Febiger, 1974, 176 23 Feild BJ, Russell RO, Dowling JT, Rackley CE: Regional left ventricular performance in the year following myocardial infarction. Circulation 1972; 46:679-689 24 Hurst JW: The heart, 4th 00. New York: McGraw-Hill, 1978, 318-322 25 Levisman JA, MacAlpin RN, Abbasi AS, Ellis N, Eber LM: Echocardiographic diagnosis of a mobile, pedunculated tumor in the left ventricular cavity. Am J Cardiol 1975; ~:957-959 26 Dejoseph RL, ShiroH RA, Levenson LW, Martin CE, Zelis RF: Echocardiographic diagnosis of intraventricular clot. Chest 1977; 71:417-419 27 DeMaria AN, Bommer W, Neumann A, et al: Left ventricular thrombi identified by cross-sectional echocardiography, Ann Intern Med 1979; 90:14-18 28 Rogers PH, Sherry S: Current status of antithrombotic therapy in cardiovascular disease. Prog Cardiovasc Dis 1976; 19:235-253
CHEST, 77: 4, APRIl, 1980
ANTICOAGULATION IN LEFT VENTRICULAR ANEURYSM 488
mented basis for this, the short-term anticoagulation is advised to promote endothelialization of the thrombus known to be present in over one half of the aneurysms. Anticoagulation therapy is not routinely advised for the patient undergoing angiography and found to have a ventricular aneurysm as a result of a remote infarction even if a thrombus is suspected at angiography. The present study is subject to the limitations inherent in retrospective studies, and results should be carefully considered when formulating clinical policies and decisions. Further studies of a prospective nature are needed to further define the problem of management of patients with LV aneurysms. ACKNOWLEDGMENTS: The authors gratefully acknowledge the secretarial assistance of Ms. Dana Murray. Gratitude is expressed to cardiovascular surgeons John W. Kirklin, M.D., Robert B. Karp, M.D., and Albert D. Pacifico, M.D., for the opportunity to include their patients in this study.