Acute hyperglycaemia prevents the protective effect of pre-infarction angina on microvascular function after primary angioplasty for acute myocardial infarction.

BACKGROUND: Acute hyperglycaemia has been associated with impaired microvascular function after acute myocardial infarction (AMI), whereas pre-infarction angina (PIA) occurring shortly before the onset of AMI has been shown to reduce microvascular injury after reperfusion. OBJECTIVE: To examine whether acute hyperglycaemia prevents the protective effect of PIA on microvascular function after AMI. METHODS: We studied 205 patients with a first anterior wall AMI who underwent primary angioplasty within 12 hours of onset. Coronary flow velocity parameters were assessed immediately after reperfusion using a Doppler guidewire. Severe microvascular injury was defined as the presence of systolic flow reversal and diastolic deceleration time <600 ms. Echocardiographic wall motion was analysed before revascularisation and 4 weeks later. RESULTS: Acute hyperglycaemia, defined as a blood glucose level of >or=198 mg/dl on admission, was found in 67 (33%) patients. In patients without acute hyperglycaemia, PIA was associated with a lower incidence of systolic flow reversal, a longer diastolic deceleration time and a higher coronary flow reserve. However, in patients with acute hyperglycaemia there was no significant difference in these same parameters between patients with and without PIA. In the presence of acute hyperglycaemia PIA did not improve the change in wall motion score. In a multivariate model, the absence of PIA was an independent determinant of severe microvascular injury in patients without acute hyperglycaemia (odds ratio 6.28, p = 0.001), but not in patients with acute hyperglycaemia. CONCLUSION: The protective effect of PIA on microvascular function was attenuated in patients with acute hyperglycaemia, resulting in unfavourable functional recovery.

Relation between the TIMI frame count and the degree of microvascular injury after primary coronary angioplasty in patients with acute anterior myocardial infarction.

OBJECTIVE: To investigate the relation between thrombolysis in myocardial infarction (TIMI) frame count (TFC) and coronary blood flow velocity (CBFV) parameters reflecting the degree of microvascular injury in patients with acute myocardial infarction. RESULTS: TFC and CBFV were measured after primary coronary angioplasty in 103 consecutive patients with their first anterior wall acute myocardial infarction. TFC correlated inversely with the averaged peak velocity (r = -0.43, p < 0.0001). However, TFC did not correlate significantly with diastolic deceleration time and with the averaged systolic peak velocity (r = -0.16, p = 0.22, and r = -0.23, p = 0.16, respectively). The patients were divided into two groups according to presence (35 patients) or absence (68 patients) of systolic flow reversal. There was no significant difference in TFC between the two groups (29 (16) v 25 (13), p = 0.20). CONCLUSIONS: These findings suggest that the TFC reflects epicardial CBFV. However, it is not accurate enough to assess the degree of microvascular injury after primary coronary angioplasty.

Immunohistochemical and electronmicroscopic studies of obstructive lesions in submandibular glands.

Obstructive sialoadenitis was examined by immunohistochemical techniques for keratin (MoAb KL1, PKK1 and K8.12) and actin. Electronmicroscopy (EMS) was used to identify ultrastructural changes in myoepithelial cells and ductal basal cells. With immunohistochemistry, actin staining was used as a marker of myoepithelium, MoAbs KL1 and PKK1 for ductal luminal cells, and MoAb K8.12 for ductal basal cells. Histologic features of the lesion usually showed degenerative changes of acinar and duct cells with cell infiltration and fibrous replacement. Immunohistochemical findings indicated that actin staining in the changed myoepithelial cells was irregularly positive or negative, and also keratin staining in luminal and ductal basal cells was reduced or disappeared. Ultra-structural features of the changed myoepithelial cells indicated that these cells appeared less altered than adjacent acinar and ductal cells and showed increased amounts of lipid droplets and lipofuscin granules, and also wrinkled processes filled the prominent myofilament material.