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Coronary Artery Disease and Left Ventricular Mural Thrombi: Clinical, Hemodynamic and Angiocardiographic Aspects
Coronary Artery Disease and Left Ventricular Mural Thrombi: Clinical, Hernodynamic and Angiocardiographic Aspects* Robert I . Hamby, M.D., F.C.C.P.;B. George Wisofl, M.D., F.C.C.P.; Edward T . Dauison, M.D., F.C.C.P.;and Marvin L. Hartstein, M.D. Twenty-two patients were found, during cardiac catheterization, to have mural thrombi in the left ventricle. Their ages varied from 40 to 72; the majority wen referred for evaluation because of angina peetoris. A history of multiple infarctions was noted in 13 patients. Only eight, however, had e l e c t r o c ~ p l d evidence c of two previous myocardial infarctions. The clinical and hemodynamic features inclpded cardiomegaly in 12, electrocardiographic evidence of previous anterior wall (anterior or anteroseptal) myocardhl infarction in 21 and the uniform finding of left ventricular dysfunction as well as severe s t e m i s > 95 percent) or complete obstruction of the left anterior descending artery in all 22. The frequency of mural thrombns in the total group of 458 p a tients with arteriosclerotic beart disease evaluated during the period of time of this study was 4.8 percent. If, however, one only considers patients with evidence of previ-
mural thrombi are commonly found Cardiac at postmortem examination.I4 Arteriosclerotic
heart disease is the most frequent form of heart disease associated with mural-thrombi of the left ventricle.' It is generally appreciated that mural thrombi in the left ventricle are commonly associated with ventricular aneurysm^.^,^ Pathologic studies, however, have documented the frequent occurrence of mural thrombi with acute and healed transmural myocardial infar~tion.'~,~ Mural thrombi of the heart can be suspected clinically during an acute myocardial infarction complicated by a systemic e m b ~ l u s . ~It - ' ~has been estimated that 1 percent of all acute myocardial infarctions are complicated by such systemic thromboembolic manifestations. Indeed, acute myocardial infarction has presented initially with a thromboembolic complication. All studies on mural thrombi of the heart are based on postmortem studies. The purpose of the present paper is to give the clinical, hemodynamic and angiographic findings in 22 patients who were found, at the time of study, to have mural thrombi of the left ventricle. These patients win be compared to "From the Department of Medicine, Cardiology Division and Department of Sur ery, Cardiovascular Division, Long Island Jewish-Hillsicf? Medical Center, New Hyde Park, Queens Hospital Center AfNiation, Jamaica; and the School of Medicine, Health Sciences Center, State University of New York at Stony Brook. Manuscript received September 7, 1973; revision accepted April 19. Reprint requests: Dr. Hamby, Long lslund ]&h-HtUskle Medfcal Center, New Hyde Park, New York 11040
488 HAMBY ET A1
ous anterior wan myocardial infarction, the frequency varies from 19.7 to 29.6 percent. The left ventricular angiogram demonstrated a ventricular aneurysm in one patient, while the remaining 21 patients with mural thrombi of the left ventricle had apical akinesia with or without aLInesia of the adjacent walls. The left ventricular mgiogmm revealed dhPtortion of the normal apical contour by a filling defect which varied in size and appeared smooth or ragged, with the appearance of a mam projecting ido the left ventricular cavity. Six patients underwent inhctectomy combined with aortocoronary bypass surgely and one patient had an aneurymectomy. A mural thrombus was found in all these patients at the time of surgery. Another patient died and postmortem examination confirmed the presence of a mural Uuombns. Systemic emboli presumably occurred in three patients and contributed to death in a fourth.
a larger number of patients evaluated at the same time who were also referred for symptomatic coronary artery disease but who did not have mural thrombi.
PATIENTS AND METHODS The 22 patients who form the basis of this report were referred by-their physicians because of symptomatic coronary artery disease. On admission to the hospital, all underwent a complete history and physical examination. A history of myocardial infarction was accepted if documented by the referring doctor, by serial electrocardiograms, or if the patient had a history of prolonged chest pain requiring hospitalization of three or more weeks. A history of congestive heart failure was based on a prior hospital admission for congestive heart failure or shortness of breath not associated with angina pectoris and responding to digitalis or diuretic therapy or both. A diagnosis of hypertension required either a history of antihypertensive therapy or a diastolic pressure over 90 mm Hg when admitted for evaluation. Cardiac roentgenographic studies were obtained on all patients and interpreted by a radiologist to define the presence or absence of cardiomegaly. Twelve lead electrocardiograms were taken on all patients and criteria of transmural myocardial infarction and interventricular conduction disturbance were based on accepted criteria.16 The technique for hemodynamic studies performed on these patients has been previously described.16 Right, transseptal and retrograde left heart procedures were performed on all patients. Pressures were measured in all chambers of the heart and cardiac output was obtained by the direct Fick principle. A left ventricular end-diastolic pressure above 11 mm Hg was considered abnormal. The cardiac output divided by the body surface area was expressed as an index, with a normal value for this laboratory being 3.320.8
CHEST, 66: 5, NOVEMBER, 1974
Umin/h@. Left ventricular angiograms were obtained by injecting 0.50 to 075 ml/kg of 90 percent sodium meglumine diatrizoate into the left ventricle through either the transseptal or retrograde catheter. Injection of the amtrast material was performed with a power injector (Viamonte-Hobbs) over a 2 to 2.5 second interval. The left ventricular angiographic study was performed with the patient in the right anterior oblique position, utilizing a dual field ( 9 and 6 inch ) image intensifier ( General Electric) with 35 mrn film, taken at 60 frames a second. At the completion of the left ventricular angiogram, selective coronary angiograms were performed in multiple views, using methods described by Sones and Shireyl7 or Judkins.18 Left ventricular volumes were obtained, by use of a modification of the area-leagtb method of Dodge and associates.'* The largest calculated volume was considered the end-diastolic volume which, divided into the stroke volume, defined the ejection fraction. The normal left ventricular end-diastolic volume index ( EDV ) and ejection fraction ( EF) determined by utilizing this method was 70+20 ml/M2 and 0.68+0.11, respectively. The pattern of left ventricular contraction was determined by reviewing the cineangiogram and utilizing the terminology defined by Herman and associates.20 A ventricular aneurysm was defined as a defect in the ventricular wall, presenting as a definite bulge in the external contour of the heart596 during diastole and which persists and may paradoxically bulge further during systole. Significant coronary artery disease was considered present if the arterial lumen was judged occluded by more than 50 percent.21 Since there is no mention in the literature of the andographic findings and criteria for making a diagnosis of a mural thrombus, the following criteria were
utilized on the basis of our experience in cases documented with a prior left ventricular angiogram at surgery or postmortem to have a mural thrombus present. A mural thrombus of the left ventricle was diagnosed if there was evidence of a
persistent filling defect in the left ventricular cavity during both systole and diastole, which distorts the normal contour of the left ventricular chamber.
