Falai M

Postprocedural PAI-1 activity is a risk marker of subsequent clinical restenosis in patients both with and without stent implantation after elective balloon PTCA.

Stent implantation after balloon dilation of coronary arteries has improved clinical prognosis in patients undergoing transluminal coronary angioplasty (PTCA), but late restenosis remains a relevant problem. A previous study has indicated that PAI-1 activity changes immediately after PTCA without stent implantation are predictive of clinical restenosis. The present study was aimed to investigate the early PAI-1 changes and fibrin formation in patients undergoing elective PTCA with stent implantation. PAI-1 activity and D-dimer plasma levels were evaluated in two groups of patients (G1 underwent only elective balloon PTCA and G2 underwent elective PTCA with stent implantation) before and after the procedure. At the end of the procedure, PAI-1 activity significantly decreased, while D-dimer levels significantly increased in both groups. Post-PTCA D-dimer levels in the group with stent implantation were significantly higher than in the other group (P<.05). In both groups of patients, the post-PTCA PAI-1 activity was higher in patients with subsequent clinical recurrence with restenosis (P<.005 in G1 and P<.0005 in G2) than in those without, whereas no differences were found in D-dimer levels. In conclusion, our results demonstrate that fibrin formation assessed by D-dimer levels is enhanced by stent implantation. However, this behaviour is not related, differently from PAI-1 changes, to subsequent occurrence of clinical restenosis.

Myocardial stunning associated with a myocardial bridge.

A myocardial bridge is a discrete systolic constricnormal and tests for viral infections screened negation of a coronary artery, most commonly the left tive. She received oral aspirin (100 mg daily) and anterior descending, caused by some myocardial propranolol (20 mg t.i.d.) and remained asymptomattissue ‘bridging’ the vessel [1]. Regarded for long ic until discharge, 4 days later. time as innocent anatomic variants [1], myocardial ECG evolutionary changes consisted of a slow bridges have been subsequently acknowledged as regression of ST-segment elevation with appearance potential causes of angina, myocardial infarction and of negative T waves and no Q waves (Fig. 1B). At sudden death [2,3]. pre-discharge echocardiography, the left ventricular A 67-year-old woman with no coronary risk factor apex was no longer dyskinetic but rather akinetic, and a 2-year history of substernal pain on effort never with other findings unchanged, while viability of previously evaluated, was referred to our Department after recurrent episodes of pain that had been attenuating or exacerbating over a 2-h period, with reduced or increased intensity of physical exercise. On first examination, the pain had resolved and a 1–4-mm ST segment elevation in DI–DIII and V3–6 leads (Fig. 1A) was recorded, while echocardiography demonstrated a left ventricular antero-lateral akinesia with apical dyskinesia (LVEF 47%). At coronary angiography an isolated, 20-mm long myocardial bridge was causing a 75–80% systolic constriction of the mid left anterior descending branch (Fig. 2A,B). Serial myocardial enzymes were

Timing, setting and incidence of cardiovascular complications in patients with acute myocardial infarction submitted to primary percutaneous coronary intervention

BACKGROUND At the Istituto di Clinica Medica Generale e Cardiologia (Florence, Italy), the widespread use of percutaneous coronary intervention (PCI) has markedly changed the hospital course of patients with acute myocardial infarction (AMI). These patients are typically transferred to the coronary care unit (CCU) only after primary PCI, whereas during the thrombolytic era, patients were first admitted to CCU before reperfusion. OBJECTIVES AND METHODS The incidence, timing and setting of complications from symptom onset to hospital discharge in 689 consecutive AMI patients undergoing PCI were evaluated. RESULTS Ventricular fibrillation occurred in 11% of patients, and most episodes (94.7%) occurred before or during PCI. Of all patients, 6.3% developed complete atrioventricular block (CAVB), and in 86.3% of these cases, the CAVB occurred before or during PCI; in 94.5%, a CAVB resolution occurred in the catheterization laboratory (CL). Thirty-one patients (4.5%) had impending shock on admission to the CL. Cardiogenic shock developed in 2 9 patients (4.2%), mostly in the prehospital phase or in the CL. Only four patients (less than 1%) developed cardiogenic shock later during their hospital course. Similarly, circulatory and ventilatory support, as well as temporary pacing and cardiac defibrillation, were used mostly in the prehospital phase or in the CL. During the CCU stay, 45 patients (6.5%) had hemorrhagic or vascular complications, and the incidence of post-PCI ischemia and early reocclusion of the culprit vessel were low (2.1% and 0.6%, respectively). Thus, cardiac complications usually associated with AMI were observed mainly before hospital admission or in the CL during the reopening of the target vessel. These complications were rarely observed after a successful PCI. CONCLUSIONS For AMI patients, the CL is not only the site of PCI, it is also where most life-threatening cardiac complications are observed and treated.

Relevance of post-methionine homocysteine and lipoprotein (a) in evaluating the cardiovascular risk in young CAD patients.

Background  Aims of our study were to evaluate the prevalence of high lipoprotein (a) [Lp(a)] and homocysteine levels – both in the fasting state (FHcy) and post‐methionine (PMHcy) – in young coronary artery disease (CAD) patients, and to investigate the role of genetic and environmental factors for hyperhomocysteinaemia.