clinical application, especially in coronary care units where echocardiographic study is not available for every patient with AMI. Persistent ST-segment elevation and positive T waves should alert the physician to the possibility of LV thrombus and the need for echocardiographic study, whereas LV thrombus can be excluded almost safely in those with isoelectric ST segment and inverted T waves. 1. Lamas GA, Vaughan after first anterior wall
DE, Pfeffer MA. acute myocardial
Platelet Function Unstable Angina
Left ventricular thrombus infarction. Am I Cardiol
and Plasma Pectoris
formation 1988;62:
Lipid
31-35. 2. Weinrich DJ, Burke JF, Paulette FJ. Left ventricular thrombi complicating acute myocardial infarction. Long-term followup with serial echocardiography. Ann Intern Med 1984;100:789-794. 3. Lamas GA, Vaughan DE, Pfeffer MA. Significance of a lateral Q wave following first anterior wall acute myocardial infarction. Am J Cardiol 1990;6: 674-675. 4. Mel&r RS, Visser CA, Faster V. Intracardiac thrombi and systemic embolization. Ann Intern Med 1986;104:689-698. 5. Stratton JR, Lighty GW, Pearlman AS, Ritchie JL. Detection of left ventricular thrombus by two-dimensional echocardiography. Sensitivity, specificity and cause of uncertainty. Circulation 1928;66:156-166. 6. Kircher BJ, Top01 EJ, O’Neill WW, Pitt B. Prediction of infarct coronary artery recanalization after intravenous thrombolytic therapy. Am J Cardiol 1987;59:513-515.
Levels in Patients
Elena J. Vasilieva, MD, Alexander V. Shpector, MD, Aleksey B. Raskuragev, Lekochmacher, PhD, and lnna A. Bespalko, MD e investigated 2 groups of patients with angina pectoris - those with chest pain only on exertion (stable) and those with chest pain at rest (unstable) - to determine if platelet function and serum lipid levels were similar or different between the 2 groups. We studied 25patients (22 men and 3 women, aged 3.5 to 70 years) with coronary artery disease; the diagnosis was established on the basis of typical clinical manifestations, and exercise stress testing following the Bruce protocol t and data from 24-hour Holter monitoring. Monitoring was performed using a Medilog MA-14 monitor (Oxford Medical Systems). The electrocardiogram was recorded using 2 leads: the first pair of electrodes was placed under the second rib to the right of the chest and at the heart apex; the second one was placed under the fourth rib to the right of the chest and under the left clavicle. All patients kept a detailed diary and were instructed to activate the event button on the tape recorder when experiencing angina1 chest pain so as to identify possible symptomatic ischemic episodes. The tapes were analyzed visually by 2 experts at 60 times normal speed and trend curves of ST-segment deviation and heart rate were obtained for the entire monitoring period. Episodes of interest were printed forjnal evaluation. We considered transient ST-segment deviation > 1 mm, 80 ms after the J point, and a duration of at least 1 minute as ischemic.
W
From the Moscow Medical-Stomatological Institute, Moscow, Russia. Dr. Vasilieva’s address is: Second Division of Cardiology, Moscow General Hospital #52, Pehotnaya Street 3, Moscow 123436, Russia. Manuscript received January 14,199 1; revised manuscript received June 13,1991, and accepted June 14.
with Stable MD, Svetlana
and
S.
At all examinations, blood was collected by venapuncture of the cubital vein with a 19-gauge needle in the morning after I4 hours of fasting. Blood was collected without an anticoagulant for lipid analysis and with 3.8% sodium citrate (9:l) for all other analyses. Total cholesterol, low- and high-density lipoprotein cholesterol and total triglycerides were measured in plasma samples using a Boehringer Mannheim kit on an Opton spectrophotometer. Platelet aggregation was induced by adenosine diphosphate (2 X 1Om5M) and by ristocetin (1.5 mg/ml) using Born’s technique,2 and measured using an Elvi840 aggregometer. The aggregation was estimated by its half-maximal amplitude and the time required to achieve it. The Von Willebrand factor activity was measured using formaldehyde-fixed platelets and the microtitration technique.3 Fibrinogen was measured using the Boehringer Mannheim kit and hematocrit was determined by the standard method. Statistical analysis was performed by means of Student’s t test and the chi-square method. According to patient’s complaints, in 6 angina was effort-related (stable) and in 19 angina occurred at rest (unstable). For more accurate division into these groups, we used Holter 24-hour monitoring. Patients who had an increase in heart rate before attacks of angina or episodes of silent myocardial ischemia, or both, formed group I (stable angina). Others were included in group 2. Each patient in this group had at least 1 episode of angina (in which there was no increase in heart rate before such attacks) or episodes of silent myocardial ischemia, or both. Patients whose increase in heart rate started simultaneously with attacks of angina or started laterformed BRIEF
REPORTS
959
TABLE
I Platelet Function and Plasma Lipid Level in Patients with Stable and Unstable Angina Pectoris Platelet
Aggregation Ristocetin (1.5 mg/ml)
Angina ADP (10M5 Pt.
