[Postischemic dysfunction and persistent ischemia in the early postinfarction period. Evaluation by echo-dobutamine-atropine test].

Aim: To study post-ischemic dysfunction and persistent ischemia in early post-infarction, by means of Echo-dobutamine-Atropine stress test (ECHO-DOB). Methods. We studied 138 patients (pts) aged < or = 75 yrs (mean 59.2 +/- 9.8) at their first uncomplicated myocardial infarction (AMI), treated with systemic thrombolysis. All pts underwent the test within 2 weeks since the onset of the attack and they were reevaluated in follow-up 3 months later. Under Echo and ECG monitoring, ECHO-DOB was performed according to EDICS protocol. Low doses was infused (5-10 mcg/Kg/min every 3') to assess the viability and high doses (20 > or = 40 mg/Kg/min + Atropine) to assess a possible persistent ischemia. The Wall Motion Score Index (WMSI) was used for the semiquantitative analysis of kinesis in a model of left ventricle divided into 16 segments. coronary angiography was performed within 30 days from the AMI, in 82.3% of pts. Results. Low dose of Dobutamine (DOB) induced in 92/136 (67.6%) pts an improvement in the contractile dysfunction in the region of necrosis; in 31.5% (29/92) it remained until the end of the test, suggesting the presence of viable myocardium, In absence of myocardium "at risk". High doses DOB induced worsening of contractile dysfunction in 64 pts (47%); in 40 (62.5%) viability had been previously detected (viable but ischemic myocardium); In 30 (75%) it was homozone or adjacent (viable but ischemic myocardium in the region of the coronary artery or in the tributary vessels correlated to the necrosis). In 24/64 (37.5%) pts the absence of modification of WMSI (no improvement and no worsening), suggested the presence of necrotic tissue in the tributary region of the vessel of necrosis. The significant improvement in kinesis revealed in 92 pts, by the follow-up control was confirmed in 64 (p < 0.001) (69.5%). Forty-four pts without hyperkinesia showed no significant improvement compared with the base line (stunned or hibernating myocardium). The sensitivity of low doses for viable myocardium (gold standard follow-up) was 69%; specificity was 77%. The sensitivity of high doses for ischemia (gold standard coronary arteriography) was 78%; specificity was 100%. No major side effects during the Dobutamine Atropine test were observed.
Conclusions: The ECHO-DOB test in the post-infarction period allow the assessment of the functional significance of what is the objectified by coronary angiography and identifies pts at risk of more serious events. An integration of the test with the angiographic data can direct towards more suitable therapeutical or surgical choices.