Morrison Hodges

Incidence of left-ventricular thrombosis after acute transmural myocardial infarction. Serial evaluation by two-dimensional echocardiography.

To study the incidence of left-ventricular thrombosis after transmural myocardial infarction, we performed serial two-dimensional echocardiography in 70 consecutive patients. Thirty-five patients had inferior-wall infarction: none had a left-ventricular thrombus. The other 35 had anterior-wall infarction: 12 had left-ventricular thrombi. Thrombi were diagnosed an average of five days after the infarction (range, one to 11 days). All patients with left-ventricular thrombi had severe apical-wall-motion abnormalities (akinesis or dyskinesis). Twenty-six of the 35 patients with anterior infarctions had apical akinesis or dyskinesis on echocardiography; left-ventricular thrombi developed in 12 of these 26 (46 per cent). We conclude that patients with severe apical-wall-motion abnormalities during acute transmural anterior myocardial infarction are at high risk for left-ventricular thrombosis. This high-risk group can be identified before the development of left-ventricular thrombi. Patients with inferior infarction or anterior infarction without a severe apical-wall-motion abnormality are at low risk.

Observations on detecting left ventricular thrombus with two dimensional echocardiography: emphasis on avoidance of false positive diagnoses.

Observations made in detecting left ventricular thrombus with two dimensional echocardiography in 25 patients are reviewed. In 20 patients thrombus was documented on angiography, surgery postmortem examination or serial two dimensional echocardiographic findings; in the remaining five patients two dimensional echocardiographic findings of thrombus were unequivocal. In all 25 patients wall motion abnormalities ranging from hypokinesia to frank dyskinesia were present at the site of the thrombus. Twenty-three patients had an apical thrombus; two had thrombus adjacent to the inferior wall. Clear delineation of the endocardium and thrombus margin was considered essential to the correct diagnosis of thrombus. Both intracavitary motion of the thrombus margin and a layering effect were noted infrequently although they were of benefit in identifying an intracardiac mass as thrombus. In addition, serial evaluations were helpful in establishing the correct diagnosis. False positive diagnoses can be minimized if one understands certain technical limitations of this method and correctly identifies apical structures that are not thrombi. Axial and lateral resolution problems inherent with this technique can produce intracavitary echoes that may simulate thrombi. In addition, normal or pathologic structures at the apex may also simulate thrombi. These structures include the papillary muscles, muscular trabeculae, chordal structures and tangential information from normal myocardium. Varying the sector orientation or acoustic window, or both, will aid in correctly identifying these structures and distinguishing them from left ventricular thrombi.

Utility of current risk stratification tests for predicting major arrhythmic events after myocardial infarction

OBJECTIVES We surveyed the literature to estimate prediction values for five common tests for risk of major arrhythmic events (MAEs) after myocardial infarction. We then determined feasibility of a staged risk stratification using combinations of noninvasive tests, reserving an electrophysiologic study (EPS) as the final test. BACKGROUND Improved approaches are needed for identifying those patients at highest risk for subsequent MAE and candidates for implantable cardioverter-defibrillators. METHODS We located 44 reports for which values of MAE incidence and predictive accuracy could be inferred: signal-averaged electrocardiography; heart rate variability; severe ventricular arrhythmia on ambulatory electrocardiography; left ventricular ejection fraction; and EPS. A meta-analysis of reports used receiver-operating characteristic curves to estimate mean values for sensitivity and specificity for each test and 95% confidence limits. We then simulated a clinical situation in which risk was estimated by combining tests in three stages. RESULTS Test sensitivities ranged from 42.8% to 62.4%; specificities from 77.4% to 85.8%. A three-stage stratification yielded a low-risk group (80.0% with a two-year MAE risk of 2.9%), a high-risk group (11.8% with a 41.4% risk) and an unstratified group (8.2% with an 8.9% risk equivalent to a two-year incidence of 7.9%). CONCLUSIONS Sensitivities and specificities for the five tests were relatively similar. No one test was satisfactory alone for predicting risk. Combinations of tests in stages allowed us to stratify 91.8% of patients as either high-risk or low-risk. These data suggest that a large prospective study to develop a robust prediction model is feasible and desirable.

Regional stasis of blood in the dysfunctional left ventricle: echocardiographic detection and differentiation from early thrombosis.