Age (yr) &Sex
Duration (yr)
Cornplaints
vWf %
Ht % Group
1 2 3 4 5
46M 50M 62M 54M 62F
6 7 8 9
ia 1 (effort-related
ta
ia
ta
stable
angina
according
to Holter
43 45 43 45 41
0 12 55 5 30
0
6 5
126 151 186 205 218
10
45M 46M 57M 70M 58M
6 5 8 6 2
E E R E E
221 235 247 248 274
48 41 48 47 49
55 58 80 50 85
Mean
5523
5k
211 f 14
45 2 1 43 f 11 4 f 1 79 + 4 4 f 0.4
1 1
5
13 14 15
50M 58M 58F 54M 53F 60M 52M 35M 48M 52M 56M 49M 40M 35M 57M
Mean
51k2
4kl
11 12
1 7
1 3
1 4
1 6 4 6 4 4 5 5
1
R R R R R R R R R R R R R R R
Total Chol. (mg/dU
Fibrinogen (mg/dl)
E R R E R
1 2 3 4 5 6 7 8 9 10
7
M)
Trigl. (mg/dl)
311 320 266 333 266
263
4 2 2
5 4 3 5 4
252 240 202
221 253 135 154 180
4 7 4 8 4
66 70 95 80 90
3 4 2 5 2
340 303 377 311 333
290 259 306 272 244
224 171 171 138 76
Group
2 (unstable
angina
at rest according
123 234 248 253 274 284 303 330 343 356 380 385 413 444 444
52 44 49 39 43 42 50 51 44 51 53 50 59 49 48
9 53 17 30 5 9 50 55 7 31 40 15 3 45 23
4 2 3 4 7 5 7 5 3 4 3 2 4 5 5
100
1
75 95 90 95 69 75
4 3 2 3 4 2
100
321?24*
4821
2627
421
87~3
75 85 88 100 79 82 90
to Holter 3 2 2 2 3 7 3
HDL Chol. (mg/dl)
184 291 200 168
129
34 49 25 41 37
212 183 226 207 175
34 42 46 38 54
monitoring)
85 60 66 95 81
1
LDL Chol. (mg/dl)
391
316 2 10 272 + 13
172 2 16 198k
13 40 + 3
monitoring)
2
340 280 399 311 311 280 266 400 377 330 288 355 377 400 266
232 212 260 240 274 224 176 230 240 137 237 267 204 260 182
2?0.3t
332214
225klO$
21
173
111
145 194 169
55 45 28 20 32 58 44 36 30
190 257 174 74 137 273 180 98
207 151 105 139 174 107
129
184
11 29
258 107 310 356
225 177 182 82
35 38 16 29
178225
161tlO
3423
*p < 0.001; tp < 0.02; *p < 0.01. ADP = adenosine diphosphate; Chol. = cholesterol; E E complains only of effort-related angina,; HDL = highdensity olatelet aggregation (percent); LDL = low-density lipoprotein: R = complains of angina at rest; ta = time (minutes) required iactor.
