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Thrombosis of epicardial coronary veins in acute myocardial infarction
Thrombosis acute
Birgit
of epicardial
myocardial
Fischer
Copenhagen,
coronary
veins
infarction
Hansen,
M.D.
Denmark
The incidence, cause, and significance-if any-of thrombosis of epicardial coronary veins in patients with AM1 is unknown. Venous thrombosis is related to increased platelet aggregation which is known to occur in various forms of stress7 and after tissue damage.6 Increased platelet aggregation is found in patients with coronary artery disease” and AMI.‘” Involvement of platelets is an initial event in the formation of thrombi” and early thrombi may consist purely of platelets.‘” Thrombosis of epicardial coronary arteries in AM1 has been described in innumerable papers whereas pathological changes in epicardial coronary veins have almost escaped notice. The purpose of this paper is to draw attention to the presence of thrombosis of epicardial coronary veins in cases of AM1 and to evaluate some factors of importance to the development of such thrombi. Material
in
and
methods
In a consecutive autopsy series of 63 patients with clinically definite or possible AMP” it was found, that 32 had transmural and 16 had subendocardial AMI. Two had recent occlusive coronary artery thrombosis but both survived too briefly-less than 8 hours-for postmortem demonstration of AMI.” These 50 patients are the material for this study. The autopsy technique has been described From the Department of Pathology, R&hospital&, vej 11, DK-2100 Copenhagen, Denmark. This study was supported Danish Medical Research
by the Council.
Danish
Received
for publication
July
10, 1978.
Accepted
for publication
Nov.
21, 1978
Reprint Hellerup,
requests: Dr. Birgit Fischer Copenhagen, Denmark.
696
June,
1979,
Vol.
Heart
Hansen,
97, No.
6
Frederik Foundation
Henningsens
Alle
den
V’s
and
the
62,290O
previously.* It includes a meticulous histological examination of cross-sectioned epicardial coronary vessels. The patho-anatomic diagnosis of AM1 is based on naked eye findings,‘“, Ii Nitro-BT test,“. ‘I3 and light microscopy.lo. ” The AM1 is quantitated by the point-counting technique”. ‘q and is recorded in per cent of ventricular mass. A transmural AM1 extends through more than the inner half of the ventricular wall, and a subendocardial AM1 is limited to the inner half of the wall. Combined AMI’s are transmural with additional subendocardial extension. Arterial and venous thrombosis is defined as occlusion of the vessel lumen by admixture of platelets, fibrin, leukocytes and erythrocytes seen in a laminated arrangement, i.e., lines of Zahn. In the arteries (Fig. 1) the thrombi are adherent to the luminal surface and atheromatosis is present. In the veins (Fig. 2) no structural changes are demonstrated in the vessel wall. The venous thrombi appear to be of more recent date than the arterial thrombi: the relative amount of platelets is higher, they are looser in texture, and they show more pronounced shrinkage due to fixation. Thus venous thrombi often appear as “freely floating” but attachment to the vessel wall can be demonstrated. Statistical evaluation is performed by Fisher’s and Mann-Whitney’s test.” Results
In 16 of 50 cases thrombosis of epicardial coronary veins was demonstrated. Five patients had aortic and one had mitral valve stenosis. In all six casesvenous thrombosis was demonstrated (Table I). Three had transmural and two had subendocardial AMI, and one had recent arterial thrombosis. Of the 44 patients without valvular heart
0002-8703/79/C&0696
+ 05$00.50/O
0 1979
The
C. V. Mosby
Co.
Fig.
1. Cross-section
luminal
surface.