In two-dimensional echocardiographic studies of left ventricular thrombus in patients, an unusual pattern of dynamic left ventricular intracavitary echoes was identified in some hearts with severe apical dysfunction. These intracavitary echoes were noted in the apical region and were distinct from left ventricular thrombi. Certain features of the intracavitary echoes suggested that they were generated by regional stasis of blood. To study this phenomenon, echocardiography was performed in 1I dogs with experimental anteroapical infarction and associated left ventricular thrombus and in six dogs with infarction but no thrombus. The dynamic intracavitary echo pattern suggesting blood stasis was identified in the ischemic apex in dogs of both groups. These echoes had characteristics suggesting a fluid or semifluid state and could be distinguished from thrombi. In real time, the echoes moved in a slow, circular fashion at the apex and lacked well-defined borders; their configuration and acoustic intensity changed over short periods of time, and they could be rapidly altered bv ectopic or mechanical contraction of the heart and by dopamine infusion. Postmortem examination showed that liquid blood produced the echoes. Additional studies demonstrated the echogenicitv of static blood. Echocardiography of dog hearts with KCI-induced mechanical-asystole showed the rapid development of diffuse echogenicity of the intraventricular rontents; in vitro studies confirmed the echogenicity of static blood.These observations indicate that a spectrum of echocardiographic features characterizes ventricular blood under various conditions of flow and with frank thrombosis. The ability of echocardiographv to detect in vivo stasis of blood in the left ventricle and to distinguish this from thrombosis has important clinical and investigational implications.

Embolic potential of left ventricular thrombi detected by two-dimensional echocardiography.

We sought to determine whether an association existed between the echocardiographic appearance of left ventricular thrombi and systemic embolization. We reviewed the clinical and echocardiographic characteristics of 60 patients who underwent diagnostic two-dimensional echocardiography for left ventricular thrombi. Sixteen of these 60 patients (27%) had evidence of systemic embolization. Multiple echocardiographic characteristics of left ventricular thrombi were analyzed, including mobility, shape, heterogeneity, echo density, layering, central echo lucency, presence within an aneurysm, and association with low-density swirling echoes. Incidence of embolization was significantly higher in patients with thrombi that were mobile or protruded into the left ventricular cavity (p less than .002 and p less than .05, respectively). Bayesian analysis indicated that the pretest likelihood for embolization was 27% and increased in the presence of mobility, central echo lucency, and protrusion to 60%, 50%, and 40%, respectively. A stepwise regression indicated that mobility was the first and protrusion the second most helpful echocardiographic characteristic in identifying patients with embolic phenomena. Clinical features were of less help in identifying the risk for embolization of patients with left ventricular thrombi. Nine of 31 patients (29%) with recent myocardial infarction (less than 3 weeks) has emboli in contrast to five of 26 patients (19%) with remote myocardial infarction (greater than 3 weeks) (p = NS). The three patients without infarction had congestive cardiomyopathy and two had emboli.

A controlled trial of propafenone for treatment of frequent and repetitive ventricular premature complexes

The effectiveness of oral propafenone was evaluated for the treatment of ventricular premature complexes (VPCs) in 12 patients, using a single-blind, dose-ranging trial followed by a double-blind comparison with placebo, and then an open-label, long-term protocol. During dose ranging, 8 of 12 patients achieved greater than or equal to 80% suppression of total VPCs (mean 83%) (p less than 0.01 vs single-blind placebo). Paired VPCs were suppressed greater than or equal to 90% and ventricular tachycardia was eliminated in 11 of the 12 patients (p less than 0.01). The effectiveness of propafenone for treatment of VPCs was confirmed during the double-blind trial (p less than 0.05 vs double-blind placebo) and during treatment for 6 months (p less than 0.05 vs initial single-blind placebo). Propafenone prolonged the PR interval by 16% (p less than 0.01 vs single-blind placebo) and the QRS interval by 18% (p less than 0.001). Left ventricular systolic performance decreased as assessed by 2-dimensional echocardiography (p less than 0.01 vs single-blind placebo). Propafenone increased serum digoxin levels in 5 of 5 patients (mean increase of 83%). Side effects included exacerbation of congestive heart failure (1 patient) and conduction abnormalities (2 patients). Thus, propafenone is effective for treatment of total and repetitive VPCs. Although generally well tolerated, the drug reduces left ventricular systolic function and atrioventricular conduction and increases serum digoxin levels.