Clinical Findings The pertinent clinical background of the 22 patients with a mural thrombus of the left ventricle is given in Table 1. All the patients had a history of a myocardial infarction and more than half had two or more. Two patients were referred three months after their last myocardial infarction (cases 7 and 12). Patients 3 and 20 had a cerebral vascular accident six and nine months, respectively, prior to evaluation and had no permanent neurologic impairment. Patients 4 and 5 had apical systolic murmurs and a third heart sound. Patient 3 had a third heart sound and patient 8 a double gallop. Cardiomegaly was present in 12. All the patients were in sinus rhythm A myocardial infarction on the electrocardiogram involving the anterior wall (anterior or anteroseptal infarction) of the left ventricle was present in 21
Table 1 4 l i n i c a l A w e c u of the 22 Patisntr with Mural Thrombi Last Conge Duration of Number of Myocardial tive Symptoms Myocardial Infarction Hyper- Heart Cardio(yrs) Infarctions (yrs) tension Failure megaly SPP~O~~
Patient Age/Sex
Angina pectoria Angina pectoris Congestive heart failure Angina pectoris Congestive heart failure Angina pectoris Angina pectoris Congestive heart failure Angina pectoris Angina pectoris Angina pectoris Angina pectoris Arrhythmia Arrhythmia Angina pectoris Angina pectoris Angina pectoris and shortness of breath Angina pectoris Angina pectoria Angina pectoris Angina pectoris Angina pectoris Angina pectoria
Abbreviations:
CHEST,
+
Electrocardiogram AMI, LAH AM1 AMI, IMI AMI, RBBB AM1 AMI, IMI AMI, IMI ASMI AMI, LAH, RBBB ASMI, IMI AMI, IMI AMI, IMI AMI, RBBB AMI, LAH ASMI AMI, LAH ASMI, IMI
AMI: LAH AMI, LAH IMI ASMI AMI. IMI
=present; 0 =absent. AMI, anterior myocardial infarction; LAH, left anterior hemiblock; IMI, inferior myocardial infarction; ASMI, anteroseptal myocardial infarction; RBBB, right bundle branch block
66: 5, NOVEMBER, 1974
CORONARY ARTERY MSEASE AND LEFT VENTRICULAR MURAL THROMBI 488
patients, with inferior wall myocardial infarction present as well in eight. Patient 20 was the only patient with an isolated inferior wall myocardial infarction on the electrocardiogram. This same patient had a double Vineberg procedure performed five years prior to the present study. ST segment elevation was not present in any of the 22 patients. H e m o d ~ m m kFindings and Angiographk 0bsertions
As indicated in Table 2, evidence of left ventricular dysfunction was present in all patients to a variable degree. All had one and, in most cases, two or more parameters (cardiac output, left ventricular end-diastolic pressure and volume, ejection fraction) of abnormal left ventricular function. The uniform finding of severe involvement of the left
anterior descending artery in all of the patients was striking and was characterized by complete proximal obstruction with little if any distal runoff in 15 patients and over 95 percent proximal stenosis in the remaining seven patients. Four patients had single vessel and nine had triple vessel disease. Left ventricular angiographic studies demonstrated abnormal contractile patterns in all patients, predominantlyinvolving the anterior and apical walls. In only one patient was a definite diastolic bulge present ( case 12), indicative of an aneurysm (see Method). In all patients, injection of contrast material into the left ventricle demonstrated Wing defects of variable size involving the apex of the left ventricle, which, in some cases, extended to the anterior or inferior wall. Six patients (cases 6, 9, 13, 17,21,20) had small apical filling defects. In
Table 2--Remodynamie a d Angiographic F i n d i w of the 22 P d e with ~ Mural Thrombi Patient, Cardiac Case Index No. (L/min/M')
-
LV, S/D (mm Hg)
EDV (ml/M1)
Mural Thrombus, Ejection Coronary Artery Disease Fraction Cx RCA LAD LV Wall Abnormality Location Anterior and apical akineaia Anterior and apical akinesia Antero-apical akineaia, inferior auyneresis Anterior and apical akineaia Anterior and apical akinesia Apical akineaia Antero-apical akineaia, inferior asynereais Difiuse hypokineaia Inferior-apical akinesia Anteroseptal akineaia Anteroaeptal akineaia Large apical aneurym Anterior akinesia Anterior and apical akineaia Antero-apical akineaia Antero-apical akineaia Inferior and apical akineaia , Anterior and apical akineaia Anterior and apical akineaia Apical and inferior akineaia Antero-apical akineaia Anterior and apical akinesia
Apex, large Apex and lower anterior, large Apex and inferior, large Apex, emall Lower anteroapical, small Apex, small Apex and lower anterior, large Apex, large Apex, small Apex, large Apex, small Within aneurysm Apex, small Apex, moderate Apex, large Apex, moderate Apex, small Apex, h
e
Apex, large Apex, small Apex, small Apex, small
Abbreviations: LV, S/D, left ventricular pressure, syetolic/diaatolic; EDV, end-diastolic volume, Cx, circumflex; RCA, right coronary artery; LAD, left anterior deecending
490 HAMBY ET A 1
CHEST,
66: 5, NOVEMBER, 1974
End - diastola
Infarctectomy and aortocoronary bypass were performed on six patients (cases 2,6, 8, 11, 13, 18). Aneurysmectomy alone was performed in case 12. A mural thrombus was found' at surgery in all the patients. Patient 8 died at surgery as a result of pump failure, whereas the remaining six patients had satisfactory postoperative courses and were discharged from the hospital. Four patients (cases3,4, 5, 10) died within nine months of evaluation. Patient 5 died of a massive cerebral vascular accident complicated by heart failure. Postmortem findings revealed marked myocardial fibrosis, a large, partially organized mural thrombus and thromboembolic obliteration of multiple vessels, including the internal carotid arteries. In the other three patients, no information was available as to the events leading to death and no postmortem was obtained. Patient 9
w
.
I
FIGURE 1. Left ventricular angiogram as viewed in the right anterior oblique projection. A. Patient 6. During enddiastole a slight apical irregularity is noted (arrow).Two cycles later, after dilution of contrast material, a filling defect at the apex is noted during end-systole (arrow). At surgery an apical thrombus was found. B and C. Patients 4 and 11,respectively, with arrow pointing to obliteration of the normal apical contour during both end-diastole and end-systole. At surgery an apical thrombus was found in patient 11.D. Patient 8. A large, irregular apical filling is noted, which, at surgery, was noted to be a partially organized friable thrombus.
three of these patients, during the early phase of the left ventricular angiogram, only an apical irregularity was noted (Fig 1A). As the contrast material was diluted during later cycles, however, a constant apical defect became evident. In other patients (cases 4, 10, 11, 14, 16, 18, 19), the apex appeared sharply cut off during both diastole and systole ( Fig 1B and C ). In three patients (cases 1, 8, 15), the apex appeared completely obliterated by an irregular, nonuniform density (Fig ID). Extension of the filling defect to the lower anterior wall (Fig 2A and B) was noted in three patients (cases 2, 5, 7) and in one patient (case 3 ) this extended to the inferior wall (Fig 2C). In patient 12, the entire anteroapical aneurysm was obliterated by a thrombus ( Fig 2D ) . Patient 20 ( Fig 3 ), the only patient with an isolated inferior wall myocardial infarction, had a history of a cerebral vascular accident and had, on left ventricular angiogram, a globular apical fillingdefect. CHEST, 66: 5, NOVEMBER, 1974
FIGURE2. Left ventricular angiogram as viewed in the right anterior oblique projection. A and B. Patients 2 and 5, with apical filling defect extending to the lower anterior wall. In patient 2, at surgery, the angiographic &dings were conh e d . C. Patient 3 has a mural thrombus extending to the inferior wall. D. Patient 12 with a chest x-ray film demonstrating cardiomegaly. The enddiastolic silhouette, however, did not reveal a large cardiac chamber. This was due to the presence of a large thrombus (arrow) obliterating an aneurysm, which was codinned at surgery.
