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BACKGROUND: The aim of this work was to study changes in end-diastolic volume 6 months after Q-wave and non-Q-wave anterior ST-elevation myocardial infarction by echocardiography. Ventricular dilation after anterior Q-wave myocardial infarction is well-recognized. However, there is a dearth of information about the natural history of ventricular volumes after non-Q-wave myocardial infarction. METHODS: One hundred ninety patients receiving thrombolytic therapy after anterior ST-elevation myocardial infarction were studied. All patients had 2D echocardiograms and 12-lead electrocardiograms recorded within 24 hours of symptoms and at 3, 42, and 180 days later. In addition, a further electrocardiogram was recorded on day 7 to assess patients for the presence of Q waves. Peak creatine kinase over the first 3 days of admission was recorded. End-diastolic volume index was the study end point. RESULTS: Peak creatine kinase was strongly associated with ventricular dilation in both groups (P <.001). Mean end-diastolic volume in the Q-wave group increased significantly from day 1 to 6 months (P <.05) but did not alter after non-Q-wave infarction. However, when patients were selected on predefined criteria for significant change in ventricular dilation (>10 mL/m(2)), then 35% of those with and 15% of those without Q waves fell into this category. Within this group, the increase in end-diastolic volume followed a similar pattern, with the maximum percentage increase occurring between day 1 and 6 weeks. CONCLUSIONS: In the postthrombolytic group of anterior ST-elevation myocardial infarction, a minority of patients without Q-wave development also undergo significant ventricular dilation.

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OBJECTIVE: To assess the possible benefits of intravenous isosorbide dinitrate in acute myocardial infarction and oral isosorbide mononitrate in subacute myocardial infarction. METHODS: 316 patients presenting with acute myocardial infarction were entered into double blind placebo controlled clinical trials assessing infarct size by enzyme release, ventricular size and function by echocardiography, reperfusion by continuous 12 lead ST segment monitoring and late potentials by high resolution electrocardiography. RESULTS: 301 patients, of whom 292 (97%) received thrombolytic treatment, were randomised on admission to intravenous isosorbide dinitrate or placebo. Overall, there was no significant effect of treatment on infarct size, ST segment resolution, ventricular remodelling, or late potentials at day 3. A trend was observed towards a reduction in infarct size in patients with non-Q wave infarction treated with isosorbide dinitrate. Heterogeneity of nitrate effect was observed in relation to the degree of ST segment elevation on presentation with a clear benefit of isosorbide dinitrate in patients with moderate ST segment elevation (472 U/l v 704 U/l, P = 0.003) and a trend towards a deleterious effect in patients with marked ST segment elevation (1152 U/l v 1058 U/l, P = 0.2). ST segment re-elevation was more common among patients receiving nitrate treatment than in those assigned to placebo (29 v 16, P < 0.05). Some 160 patients underwent a further randomisation to sustained release isosorbide mononitrate or placebo on day 3. Echocardiographic volumes after 6 weeks of treatment were similar in the two groups. CONCLUSIONS: No benefit was observed with administration of nitrates in the treatment groups as a whole for either acute or subacute infarction. There was, however, evidence of heterogeneity of effect in the different subgroups of acute infarction, and the possibility that nitrates may have differing actions in different groups of patients should be considered.

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BACKGROUND: Arrhythmias are common in patients who have developed ventricular enlargement after myocardial infarction. METHODS AND RESULTS: A prospective study was undertaken to assess the relation between ventricular dilatation and the development of late potentials after myocardial infarction. Echocardiograms and signal-averaged ECGs were recorded on days 1,3,7, and 42 in 52 patients with a first anterior myocardial infarction. Twenty-nine percent of patients were late potential-positive on their initial signal-averaged ECG recorded on the day of admission. The incidence of late potentials rose during the next week to a peak of 42% at day 7, declining to 13% by day 42. The presence of late potentials on the day of admission was associated with an increase in end-diastolic volume index of 16.1 +/- 6.0 mL/m2 (mean +/- SEM), compared with a decreased of 4.7 +/- 2.7 mL/m2 among late potential-negative patients (P < .006). Qualitatively similar results were evident for late potentials on day 3 and day 7. By contrast, there was no association between late potentials on day 42 and ventricular dilatation. Marked dynamic changes in late potentials were evident during the first week. Patients with persistent late potentials (n = 9) on all three recordings in the first week showed a marked increase in end-diastolic volume index of 21.3 +/- 8.1 mL/m2 (P < .005 in comparison with patients who were persistently negative [n = 20]). Patients demonstrating dynamic positivity (n = 15) not present on all three recordings in the first week showed no significant increase in end-diastolic volume index. CONCLUSION: It is concluded that late potentials during the first week after infarction are associated with subsequent ventricular dilatation. These early-phase late potentials may be a manifestation of cell slippage. They arise before gross topographical enlargement and may serve as a predictor of ventricular dilatation.

