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Objective: To compare the ability of dobutamine and dipyridamole stress echocardiography to detect functional recovery of stunned but viable myocardial regions early after acute myocardial infarction, and to predict late functional recovery of the reperfusion salvaged myocardium within the infarct area., Methods: Within 10 d of acute myocardial infarction, 51 patients--30 anterior and 21 inferior, 44 Q wave and seven non-Q-wave infarction--were submitted to a dobutamine echocardiography test at low dose (5-10 micrograms/kg/min over 5 min) and high dose (20-40 micrograms/kg/min over 3 min) and to dipyridamole echocardiography test (0.56 mg/kg over 4 min + 0.28 mg/kg over 2 min) on different days and in random order, after interruption of any vasoactive drug. Resting echocardiography was repeated at two months in 41 of 51 patients (80%). Regional wall motion of the left ventricle was analysed in a semiquantitative manner on a 14-segment model. Viability was defined as improvement of one grade or more of at least two basally asynergic segments in the infarcted area., Results: Regional functional recovery was detected by low dose dobutamine in 38/51 patients (75%) and in 147/308 (48%) of basally asynergic segments, compared to 25/51 patients (49%; P < 0.001) and 78/308 segments (25%; P < 0.001) only identified by dipyridamole. Late spontaneous functional recovery was detected in 24/41 patients (59%) and in 78/254 basally asynergic segments (31%). The sensitivity of dobutamine and dipyridamole echocardiography for predicting spontaneous functional recovery was 72% and 51% respectively (P < 0.001), specificity 68% and 82% (P < 0.001), positive predictive value 50% and 56%, and negative predictive value 85% and 79%., Conclusions: In comparison with dipyridamole in patients with thrombolysed myocardial infarction, dobutamine induces regional functional recovery. This suggests that dobutamine is more sensitive in showing the presence of viable myocardium within the infarct zone, though it has a lower specificity in predicting delayed spontaneous functional recovery of non-contractile but still viable areas.

Background: Patients with non-Q wave myocardial infarction (NQ AMI) are usually considered to have an increased risk of recurrent ischemic events and reinfarction. We wished to assess whether dobutamine stress echocardiography with the addition of atropine (DOB-E + ATRO) can detect jeopardized myocardium after a recent NQ AMI and to assess the prognostic significance of this test in a group of patients with a first uncomplicated NQ AMI:, Methods and Results: Fourty-one consecutive patients (38 men, mean age 52 +/- 9 years, 31 anterior, 68% treated with thrombolysis) underwent low and high-dose DOB-E (from 5 to 40 mcg/kg/min); ATRO was added in 14/41 (34%) patients. A significant deterioration of wall motion in the infarcted region (IR) indicative of residual myocardial ischemia was present in 36/41 patients (88%). Significant electrocardiographic changes and angina developed in 61% and 32% of patients, respectively. Coronary angiography was performed in 30/41 patients (73%) and showed 1-vessel coronary artery disease (CAD) in 70% of cases, multivessel CAD in 23% of cases and no significant CAD in 7% of patients. Three patients were lost at follow-up and 10 other patients were excluded from the analysis because a revascularization procedure was performed during diagnostic angiography. On a mean follow-up period of 9.5 +/- 9 months, the incidence of coronary events (re-infarction, recurrent angina, revascularization procedures) was higher (15/36 vs 1/5, 42% vs 20%) in patients with a DOB-E + ATRO positive test (1 reinfarction, 9 recurrent angina, 5 revascularized) than in those with a negative test (1 recurrent angina)., Conclusions: DOB-E + ATRO early after a first uncomplicated NQ AMI documents the presence of myocardial ischemia in the IR in the great majority of patients. A positive DOB-E + ATRO was found to be associated with a higher incidence of cardiac events at follow-up, but the results of this non prospective study (high sensitivity but low specificity and predictive value for cardiac events at follow-up) suggest to utilize with caution this test for risk stratification of patients with recent NQ AMI until prospective and larger studies are performed.