CORONARY ARTEIRY DISEASE AND LEFT VENTRICULAR MURAL THROMBI 491
FIGURE3. Left ventricular angiogram as viewed in the right anterior oblique projection in patient 20. This is the only patient with an isolated inferior wall myocardial infarction. Note the distorted inferior wall of the left ventride during diastole, probably from a prior Vineberg procedure. The arrow points to a distinct globular apical filling defect.
sustained a cerebrovascular accident three months after discharge from the hospital. Patients 19,21 and 22 were not considered candidates for surgery and, on follow-up of over six months, they still have incapacitating angina pectoris. In the remaining six patients (cases 1, 7, 14 -17), no follow-up information was available. Cornparatioe Stud@
Since all the patients with mural thrombi had electrocardiographic evidence of a transmural myocardial infarction, a comparisdn was made only with patients who had evidence of an infarction on the electrocardiogram. Thus, of a total of 458 patients with coronary disease during the period of this study, 228 had evidence of a transmural myocardial infarction. Of the total group of patients with prior transmural myocardial infarction, 22 had mural thrombi, while 206 did not have evidence of a mural thrombus. No significant differences were noted in the duration of symptoms or incidence of hypertension or congestive heart failure when comparing those with mural thrombi and those without mural thrombi and a prior transmural infarction. Cardiomegaly was present in 55 percent of the patients with mural thrombi but in only 24 percent of the patients with prior infarction but no mural thrombi (p<0.001). A review of the electrocardiographic findings of the entire group of 458 patients (Table 3) seen indicated that approximately 20 percent of Table 3-8leetrocardiographic Finding* cu Related to the Presence of Mural Thrombi No.
Mural Thrombus Present Percent
No transmural infarction
230
0
0
Inferior transmural infarction (isolated)
135
1
0.7
Anterior transmural infarction (isolated)
86
1%
19.7
Combined inferior and anterior infarction
27
8
29.6
the patients with anterior wall (anterior or anteroseptal) myocardial infarction had mural thrombi. The highest incidence of mural thrombi occurred in patients with electrocardiographic evidence of multiple myocardial infarctions (29.6 percent ) . Left ventricular dysfunction, as indicated by hemodynamic findings and abnormal contractile patterns, was found in all 22 patients with mural thrombi, while 61 percent of the patients without mural thrombi, however, had at least one abnormal hemodynamic parameter and, in 93 percent, abnormal left ventricular systolic wall movement was present. Seven patients with electrocardiographic evidence of a transmural myocardial infarction had a persistent diastolic and systolic bulge of the left ventricular wall consistent with a true ventricular aneurysm. Finally, high grade stenosis ( >95 percent narrowing of lumen) or complete obstruction of the left anterior descending artery found in all the patients with mural thrombi was observed in 65 percent of the remaining 179 patients. In the past, the recognition of mural thrombi in the heart was dependent on the postmortem study1+' and could only be clhically inferred in patients with arteriosclerotic heart disease if the clinical course was complicated by a systemic embolus.'-l4 Such systemic emboli complicating coronary artery disease occur predominantly during acute myocardial infarction. Such complications during acute myocardial infarction could be reduced,22although not preventede with anticoagulants. A thromboembolic complication may, furthermore, precede clinical recognition of acute myocardial infarction.18.14 In the present cases, information was only available in seven patients during their last hospitalization for an acute myocardial infarction and revealed that five were receiving anticoagulants, while two patients did not. Thromboembolism was documented in one patient and presumably occurred in three other patients with cerebral vascular accidents. It is rather surprising that, in spite of the very high frequency of mural thrombi of the left ventricle reported at postmortem examination in patients with arteriosclerotic heart disease,'+' there is no mention in the literature of angiographic documentation in patients evaluated with coronary artery disease. The frequency of mural thrombi in the heart, observed at postmortem examination, ranges from 21 to 67 percent1" of all patients with arteriosclerotic heart disease. Although mural thrombi occur more frequently in patients who die of acute myocardial infarction, thrombi have been noted in 24 percent of patients dying with healed infarcti~ns.'.~Ventricular aneurysms have been reCHEST, 66: 5, NOVEMBER, 1974
ported in association with mural thrombi, in an incidence of from 54 percents to as high as 68 percent.5 Mural thrombi in the absence of a ventricular aneurysm are found in one-third of the patients dying with arteriosclerotic heart disease.'-' The frequency of mural thrombi in the left ventricle was only 4.8 percent of the total patients evaluated. More than half of these patients, however, had no evidence of previous transmural myocardial infarction. As indicated in Table 3, if one considers the location of the infarction, evidence of an anterior wall infarction (anterior or anteroseptal), whether isolated or combined with inferior wall myocardial infarction, wries a frequency varying from 19.7 percent to 29.6 percent incidence of mural thrombus. This supports the work of Jordan and co-workers2of the greater propensity of anterior myocardial infarctions for complication by mural thrombi. These authors found that 31 percent of healed anterior myocardial infarctions were complicated by mural thrombi as compared to 16.3 percent with healed inferior wall myocardial infarctions. The increased incidence of mural thrombi noted with anterior wall infarctions can, in part, be explained by the larger size of anterior infarctions as compared to posterior wall myocardial infarction. The size of the infarction has been directly related to the frequency of mural t h r ~ m b iEstimating .~ the area of the infarction, it was noted that in small infarctions ( <20 sq cm) the frequency of mural thrombi was 15 percent, whereas in large infarctions ( <80 sq em) the frequency was 93 percent. Multiple infarctions are more likely associated with extensive myocardial damage than are single infarctions. The frequency of mural thrombi in a heart with two or more myocardial infarctions present is greater than that found with single myocardial infarcts.' In the present series of 22 patients with mural thrombi, 13 had a history of two or more myocardial infarctions. Only eight, however, had electrocardiographic documentation of multiple infarctions. The left anterior descending artery is the major source of blood supply to the interventricular septum and anterior and apical wall of the left ventricle.16 Obstructive disease of the left anterior descending artery is #us more likely to be associated with a large myocardial infarction complicated by significant hemodynamic impairment.16 Thus, the uniform finding of significant stenotic or obstructive disease of the left anterior descending artery in all of our patients complicated uniformly by marked impairment of left ventricular function probably indicates the presence of a large myocardial infarction. In one series of patients reported, older age appeared as a factor favoring the frequency of mural thrombiSsIn the present group of patients, however, the age range was 40 to 72 years, not significantly CHEST, 66: 5, NOVEMBER, 1974