group 2, because it seemed that tachycardia developed secondary to pain and was not the cause of ischemia. According to this division, 10 patients formed group I and 15 patients group 2. Holter monitoring identified effort-related (stable) angina in 4 of 10 patients. The complaints of these 4 were previously thought to be angina at rest (patients 2, 3, 5 and 8 from group 1) (Table I). Wefound the levels of von Willebrand to be much higher in group 2 than in group 1 patients (Table I). No patient from group 1 had von Willebrand factor >300% of the average value for control donors, whereas 9 of 15 patients from group 2 had von Willebrand factor higher than that level (p KO.01, chisquare). The level of-fibrinogen, hematocrit and adenosine diphosphate-induced platelet aggregation did not differ much in both groups, but platelet aggregation using ristocetin was higher in group 2. The levels 960
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
lipoprotein; Ht = hematocrit: ia = maximal amplitude of to achieve ia: Trigl. = triglycerides; vWF = van Willebrand
of total cholesterol and low-density lipoprotein cholesterol were higher in group 1 than in group 2 (Table I).
It wasshown in this study that changes in plasma lipid levels were greater in patients with stable than unstable angina. In contrast, the parameters of platelet hemostasis were more altered in patients with unstable angina. The most striking difference between groups was in the average level of the von Willebrand factor: much higher in group 2 than in group 1. This protein plays a major role in platelet adhesion. We previously showed an increase in the von Willebrand factor and in platelet adhesion and spreading in more than half of our patients with coronary artery disease.435 It is known that the reason for effort angina (or effortrelated silent ischemia) is the imbalance between oxygen demand and coronary blood flow due to the atherosclerotic changes in coronary arteria.6*7 The reason for atOCTOBER 1, 1991
tacks of angina at rest may be transient reduction of coronary blood flow due to coronary spasm or thrombus formation.*T9 The activation of platelets in group 2 can play a major role not only in the formation of platelet aggregates, but also in the development of coronary spasm, producing such vasoconstrictors as thromboxane AZ, serotonine and others.9,10 This study suggests that alteration of plasma lipid levels plays a main role in the development of effortrelated angina due to increased oxygen demand, and changes in platelet function may be of major importance in the episodes of angina at rest due to transient reduction in coronary blood flow. Acknowledgment: We are very grateful to Vladimir I. Gelfand and Juri M. Vasiliev for help and constructive criticism.
1. Bruce RA, Blackman JR, Jones JW, Strait G. Exercising testing in adult normal subjects and cardiac patients. Pediatrics 1963;32:742-749. 2. Born GVR. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962;194:927-929. 3. Ramsey MS, Evatt MD. Rapid assay for van Wilebrand factor activity using formalin-fixed platelets and microtitration technique. Am J C/in Pathol 1979;72:996-999. 4. Orlov VN, Bespalko IA, Vasilieva EJ. Platelets and van W&brand factor in patients with acute myocardial infarction (in Russian). Sou Med 1988;1:9-13. 5. Vasilieva EJ, Orlov VN, Barkagan ZS. Shape and spreading of platelets from the blood of patients with acute myocardial infarction. Thromb Haemost 1984;52:201-204. 6. Gotto AM, Thompson JR, Gorry GA. Relationship between plasma lipid concentration and coronary disease in 496 patients. Circulation 1977;56:875-883. 7. Raab W. The neurogenic metabolic factor in ischemic heart disease. Dis Chest 1964;42:150-157. 6. Sherman CT, Zitvack F, Grundfest W. Coronary angioscopy in patients with unstable angina pectoris. N Engl J Med 1986;315:913-919. 9. Vetroves GW. Changing concepts in pathophysiology of myocardial ischemia. Am J Cm-dial 1989;64:3Fm9F. 10. Mehta J, Mehta P. Role of blood platelets and prostaglandins in coronary artery disease. Am J Cardiol 1981;48:366-373.
Two-Dimensional Echocardiographic Characteristics of Pericardial Hematoma Secondary to Left Ventricular Free Wall Rupture Complicating Acute Myocardial Infarction Martin Brack, MD, Richard W. Asinger, MD, Scott W. Sharkey, MD, Charles A. Herzog, MD, and Morrison Hodges, MD upture of the left ventricular (LV) free wall is a common complication of acute myocardial infarction (AMI) and accounts for up to 10% of hospital deaths.’ Infarct expansion may precede rupture,2 whereas the rupture itself is usually associated with rapid hemodynamic deterioration from cardiac tamponade and leads to death. The potential for salvage of such patients is poor; however, under favorable circumstances (early identification and optimal hemodynamic support), some patients survive emergency surgical repair.3 Cases have been reported where echocardiography contributed to the diagnosis by demonstrating intrapericardial echodensities and moderate effusion.4-10 This report describes our observations of the 2-dimensional echocardiographic characteristics of LV free wall rupture in 7 patients with AMI.
