Management of postinfarct ventricular tachycardias.

The clinical profile of patients with postinfarct VT has changed in the past two decades. Along with these changes, existing treatments have improved, and entirely new therapeutic approaches have been developed. The expanded range of treatment options has made postinfarct VT a less imposing clinical problem than it once was. Emerging therapies promise to make an even greater beneficial impact. The challenge in treating patients with postinfarct VT has changed from merely keeping patients alive to keeping up with innovations in therapy that can provide them with a better quantity and quality of life.

[MIBI-echocardiography with dobutamine: Significance of changes of contractility in patients with changes in perfusion]. / Ecocardiografía-MIBI con dobutamina: significado de las alteraciones de la contractilidad en pacientes con alteraciones de la perfusión.

BACKGROUND AND OBJECTIVES: In the presence of coronary artery disease and with an appropriate stressor, perfusion defects precede contractility abnormalities. Perfusion defects without contractility abnormalities may be due to the absence of ischemia or mild ischemia. Our purpose has been to compare the clinical characteristics, hemodynamic response and severity of perfusion defects in patients with coronary artery disease and perfusion defects with and without wall motion abnormalities during dobutamine infusion. PATIENTS AND METHODS: Eighty two patients with significant coronary artery disease demonstrated by angiography without previous myocardial infarction underwent dobutamine infusion (up to 40 mg/kg/min). Atropine was given when necessary. Stress scientigraphic MIBI-SPECT images were acquired 1 hour after peak stress and rest studies were obtained 24 hours after stress testing. The perfusion score was calculated by dividing the total uptake score between the number of segments affected. RESULTS: Among the 73 patients with perfusion defects, stress echocardiography was positive in 59 (Group A) and was negative in the remaining 14 (Group B). There were more hypertensive patients in Group A (33 vs 4; p = 0.04). There was no significant difference between the two groups with respect to other clinical characteristics. The peak rate-pressure product was similar in both groups (18.520 +/- 5.691 vs 18.680 +/- 5.329; p = NS). The development of electric abnormalities and angina was more common in Group A (42 vs 3, p < 0.001 and 33 vs 1; p < 0.001). Perfusion defects were not more extensive in Group A (abnormal segments 2.15 vs 2.21; p = NS) but they were more severe (segments with severe uptake reduction or no uptake 1.10 vs 0.28; p < 0.05; perfusion score 2.62 vs 2.21; p < 0.05). CONCLUSION: In patients with severe coronary artery disease and perfusion defects during dobutamine-MIBI-SPECT, the presence of wall motion abnormalities defines patients with more severe perfusion defects.