different from the 206 patients with electrocardic+ graphic evidence of a transmural myocardial infarction and no evidence of a mural thrombus. Duration of symptoms, presence of hypertension and a history of congestive heart failure could not be related to the presence of a mural thrombus. This agrees with the observations of Garvin.' Jordan and co-worke r ~ ?however, did observe an increased frequency of mural thrombi in patients with hypertension and congestive heart failure. In the present group of patients, cardiomegaly did appear related to mural thrombi, probably reflecting the extensive rnyocar&a1 damage present. The location of the mural thrombus in general is on the endocardial surface adjacent to the myocardial infarction,'3,hually at the apex of the heart and often extending to the anterior free wall or the anterior aspect of the interventricular septum. Left ventricular dysfunction in patients with mural thrombi, as noted in the present series, includes a decreased left ventricular ejection fraction and stasis of blood in the apex of the left ventricle. Left ventricular angiograms in our patients did suggest apical stasis as indicated by pooling of contrast material in the apex during three or four cardiac cycles after the completion of injection. In the present group of patients, all had apical filling defects of varying size, with extension in some to the lower anterior wall. As indicated in Figures 1 and 2, the angiographic pattern appears quite distinctive, with loss of the normal apical contour of the left ventricle by a filling defect. The margin of the filling defect may appear smooth or ragged, appearing as a mass projecting into the cavity of the left ventricle. It should be emphasized that the true incidence of mural thrombi is probably higher than noted in this study since angiographic methods are probably not sensitive enough to appreciate small thrombi. Furthermore, angiograms were only performed in the right anterior oblique projection. A more satisfactory approach would have been biplane angiographic studies. Although no thromboembolic complications occurred during the diagnostic evaluations, the high incidence of thrombus noted in association with infarction of the anterior wall of the left ventricle suggests caution when performing left ventricular angiograms on such patients. ACKNOWLEDGMENT: We thank Dr. Irwin H o h for his critical review of this manuscript. Assistance in preparin this manuscript was also given by Jarmila Dvorak, Ph.D. staff and Mrs. Brenda Hamby.
an1
1 Canin CF: Mural thrombi in the heart. Am Heart J 21:713-720, 1941 2 Jordan RA, Miller FU3, Edwards JE,et al: Thromboembolism in acute and in healed myocardial infarction. I. Intracardiac mural thrombosis. Circulation 6:l-6, 1952
CORONARY A1ITERY DISEASE AND LEFT VENTRICULAR MURAL THROMBI 493
3 Yater WM,Welsh PP, Stapleton JF, et al: Comparison of clinical and pathologic aspects of coronary artery disease in men of various age groups: A study of 950 autopsied
cases from the Armed Forces Institute of Pathology. AM 1ntem.Med 34 :352-392, 1951 4 Bean WB: Infarction of the heart. 111. Clinical come and morphological findings. Ann Intern Med 12:71-94, 1938 5 Phares WS, Edwards JE, Burchell HB: Cardiac aneurysms: Clinicopathologic studies. Proc Staff Meet Mayo Clinic 28:204-271, 1953 6 Schlichter J, Hellerstein HK, Katz LN: Aneurysm of the heart: A correlative study of 102 proved cases. Medicine 33:43-78, 1954 7 Young JR, Humphries AW, D e Wolfe VG, et al: Peripheral arterial embolism. JAMA 185:621-627, 1963 8 Deterling RA Jr, Vargas LL, Mc Allister FF: Follow-up studies of patients with embolic occlusion of the aortic bifurcation. Ann Surg 155:383-391. 1962 9 Thompson JE, Weston AS, Sigler L, et al: Arterial embolectomy after acute myocardial infarction: A study of 31 patients. AM Surg 171:979-986, 1970 10 Darling RC, Austen WG, Linton RR: Arterial embolism. Surg Gynec Obstet 124:106-114,1967 11 Miller RD,Jordan RA, Parker RL, et a]: Thromboembolism in acute and in healed myocardial infarction. 11. Systemic and pulmonary arterial occlusion. Circulation 6:7-15, 1952 12 Nielsen GL, Sorensen HR: The operative treatment of emboli in the extremities of patients with acute coronary occlusion. Danish Med Bull 15:249-252, 1968
13 Harrison CE Jr, Spittell JA Jr, Mankin HT: Sudden arterial occlusion: A clue to silent myocardial infarction. Proc Staff Meet Mayo Clin 37:293-300, 1962 14 Lazy BG, de Takats G: Peripheral arterial embolism after myocardial infarction: Occurrence in unsuspected cases and ambulatory patients. JAMA 155:10-13, 1954 15 Massie E, Walsh TJ: Clinical Vectorcardiography and Electrocardiography. Chicago, Year Book Publishers Inc, 1980 16 Hamby RI, Gupta MP,Young MW: Clinical and hemodynamic aspects of single vessel coronary artery disease. Am Heart J in press 17 Sones FM Jr, Shirey EK: Cine coronary arteriography. Mod Conc Cardiovasc Dis 31:735-738, 1962 18 Judkins MP: Percutaneous transfemoral selective corn nary arteriography. Radio1 Clin N Am 6:467-492, 1968 19 Dodge HT, Sandler H, Ballew DW, et al: The use of biplane angiocardiography for the measurement of left ventricular volume in man. Am Heart J 60:762-776, 1960 20 Herman MV, Heinle RA, Klein MD, et al: Localized disorders in myocardial contraction. Asynergy and its role in congestive heart failure. N Engl277:222-232, 1967 21 Proudfit WL, Shirey EK, Sones FM Jr: Selective cine coronary arteriography. Correlation with clinical findings in 1000 patients. Circulation 33:901-910,1968 22 Wright IS, Marple C, Beck DF: Myocardial Infarction: Report of the Anticoagulant Committee of the American Heart Association, New York, Grune and Stratton, Inc 1954 '
Mysterious Migration of Fishes The most adventurous journey of all is that of the fresh water eel. From the contents of plankton nets towed in various parts of the Atlantic Ocean aboard the
Thor and Dana, Johannes Schmidt, a Danish scientist, found that younger and younger stages of the tiny eels could be traced farther and farther back t o the deep central part of the North Atlantic Ocean southeast of Bermuda. Transparent eggs about the size of a pea are found there in the spring about 500 feet below the surface, so that mating probably takes place near the deep sea floor beneath. When the flat leaf-like larva is first hatched it is only a quarter. of inch long. These bizarre creatures grow slowly, and meanwhile travel on the long path toward fresh water. The baby eel takes three years to reach European waters. We cannot be
