Prognostic value of residual ischaemia assessed by exercise electrocardiography and dobutamine stress echocardiography in low-risk patients following acute myocardial infarction.

BACKGROUND: Risk stratification after uncomplicated myocardial infarction is major clinical problem. In particular, the prognostic value of residual inducible ischaemia is still controversial. We compared the relative prognostic value of exercise ECG and dobutamine stress echocardiography performed in the early post-infarction period. METHODS: Four hundred and six patients (53 female) aged 57 +/- 9 years, undergoing maximal exercise ECG and dobutamine stress echocardiography within 10 days of an uncomplicated myocardial infarction off therapy, were prospectively followed-up for 8.8 months. Age, sex, diabetes, smoking habit, hypertension, dyslipidaemia, infarct location, thrombolysis and resting wall motion score index were taken into account among clinical variables. Prognostic correlations were made vs spontaneous events (cardiac death, non-fatal reinfarction and unstable angina requiring hospitalization) whilst patients undergoing revascularization (by means of percutaneous transluminal coronary angioplasty or coronary artery bypass surgery) at the time of the procedure were censored. RESULTS: One hundred and twenty-seven events occurred during the follow-up: 41 (10%) were spontaneous (five deaths, 12 reinfarctions and 24 unstable angina) and 86 procedural (27 angioplasty and 59 bypass surgery). Spontaneous events were not predicted by any clinical, exercise ECG or dobutamine stress echocardiography variable, but the negative predictive value of both tests was excellent (91% and 90% respectively). With a multivariate Cox analysis, male gender, positive low-workload (< 100 W) exercise ECG (P < 0.0001), positive low-dose dobutamine stress echocardiography (P < 0.0001) and rest-stress wall motion score index variation (P < 0.001) were found to predict cumulative cardiac events with an independent and additive value. Dobutamine stress echocardiography was significantly more sensitive (P < 0.05) and less specific (P < 0.01) in predicting the outcome of patients with anterior infarction, whilst exercise ECG was significantly more sensitive (P < 0.05) in patients with non-Q wave infarction. CONCLUSIONS: (1) Spontaneous events are poorly predicted by provocative tests in low-risk patients after uncomplicated myocardial infarction. (2) However, both exercise ECG and dobutamine stress echocardiography can predict a favourable outcome with a very high negative predictive value. (3) Dobutamine stress echocardiography should be considered a secondary option in cases where the exercise ECG is equivocal or when the location of ischaemia is a relevant issue. (4) The possibility that the two tests have a differential utility depending on the infarct location and type (Q wave vs non-Q wave) may be clinically relevant and deserves further evaluation.

Incidence and correlates of complex ventricular arrhythmias during dobutamine stress echocardiography after acute myocardial infarction.

Although previous studies have confirmed the safety of dobutamine stress echocardiography, complex ventricular arrhythmias have been reported. Our aim was (1) to identify the markers of increased arrhythmic risk during dobutamine stress echocardiography and (2) to assess whether the occurrence of major ventricular arrhythmias during the test may represent a clinically useful marker of electrical instability. Three hundred and seventy-seven consecutive survivors from acute myocardial infarction, off cardioactive therapy, underwent dobutamine stress echocardiography 11.4 days after the acute event. Holter monitoring with assessment of heart rate variability and echocardiographic determination of left ventricular ejection fraction. In addition, exercise stress testing, signal averaged ECG and coronary angiography were carried out, respectively, in 357, 150 and 273 patients. Ten subjects showed complex ventricular arrhythmias (eight non-sustained and one sustained ventricular tachycardia and one ventricular fibrillation) during dobutamine stress echocardiography (group A), whilst 366 did not (group B). Complex ventricular arrhythmias were detected by Holter monitoring in 8/10 patients in group A and 45/367 patients in group B (odds ratio 28.6, 95% CI 5.4-92.2) and by exercise testing in 4/10 patients in group A and 33/347 patients in group B (odds ratio 6.3, 95% CI 1.4-27.2). Ejection fraction < 40% was present in 3/10 patients in group A and 50/367 in group B (odds ratio 2.7, 95% CI 0.3-12.2), whilst multivessel disease was present, respectively, in 8/10 and 176/263 patients (odds ratio 1.9, 95% CI 0.3-25.5). Reduced heart rate variability and the presence of late potentials on signal averaged ECG were found in, respectively, 40/367 and 13/140 patients in group B, but none were found in group A. A total of 61 events (35 CABG, 15 PTCA, four cardiac deaths and seven non-fatal reinfarctions) occurred during the follow-up (11.4 months, range 6 to 20): four in group A and 57 in group B. No documented major arrhythmic event was reported. We conclude that (1) complex arrhythmias during dobutamine stress may occur in patients early after acute myocardial infarction; (2) the preexisting evidence of frequent, as well as repetitive, arrhythmias represents a potential marker of increased risk in this connection and, finally, (3) dobutamine-induced arrhythmias seem to represent an uncommon, even though potentially dangerous, event but not a useful new "window' on electrical instability of post-MI patients.