of epicardial coronary artery showing atheromatosis (Verhoeff elastica-van Gieson stain; original magnification
disease(Table I), 10 with transmural AM1 involving at least 30 per cent of the left ventricular mass had venous thrombosis, and six of these had very large AMI’s involving at least 70 per cent of the left ventricle. None of the seven patients with transmural AM1 less than 30 per cent and none of the 14 patients with subendocardial AM1 had venous thrombosis. There is no statistical difference in the size of AM1 between transmural AMI’s less than 30 per cent and subendocardial AMI’s. Thus venous thrombosis was demonstrated in 10 of 22 caseswith large and in none of 22 cases with small AMI’s (p < 0.002). Mean post-attack survival time in patients with transmural AM1 without valvular heart disease was the same in patients with (7.2 days, N = 10) as in patients without venous thrombosis (7.0 days, N = 19). However, none of the nine patients who died within 24 hours after the acute admission had venous thrombosis, while 10 of the remaining 20 patients had venous thrombosis (p < 0.002). Among the 44 patients no statistically significant difference was found in the incidence and severity of coronary artery diseasebetween those with and those without venous thrombosis. At least 75 per cent stenosis of 1 main artery was
American
Heart
Journal
Thrombosis
of coronary
veins in acute MI
and occlusion x 16).
by thrombus
adherent
to
found in 10 patients (100 per cent) with, and in 33 of 34 patients (94 per cent) without venous thrombosis. At least 75 per cent stenosis of two or three main arteries was found in 60 per cent and 82 per cent, respectively. Localization of venous thrombosis in relation to arterial thrombosis and to type of left ventricular AM1 appears in Table II. Arterial thrombosiswas seenin 12 of 15 casesof AM1 and was in all cases localized to the arteries supplying the infarcted area. Three AMI’s were non-thrombotic and they all had aortic valve stenosis. In all 15 cases of AM1 the venous thrombi were localized to veins draining the infarcted myocardium. In case No. 6 the vein accompanying the circumflex artery was thrombosed but the anteroseptal AM1 also involved the marginal wall in the apical part of the left ventricle. In case No. 29 the circumflex artery continued as a posterior descending artery. In seven cases there was thrombosis of two coronary veins; in four of these cases both veins drained infarcted myocardium, and in another three cases one of the veins drained an area without demonstrable AMI. Two of these latter patients died in cardiogenic shock. In all, 12 of 50 patients died in cardiogenic shock. Seven had transmural and four had suben-
697
Hansen
Fig. 2. Cross-section of epicardial coronary vein structural changes in the vessel wall. (Hematoxylin
occluded by thrombus showing lines and eosin stain; original magnification
I. Thrombosis of epicardial coronary veins in relation to valvular heart disease and to type and size of left ventricular AM1 Table
b Valvular heart disease present Transmural AM1 > 30% < 30% Subendocardial AM1 Recent arterial thrombosis Total
2 1 2 1 6
2 1 2 1 6
6 16 7 14 1 44
6 4
docardial AMI’s and one had recent without demonstrable AMI. Five of with venous thrombosis and seven of without venous thrombosis died in shock (p > 0.2). 698
10
are no
Myocardial rupture was seen in four of 10 cases of transmural AM1 with, and in three of 19 transmural AMI’s without venous thrombosis (p > 0.2). There was no statistically significant difference in heart weight between the two groups. During their stay in hospital four of 16 patients with venous thrombosis were in the therapeutic level on anticoagulant medication compared to four of 34 patients without venous thrombosis (p > 0.2). Discussion
No valvular heart disease present Transmural AM1 2 70% 30-70% < 30% Subendocardial AM1 Recent arterial thrombosis Total
of Zahn. There x 80).
12 7 14 1 34
thrombosis 16 patients 34 patients cardiogenic
The patho-anatomic diagnosis of very early AM1 is difficult. Light microscopy has little to offer since specific changes will not be visible until after at least 12 hours.“‘, I7 Demonstration of loss of dehydrogenases in the infarcted myocardium (Nitro-BT test) will reveal AMI’s of 6 to 8 hours duration.’ It has been suggested that the presence of wavy muscle fibers’ should indicate very early (1 hour duration) AMI, but this phenomenon remains to be clarified and has not been applied in this study. Rigid criteria must be applied to avoid confusion of true thrombi with postmortem clots which are composed of the normal elements of the blood in more or less normal proportions. The formation of true thrombi require circulating blood, June, 1979, Vol. 97, No. 6
Thrombosis
II. Localization ventricular AM1
Thrombosis No.