sure, but it seems likely that the newly-hatched leptocephalus rising part way to the surface is caught by the Gulf Stream and thus is canied to the European shores. By the time it reaches there it has become of age. It is strongly attracted by fresh waters draining out of rivers. When it amves at its destination at the river's mouth, the leaf-like shape disappears and it becomes narrow and round. In the rivers it grows to be a foot or more in length. Then as much as twenty years later, it begins to journey back to the spawning grounds of the Sargasso Sea, where a new generation begins the long ocean circuit. Chapin H, Smith FGH:The Ocean River. New York, Charles Scribneis Sons, 1952
CHEST, 66: 5, NOVEMBER, 1974
mural thrombi are commonly found Cardiac at postmortem examination.I4 Arteriosclerotic
heart disease is the most frequent form of heart disease associated with mural-thrombi of the left ventricle.' It is generally appreciated that mural thrombi in the left ventricle are commonly associated with ventricular aneurysm^.^,^ Pathologic studies, however, have documented the frequent occurrence of mural thrombi with acute and healed transmural myocardial infar~tion.'~,~ Mural thrombi of the heart can be suspected clinically during an acute myocardial infarction complicated by a systemic e m b ~ l u s . ~It - ' ~has been estimated that 1 percent of all acute myocardial infarctions are complicated by such systemic thromboembolic manifestations. Indeed, acute myocardial infarction has presented initially with a thromboembolic complication. All studies on mural thrombi of the heart are based on postmortem studies. The purpose of the present paper is to give the clinical, hemodynamic and angiographic findings in 22 patients who were found, at the time of study, to have mural thrombi of the left ventricle. These patients win be compared to "From the Department of Medicine, Cardiology Division and Department of Sur ery, Cardiovascular Division, Long Island Jewish-Hillsicf? Medical Center, New Hyde Park, Queens Hospital Center AfNiation, Jamaica; and the School of Medicine, Health Sciences Center, State University of New York at Stony Brook. Manuscript received September 7, 1973; revision accepted April 19. Reprint requests: Dr. Hamby, Long lslund ]&h-HtUskle Medfcal Center, New Hyde Park, New York 11040
488 HAMBY ET A1
ous anterior wan myocardial infarction, the frequency varies from 19.7 to 29.6 percent. The left ventricular angiogram demonstrated a ventricular aneurysm in one patient, while the remaining 21 patients with mural thrombi of the left ventricle had apical akinesia with or without aLInesia of the adjacent walls. The left ventricular mgiogmm revealed dhPtortion of the normal apical contour by a filling defect which varied in size and appeared smooth or ragged, with the appearance of a mam projecting ido the left ventricular cavity. Six patients underwent inhctectomy combined with aortocoronary bypass surgely and one patient had an aneurymectomy. A mural thrombus was found in all these patients at the time of surgery. Another patient died and postmortem examination confirmed the presence of a mural Uuombns. Systemic emboli presumably occurred in three patients and contributed to death in a fourth.
a larger number of patients evaluated at the same time who were also referred for symptomatic coronary artery disease but who did not have mural thrombi.
PATIENTS AND METHODS The 22 patients who form the basis of this report were referred by-their physicians because of symptomatic coronary artery disease. On admission to the hospital, all underwent a complete history and physical examination. A history of myocardial infarction was accepted if documented by the referring doctor, by serial electrocardiograms, or if the patient had a history of prolonged chest pain requiring hospitalization of three or more weeks. A history of congestive heart failure was based on a prior hospital admission for congestive heart failure or shortness of breath not associated with angina pectoris and responding to digitalis or diuretic therapy or both. A diagnosis of hypertension required either a history of antihypertensive therapy or a diastolic pressure over 90 mm Hg when admitted for evaluation. Cardiac roentgenographic studies were obtained on all patients and interpreted by a radiologist to define the presence or absence of cardiomegaly. Twelve lead electrocardiograms were taken on all patients and criteria of transmural myocardial infarction and interventricular conduction disturbance were based on accepted criteria.16 The technique for hemodynamic studies performed on these patients has been previously described.16 Right, transseptal and retrograde left heart procedures were performed on all patients. Pressures were measured in all chambers of the heart and cardiac output was obtained by the direct Fick principle. A left ventricular end-diastolic pressure above 11 mm Hg was considered abnormal. The cardiac output divided by the body surface area was expressed as an index, with a normal value for this laboratory being 3.320.8
CHEST, 66: 5, NOVEMBER, 1974
Umin/h@. Left ventricular angiograms were obtained by injecting 0.50 to 075 ml/kg of 90 percent sodium meglumine diatrizoate into the left ventricle through either the transseptal or retrograde catheter. Injection of the amtrast material was performed with a power injector (Viamonte-Hobbs) over a 2 to 2.5 second interval. The left ventricular angiographic study was performed with the patient in the right anterior oblique position, utilizing a dual field ( 9 and 6 inch ) image intensifier ( General Electric) with 35 mrn film, taken at 60 frames a second. At the completion of the left ventricular angiogram, selective coronary angiograms were performed in multiple views, using methods described by Sones and Shireyl7 or Judkins.18 Left ventricular volumes were obtained, by use of a modification of the area-leagtb method of Dodge and associates.'* The largest calculated volume was considered the end-diastolic volume which, divided into the stroke volume, defined the ejection fraction. The normal left ventricular end-diastolic volume index ( EDV ) and ejection fraction ( EF) determined by utilizing this method was 70+20 ml/M2 and 0.68+0.11, respectively. The pattern of left ventricular contraction was determined by reviewing the cineangiogram and utilizing the terminology defined by Herman and associates.20 A ventricular aneurysm was defined as a defect in the ventricular wall, presenting as a definite bulge in the external contour of the heart596 during diastole and which persists and may paradoxically bulge further during systole. Significant coronary artery disease was considered present if the arterial lumen was judged occluded by more than 50 percent.21 Since there is no mention in the literature of the andographic findings and criteria for making a diagnosis of a mural thrombus, the following criteria were
utilized on the basis of our experience in cases documented with a prior left ventricular angiogram at surgery or postmortem to have a mural thrombus present. A mural thrombus of the left ventricle was diagnosed if there was evidence of a
persistent filling defect in the left ventricular cavity during both systole and diastole, which distorts the normal contour of the left ventricular chamber.
