1180 BRIEF REPORTS

are listed in Table II. Systemic and pulmonary arteri- al, pulmonary artery wedge and right atrial pressures, and systemic and pulmonary arterial resistances were not significantly different in group A compared with group B. However, cardiac and stroke indexes were lower in group B than in group A, whereas heart rate was higher. As shown in Figure 2, no correlation was found between plasma AVP level and osmolality, sys- temic blood pressure and cardiac index. However, there were significant correlations between plasma AVP and norepinephrine levels, renin activity and right atria1 pressure.

Our results suggest, therefore, that plasma AVP can be highly elevated in some patients after AMI, partic- ularly in those who do not survive their initial hos- pitalization. As expected, nonsurvivors also showed an increased activation of their sympathetic and renin- angiotensin systems and had more severe cardiac fail- ure compared with survivors. The stimulus for such a marked increase in AVP levels is unknown, but may include several factors such as high plasma osmolality, pain, nausea, cardiac failure, hypotension, increased angiotensin II production and medications. The lack of correlation between plasma AVP level and osmolality suggests that osmolality was not a major stimulus for AVP secretion. Morphine, given to 20 patients in both groups, is an unlikely cause of elevation of plasma vasopressin because its acute administration does not usually influence plasma AVP levels, according to re- cent studies. Chronic congestive heart failure is known to be associated with an increase in plasma AVP.3v4 The significant correlations seen in our study between plasma AVP and norepinephrine, renin activity and right atria1 pressure suggest that cardiac failure after

AMI may be one of the major stimuli for AVP release. The lack of correlation between plasma AVP and car- diac index may be attributed to the small number of patients studied invasively. However, other factors such as pain or nausea may have resulted in increased AVP secretion after AMI. Whether these high plasma AVP levels produce global or regional peripheral va- soconstriction is unknown. Previous studies of patients with chronic congestive heart failure have suggested that only marked increase in plasma AVP levels seen in rare subjects with severe heart failure could con- tribute to peripheral vasoconstriction.4 It is, therefore, possible that the highest AVP levels seen in a few patients of our present study could exert some vaso- constrictive effect. The action of AVP on the coronary arteries is still debatede5p6 Further studies are needed to determine whether markedly elevated plasma AVP levels such as those found in some patients after AM1 can further limit coronary blood flow and aggravate myocardial injury.

1. Jewitt DE, Mercer CJ, Reid D, Valori C, Thomas M, Schillingford JP. Free noradrenaline and adrenaline excretion in relation to the development of cardiac arrhythmias and heart-failure in patients with acute myocardial in- farction. Lancet 1969;1:635-641. 2. Vaney C, Waeber B, Turini G, Margalith D, Bnmner HR, Perret C. Renin and the complications of acute myocardial infarction. Chest 1984;86:40-43. 3. Goldsmith SR, Francis GS, Cowley AW, Levine TB, Cohn JN. Increased plasma arginine vasopressin levels in patients with congestive heart failure. JACC 1983;1:1385-1390. 4. Nicod P, Waeber B. Bussien JP, Goy JJ, Turini GA, Nussberger J, Hofbauer KG, Brunner HR. Acute hemodynamic effect of a vascular antagonist of vasopressin in patients with congestive heart failure. Am J Cardiol 1985; 55:1043-1047. 5. Heyndrickx GR, Boettcher DH, Vatner SF. Effects of angiotensin, vasopres- sin, and methoxamine on cardiac function and blood flow distribution in conscious dogs. Am r Physiol 1976;231:1579-1587. 6. Nicod P, Winniford MD, Campbell WB, Rehr RB, Firth BG, Hillis LD. Alteration of coronary blood flow induced by cigarette smoking: lack of rela- tion to plasma arginine vasopressin concentrations. Am J Cardiol1984;54:667- 668.

Lysis of Mobile left Ventricular Thrombi During Acute Myocardial

Infarction with Urokinase ANDRE KEREN, MD

AHARON MEDINA, MD SHMUEL GO-ITLIEB, MD

SHMUEL BANAI, MD SHLOMO STERN, MD

1 eft ventricular (LV) thrombi occur in about one- third of patients who have had an acute myocardial infarction (AMI) .ls2 Autopsy3 and echocardiographic studies1s2 suggest that patients with protruding and mo- bile LV thrombi are at risk of systemic embolization. Kremer et al4 reported the successful use of urokinase

From the Heiden Department of Cardiology, Bikur Cholim Hos- pital and Hebrew University-Hadassah Medical School, P.O. Box 492, Jerusalem, Israel. Manuscript received March 16,1987; revised manuscript received and accepted June Z&1987.

for lysis of protruding and mobile LV thrombi during AM1 but no further reports followed this initial com- munication. We report the effect of urokinase on mo- bile LV thrombi in a patient with AMI.