R
Over a 7-year period, 7 patients (5 men and 2 women, mean age 67 years, range 60 to 85) had documented or probable myocardial rupture complicating AMI with 2-dimensional echocardiography during acute hemodynamic deterioration. In 6patients, a tear of the LVfree wall was seenby surgery or autopsy. In the remaining patient, an expanding infarct was noted From County 55415, Brack Berne, revised
the Cardiology Division, Department of Medicine, Hennepin Medical Center, 701 Park Avenue, Minneapolis, Minnesota and the University of Minnesota, Minneapolis, Minnesota. Dr. is supported by a grant from Tiefenau Hospital, University of Berne, Switzerland. Manuscript received December 17, 1990; manuscript received and accepted June 4, 199 1.
echocardiographically culminating in sudden hemodynamic compromise with echocardiographic features typical of pericardial hematoma. The diagnosis of AMI was based on history of chest pain, serial electrocardiograms and serum cardiac enzyme levels. Three patients underwent emergent angiography, and each showed an occludedproximal epicardial coronary artery. Inpatients 2,6 and 7, chest pain was followed immediately by cardiogenic shock, suggesting that infarction may have occurred earlier and that their initial clinical presentation was myocardial rupture. Acute hemodynamic deterioration occurred 1 day after admission in patient 5, and at jive days in patients 1 and 3. Patient 4 collapsed during the recovery period after an exercise test on the tenth day of an otherwise uncomplicated inferior wall AMI. The time from the initial onset of chest pain to the apparent rupture ranged from 10 hours to 10 days. In all 7 patients, hemodynamic deterioration was rapid, but the patients could be supported for at least I hour after echocardiographic detection of pericardial hematoma in 6 patients. Two-dimensional echocardiograms were obtained with either an ATL Mark III mechanical sector scanner (Advanced Technology Laboratories) or an HP 77020Aphased-array sector scanner (Hewlett-Packard). A limited echocardiographic examination was performed using at least the subcostal window (modiBRIEF REPORTS
961
DE, Pfeffer MA. acute myocardial
Platelet Function Unstable Angina
Left ventricular thrombus infarction. Am I Cardiol
and Plasma Pectoris
formation 1988;62:
Lipid
31-35. 2. Weinrich DJ, Burke JF, Paulette FJ. Left ventricular thrombi complicating acute myocardial infarction. Long-term followup with serial echocardiography. Ann Intern Med 1984;100:789-794. 3. Lamas GA, Vaughan DE, Pfeffer MA. Significance of a lateral Q wave following first anterior wall acute myocardial infarction. Am J Cardiol 1990;6: 674-675. 4. Mel&r RS, Visser CA, Faster V. Intracardiac thrombi and systemic embolization. Ann Intern Med 1986;104:689-698. 5. Stratton JR, Lighty GW, Pearlman AS, Ritchie JL. Detection of left ventricular thrombus by two-dimensional echocardiography. Sensitivity, specificity and cause of uncertainty. Circulation 1928;66:156-166. 6. Kircher BJ, Top01 EJ, O’Neill WW, Pitt B. Prediction of infarct coronary artery recanalization after intravenous thrombolytic therapy. Am J Cardiol 1987;59:513-515.
Levels in Patients
Elena J. Vasilieva, MD, Alexander V. Shpector, MD, Aleksey B. Raskuragev, Lekochmacher, PhD, and lnna A. Bespalko, MD e investigated 2 groups of patients with angina pectoris - those with chest pain only on exertion (stable) and those with chest pain at rest (unstable) - to determine if platelet function and serum lipid levels were similar or different between the 2 groups. We studied 25patients (22 men and 3 women, aged 3.5 to 70 years) with coronary artery disease; the diagnosis was established on the basis of typical clinical manifestations, and exercise stress testing following the Bruce protocol t and data from 24-hour Holter monitoring. Monitoring was performed using a Medilog MA-14 monitor (Oxford Medical Systems). The electrocardiogram was recorded using 2 leads: the first pair of electrodes was placed under the second rib to the right of the chest and at the heart apex; the second one was placed under the fourth rib to the right of the chest and under the left clavicle. All patients kept a detailed diary and were instructed to activate the event button on the tape recorder when experiencing angina1 chest pain so as to identify possible symptomatic ischemic episodes. The tapes were analyzed visually by 2 experts at 60 times normal speed and trend curves of ST-segment deviation and heart rate were obtained for the entire monitoring period. Episodes of interest were printed forjnal evaluation. We considered transient ST-segment deviation > 1 mm, 80 ms after the J point, and a duration of at least 1 minute as ischemic.