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The acute hemodynamic and echocardiographic effects of pericardial closure on cardiac function were studied in 11 pigs during steady-state anesthesia and ventilation. Observations were made after sternotomy, both while the pericardium was open and after it had been closed, and then after closure of the chest, after the pericardium had been reopened by removing the pericardial suture through the chest wall. In five pigs, further observations were made when a suture was tightened to close the pericardium while the chest remained closed. Closure of the pericardium when the chest was open reduced cardiac output by 14% and mean stroke volume by 19% (both p less than 0.05). Systemic vascular resistance increased by 15% when the pericardium was closed while the chest was open (NS), and increased by 19% when it was closed while the chest was closed (p less than 0.05). Heart rate did not change significantly, and the systemic blood pressure was maintained (-8%, NS). All these effects were reversed by opening the pericardium. Intrathoracic epicardial echocardiographic monitoring of the left ventricle showed that its end-diastolic dimension increased (by 11%, p less than 0.05) when the pericardium was opened. After chest closure, paradoxical motion of the interventricular septum was consistently demonstrated only during ventilation, and it was not related to whether or not the pericardium was open. This study suggests that cardiac function may be impaired by pericardial closure after cardiac surgery because of some degree of constriction of the heart chambers, although acute circulatory responses compensate for the mild decrease in stroke volume. Monitoring of blood pressure alone cannot document the subtle circulatory changes induced by pericardial closure, and therefore it is not a reliable guide to decisions of whether to close the pericardium or leave it open in individual patients.

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The total surgical experience of a supraregional paediatric cardiology unit over a nine year period (January 1980 to December 1988) was reviewed to assess the effect of the introduction of the full range of ultrasound techniques. A total of 1517 patients underwent cardiac surgery (955 cardiopulmonary bypass, 562 closed procedures). Of these, 485 patients (32%) did not undergo cardiac catheterisation before operation: 217 bypass (23% of all procedures under cardiopulmonary bypass) and 268 closed procedures (48%). The overall ratio of catheterisations to operations for patients undergoing palliative or corrective surgery fell from 0.97 (1980) to 0.38 (1988). The patients were classified as (a) neonates (0-28 days), (b) infants (one to 12 months), and (c) children (one to 14 years). The main impact of non-invasive surgical referral was in neonates (total catheter:operation ratio 0.38; neonates 0.2 for 1988). The surgical population was further divided according to the principal echocardiographic technique available: (a) 1980-4 cross sectional imaging; (b) 1985-6; imaging plus spectral Doppler ultrasound; (c) 1987-8; imaging plus spectral Doppler ultrasound and colour flow mapping. A fall in the catheter:operation ratio for all age groups was most pronounced in the last four years. This reflects increased familiarity and surgical confidence with non-invasive diagnostic assessment. The introduction of each new echocardiographic technique was associated with a significant fall in the total catheter:operation ratio compared with the preceding period. Six incorrect ultrasound diagnoses were made during the entire period; one of these patients died in the early postoperative period. The integration of Doppler ultrasound with cross sectional imaging has made non-invasive assessment an increasingly practical alternative to preoperative cardiac catheterization.

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Fifty consecutive patients with a newly acquired systolic murmur and severe cardiac decompensation following a recent myocardial infarction (27 with an anterior and 23 with an inferior infarct) were studied by a combination of two-dimensional echocardiography, spectral Doppler and Doppler color flow mapping. The initial ultrasound study defined a ventricular septal rupture in 43 patients and severe isolated mitral regurgitation in 7 patients (5 with papillary muscle rupture and 2 with severe papillary muscle dysfunction). All 50 patients had subsequent confirmation of the diagnosis by either cardiac catheterization or surgical inspection, or both. Two-dimensional echocardiography alone directly visualized a septal defect in only 17 (40%) of the 43 patients with ventricular septal rupture. In all 43 patients the mitral valve appeared normal on imaging. In six of the seven patients with isolated mitral regurgitation, two-dimensional echocardiography correctly demonstrated the structural abnormality of the mitral valve (five with flail anterior leaflet and one with posterior leaflet prolapse). The addition of Doppler color flow mapping greatly improved the diagnostic information in both patient groups. In all 43 patients with ventricular septal rupture, Doppler color flow mapping demonstrated both an area of turbulent transseptal flow and a diagnostic systolic flow disturbance within the right ventricle. In the seven patients with isolated papillary muscle rupture or dysfunction, Doppler color flow mapping not only demonstrated the presence of mitral regurgitation in all cases, but also identified the specific mitral leaflet abnormality by defining the direction of the regurgitant jet.(ABSTRACT TRUNCATED AT 250 WORDS)

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A small probe for cardiac surgery was developed and clinically tested. The probe is built as a phased array transducer with 64 elements with a centerfrequency of 5 MHz. The transducertip is connected with a handle by a flexible yet steerable shaft. This shaft has a length of 10 cm and can be set in a desired shape. Good quality images were obtained in all patients. The first study suggest many applications for a small probe in intraoperative echocardiography.