Coronary
43 9 39 6 38 46 29 14 4 34 44 62 58 54
LAD DXT, DXT, FX DXT, DXT LAD, DXT LAD, LAD LAD DXT LAD, DXT,
53
DXT
23
LAD,
*DXT: right accompany. tTransmura1
coronary AM1
artery;
of anterior
veins
Coronary
Heart
Journal
Type of left ventricular AMI
arteries*
LAD LAD LAD LAD
LAD LAD
Combined Inferior Combined Subtotalt
DXT FX DXT LAD LAD LAD DXT, LAD DXT
FX
FX FX
FX
DXT, left
posterior
anterior wall
descending and
Combining
Antero-septal -I’-
LAD
LAD: and
of manifestation
External
rupture
Internal rupture Aortic stenosis Mitral stenosis Aortic stenosis Internal rupture Internal rupture
anterior inferior
-“_ -I’-
LAD Posterior papillary muscle Postero-septal subendocardial LAD artery;
of interventricular
and the ratio of formed elements is-totally out of proportion to that in circulating blood. Early arterial thrombi may be composed purely of platelets’” and involvement of platelets was shown by Erhardt and associatesJto be an initial event. The demonstrated high incidence of venous thrombosis in large AMI’s is probably due to the pronounced tissue damage. Gjesdal and Stirlie,” in their experimental study on regional ischemia during vascular surgery, found that increased platelet aggregation was related to metabolites from the ischemia area, especially platelet factor 4, and to duration of the ischemic period. This is in agreement with the findings in this study where venous thrombosis was found in veins draining large infarctions and only in patients surviving the acute attack for more than 24 hours. Jergensen” found that infusion of ADP resulted in platelet aggregation and that these were formed in the flowing blood independent of the vessel wall, as also demonstrated in this study. In patients with valvular heart disease, damage to the platelets with resulting ADP release might explain the formation of venous thrombi. It was previously suggested by us’ that thrombosis of coronary veins might explain false-negaAmerican
veins in acute MI
of venous thrombosis in relation to arterial thrombosis and to type of left
Table
Patient
of coronary
FX: septum
left
circumflex
involving
artery.
The
3 70% of ventricular
veins
are
Aortic
stenosis
Aortic
stenosis
Aortic
stenosis
named
by
the
arteries
they
mass.
tive Nitro-BT tests seen in large AMI’s and in caseswith myocardial rupture. In this series with four cases of false-negative Nitro-BT tests, two had venous thrombosis and two had myocardial rupture, but in the remaining 14 cases of venous thrombosis and in five cases of myocardial rupture the Nitro-BT test was clear-cut and in agreement with naked eye findings and/or light microscopy. Thus venous thrombosis does not explain. the false-negative Nitro-BT tests. Incidence and severity of coronary artery disease, heart weight, anticoagulant medication, and cardiogenic shock seem to be of no importance to the development of coronary vein thrombosis. Summary
Thrombosis of epicardial coronary veins was demonstrated in 16 of 50 casesof left ventricular acute myocardial infarction and/or recent coronary arterial thrombosis. All patients with valvular heart diseasehad venous thrombosis. In cases without valvular heart disease, venous thrombosis was seen in infarctions involving more than 30 per cent of the left ventricular myocardial mass with a post-attack survival time of at least 24 hours. The veins thrombosed were in all cases 699
Hansen
those draining the infarcted myocardium. Coronary vein thrombosis seems not to be prevented by anticoagulant medication. The author of Lis Annette
wishes to acknowledge Tovgaard.
the technical
assistance
REFERENCES 1.
2. 3.
4.
5. 6.
7.
8.
700
Andersen, J. A., and Hansen, B. F.: The value of the Nitro-BT method in fresh myocardial infarction, AM. HEART J. 85:611, 1973. Bouchardy, B., and Majno, G.: Histopathology of early myocardial infarcts, Am. J. Pathol. 74:301, 1974. Ehrlich, J. C., and Shinohara, Y.: Low incidence of coronary thrombosis in myocardial infarction, Arch. Pathol. 78:432, 1964. Erhardt, L. R., Unge, G., and Boman, G.: Formation of coronary arterial thrombi in relation to onset of necrosis in acute myocardial infarction in man, AM. HEART J. 91592, 1976. Documenta Geigy Wissenschaftliche Tabellen. 6th ed, Basle, Switzerland, 1960, J. R. Geigy S. A., pp. 109-127. Gjesdal, K., and S&lie, D.: Platelet function during reconstructive peripheral arterial surgery, Acta Chir. Stand. 143:329, 1977. Haft, J. I., and Fani, K.: Stress and the induction of intravascular platelet aggregation in the heart, Circulation 48: 164, 1973. Hansen, B. F.: Heart autopsy in ischemic heart disease, an autopsy protocol, Acta Pathol. Microbial. Stand. Sect. A. 86:241, 1978.
