A negative myocardial perfusion scintigram after coronary angioplasty confers benign long-term prognosis.

BACKGROUND: Myocardial perfusion SPECT is often used to exclude late restenosis or disease progression after coronary angioplasty (PTCA), but few studies have been published regarding the prognostic value of a negative study. AIM: To examine the long-term prognostic value of a non-ischemic SPECT result after successful PTCA. METHODS: We retrospectively reviewed 783 patients (pts) who underwent scintigraphy 3 months to 3 years after successful PTCA. In 118 no significant myocardial ischemia (moderate or severe) was observed. There was a history of myocardial infarction (MI) in 38.1%, multivessel disease in 36.8% and LVEF < 50% in 15.3%. Referral for SPECT was chronic angina in 50.5% and acute coronary syndrome in 32.2%. SPECT was performed using a treadmill exercise test in 72%, adenosine in 21%, dipyridamole in 3% and dobutamine in 4%. Fifty-three percent of pts were under anti-ischemic medication. Patients were divided into two groups according to the SPECT result: group A pts (n = 70) had mild or no ischemia and group B pts (n = 48) had non-reversible defects of small or moderate size. The endpoint was the combined occurrence of death, MI, unstable angina (UA) and repeated revascularization. RESULTS: There were one MI, 2 UA episodes and 4 repeated PTCAs (1 for UA). Event-free survival rate at two-year follow-up was slightly lower in patients from group B compared with group A, respectively 91.7% versus 97.1% (p = 0.16, log rank test). CONCLUSIONS: This study suggests an excellent prognosis for patients with no or mild ischemia as assessed by SPECT performed more than 3 months after coronary angioplasty. Those patients with mild persistent defects did not present a significantly worse outcome.

[Molecular pathobiology in heart failure]. / Patobiologia molecular na insuficiência cardíaca.

Heart failure is a pathophysiological state resulting from disturbed cardiac function. It is based on complex molecular processes, many of which are not fully understood. During heart failure adaptive mechanisms, that reinstall altered cardiac function, are activated. The main mechanisms are: a) Alteration of the structure and composition of myocytes by myocardial hypertrophy, reexpression of fetal and neo-natal proteins and the expression of certain proto-oncogenes; b) Activation of the neuroendocrinal system, specifically the sympathetic nervous system, renin-angiotensin-aldosterone system and vasopressin release; c) Activation of autocrine and paracrine systems. However, when these systems are activated beyond a certain limit they contribute to heart failure aggravation. This can also be promoted by alteration of the calcium metabolism inherent in heart failure. The synthesis of the counterregulator atrial natriuretic factor is also increased.