A 41-year-old man with previous inferior wall AM1 treated with streptokinase was hospitalized with ante- rior wall AMI. On admission, blood pressure and pulses were normal, apex beat was dyskinetic and on auscultation, a fourth heart sound was detected. Peak creatine phosphokinase was 5,860 U (normal less than 160 U). The first days of his hospitalization were com- plicated by cardiogenic shock, acute pulmonary ede- ma and ventricular arrhythmias, and the patient was treated with dopamine, dobutamine, diuretics and lignocaine. Bedside 2-dimensional echocardiography showed LV enlargement, apical, septal and inferior wall akinesia, and severely decreased LV function. Nuclear LV ejection fraction was 23%. The patient gradually improved and 26 days after admission, nu- clear LV ejection fraction was 32%. Repeat echocar- diogram showed improvement in segmental wall mo- tion but also revealed 3 protruding and mobile thrombi in the apex of the left ventricle. After detection of the

November 15, 1967 THE AMERICAN JOURNAL OF CARDlObOGY Volume 60

FIGURE 1. A, apical 4-chamber view showing the presence of 2 mobile thrombi before administration of urokinase (large arrows); B, significant decrease in size of thrombi 12 hours after initiation of urokinase therapy; C, echocardiogram recorded 36 hours after initiation of urokinase therapy. The area previously occupied by thrombi is marked by smallarrows. LV = left ventricle; RA = right atri- um; RV = right ventricle; Th = thrombi.

thrombi, echocardiographic studies were performed at least twice a day. Intravenous heparin, 10,000 U bolus and 1,000 to 1,200 U/hour, was started. Forty- eight hours later the patient had a transient cerebral ischemic episode with dysarthria and left hemiparesis lasting 6 hours. Echocardiography showed almost complete disappearance of the smallest thrombus pre- viously attached to the LV wall by a thin stalk. No changes in the size and the mobility of the 2 other thrombi were found that time or after 1 week of thera- py with heparin [Figure IA). Therefore, urokinase was given using the protocol of Kremer et ai. After an intravenous bolus of 250,000 U, 60,000 U/hour of uroki- nose and 1,000 units/hour of heparin were adminis- tered for 48 hours. A significant decrease in the size of the 2 thrombi was documented after 12 hours [Figure ZB], and LV thrombi were not detected by echocardi- ography 36 hours after initiation of the urokinase (Fig- ure 1C). Therapy with heparin was continued for 4 more days until oral anticoagulation reached thera- peutic range. No complications were associated with this therapy and the patient was discharged after ther- apy with diltiazem, diuretics, dicumarol and aspirin. Four months later he is free of symptoms and echocar- diography detected no recurrence of thrombi.

The lysis of fresh mobile thrombi by urokinase without any complications in our patient is in accor-

dance with the previous experience of Kremer et aL4 These investigators reported the successful lysis of protruding LV thrombi in 8 of 9 patients treated with urokinase less than 4 weeks after an AMI. An unspeci- fied number of patients in Kremer’s study had mobile thrombie4 Recently, Blazer et al5 reported embolization of an organized left atria1 thrombus in a patient both before and after administration of streptokinase. Con- sidering the high risk of thrombectomy after a recent infarction,l the safety of lysing fresh mobile thrombi and thrombolytic agents should be investigated further in these patients.

Addendum: Since we submitted our manuscript for publication, we used streptokinase infusion in a young patient with a large protruding apical thrombus found 10 days after acute myocardial infarction. Com- plete lysis of the thrombus was achieved without complications.

1. Meltzer RS, Visser CA, Fuster V. Intracordioc thrombi and systemic embo- lizotion. Ann Intern Med 1986:104x%9-698. 2. Haugland JM, Asinger RW, Mike11 FL, Elsperger J, Hodges M. Embolic potential of left ventricular thrombus detected by two-dimensional echocar- diogrophy. Circulation 1984;70:588-598. 3. Cabin HS, Roberts WC. Left ventricular aneurysm, introaneurysmol thrombus and systemic embolus in coronary heart disease. Chest 1980;77: 586-590. 4. Kremer P, Fiebig R, Tilsner V, Bleifeld W, Mathey DG. Lysis of left ventric- ular thrombi with urokinose. Circulation 1985;72:112-118.

5. Blazer D, Degroat T, Kotler MN, Nakhjavan F, Parameswaran R, McGow- an C, Parry WR. Peripheral embolization during thrombolytic therapy for left atria1 thrombus. Am J Cardiol 1986;58:554-555.