9. Jergensen, 10.
11.
12.
13.
14.
15.
16. 17.
18.
L.: Experimental platelet and coagulation thrombi, Acta Pathol. Microbibl. Stand. 62:189: 1964. Mallorv. G. K.. White. P. D.. and Salcedo-Salear. J.: The speed of’healing of myocardial infarction, A1lI’. &ART J. 18:647, 1939. Mitchell, J. R., and Cranston, W. I.: A simple method for the quantitative assessment of aortic disease, J. Atheroscler. Res. 6:135, 1965. Murphy, E. A., and Mustard, J. F.: Coagulation test and platelet economy in atherosclerotic and control subjects, Circulation 25:114, 1962. Nachlas, M. M., and Shnitka, T. K.: Macroscopic identification of early myocardial infarcts by alterations in dehydrogenase activity, Am. J. Pathol. 42:379, 1963. Rissanen, V., and Pyorala, K.: Application of pointcounting technique to the quantitative assessment of coronary and aortic atherosclerosis, Acta Pathol. Microbiol. Stand. 80:412, 1972. Roberts, W. C., and Buja, L. M.: The frequency and significance of coronary arterial thrombi and other observations in fatal acute myocardial infarction, Am. J. Med. 52:425, 1972. World Health Organization: Ischemic heart disease registers. Annex II: 30-33, Copenhagen, 1970. World Health Organization: The pathological diagnosis of acute ischemic heart disease. Technical report series No. 441, Geneva, 1970. Zahavi, J., and Dreyfuss, I.: An abnormal pattern of adenosine diphosphate-induced platelet aggregation in acute myocardial infarction, Thromb. Diath. Haemorrh. 2 1:76, 1969.
June,
1979,
Vol.
97, No.
6
Birgit
of epicardial
myocardial
Fischer
Copenhagen,
coronary
veins
infarction
Hansen,
M.D.
Denmark
The incidence, cause, and significance-if any-of thrombosis of epicardial coronary veins in patients with AM1 is unknown. Venous thrombosis is related to increased platelet aggregation which is known to occur in various forms of stress7 and after tissue damage.6 Increased platelet aggregation is found in patients with coronary artery disease” and AMI.‘” Involvement of platelets is an initial event in the formation of thrombi” and early thrombi may consist purely of platelets.‘” Thrombosis of epicardial coronary arteries in AM1 has been described in innumerable papers whereas pathological changes in epicardial coronary veins have almost escaped notice. The purpose of this paper is to draw attention to the presence of thrombosis of epicardial coronary veins in cases of AM1 and to evaluate some factors of importance to the development of such thrombi. Material
in
and
methods
In a consecutive autopsy series of 63 patients with clinically definite or possible AMP” it was found, that 32 had transmural and 16 had subendocardial AMI. Two had recent occlusive coronary artery thrombosis but both survived too briefly-less than 8 hours-for postmortem demonstration of AMI.” These 50 patients are the material for this study. The autopsy technique has been described From the Department of Pathology, R&hospital&, vej 11, DK-2100 Copenhagen, Denmark. This study was supported Danish Medical Research
by the Council.
Danish
Received
for publication
July
10, 1978.
Accepted
for publication
Nov.
21, 1978
Reprint Hellerup,
requests: Dr. Birgit Fischer Copenhagen, Denmark.
696
June,
1979,
Vol.
Heart
Hansen,
97, No.