Clinical Findings The pertinent clinical background of the 22 patients with a mural thrombus of the left ventricle is given in Table 1. All the patients had a history of a myocardial infarction and more than half had two or more. Two patients were referred three months after their last myocardial infarction (cases 7 and 12). Patients 3 and 20 had a cerebral vascular accident six and nine months, respectively, prior to evaluation and had no permanent neurologic impairment. Patients 4 and 5 had apical systolic murmurs and a third heart sound. Patient 3 had a third heart sound and patient 8 a double gallop. Cardiomegaly was present in 12. All the patients were in sinus rhythm A myocardial infarction on the electrocardiogram involving the anterior wall (anterior or anteroseptal infarction) of the left ventricle was present in 21
Table 1 4 l i n i c a l A w e c u of the 22 Patisntr with Mural Thrombi Last Conge Duration of Number of Myocardial tive Symptoms Myocardial Infarction Hyper- Heart Cardio(yrs) Infarctions (yrs) tension Failure megaly SPP~O~~
Patient Age/Sex
Angina pectoria Angina pectoris Congestive heart failure Angina pectoris Congestive heart failure Angina pectoris Angina pectoris Congestive heart failure Angina pectoris Angina pectoris Angina pectoris Angina pectoris Arrhythmia Arrhythmia Angina pectoris Angina pectoris Angina pectoris and shortness of breath Angina pectoris Angina pectoria Angina pectoris Angina pectoris Angina pectoris Angina pectoria
Abbreviations:
CHEST,
+
Electrocardiogram AMI, LAH AM1 AMI, IMI AMI, RBBB AM1 AMI, IMI AMI, IMI ASMI AMI, LAH, RBBB ASMI, IMI AMI, IMI AMI, IMI AMI, RBBB AMI, LAH ASMI AMI, LAH ASMI, IMI
AMI: LAH AMI, LAH IMI ASMI AMI. IMI
=present; 0 =absent. AMI, anterior myocardial infarction; LAH, left anterior hemiblock; IMI, inferior myocardial infarction; ASMI, anteroseptal myocardial infarction; RBBB, right bundle branch block
66: 5, NOVEMBER, 1974
CORONARY ARTERY MSEASE AND LEFT VENTRICULAR MURAL THROMBI 488
patients, with inferior wall myocardial infarction present as well in eight. Patient 20 was the only patient with an isolated inferior wall myocardial infarction on the electrocardiogram. This same patient had a double Vineberg procedure performed five years prior to the present study. ST segment elevation was not present in any of the 22 patients. H e m o d ~ m m kFindings and Angiographk 0bsertions
As indicated in Table 2, evidence of left ventricular dysfunction was present in all patients to a variable degree. All had one and, in most cases, two or more parameters (cardiac output, left ventricular end-diastolic pressure and volume, ejection fraction) of abnormal left ventricular function. The uniform finding of severe involvement of the left
anterior descending artery in all of the patients was striking and was characterized by complete proximal obstruction with little if any distal runoff in 15 patients and over 95 percent proximal stenosis in the remaining seven patients. Four patients had single vessel and nine had triple vessel disease. Left ventricular angiographic studies demonstrated abnormal contractile patterns in all patients, predominantlyinvolving the anterior and apical walls. In only one patient was a definite diastolic bulge present ( case 12), indicative of an aneurysm (see Method). In all patients, injection of contrast material into the left ventricle demonstrated Wing defects of variable size involving the apex of the left ventricle, which, in some cases, extended to the anterior or inferior wall. Six patients (cases 6, 9, 13, 17,21,20) had small apical filling defects. In
Table 2--Remodynamie a d Angiographic F i n d i w of the 22 P d e with ~ Mural Thrombi Patient, Cardiac Case Index No. (L/min/M')
-
LV, S/D (mm Hg)
EDV (ml/M1)
Mural Thrombus, Ejection Coronary Artery Disease Fraction Cx RCA LAD LV Wall Abnormality Location Anterior and apical akineaia Anterior and apical akinesia Antero-apical akineaia, inferior auyneresis Anterior and apical akineaia Anterior and apical akinesia Apical akineaia Antero-apical akineaia, inferior asynereais Difiuse hypokineaia Inferior-apical akinesia Anteroseptal akineaia Anteroaeptal akineaia Large apical aneurym Anterior akinesia Anterior and apical akineaia Antero-apical akineaia Antero-apical akineaia Inferior and apical akineaia , Anterior and apical akineaia Anterior and apical akineaia Apical and inferior akineaia Antero-apical akineaia Anterior and apical akinesia
Apex, large Apex and lower anterior, large Apex and inferior, large Apex, emall Lower anteroapical, small Apex, small Apex and lower anterior, large Apex, large Apex, small Apex, large Apex, small Within aneurysm Apex, small Apex, moderate Apex, large Apex, moderate Apex, small Apex, h
e
Apex, large Apex, small Apex, small Apex, small
Abbreviations: LV, S/D, left ventricular pressure, syetolic/diaatolic; EDV, end-diastolic volume, Cx, circumflex; RCA, right coronary artery; LAD, left anterior deecending
490 HAMBY ET A 1
CHEST,
66: 5, NOVEMBER, 1974
End - diastola
Infarctectomy and aortocoronary bypass were performed on six patients (cases 2,6, 8, 11, 13, 18). Aneurysmectomy alone was performed in case 12. A mural thrombus was found' at surgery in all the patients. Patient 8 died at surgery as a result of pump failure, whereas the remaining six patients had satisfactory postoperative courses and were discharged from the hospital. Four patients (cases3,4, 5, 10) died within nine months of evaluation. Patient 5 died of a massive cerebral vascular accident complicated by heart failure. Postmortem findings revealed marked myocardial fibrosis, a large, partially organized mural thrombus and thromboembolic obliteration of multiple vessels, including the internal carotid arteries. In the other three patients, no information was available as to the events leading to death and no postmortem was obtained. Patient 9
w
.
I
FIGURE 1. Left ventricular angiogram as viewed in the right anterior oblique projection. A. Patient 6. During enddiastole a slight apical irregularity is noted (arrow).Two cycles later, after dilution of contrast material, a filling defect at the apex is noted during end-systole (arrow). At surgery an apical thrombus was found. B and C. Patients 4 and 11,respectively, with arrow pointing to obliteration of the normal apical contour during both end-diastole and end-systole. At surgery an apical thrombus was found in patient 11.D. Patient 8. A large, irregular apical filling is noted, which, at surgery, was noted to be a partially organized friable thrombus.
three of these patients, during the early phase of the left ventricular angiogram, only an apical irregularity was noted (Fig 1A). As the contrast material was diluted during later cycles, however, a constant apical defect became evident. In other patients (cases 4, 10, 11, 14, 16, 18, 19), the apex appeared sharply cut off during both diastole and systole ( Fig 1B and C ). In three patients (cases 1, 8, 15), the apex appeared completely obliterated by an irregular, nonuniform density (Fig ID). Extension of the filling defect to the lower anterior wall (Fig 2A and B) was noted in three patients (cases 2, 5, 7) and in one patient (case 3 ) this extended to the inferior wall (Fig 2C). In patient 12, the entire anteroapical aneurysm was obliterated by a thrombus ( Fig 2D ) . Patient 20 ( Fig 3 ), the only patient with an isolated inferior wall myocardial infarction, had a history of a cerebral vascular accident and had, on left ventricular angiogram, a globular apical fillingdefect. CHEST, 66: 5, NOVEMBER, 1974
FIGURE2. Left ventricular angiogram as viewed in the right anterior oblique projection. A and B. Patients 2 and 5, with apical filling defect extending to the lower anterior wall. In patient 2, at surgery, the angiographic &dings were conh e d . C. Patient 3 has a mural thrombus extending to the inferior wall. D. Patient 12 with a chest x-ray film demonstrating cardiomegaly. The enddiastolic silhouette, however, did not reveal a large cardiac chamber. This was due to the presence of a large thrombus (arrow) obliterating an aneurysm, which was codinned at surgery.
