The effect of ultrasound on the rate of fibrinolysis has been investigated using an in vitro system. Plasma or blood clots containing a trace label of 125I fibrin were suspended in plasma containing plasminogen activator and intermittently exposed to continuous wave 1-MHz ultrasound at intensities up to 8 W/ cm2. Plasma clot lysis at 1 h with 1 igg/ml recombinant tissue plasminogen activator (rt-PA) was 12.8±1.2% without ultrasound and was significantly (P = 0.0001) increased by exposure to ultrasound with greater lysis at 1 W/cm2 (18.0 ± 1.4%), 2 W/cm2 (19.3 ± 0.7%), 4 W/cm2 (22.8 ± 1.8%), and 8 W/cm2 (58.7 ± 7.1%). Significant increases in lysis were also seen with urokinase at ultrasound intensities of 2 W/cm2 and above. Exposure of clots to ultrasound in the absence of plasminogen activator did not increase lysis. Ultrasound exposure resulted in a marked reduction in the rt-PA concentration required to achieve an equivalent degree of lysis to that seen without ultrasound. For example, 15% lysis occurred in 1 h at 1 gg/ml rt-PA without ultrasound or with 0.2 ug/ml with ultrasound, a fivefold reduction in concentration. Ultrasound at 1 W/cm2 and above also potentiated lysis of retracted whole blood clots mediated by rt-PA or urokinase. The maximum temperature increase of plasma clots exposed to 4 W/cm2 ultrasound was only 1.7°C, which could not explain the enhancement offibrinolysis. Ultrasound exposure did not cause mechanical fragmentation of the clot into sedimentable fragments, nor did it alter the sizes of plasmic derivatives as demonstrated by SDS polyacrylamide gel electrophoresis. We conclude that ultrasound at 1 MHz potentiates enzymatic fibrinolysis by a nonthermal mechanism at energies that can potentially be applied and tolerated in vivo to accelerate therapeutic fibrinolysis. (J.

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Left ventricular thrombus complicating myocardial infarction was diagnosed by two-dimensional echocardiography in 119 patients. The infarct site was anterior in 98 patients and inferior in 11. Systemic embolism occurred in 26 patients (stroke in 18, lower limb embolism in 7 and mesenteric embolism in 1). A protruding configuration of the thrombus was more common in the patients with embolism than in those without (23 [88%] of 26 versus 17 [18%] of 93) (p less than 0.01). Free mobility of the thrombus was found in 15 (58%) of 26 and 3 (3%) of 93 cases, respectively (p less than 0.01). In predicting embolism, protruding thrombus configuration had a sensitivity of 88% and a specificity of 82%, and positive and negative predictive accuracy was 57 and 96%, respectively. For free mobility of the thrombus, sensitivity was 58%, specificity 97%, positive predictive accuracy 85% and negative predictive accuracy 89%. In the 46 patients whose echocardiogram was obtained during the hospital admission for the index infarct, repeat echocardiograms were obtained during oral anticoagulant therapy. Twelve of these 46 patients had embolism and 2 of the 12 died. In seven of these patients, full dose oral anticoagulant therapy had been given before embolism occurred and in five it was started after an embolic event. The thrombus decreased in size or disappeared in six patients; in four the thrombus showed no change, and in two of these four emboli recurred despite anticoagulation. It is concluded that two-dimensional echocardiography may help delineate the embolic potential of left ventricular thrombus complicating myocardial infarction and may be of value in weighing the benefits and disadvantages of oral anticoagulant therapy.

Recent progress has been made in diagnosing and tracing the natural history of intracardiac thrombi by echocardiography. Left ventricular thrombi occur and cause emboli in three clinical conditions: acute myocardial infarction, left ventricular aneurysm as a sequel to infarction, and idiopathic dilated cardiomyopathy. Echocardiographic studies have shown that one third of patients with acute anterior myocardial infarction have left ventricular thrombi; only a small percentage of these patients have emboli. Administration of anticoagulants decreases the prevalence of left ventricular thrombi and the frequency of embolization in this group. Thrombi that are protruding and mobile are most likely to embolize. Anticoagulation treatment decreases the prevalence of embolization in idiopathic dilated cardiomyopathy and should be instituted regardless of whether atrial or ventricular thrombi are detected by two-dimensional echocardiography. In patients with chronic left ventricular aneurysm, thrombi occur commonly, but emboli, infrequently. Therefore, data are insufficient to suggest that anticoagulation treatment is indicated, even if left ventricular thrombi are detected by two-dimensional echocardiography.

The accuracy of electrocardiography, M-mode echocardiography and two-dimensional echocardiography in predicting left ventricular hypertrophy was compared in 50 patients who came to autopsy within 6 months after the studies were performed. Several methods for determining left ventricular hypertrophy were examined for each of the three techniques. M-mode echocardiography was technically adequate to evaluate the presence or absence of left ventricular hypertrophy more often than either electrocardiography or two-dimensional echocardiography. Measurements from M-mode echocardiography also correlated best with autopsy measurements. Both echocardiographic techniques had a higher sensitivity than electrocardiographic criteria in diagnosing left ventricular hypertrophy. Two-dimensional echocardiography was not shown to improve the M-mode assessment of left ventricular hypertrophy. In an attempt to simplify both M-mode left ventricular mass calculations and the diagnosis of left ventricular hypertrophy for the clinician, a left ventricular mass nomogram was constructed, enabling quick insertion of standard M-mode echocardiographic measurements.