6
Frederik Foundation
Henningsens
Alle
den
V’s
and
the
62,290O
previously.* It includes a meticulous histological examination of cross-sectioned epicardial coronary vessels. The patho-anatomic diagnosis of AM1 is based on naked eye findings,‘“, Ii Nitro-BT test,“. ‘I3 and light microscopy.lo. ” The AM1 is quantitated by the point-counting technique”. ‘q and is recorded in per cent of ventricular mass. A transmural AM1 extends through more than the inner half of the ventricular wall, and a subendocardial AM1 is limited to the inner half of the wall. Combined AMI’s are transmural with additional subendocardial extension. Arterial and venous thrombosis is defined as occlusion of the vessel lumen by admixture of platelets, fibrin, leukocytes and erythrocytes seen in a laminated arrangement, i.e., lines of Zahn. In the arteries (Fig. 1) the thrombi are adherent to the luminal surface and atheromatosis is present. In the veins (Fig. 2) no structural changes are demonstrated in the vessel wall. The venous thrombi appear to be of more recent date than the arterial thrombi: the relative amount of platelets is higher, they are looser in texture, and they show more pronounced shrinkage due to fixation. Thus venous thrombi often appear as “freely floating” but attachment to the vessel wall can be demonstrated. Statistical evaluation is performed by Fisher’s and Mann-Whitney’s test.” Results
In 16 of 50 cases thrombosis of epicardial coronary veins was demonstrated. Five patients had aortic and one had mitral valve stenosis. In all six casesvenous thrombosis was demonstrated (Table I). Three had transmural and two had subendocardial AMI, and one had recent arterial thrombosis. Of the 44 patients without valvular heart
0002-8703/79/C&0696
+ 05$00.50/O
0 1979
The
C. V. Mosby
Co.
Fig.
1. Cross-section
luminal
surface.
of epicardial coronary artery showing atheromatosis (Verhoeff elastica-van Gieson stain; original magnification
disease(Table I), 10 with transmural AM1 involving at least 30 per cent of the left ventricular mass had venous thrombosis, and six of these had very large AMI’s involving at least 70 per cent of the left ventricle. None of the seven patients with transmural AM1 less than 30 per cent and none of the 14 patients with subendocardial AM1 had venous thrombosis. There is no statistical difference in the size of AM1 between transmural AMI’s less than 30 per cent and subendocardial AMI’s. Thus venous thrombosis was demonstrated in 10 of 22 caseswith large and in none of 22 cases with small AMI’s (p < 0.002). Mean post-attack survival time in patients with transmural AM1 without valvular heart disease was the same in patients with (7.2 days, N = 10) as in patients without venous thrombosis (7.0 days, N = 19). However, none of the nine patients who died within 24 hours after the acute admission had venous thrombosis, while 10 of the remaining 20 patients had venous thrombosis (p < 0.002). Among the 44 patients no statistically significant difference was found in the incidence and severity of coronary artery diseasebetween those with and those without venous thrombosis. At least 75 per cent stenosis of 1 main artery was
American
Heart
Journal
Thrombosis
of coronary
veins in acute MI
and occlusion x 16).
by thrombus
adherent
to
found in 10 patients (100 per cent) with, and in 33 of 34 patients (94 per cent) without venous thrombosis. At least 75 per cent stenosis of two or three main arteries was found in 60 per cent and 82 per cent, respectively. Localization of venous thrombosis in relation to arterial thrombosis and to type of left ventricular AM1 appears in Table II. Arterial thrombosiswas seenin 12 of 15 casesof AM1 and was in all cases localized to the arteries supplying the infarcted area. Three AMI’s were non-thrombotic and they all had aortic valve stenosis. In all 15 cases of AM1 the venous thrombi were localized to veins draining the infarcted myocardium. In case No. 6 the vein accompanying the circumflex artery was thrombosed but the anteroseptal AM1 also involved the marginal wall in the apical part of the left ventricle. In case No. 29 the circumflex artery continued as a posterior descending artery. In seven cases there was thrombosis of two coronary veins; in four of these cases both veins drained infarcted myocardium, and in another three cases one of the veins drained an area without demonstrable AMI. Two of these latter patients died in cardiogenic shock. In all, 12 of 50 patients died in cardiogenic shock. Seven had transmural and four had suben-
697
Hansen
Fig. 2. Cross-section of epicardial coronary vein structural changes in the vessel wall. (Hematoxylin
occluded by thrombus showing lines and eosin stain; original magnification
I. Thrombosis of epicardial coronary veins in relation to valvular heart disease and to type and size of left ventricular AM1 Table
b Valvular heart disease present Transmural AM1 > 30% < 30% Subendocardial AM1 Recent arterial thrombosis Total
2 1 2 1 6
2 1 2 1 6
6 16 7 14 1 44
6 4
docardial AMI’s and one had recent without demonstrable AMI. Five of with venous thrombosis and seven of without venous thrombosis died in shock (p > 0.2). 698
10
are no
Myocardial rupture was seen in four of 10 cases of transmural AM1 with, and in three of 19 transmural AMI’s without venous thrombosis (p > 0.2). There was no statistically significant difference in heart weight between the two groups. During their stay in hospital four of 16 patients with venous thrombosis were in the therapeutic level on anticoagulant medication compared to four of 34 patients without venous thrombosis (p > 0.2). Discussion
No valvular heart disease present Transmural AM1 2 70% 30-70% < 30% Subendocardial AM1 Recent arterial thrombosis Total
of Zahn. There x 80).