The thrombolysis in myocardial infarction (TIMI) phase II pilot study: Tissue plasminogen activator followed by percutaneous transluminal coronary angioplasty

The Thrombolysis in Myocardial Infarction (TIMI) Study Group is investigating whether percutaneous transluminal coronary angioplasty or intravenous beta-receptor blockers, or both, are useful adjuncts to recombinant tissue-type plasminogen activator (rt-PA) in the treatment of patients with acute myocardial infarction (TIMI II study). A total of 317 patients with acute myocardial infarction were treated an average of 2.7 hours after the onset of chest pain during the course of a nonrandomized pilot investigation with 150 mg of rt-PA given over 6 hours. This dose of rt-PA resulted in a high rate of infarct-related coronary artery patency (82 and 87% of patients catheterized an average of either 1 or 32 hours after entry, respectively) and a low 21 day mortality rate of 4.4%. Coronary angioplasty was performed successfully in greater than 90% of patients with appropriate anatomy and in greater than 50% of those treated with rt-PA. In 75 patients treated within 2 hours of the onset of chest pain only 2 (2.7%) were dead by 6 weeks. However, five cases of intracranial hemorrhage were noted, and the rt-PA dose was subsequently reduced to 100 mg given over 6 hours. The TIMI II design and the results of the TIMI II pilot study are discussed.

Comparative hemodynamic effects of dopamine and dobutamine in patients with acute cardiogenic circulatory collapse

The hemodynamic effects of dopamine (DPM) and dobutamine (DBM) were compared in 13 patients with acute cardiogenic circulatory collapse. All patients presented with acute pump failure and inadequate systemic perfusion, and most were hypotensive. Nine patients had an acute myocardial infarction (AMI); the other four patients had an acute decompensation of a previously stable ischemic cardiomyopathy, and presented with a low-output syndrome in the absence of documented AMI. Patients were studied with a randomized single crossover design using each patient as his own control. Both drugs were given at doses of 2.5, 5, and 10 micrograms/kg/min for periods of 10 minutes at each dose while hemodynamics were monitored. No other vasoactive drugs were used during the study. Because of advanced age or severe peripheral vascular disease, no patient was considered suitable for intra-aortic balloon counterpulsation. There were no significant differences between the two drugs with regard to heart rate, mean-arterial pressure, systemic vascular resistance, stroke work index, or mean right atrial pressure. DBM improved stroke index and cardiac index significantly (p less than 0.05) more than DPM at doses of 5 micrograms/kg/min. DPM increased left ventricular filling pressure (LVFP) more than DMB at 5 micrograms/kg/min (p less than 0.001) and at 10 micrograms/kg/min (p less than 0.05). Although both DPM and DBM are useful in acute cardiogenic circulatory collapse, there appear to be important differences in their effect on LVFP and in the mechanisms whereby they increase blood pressure.

Demonstration of exercise-induced painless myocardial ischemia in survivors of out-of-hospital ventricular fibrillation

To ascertain if myocardial ischemia is the mechanism of out-of-hospital ventricular fibrillation (VF), left ventricular (LV) function was assessed at rest and during submaximal exercise in 15 patients who survived out-of-hospital VF. They were separated into asymptomatic (9 patients, group A) and symptomatic (6 patients, group S) groups for a history of angina or myocardial infarction. Both groups had significant (at least 70% diameter stenosis) coronary artery disease. At catheterization no patient had angina during exercise, but 12 of 15 had ST depression or increased ST depression (group A, 1.9 +/- 1.4 mm; group S, 1.1 +/- 1.2 mm) and 11 had abnormal wall motion. From rest to exercise, patients in group S had increased LV end-diastolic pressure (from 21 +/- 9 to 37 +/- 11 mm Hg, p = 0.009) and volume (from 100 +/- 25 to 107 +/- 26 ml/m2, p = 0.006), with no significant change in LV ejection fraction (from 40 +/- 13 to 42 +/- 12%). In group A LV end-diastolic pressure increased from 19 +/- 4 to 31 +/- 8 mm Hg (p = 0.001), but neither end-diastolic volume nor ejection fraction changed significantly (from 83 +/- 13 to 92 +/- 23 ml/m2 and from 55 +/- 13% to 46 +/- 13%, respectively). Thus, patients with coronary artery disease who survive out-of-hospital VF may have evidence of myocardial ischemia during exercise without pain. Painless ischemia may have a role in out-of-hospital VF.

Two-dimensional echocardiographic demonstration of left atrial thrombi in patients with prosthetic mitral valves

Although M-mode echocardiography (MME) is not a reliable method for detecting left atrial thrombi, recent reports suggest that two-dimensional echo (2DE) may be more effective than MME in identifying intracardiac thrombi. In three patients with prosthetic mitral valves who presented with either arterial embolization or prosthetic valvular dysfunction, 2DE demonstrated left atrial masses consistent with thrombi, while MME was either negative (two patients) or suspicious (one patient) for left atrial thrombus. Thrombi were documented by surgical or postmortem examination in all cases. Clear delineation of the atrial cavity and the margins of the masses, visualization on multiple echocardiographic views and comparison of serial examinations were helpful in identifying these masses as thrombi. In addition, the masses visualized had certain patterns of motion which seem unique and may allow characterization of atrial masses as thrombi.