To compare the hemodynamic effect of volume loading with that of dobutamine infusion in severe ischemic right ventricular (RV) dysfunction, 11 patients with inferior and RV infarction complicated by low cardiac output syndrome and important hemodynamic derangement (systolic blood pressure < 100 mm Hg, cardiac index < 2.0 liters/min/m2, right atrial pressure > 10 mm Hg) were prospectively studied within 48 hours of symptom onset. After right heart catheterization, volume loading (mean 400 ml saline solution) and dobutamine infusion (5 and 10 micrograms/kg/min over 10 minutes) were performed according to a randomized, crossover design. Volume loading resulted in increased right atrial (from 15 +/- 2 to 19 +/- 3 mm Hg, p < 0.05) and pulmonary capillary (from 15 +/- 2 to 19 +/- 3 mm Hg, p < 0.05) pressures, without increasing cardiac index, heart rate, aortic pressure, or right and left ventricular stroke work index. Dobutamine (5 micrograms/kg/min) increased cardiac index (from 1.5 +/- 0.3 to 1.9 +/- 0.5 liters/min/m2, p < 0.05), incrementing both heart rate (from 61 +/- 12 to 70 +/- 13 beats/min, p < 0.05) and stroke volume index (from 25 +/- 6 to 27 +/- 5 ml/beat/m2, p < 0.05), as well as right (from 1.4 +/- 1.6 to 2.3 +/- 2.2 g.m/m2, p < 0.05) and left (from 21 +/- 7 to 27 +/- 10 g.m/m2, p < 0.05) stroke work indexes; right and left ventricular filling pressures did not decrease. Dobutamine (10 micrograms/kg/min) significantly improved myocardial performance.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of the study was to compare the ability of dobutamine and dipyridamole echocardiography to detect stunned but viable myocardium early after acute myocardial infarction, to predict spontaneous functional recovery of the reperfused myocardium at 2 months and to detect myocardial ischemia in the infarcted area. Within 10 days from acute myocardial infarction, 47 patients, 29 anterior and 18 inferior, 41 Q-wave and 6 non Q-wave infarctions, underwent dobutamine echocardiography test at low-dose (5-10 mcg/kg/min over 5 min) and high-dose (20-40 mgc/kg/min over 3 min) and to dipyridamole echocardiography test (0.56 mg/kg over 4 min + 0.28 mg/kg over 2 min) in different days and in random order, after interruption of any vasoactive drug. Resting echocardiography was repeated at 2 months in 38/47 patients. Regional wall motion analysis was performed in a qualitative manner on a 14-segment model; viability was defined as improvement of 1 grade or more of at least 2 basally asynergic segments in the infarcted area. Ischemia was defined as an improvement followed by significant deterioration of contractility of the infarcted segments or deterioration of the infarcted area. All patients underwent coronary arteriography within 1 month from admission. Viability was detected by low-dose dobutamine in 34/47 patients (72%) and in 131/297 (44%) of basally asynergic segments compared to only 21/47 patients (45%) and in 66/297 segments (22%) detected by dipyridamole; myocardial ischemia was induced by dobutamine in 64% of patients compared to 36% by dipyridamole. Late spontaneous functional recovery was detected in 21/38 patients (57%) and in 70/244 (29%) of asynergic segments. Sensitivity of dobutamine and dipyridamole echocardiography for predicting spontaneous functional recovery was 70% and 46% specificity 69% and 83%, positive predictive value 48% and 52%, negative predictive value 85% and 79% respectively. Dobutamine correctly identified the presence of a significant stenosis of the infarct-related artery in 74% of cases compared with 43% of dipyridamole; specificity for detecting stenosis was 67% for dobutamine and 83% for dipyridamole. In conclusion, in patients with thrombolyzed myocardial infarction dobutamine echocardiography detects viable myocardium with late spontaneous recovery in a greater proportion of patients and segments than dipyridamole; dobutamine has a higher sensitivity but a lower specificity compared to dipyridamole for identifying a residual stenosis of the infarct-related artery that may jeopardize myocardium in the area at risk.

To evaluate the hemodynamic effects of the first oral administration of enalapril maleate, a long-acting ACE-inhibitor, in the early phase of an acute uncomplicated myocardial infarction, we studied 15 patients, in Killip class I or II, within 72 hours from the onset of symptoms. Hemodynamic measurements were obtained by a triple lumen 7 F Swan-Ganz catheter, inserted into the pulmonary artery, under control conditions and 2, 4, 6, 8 and 12 hours after 10 mg (15 patients) and 20 mg (11 patients) of the drug. Ten milligrams of enalapril reduced systolic and mean arterial blood pressure (from 118 +/- 17 to 111 +/- 18 mmHg, p < .05, and from 92 +/- 12 to 83 +/- 12 mmHg, p < .01, respectively), with a maximum effect after 4 hours from administration. Heart rate and vascular resistances showed an insignificant trend toward reduction, and no changes were observed in left ventricular systolic work index, right and left ventricular filling pressures or cardiac index. Hemodynamic changes induced by 20 mg of the drug, in a smaller group of patients, had a similar trend, which did not reach a statistical significance. In conclusion, in patients with acute uncomplicated myocardial infarction, a single oral dose of enalapril maleate is safe and well tolerated, does not induce severe hypotension, and produces potentially beneficial changes in hemodynamics.

Forty-five patients with a first anterior myocardial infarction were studied by serial two-dimensional echocardiographic examinations to evaluate the incidence, short-term evolution and clinical significance of infarct expansion. Infarct expansion was found in 26 patients (58%); in 22 cases it was detected at the first examination 24 hours after the onset of symptoms, while in the other 4 it developed later. In 20 (77%) patients expansion involved only the septal and apical regions, while in 6 (23%) it extended to the antero-lateral wall. Two out of 22 patients with early expansion died of cardiogenic shock; expansion of the infarcted area progressively increased in 10 of the remaining 20 patients and remained stable in the other 10. Compared to the patients without expansion those with expansion had a higher CK peak level, a greater number of pathological Q waves and a greater echocardiographic asynergy score; moreover, in-hospital mortality and the incidence of left ventricular failure were higher in the group with expansion (8% vs 0% and 54% vs 10% respectively). Thus our results show that in patients with anterior infarction, expansion is a frequent event which usually develops early and may have a progressive course; infarct expansion, especially when it is large and progressive, is associated with a high incidence of early left ventricular failure and has a poor prognostic significance.