W
From the Moscow Medical-Stomatological Institute, Moscow, Russia. Dr. Vasilieva’s address is: Second Division of Cardiology, Moscow General Hospital #52, Pehotnaya Street 3, Moscow 123436, Russia. Manuscript received January 14,199 1; revised manuscript received June 13,1991, and accepted June 14.
with Stable MD, Svetlana
and
S.
At all examinations, blood was collected by venapuncture of the cubital vein with a 19-gauge needle in the morning after I4 hours of fasting. Blood was collected without an anticoagulant for lipid analysis and with 3.8% sodium citrate (9:l) for all other analyses. Total cholesterol, low- and high-density lipoprotein cholesterol and total triglycerides were measured in plasma samples using a Boehringer Mannheim kit on an Opton spectrophotometer. Platelet aggregation was induced by adenosine diphosphate (2 X 1Om5M) and by ristocetin (1.5 mg/ml) using Born’s technique,2 and measured using an Elvi840 aggregometer. The aggregation was estimated by its half-maximal amplitude and the time required to achieve it. The Von Willebrand factor activity was measured using formaldehyde-fixed platelets and the microtitration technique.3 Fibrinogen was measured using the Boehringer Mannheim kit and hematocrit was determined by the standard method. Statistical analysis was performed by means of Student’s t test and the chi-square method. According to patient’s complaints, in 6 angina was effort-related (stable) and in 19 angina occurred at rest (unstable). For more accurate division into these groups, we used Holter 24-hour monitoring. Patients who had an increase in heart rate before attacks of angina or episodes of silent myocardial ischemia, or both, formed group I (stable angina). Others were included in group 2. Each patient in this group had at least 1 episode of angina (in which there was no increase in heart rate before such attacks) or episodes of silent myocardial ischemia, or both. Patients whose increase in heart rate started simultaneously with attacks of angina or started laterformed BRIEF
REPORTS
959
TABLE
I Platelet Function and Plasma Lipid Level in Patients with Stable and Unstable Angina Pectoris Platelet
Aggregation Ristocetin (1.5 mg/ml)
Angina ADP (10M5 Pt.
Age (yr) &Sex
Duration (yr)
Cornplaints
vWf %
Ht % Group
1 2 3 4 5
46M 50M 62M 54M 62F
6 7 8 9
ia 1 (effort-related
ta
ia
ta
stable
angina
according
to Holter
43 45 43 45 41
0 12 55 5 30
0
6 5
126 151 186 205 218
10
45M 46M 57M 70M 58M
6 5 8 6 2
E E R E E
221 235 247 248 274
48 41 48 47 49
55 58 80 50 85
Mean
5523
5k
211 f 14
45 2 1 43 f 11 4 f 1 79 + 4 4 f 0.4
1 1
5
13 14 15
50M 58M 58F 54M 53F 60M 52M 35M 48M 52M 56M 49M 40M 35M 57M
Mean
51k2
4kl
11 12
1 7
1 3
1 4
1 6 4 6 4 4 5 5
1
R R R R R R R R R R R R R R R
Total Chol. (mg/dU
Fibrinogen (mg/dl)
E R R E R
1 2 3 4 5 6 7 8 9 10
7
M)
Trigl. (mg/dl)
311 320 266 333 266
263
4 2 2
5 4 3 5 4
252 240 202
221 253 135 154 180
4 7 4 8 4
66 70 95 80 90
3 4 2 5 2
340 303 377 311 333
290 259 306 272 244
224 171 171 138 76
Group
2 (unstable
angina
at rest according
123 234 248 253 274 284 303 330 343 356 380 385 413 444 444
52 44 49 39 43 42 50 51 44 51 53 50 59 49 48
9 53 17 30 5 9 50 55 7 31 40 15 3 45 23
4 2 3 4 7 5 7 5 3 4 3 2 4 5 5
100
1
75 95 90 95 69 75
4 3 2 3 4 2
100
321?24*
4821
2627
421
87~3
75 85 88 100 79 82 90
to Holter 3 2 2 2 3 7 3
HDL Chol. (mg/dl)
184 291 200 168
129
34 49 25 41 37
212 183 226 207 175
34 42 46 38 54
monitoring)
85 60 66 95 81
1