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Thirty-two neonates and infants with pulmonary atresia with ventricular septal defect were initially investigated with cross-sectional and spectral Doppler echocardiography and Doppler color flow mapping. All 32 had subsequent correlative angiography. This demonstrated that 24 infants had adequate-sized right and left pulmonary arteries (19 confluent, 5 nonconfluent). Of the five infants with nonconfluent pulmonary arteries, four had bilateral ductus arteriosus and one had a single left-sided ductus with anomalous origin of the right pulmonary artery from the ascending aorta. Nineteen infants had confluent pulmonary arteries, all of which were supplied by a single ductus. Eight infants had complete absence of or inadequate pulmonary arteries; all had multiple aortopulmonary collateral vessels arising from the descending aorta. The presence of adequate-sized right and left pulmonary arteries was correctly predicted in 21 of 24 infants by cross-sectional echocardiography alone and in all 24 by Doppler color flow mapping. Confluence of the right and left pulmonary arteries was predicted by cross-sectional imaging in 14 of the 19 infants in whom it occurred, and by Doppler color flow mapping in all 19 infants. The precise definition of the pulmonary blood supply was correctly predicted by Doppler color flow mapping in 16 of the 19 infants with confluent pulmonary arteries and a single ductus. However, in three infants in this group, Doppler color flow mapping made a false diagnosis of multiple aortopulmonary collateral vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

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Thirty one patients with multiple ventricular septal defects were studied by cross sectional echocardiography, conventional pulsed and continuous wave Doppler, colour flow imaging, and left ventriculography to determine the relative diagnostic benefits and pitfalls of each technique. The patients studied had a wide range of congenital heart defects with 19 patients having isolated multiple ventricular septal defects, three with associated tetralogy of Fallot, five with double outlet right ventricle, three with complete transposition and ventricular septal defect, and one with a complete atrioventricular septal defect. In 23 patients the defects were inspected at operation. Cross sectional imaging with integrated pulsed and continuous wave Doppler correctly identified multiple defects in only 12 (39%) patients. In contrast, colour flow imaging was accurate in 24 (77%) patients and left ventriculography in 20 (65%) patients. When patients were subdivided on the basis of relative peak systolic ventricular pressures into restrictive defects (18 patients) and non-restrictive defects (13 patients) the diagnostic value of colour flow imaging was different for each group. Colour flow mapping correctly identified multiple ventricular septal defects in 16/18 (89%) patients with restrictive defects but only 8/13 (62%) with non-restrictive defects. The comparative diagnostic accuracy of left ventriculography was 15/18 (83%) in the restrictive group and 5/13 (38%) in the non-restrictive group. Colour flow imaging was the single investigative technique with the greatest diagnostic accuracy in the diagnosis of multiple ventricular septal defects. It failed to be consistently accurate in defined subgroups with non-restrictive defects as did left ventriculography. The greatest overall diagnostic accuracy in this series was obtained when both colour flow imaging and ventriculography techniques were used in combination in a complementary fashion.

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Two-dimensional echocardiography in combination with Doppler and color Doppler flow mapping is now considered the technique of choice for the early diagnosis and assessment of the 'surgical' complications of acute myocardial infarction. It has the advantage of being a rapid, safe technique with ease of portability and repeatability, at relatively low cost. Transesophageal echocardiography may provide an alternative 'window' for imaging cardiac structure and function, but as yet its value in the diagnosis of the complications of myocardial function is not proven. In the acute phase, color Doppler flow mapping can diagnose the cause of hemodynamic deterioration by distinguishing primary pump failure from the mechanical complications such as ventricular septal rupture or papillary muscle rupture. In the subacute phase, complications including left ventricular true and false aneurysms may be detected and this information allows optimal management decisions to be made. Thus, color Doppler flow mapping has become an indispensable technique in the coronary care unit. It provides a complete picture of cardiac structure and function making it superior to other methods in the clinical situation of an acute myocardial infarction which has such a volatile and unpredictable course.

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Eleven cases of left ventricular pseudoaneurysm in nine patients were studied by cross sectional echocardiography, conventional Doppler echocardiography, and colour flow imaging. In two patients recurrent pseudoaneurysms developed after cardiac surgery, three had acute rupture after myocardial infarction, two were the result of stab wounds, one was a late rupture of a true left ventricular aneurysm, one developed after surgical resection of a true left ventricular aneurysm, and two as a consequence of left ventricular venting. In all 11 cases the diagnosis was confirmed by angiographic or surgical information or both. The diagnosis was suspected clinically in only four cases. Cross sectional echocardiography alone confirmed the diagnosis in five cases. Neither pulsed wave Doppler nor continuous wave Doppler established the diagnosis when they were used without colour flow imaging in five and three cases respectively. In all 11 cases colour flow imaging showed flow in and out of the pericardial cavity at the defect site as well as the abnormal flow within the pseudoaneurysm. Subsequent use of pulsed Doppler showed a consistent "to and fro" flow pattern across the myocardial defect with characteristic respiratory variation of the peak systolic velocity. This unique intrapericardial flow pattern is diagnostic of a pseudoaneurysm. Colour flow imaging is a valuable addition to cross sectional and Doppler echocardiography, and is the best technique for detecting left ventricular pseudoaneurysms.

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