Perfusion-contraction mismatch during inotropic stimulation in hibernating myocardium.

UNLABELLED: The aims of this study were to assess the value of dobutamine echocardiography in identifying myocardial hibernation versus stunning and to elucidate the underlying pathophysiological mechanism of the contractile impairment. METHODS: Twenty-one patients with isolated stenosis of the left anterior descending artery were evaluated 1 mo after thrombolysed acute anterior infarction. Regional function and blood flow were measured using echocardiography and PET at rest and during dobutamine administration (10 microg/kg/min). RESULTS: Defined by [18F]fluorodeoxyglucose uptake, 36 of 102 dyssynergic segments were necrotic, and 66 were viable. The latter segments were subdivided according to their [13N]ammonia flow distribution: 30 hibernating regions with perfusion defects (flow of <80% of maximum) and 36 stunned areas with preserved resting perfusion (flow of > or =80% of maximum). Resting flows were similar in necrosis and hibernation (0.43 +/- 0.18 versus 0.47 +/- 0.16 ml x min(-1) x g(-1); not significant), and both resting values were lower than those seen in stunning (0.79 +/- 0.24; p < 0.05). Flow response to dobutamine was markedly reduced in necrosis (dobutamine/resting flow = 1.16 +/- 0.27), whereas it was maintained in hibernation (1.65 +/- 0.54) and stunning (1.42 +/- 0.57). Dobutamine improved function in a higher number of stunned (55%) than hibernating (16%) or necrotic (11%) segments. CONCLUSION: Dobutamine improves function mainly in stunned myocardium and does not reliably identify hibernation. The lack of functional response in hibernation is not related to an exhausted vasodilating capacity.

Perfusional and metabolic effects of nisoldipine as shown by positron emission tomography after acute myocardial infarction.

After myocardial infarction, regional dysfunction can occur in viable myocardial regions because of the presence of baseline hypoperfusion. Recent evidence suggests that these areas may maintain a residual perfusion reserve. The aim of the present study was to evaluate whether oral nisoldipine can increase regional myocardial blood flow (MBF) in dyssynergic but viable myocardium after myocardial infarction. Patients with isolated left anterior descending coronary stenosis were studied 1 month after the first myocardial infarction. Patients underwent [18F]fluorodeoxyglucose imaging, and MBF was measured, using positron emission tomography and [13N]ammonia, at baseline and following dobutamine administration (10 micrograms/kg/min over 5 minutes). MBF measurements were repeated 24 hours after nisoldipine (10 mg twice daily). Preliminary results suggest that necrotic areas showed the largest reduction in baseline MBF. Dyssynergic-viable regions showed a reduced resting MBF but maintained a residual perfusion reserve in response to inotropic stimulation. Thus, nisoldipine selectively improved basal perfusion in dyssynergic-viable myocardium.

Should we treat silent myocardial ischaemia?

Silent myocardial ischaemia has been documented in various clinical entities. Exercise testing and ambulatory ECG monitoring are the most widely used tests for documenting silent ischaemia, and both exercise-induced and daily life ischaemia have the potential to trigger prolonged functional and structural changes. Numerous clinical investigations in apparently healthy subjects, in stable and unstable angina, in patients with a previous myocardial infarction indicate that ischaemia has an adverse prognostic influence, independent of whether the ischaemia is silent or symptomatic. Methods for documenting silent ischaemia lead to different considerations according to each clinical syndrome of coronary artery disease. This review deals with the different intervention strategies derived from the unique prognostic profiles offered by silent ischaemia in a variety of clinical entities.

[Hypercholesterolemia and coronary disease: intervention strategies]. / L'ipercolesterolemia e malattia coronarica: strategie di intervento.

The decision to treat hypercholesterolemia must take into account both the risk of death and myocardial infarction and the risk/benefit ratio of treatment. Nowadays there is convincing evidence that hypercholesterolemia in patients with previous myocardial infarction is an important prognostic factor: furthermore, the excess of risk due to cholesterol is consistently higher than that in the general population. Prospective studies demonstrated that cholesterol lowering treatment obtained either with diet or drugs can improve survival and quality of life in postinfarction patients. Experimental, clinical and angiographic studies suggested that cholesterol lowering therapy can produce both stabilization and regression of the atherosclerotic plaque. In view of this, the evaluation of cholesterol level must be part of the general work-up of patients with previous myocardial infarction. The satisfactory results obtained with diet suggest to try a dietary treatment in post-infarction patients with high cholesterol level before using drugs. Since there are no clear-cut upper values, the end point of treatment should be to lower cholesterol levels to the values recommended for the general population, although we believe that threshold values to be obtained in these subjects should be lower than those requested in primary prevention.