30 patients with a previous myocardial infarction who had undergone diagnostic conventional left ventriculography and coronary arteriography had left ventriculography also performed by digital subtraction angiography after intravenous injection of contrast medium; the mean interval between the two investigations was 2.3 days. The conventional and the digital subtracted left ventricular images were computer-processed; global ejection fraction (obtained by the volumes calculated with the Dodge method) and segmental wall motion (from a quantitative analysis performed according to the Stanford method) were compared. We found a close correlation for the ejection fraction obtained by the two techniques (r = 0.89, p less than 0.01); absolute values proved to be slightly higher in the digital subtraction angiography. Segmental wall motion was significantly correlated too (p less than 0.05 for all the segments of the ventricular silhouette but for the one corresponding to the base of the heart). Digital intravenous angiography provides an accurate and less invasive method to evaluate left ventricular function.

Over a five-year period 57 patients (pts) with sustained, recurrent, post-infarction ventricular tachycardia (VT) refractory to conventional antiarrhythmic treatment were evaluated. In 28 (49%) pts VT was controlled by amiodarone (A) in a dose of 3000 mg week-1. During long-term follow-up 5/28 (18%) pts died; no severe side-effects were observed with this dosage. In 17 of the 29 pts not controlled by this regimen, the dosage of A was increased to 6000-8000 mg week-1; short-term control of VT was achieved in 9/17 (53%) pts, but over a long-term follow-up 5/9 (56%) died and severe side-effects (11% pulmonary fibrosis and 11% hepatitis) occurred in 22%. Twenty pts, resistant to a low (12 pts) or high (8 pts) doses of A, underwent map-guided surgical treatment. In conclusion A is superior to conventional drugs in the treatment of sustained, recurrent, post-infarction VT, but when high doses are necessary to prevent VT, long-term results are poor and severe side-effects frequent. In pts refractory to standard doses of A, map-guided surgery is the treatment of choice.

Thirty patients with myocardial infarction were studied using Digital Subtraction Ventriculography with Intravenous injection (DSVIV) between 3 and 6 days from myocardial infarction and were checked after 30 and 90 days. The variation of ejection fraction in the controls was not important. The wall motion provided precise indications regarding the infarctual regions. Digital subtraction ventriculography seems to be a very interesting tool in the study of the left ventricle in the evolution of myocardial infarction, thanks to a low invasivity, providing data on ventricular function.

This report addresses the problems related to surgical treatment of post-infarction ventricular tachycardia (VT) and is based on a 5 year experience of 36 consecutive patients. In every case the arrhythmia was unresponsive to pharmacological therapy. All patients were operated on after the completion of a diagnostic protocol including preoperative endocardial, intra-operative epi-endocardial mapping, the latter performed automatically when possible. Surgical techniques were: classical Guiraudon's encircling endocardial ventriculotomy (EEV); partial EEV, endocardial resection (ER); cryoablation or a combination of these procedures. The in-hospital mortality (30 days) was 8.3% (3 patients). During the follow-up period (1-68 months), 3 patients (9%) died of cardiac but not VT related causes. Of the survivors, 92% are VT-free. We consider electrophysiologically guided surgery a safe and reliable method for the treatment of post-infarction VT and suggest its more extensive use. We stress the importance of automatic mapping in pleomorphic and non-sustained VT, and the necessity of tailoring the surgical technique to the characteristics of each case.

The preliminary results of a prospective study undertaken in patients with a first episode of acute myocardial infarction are presented. The clinical, electrocardiographic and angiographic characteristics of 34 patients who developed early post-infarction angina (group I) were compared with those of 144 patients who remained asymptomatic after the acute infarct (group II). No difference was found between the two groups as to age, sex prevalence, risk factors, presence of stable angina before infarction, severe ventricular arrhythmias or transient congestive heart failure in CCU and peak CK value. Patients of group I had more frequently ecg signs of myocardial infarction in anterior leads (P less than 0.01) than patients of group II. Exercise testing, performed by 23 patients of group I and by 140 patients of group II, was positive in 14 patients with early post-infarction angina and in 37 who remained asymptomatic after the acute infarct (P less than 0.01). The two groups had similar values of left ventricular end diastolic volume index, left ventricular end diastolic pressure and ejection fraction. Patients with early post-infarction angina however had more frequently double or triple vessel disease, while single vessel disease prevailed in group II patients. Although the follow-up period was limited (average 9 months), a higher incidence of cardiac complications was found in group I patients (P less than 0.01). These data show that early post-infarction angina defines a high-risk subset of patients among those with recent myocardial infarction. A more aggressive approach, including thrombolytic therapy and coronary angioplasty, seems warranted.