LDL Chol. (mg/dl)
391
316 2 10 272 + 13
172 2 16 198k
13 40 + 3
monitoring)
2
340 280 399 311 311 280 266 400 377 330 288 355 377 400 266
232 212 260 240 274 224 176 230 240 137 237 267 204 260 182
2?0.3t
332214
225klO$
21
173
111
145 194 169
55 45 28 20 32 58 44 36 30
190 257 174 74 137 273 180 98
207 151 105 139 174 107
129
184
11 29
258 107 310 356
225 177 182 82
35 38 16 29
178225
161tlO
3423
*p < 0.001; tp < 0.02; *p < 0.01. ADP = adenosine diphosphate; Chol. = cholesterol; E E complains only of effort-related angina,; HDL = highdensity olatelet aggregation (percent); LDL = low-density lipoprotein: R = complains of angina at rest; ta = time (minutes) required iactor.
group 2, because it seemed that tachycardia developed secondary to pain and was not the cause of ischemia. According to this division, 10 patients formed group I and 15 patients group 2. Holter monitoring identified effort-related (stable) angina in 4 of 10 patients. The complaints of these 4 were previously thought to be angina at rest (patients 2, 3, 5 and 8 from group 1) (Table I). Wefound the levels of von Willebrand to be much higher in group 2 than in group 1 patients (Table I). No patient from group 1 had von Willebrand factor >300% of the average value for control donors, whereas 9 of 15 patients from group 2 had von Willebrand factor higher than that level (p KO.01, chisquare). The level of-fibrinogen, hematocrit and adenosine diphosphate-induced platelet aggregation did not differ much in both groups, but platelet aggregation using ristocetin was higher in group 2. The levels 960
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
lipoprotein; Ht = hematocrit: ia = maximal amplitude of to achieve ia: Trigl. = triglycerides; vWF = van Willebrand
of total cholesterol and low-density lipoprotein cholesterol were higher in group 1 than in group 2 (Table I).
It wasshown in this study that changes in plasma lipid levels were greater in patients with stable than unstable angina. In contrast, the parameters of platelet hemostasis were more altered in patients with unstable angina. The most striking difference between groups was in the average level of the von Willebrand factor: much higher in group 2 than in group 1. This protein plays a major role in platelet adhesion. We previously showed an increase in the von Willebrand factor and in platelet adhesion and spreading in more than half of our patients with coronary artery disease.435 It is known that the reason for effort angina (or effortrelated silent ischemia) is the imbalance between oxygen demand and coronary blood flow due to the atherosclerotic changes in coronary arteria.6*7 The reason for atOCTOBER 1, 1991
tacks of angina at rest may be transient reduction of coronary blood flow due to coronary spasm or thrombus formation.*T9 The activation of platelets in group 2 can play a major role not only in the formation of platelet aggregates, but also in the development of coronary spasm, producing such vasoconstrictors as thromboxane AZ, serotonine and others.9,10 This study suggests that alteration of plasma lipid levels plays a main role in the development of effortrelated angina due to increased oxygen demand, and changes in platelet function may be of major importance in the episodes of angina at rest due to transient reduction in coronary blood flow. Acknowledgment: We are very grateful to Vladimir I. Gelfand and Juri M. Vasiliev for help and constructive criticism.