Dobutamine stress echocardiography for the identification of multivessel coronary artery disease after uncomplicated myocardial infarction: the importance of test end-point.

Our aim was to verify whether the sensitivity of pharmachological stress echocardiography for multivessel disease after acute myocardial infarction may be improved by a more aggressive protocol, i.e. not considering the appearance of the first wall motion abnormality as the absolute end-point if it occurs in the infarcted area without clinical or instrumental markers of extensive ischemia or left ventricular dysfunction. One-hundred twenty-one consecutive patients (age 32-71 years) prospectively underwent dobutamine-atropine stress echo (dobutamine infusion up to 40 micrograms/kg/min with additional atropine 1 mg) 11.8 +/- 4.8 days after uncomplicated myocardial infarction and coronary angiography within 6 weeks. Criteria for stopping the test were: significant ST depression or elevation, typical chest pain, major arrhythmias and left ventricular dysfunction. The test was considered as positive if a deterioration of basal wall motion pattern was observed: it was defined homozonally positive (the deterioration occurred in the myocardial area fed by the culprit vessel) or heterozonally positive (the deterioration occurred in a different vascular area). A coronary stenosis > 70% of vessel lumen was defined as critical. Thirty-four patients showed a negative test result. Among the 87 patients with positive test, 65 had no further wall motion deterioration from the first-induced wall motion abnormality (WMA) to peak test (Group A), whereas nine patients showed further homozonal (Group B) and 13 further heterozonal (Group C) asynergies. Sensitivity, specificity and accuracy of dobutamine stress echocardiography for multivessel disease were, respectively, 63%, 96% and 82% using the first-induced wall motion abnormality as test end-point, whilst they were 84% (P < 0.01), 93% and 89% according to the aggressive approach previously described. Dobutamine stress time of patients with multivessel disease was higher in Groups B and C (13.1 +/- 3.6 min) than in Group A (9.8 +/- 3.7 min, P < 0.01) and, finally, the mean obstruction of non-culprit vessel was higher in Group A (62.2%) than in Group C (47.4%, P < 0.05). No major complications were found. We conclude that the sensitivity of dobutamine stress echocardiography for multivessel disease following recent myocardial infarction is critically dependent on the test end-point. It may be improved by a more aggressive approach capable to identify less severe heterozonal coronary lesions.

[Acute effects of diltiazem in pulmonary hypertension secondary to chronic obstructive bronchitis]. / Effetti acuti del diltiazem nell'ipertensione polmonare secondaria a bronchite cronica ostruttiva.

The effect of acute i.v. administration of diltiazem on pulmonary haemodynamics was compared to that produced by oxygen in 10 hypoxemic patients with chronic obstructive lung disease and pulmonary hypertension (PAPm greater than 20 mmHg), without left ventricular dysfunction. Determinations were carried out at baseline, during 100% oxygen inhalation, at least 20 minutes after oxygen withdrawal and 15 minutes after i.v. diltiazem loading dose of 0.25 mg/kg followed by the infusion of 1 mcg/kg/min. Oxygen inhalation produced no significant modifications of haemodynamic variables, whilst a significant (p less than 0.05) decrease of PAPm, pulmonary arteriolar resistance (PAR) and peripheral resistance (TPR) was observed after diltiazem administration (respectively 14%, 23% and 11.6%). Heart rate, cardiac index and blood pressure did not change significantly even with diltiazem. These results could support the inclusion of diltiazem in the therapeutic regimen of pulmonary hypertension due to chronic obstructive lung disease, but further investigations are needed to clarify the predictive value of its acute administration in assessing long term efficacy.

Decreased beta-adrenoceptors in polymorphonucleates in essential hypertension.

Number and affinity of beta-adrenoceptors in human polymorphonucleates (PMN's) have been studied in patients with essential hypertension (n = 12) and in normal subjects of the same range of age and sex (n = 16). (-)Diidroalprenolol-H3 has been utilized as ligand. Membranes preparation was performed according to Galant (5). Number of beta-adrenoceptor is significantly decreased compared with controls (p less than 0.05), both with saturation curves and Scatchard analysis. Affinity of beta-adrenoceptors toward (-)diidroalprenolol-H3 is lightly increased but not significantly. These data could be explained on the basis of the desensitization occurring in hypertensive subjects by altered plasma catecholamines level, as in experimental in vitro systems.