CORONARY ARTEIRY DISEASE AND LEFT VENTRICULAR MURAL THROMBI 491
FIGURE3. Left ventricular angiogram as viewed in the right anterior oblique projection in patient 20. This is the only patient with an isolated inferior wall myocardial infarction. Note the distorted inferior wall of the left ventride during diastole, probably from a prior Vineberg procedure. The arrow points to a distinct globular apical filling defect.
sustained a cerebrovascular accident three months after discharge from the hospital. Patients 19,21 and 22 were not considered candidates for surgery and, on follow-up of over six months, they still have incapacitating angina pectoris. In the remaining six patients (cases 1, 7, 14 -17), no follow-up information was available. Cornparatioe Stud@
Since all the patients with mural thrombi had electrocardiographic evidence of a transmural myocardial infarction, a comparisdn was made only with patients who had evidence of an infarction on the electrocardiogram. Thus, of a total of 458 patients with coronary disease during the period of this study, 228 had evidence of a transmural myocardial infarction. Of the total group of patients with prior transmural myocardial infarction, 22 had mural thrombi, while 206 did not have evidence of a mural thrombus. No significant differences were noted in the duration of symptoms or incidence of hypertension or congestive heart failure when comparing those with mural thrombi and those without mural thrombi and a prior transmural infarction. Cardiomegaly was present in 55 percent of the patients with mural thrombi but in only 24 percent of the patients with prior infarction but no mural thrombi (p<0.001). A review of the electrocardiographic findings of the entire group of 458 patients (Table 3) seen indicated that approximately 20 percent of Table 3-8leetrocardiographic Finding* cu Related to the Presence of Mural Thrombi No.
Mural Thrombus Present Percent
No transmural infarction
230
0
0
Inferior transmural infarction (isolated)
135
1
0.7
Anterior transmural infarction (isolated)
86
1%
19.7
Combined inferior and anterior infarction
27
8
29.6
the patients with anterior wall (anterior or anteroseptal) myocardial infarction had mural thrombi. The highest incidence of mural thrombi occurred in patients with electrocardiographic evidence of multiple myocardial infarctions (29.6 percent ) . Left ventricular dysfunction, as indicated by hemodynamic findings and abnormal contractile patterns, was found in all 22 patients with mural thrombi, while 61 percent of the patients without mural thrombi, however, had at least one abnormal hemodynamic parameter and, in 93 percent, abnormal left ventricular systolic wall movement was present. Seven patients with electrocardiographic evidence of a transmural myocardial infarction had a persistent diastolic and systolic bulge of the left ventricular wall consistent with a true ventricular aneurysm. Finally, high grade stenosis ( >95 percent narrowing of lumen) or complete obstruction of the left anterior descending artery found in all the patients with mural thrombi was observed in 65 percent of the remaining 179 patients. In the past, the recognition of mural thrombi in the heart was dependent on the postmortem study1+' and could only be clhically inferred in patients with arteriosclerotic heart disease if the clinical course was complicated by a systemic embolus.'-l4 Such systemic emboli complicating coronary artery disease occur predominantly during acute myocardial infarction. Such complications during acute myocardial infarction could be reduced,22although not preventede with anticoagulants. A thromboembolic complication may, furthermore, precede clinical recognition of acute myocardial infarction.18.14 In the present cases, information was only available in seven patients during their last hospitalization for an acute myocardial infarction and revealed that five were receiving anticoagulants, while two patients did not. Thromboembolism was documented in one patient and presumably occurred in three other patients with cerebral vascular accidents. It is rather surprising that, in spite of the very high frequency of mural thrombi of the left ventricle reported at postmortem examination in patients with arteriosclerotic heart disease,'+' there is no mention in the literature of angiographic documentation in patients evaluated with coronary artery disease. The frequency of mural thrombi in the heart, observed at postmortem examination, ranges from 21 to 67 percent1" of all patients with arteriosclerotic heart disease. Although mural thrombi occur more frequently in patients who die of acute myocardial infarction, thrombi have been noted in 24 percent of patients dying with healed infarcti~ns.'.~Ventricular aneurysms have been reCHEST, 66: 5, NOVEMBER, 1974
ported in association with mural thrombi, in an incidence of from 54 percents to as high as 68 percent.5 Mural thrombi in the absence of a ventricular aneurysm are found in one-third of the patients dying with arteriosclerotic heart disease.'-' The frequency of mural thrombi in the left ventricle was only 4.8 percent of the total patients evaluated. More than half of these patients, however, had no evidence of previous transmural myocardial infarction. As indicated in Table 3, if one considers the location of the infarction, evidence of an anterior wall infarction (anterior or anteroseptal), whether isolated or combined with inferior wall myocardial infarction, wries a frequency varying from 19.7 percent to 29.6 percent incidence of mural thrombus. This supports the work of Jordan and co-workers2of the greater propensity of anterior myocardial infarctions for complication by mural thrombi. These authors found that 31 percent of healed anterior myocardial infarctions were complicated by mural thrombi as compared to 16.3 percent with healed inferior wall myocardial infarctions. The increased incidence of mural thrombi noted with anterior wall infarctions can, in part, be explained by the larger size of anterior infarctions as compared to posterior wall myocardial infarction. The size of the infarction has been directly related to the frequency of mural t h r ~ m b iEstimating .~ the area of the infarction, it was noted that in small infarctions ( <20 sq cm) the frequency of mural thrombi was 15 percent, whereas in large infarctions ( <80 sq em) the frequency was 93 percent. Multiple infarctions are more likely associated with extensive myocardial damage than are single infarctions. The frequency of mural thrombi in a heart with two or more myocardial infarctions present is greater than that found with single myocardial infarcts.' In the present series of 22 patients with mural thrombi, 13 had a history of two or more myocardial infarctions. Only eight, however, had electrocardiographic documentation of multiple infarctions. The left anterior descending artery is the major source of blood supply to the interventricular septum and anterior and apical wall of the left ventricle.16 Obstructive disease of the left anterior descending artery is #us more likely to be associated with a large myocardial infarction complicated by significant hemodynamic impairment.16 Thus, the uniform finding of significant stenotic or obstructive disease of the left anterior descending artery in all of our patients complicated uniformly by marked impairment of left ventricular function probably indicates the presence of a large myocardial infarction. In one series of patients reported, older age appeared as a factor favoring the frequency of mural thrombiSsIn the present group of patients, however, the age range was 40 to 72 years, not significantly CHEST, 66: 5, NOVEMBER, 1974
different from the 206 patients with electrocardic+ graphic evidence of a transmural myocardial infarction and no evidence of a mural thrombus. Duration of symptoms, presence of hypertension and a history of congestive heart failure could not be related to the presence of a mural thrombus. This agrees with the observations of Garvin.' Jordan and co-worke r ~ ?however, did observe an increased frequency of mural thrombi in patients with hypertension and congestive heart failure. In the present group of patients, cardiomegaly did appear related to mural thrombi, probably reflecting the extensive rnyocar&a1 damage present. The location of the mural thrombus in general is on the endocardial surface adjacent to the myocardial infarction,'3,hually at the apex of the heart and often extending to the anterior free wall or the anterior aspect of the interventricular septum. Left ventricular dysfunction in patients with mural thrombi, as noted in the present series, includes a decreased left ventricular ejection fraction and stasis of blood in the apex of the left ventricle. Left ventricular angiograms in our patients did suggest apical stasis as indicated by pooling of contrast material in the apex during three or four cardiac cycles after the completion of injection. In the present group of patients, all had apical filling defects of varying size, with extension in some to the lower anterior wall. As indicated in Figures 1 and 2, the angiographic pattern appears quite distinctive, with loss of the normal apical contour of the left ventricle by a filling defect. The margin of the filling defect may appear smooth or ragged, appearing as a mass projecting into the cavity of the left ventricle. It should be emphasized that the true incidence of mural thrombi is probably higher than noted in this study since angiographic methods are probably not sensitive enough to appreciate small thrombi. Furthermore, angiograms were only performed in the right anterior oblique projection. A more satisfactory approach would have been biplane angiographic studies. Although no thromboembolic complications occurred during the diagnostic evaluations, the high incidence of thrombus noted in association with infarction of the anterior wall of the left ventricle suggests caution when performing left ventricular angiograms on such patients. ACKNOWLEDGMENT: We thank Dr. Irwin H o h for his critical review of this manuscript. Assistance in preparin this manuscript was also given by Jarmila Dvorak, Ph.D. staff and Mrs. Brenda Hamby.