1. Bruce RA, Blackman JR, Jones JW, Strait G. Exercising testing in adult normal subjects and cardiac patients. Pediatrics 1963;32:742-749. 2. Born GVR. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962;194:927-929. 3. Ramsey MS, Evatt MD. Rapid assay for van Wilebrand factor activity using formalin-fixed platelets and microtitration technique. Am J C/in Pathol 1979;72:996-999. 4. Orlov VN, Bespalko IA, Vasilieva EJ. Platelets and van W&brand factor in patients with acute myocardial infarction (in Russian). Sou Med 1988;1:9-13. 5. Vasilieva EJ, Orlov VN, Barkagan ZS. Shape and spreading of platelets from the blood of patients with acute myocardial infarction. Thromb Haemost 1984;52:201-204. 6. Gotto AM, Thompson JR, Gorry GA. Relationship between plasma lipid concentration and coronary disease in 496 patients. Circulation 1977;56:875-883. 7. Raab W. The neurogenic metabolic factor in ischemic heart disease. Dis Chest 1964;42:150-157. 6. Sherman CT, Zitvack F, Grundfest W. Coronary angioscopy in patients with unstable angina pectoris. N Engl J Med 1986;315:913-919. 9. Vetroves GW. Changing concepts in pathophysiology of myocardial ischemia. Am J Cm-dial 1989;64:3Fm9F. 10. Mehta J, Mehta P. Role of blood platelets and prostaglandins in coronary artery disease. Am J Cardiol 1981;48:366-373.
Two-Dimensional Echocardiographic Characteristics of Pericardial Hematoma Secondary to Left Ventricular Free Wall Rupture Complicating Acute Myocardial Infarction Martin Brack, MD, Richard W. Asinger, MD, Scott W. Sharkey, MD, Charles A. Herzog, MD, and Morrison Hodges, MD upture of the left ventricular (LV) free wall is a common complication of acute myocardial infarction (AMI) and accounts for up to 10% of hospital deaths.’ Infarct expansion may precede rupture,2 whereas the rupture itself is usually associated with rapid hemodynamic deterioration from cardiac tamponade and leads to death. The potential for salvage of such patients is poor; however, under favorable circumstances (early identification and optimal hemodynamic support), some patients survive emergency surgical repair.3 Cases have been reported where echocardiography contributed to the diagnosis by demonstrating intrapericardial echodensities and moderate effusion.4-10 This report describes our observations of the 2-dimensional echocardiographic characteristics of LV free wall rupture in 7 patients with AMI.
R
Over a 7-year period, 7 patients (5 men and 2 women, mean age 67 years, range 60 to 85) had documented or probable myocardial rupture complicating AMI with 2-dimensional echocardiography during acute hemodynamic deterioration. In 6patients, a tear of the LVfree wall was seenby surgery or autopsy. In the remaining patient, an expanding infarct was noted From County 55415, Brack Berne, revised
the Cardiology Division, Department of Medicine, Hennepin Medical Center, 701 Park Avenue, Minneapolis, Minnesota and the University of Minnesota, Minneapolis, Minnesota. Dr. is supported by a grant from Tiefenau Hospital, University of Berne, Switzerland. Manuscript received December 17, 1990; manuscript received and accepted June 4, 199 1.
echocardiographically culminating in sudden hemodynamic compromise with echocardiographic features typical of pericardial hematoma. The diagnosis of AMI was based on history of chest pain, serial electrocardiograms and serum cardiac enzyme levels. Three patients underwent emergent angiography, and each showed an occludedproximal epicardial coronary artery. Inpatients 2,6 and 7, chest pain was followed immediately by cardiogenic shock, suggesting that infarction may have occurred earlier and that their initial clinical presentation was myocardial rupture. Acute hemodynamic deterioration occurred 1 day after admission in patient 5, and at jive days in patients 1 and 3. Patient 4 collapsed during the recovery period after an exercise test on the tenth day of an otherwise uncomplicated inferior wall AMI. The time from the initial onset of chest pain to the apparent rupture ranged from 10 hours to 10 days. In all 7 patients, hemodynamic deterioration was rapid, but the patients could be supported for at least I hour after echocardiographic detection of pericardial hematoma in 6 patients. Two-dimensional echocardiograms were obtained with either an ATL Mark III mechanical sector scanner (Advanced Technology Laboratories) or an HP 77020Aphased-array sector scanner (Hewlett-Packard). A limited echocardiographic examination was performed using at least the subcostal window (modiBRIEF REPORTS
961