12 7 14 1 34
thrombosis 16 patients 34 patients cardiogenic
The patho-anatomic diagnosis of very early AM1 is difficult. Light microscopy has little to offer since specific changes will not be visible until after at least 12 hours.“‘, I7 Demonstration of loss of dehydrogenases in the infarcted myocardium (Nitro-BT test) will reveal AMI’s of 6 to 8 hours duration.’ It has been suggested that the presence of wavy muscle fibers’ should indicate very early (1 hour duration) AMI, but this phenomenon remains to be clarified and has not been applied in this study. Rigid criteria must be applied to avoid confusion of true thrombi with postmortem clots which are composed of the normal elements of the blood in more or less normal proportions. The formation of true thrombi require circulating blood, June, 1979, Vol. 97, No. 6
Thrombosis
II. Localization ventricular AM1
Thrombosis No.
Coronary
43 9 39 6 38 46 29 14 4 34 44 62 58 54
LAD DXT, DXT, FX DXT, DXT LAD, DXT LAD, LAD LAD DXT LAD, DXT,
53
DXT
23
LAD,
*DXT: right accompany. tTransmura1
coronary AM1
artery;
of anterior
veins
Coronary
Heart
Journal
Type of left ventricular AMI
arteries*
LAD LAD LAD LAD
LAD LAD
Combined Inferior Combined Subtotalt
DXT FX DXT LAD LAD LAD DXT, LAD DXT
FX
FX FX
FX
DXT, left
posterior
anterior wall
descending and
Combining
Antero-septal -I’-
LAD
LAD: and
of manifestation
External
rupture
Internal rupture Aortic stenosis Mitral stenosis Aortic stenosis Internal rupture Internal rupture
anterior inferior
-“_ -I’-
LAD Posterior papillary muscle Postero-septal subendocardial LAD artery;
of interventricular
and the ratio of formed elements is-totally out of proportion to that in circulating blood. Early arterial thrombi may be composed purely of platelets’” and involvement of platelets was shown by Erhardt and associatesJto be an initial event. The demonstrated high incidence of venous thrombosis in large AMI’s is probably due to the pronounced tissue damage. Gjesdal and Stirlie,” in their experimental study on regional ischemia during vascular surgery, found that increased platelet aggregation was related to metabolites from the ischemia area, especially platelet factor 4, and to duration of the ischemic period. This is in agreement with the findings in this study where venous thrombosis was found in veins draining large infarctions and only in patients surviving the acute attack for more than 24 hours. Jergensen” found that infusion of ADP resulted in platelet aggregation and that these were formed in the flowing blood independent of the vessel wall, as also demonstrated in this study. In patients with valvular heart disease, damage to the platelets with resulting ADP release might explain the formation of venous thrombi. It was previously suggested by us’ that thrombosis of coronary veins might explain false-negaAmerican
veins in acute MI
of venous thrombosis in relation to arterial thrombosis and to type of left
Table
Patient
of coronary
FX: septum
left
circumflex
involving
artery.