an1
1 Canin CF: Mural thrombi in the heart. Am Heart J 21:713-720, 1941 2 Jordan RA, Miller FU3, Edwards JE,et al: Thromboembolism in acute and in healed myocardial infarction. I. Intracardiac mural thrombosis. Circulation 6:l-6, 1952
CORONARY A1ITERY DISEASE AND LEFT VENTRICULAR MURAL THROMBI 493
3 Yater WM,Welsh PP, Stapleton JF, et al: Comparison of clinical and pathologic aspects of coronary artery disease in men of various age groups: A study of 950 autopsied
cases from the Armed Forces Institute of Pathology. AM 1ntem.Med 34 :352-392, 1951 4 Bean WB: Infarction of the heart. 111. Clinical come and morphological findings. Ann Intern Med 12:71-94, 1938 5 Phares WS, Edwards JE, Burchell HB: Cardiac aneurysms: Clinicopathologic studies. Proc Staff Meet Mayo Clinic 28:204-271, 1953 6 Schlichter J, Hellerstein HK, Katz LN: Aneurysm of the heart: A correlative study of 102 proved cases. Medicine 33:43-78, 1954 7 Young JR, Humphries AW, D e Wolfe VG, et al: Peripheral arterial embolism. JAMA 185:621-627, 1963 8 Deterling RA Jr, Vargas LL, Mc Allister FF: Follow-up studies of patients with embolic occlusion of the aortic bifurcation. Ann Surg 155:383-391. 1962 9 Thompson JE, Weston AS, Sigler L, et al: Arterial embolectomy after acute myocardial infarction: A study of 31 patients. AM Surg 171:979-986, 1970 10 Darling RC, Austen WG, Linton RR: Arterial embolism. Surg Gynec Obstet 124:106-114,1967 11 Miller RD,Jordan RA, Parker RL, et a]: Thromboembolism in acute and in healed myocardial infarction. 11. Systemic and pulmonary arterial occlusion. Circulation 6:7-15, 1952 12 Nielsen GL, Sorensen HR: The operative treatment of emboli in the extremities of patients with acute coronary occlusion. Danish Med Bull 15:249-252, 1968
13 Harrison CE Jr, Spittell JA Jr, Mankin HT: Sudden arterial occlusion: A clue to silent myocardial infarction. Proc Staff Meet Mayo Clin 37:293-300, 1962 14 Lazy BG, de Takats G: Peripheral arterial embolism after myocardial infarction: Occurrence in unsuspected cases and ambulatory patients. JAMA 155:10-13, 1954 15 Massie E, Walsh TJ: Clinical Vectorcardiography and Electrocardiography. Chicago, Year Book Publishers Inc, 1980 16 Hamby RI, Gupta MP,Young MW: Clinical and hemodynamic aspects of single vessel coronary artery disease. Am Heart J in press 17 Sones FM Jr, Shirey EK: Cine coronary arteriography. Mod Conc Cardiovasc Dis 31:735-738, 1962 18 Judkins MP: Percutaneous transfemoral selective corn nary arteriography. Radio1 Clin N Am 6:467-492, 1968 19 Dodge HT, Sandler H, Ballew DW, et al: The use of biplane angiocardiography for the measurement of left ventricular volume in man. Am Heart J 60:762-776, 1960 20 Herman MV, Heinle RA, Klein MD, et al: Localized disorders in myocardial contraction. Asynergy and its role in congestive heart failure. N Engl277:222-232, 1967 21 Proudfit WL, Shirey EK, Sones FM Jr: Selective cine coronary arteriography. Correlation with clinical findings in 1000 patients. Circulation 33:901-910,1968 22 Wright IS, Marple C, Beck DF: Myocardial Infarction: Report of the Anticoagulant Committee of the American Heart Association, New York, Grune and Stratton, Inc 1954 '
Mysterious Migration of Fishes The most adventurous journey of all is that of the fresh water eel. From the contents of plankton nets towed in various parts of the Atlantic Ocean aboard the
Thor and Dana, Johannes Schmidt, a Danish scientist, found that younger and younger stages of the tiny eels could be traced farther and farther back t o the deep central part of the North Atlantic Ocean southeast of Bermuda. Transparent eggs about the size of a pea are found there in the spring about 500 feet below the surface, so that mating probably takes place near the deep sea floor beneath. When the flat leaf-like larva is first hatched it is only a quarter. of inch long. These bizarre creatures grow slowly, and meanwhile travel on the long path toward fresh water. The baby eel takes three years to reach European waters. We cannot be
sure, but it seems likely that the newly-hatched leptocephalus rising part way to the surface is caught by the Gulf Stream and thus is canied to the European shores. By the time it reaches there it has become of age. It is strongly attracted by fresh waters draining out of rivers. When it amves at its destination at the river's mouth, the leaf-like shape disappears and it becomes narrow and round. In the rivers it grows to be a foot or more in length. Then as much as twenty years later, it begins to journey back to the spawning grounds of the Sargasso Sea, where a new generation begins the long ocean circuit. Chapin H, Smith FGH:The Ocean River. New York, Charles Scribneis Sons, 1952
CHEST, 66: 5, NOVEMBER, 1974