The
3 70% of ventricular
veins
are
Aortic
stenosis
Aortic
stenosis
Aortic
stenosis
named
by
the
arteries
they
mass.
tive Nitro-BT tests seen in large AMI’s and in caseswith myocardial rupture. In this series with four cases of false-negative Nitro-BT tests, two had venous thrombosis and two had myocardial rupture, but in the remaining 14 cases of venous thrombosis and in five cases of myocardial rupture the Nitro-BT test was clear-cut and in agreement with naked eye findings and/or light microscopy. Thus venous thrombosis does not explain. the false-negative Nitro-BT tests. Incidence and severity of coronary artery disease, heart weight, anticoagulant medication, and cardiogenic shock seem to be of no importance to the development of coronary vein thrombosis. Summary
Thrombosis of epicardial coronary veins was demonstrated in 16 of 50 casesof left ventricular acute myocardial infarction and/or recent coronary arterial thrombosis. All patients with valvular heart diseasehad venous thrombosis. In cases without valvular heart disease, venous thrombosis was seen in infarctions involving more than 30 per cent of the left ventricular myocardial mass with a post-attack survival time of at least 24 hours. The veins thrombosed were in all cases 699
Hansen
those draining the infarcted myocardium. Coronary vein thrombosis seems not to be prevented by anticoagulant medication. The author of Lis Annette
wishes to acknowledge Tovgaard.
the technical
assistance
REFERENCES 1.
2. 3.
4.
5. 6.
7.
8.
700
Andersen, J. A., and Hansen, B. F.: The value of the Nitro-BT method in fresh myocardial infarction, AM. HEART J. 85:611, 1973. Bouchardy, B., and Majno, G.: Histopathology of early myocardial infarcts, Am. J. Pathol. 74:301, 1974. Ehrlich, J. C., and Shinohara, Y.: Low incidence of coronary thrombosis in myocardial infarction, Arch. Pathol. 78:432, 1964. Erhardt, L. R., Unge, G., and Boman, G.: Formation of coronary arterial thrombi in relation to onset of necrosis in acute myocardial infarction in man, AM. HEART J. 91592, 1976. Documenta Geigy Wissenschaftliche Tabellen. 6th ed, Basle, Switzerland, 1960, J. R. Geigy S. A., pp. 109-127. Gjesdal, K., and S&lie, D.: Platelet function during reconstructive peripheral arterial surgery, Acta Chir. Stand. 143:329, 1977. Haft, J. I., and Fani, K.: Stress and the induction of intravascular platelet aggregation in the heart, Circulation 48: 164, 1973. Hansen, B. F.: Heart autopsy in ischemic heart disease, an autopsy protocol, Acta Pathol. Microbial. Stand. Sect. A. 86:241, 1978.
9. Jergensen, 10.
11.
12.
13.
14.
15.
16. 17.
18.
L.: Experimental platelet and coagulation thrombi, Acta Pathol. Microbibl. Stand. 62:189: 1964. Mallorv. G. K.. White. P. D.. and Salcedo-Salear. J.: The speed of’healing of myocardial infarction, A1lI’. &ART J. 18:647, 1939. Mitchell, J. R., and Cranston, W. I.: A simple method for the quantitative assessment of aortic disease, J. Atheroscler. Res. 6:135, 1965. Murphy, E. A., and Mustard, J. F.: Coagulation test and platelet economy in atherosclerotic and control subjects, Circulation 25:114, 1962. Nachlas, M. M., and Shnitka, T. K.: Macroscopic identification of early myocardial infarcts by alterations in dehydrogenase activity, Am. J. Pathol. 42:379, 1963. Rissanen, V., and Pyorala, K.: Application of pointcounting technique to the quantitative assessment of coronary and aortic atherosclerosis, Acta Pathol. Microbiol. Stand. 80:412, 1972. Roberts, W. C., and Buja, L. M.: The frequency and significance of coronary arterial thrombi and other observations in fatal acute myocardial infarction, Am. J. Med. 52:425, 1972. World Health Organization: Ischemic heart disease registers. Annex II: 30-33, Copenhagen, 1970. World Health Organization: The pathological diagnosis of acute ischemic heart disease. Technical report series No. 441, Geneva, 1970. Zahavi, J., and Dreyfuss, I.: An abnormal pattern of adenosine diphosphate-induced platelet aggregation in acute myocardial infarction, Thromb. Diath. Haemorrh. 2 1:76, 1969.
June,
1979,
Vol.
97, No.
6