Effect of tirofiban therapy on ST segment resolution and clinical outcomes in patients with ST segment elevated acute myocardial infarction undergoing primary angioplasty.

BACKGROUND: In our study, we assessed the effect of glycoprotein (GP) IIb/IIIa receptor inhibition on microvascular flow after acute coronary occlusion using the early sum of ST segment resolution in electrocardiography. Platelets may play a major role in the dissociation of epicardial artery recanalization and tissue level reperfusion, referred to as the 'no-reflow phenomenon'. Therefore, GP IIb/IIIa receptor inhibition might improve myocardial reperfusion, distinct from its effects on epicardial patency. METHODS AND RESULTS: One hundred and fifteen patients (mean age 57.7 +/- 12.2 years, 96 males, 19 females) with < or = 12-hour acute ST segment elevation myocardial infarction who underwent successful primary percutaneous coronary intervention were retrospectively enrolled into the study. Patients were grouped according to whether they received tirofiban therapy or not. Clinical and electrocardiographic parameters were evaluated. The first sum of ST segment elevation amounts in millimeters was obtained immediately before angioplasty and the second 60 min after restoration of thrombolysis in myocardial infarction III flow. The difference between the two measurements was accepted as resolution of the sum of ST segment elevation and expressed as SigmaSTR. There were no significant differences between the groups regarding age, gender, cardiovascular risk factors, and laboratory parameters, duration from angina onset to the emergency unit, and from door to angioplasty. SigmaSTR was higher in patients who received tirofiban than in those who did not (7.2 +/- 2.8 and 4.2 +/- 2.6 mm, respectively; p < 0.001). There was a significant and positive correlation between GP IIb/IIIa inhibition and SigmaSTR (r = 0.336, p < 0.001), as well as between ejection fraction and SigmaSTR (r = 0.310, p < 0.001). GP IIb/IIIa inhibition was the only independent determinant of SigmaSTR in a multivariate linear regression model which contains 10 variables (p < 0.001). The incidence of in-hospital post-myocardial infarction refractory angina, reinfarction, and heart failure was significantly lower in the tirofiban group (p < 0.05, p < 0.05, and p < 0.05, respectively). Additionally, after 30 days, reinfarction and heart failure were lower in the tirofiban group (p < 0.05 and p < 0.05, respectively). CONCLUSIONS: It is well known that SigmaSTR determines microvascular perfusion. This study shows that GP IIb/IIIa inhibition with tirofiban is of value in preserving microvascular perfusion after restoring coronary thrombolysis in myocardial infarction III flow.

Anxiety and P wave dispersion in a healthy young population.

BACKGROUND: P wave dispersion (P(d)), defined as the difference between the maximum (P(max)) and the minimum P wave duration (P(min)), and P(max) are electrocardiographic (ECG) markers that have been used to evaluate the discontinuous propagation of sinus impulses and the prolongation of atrial conduction time. P(d) in normal subjects has been reported to be influenced by the autonomic tone, which induces changes in atrial size and the velocity of impulse propagation. However, the association between P(d) and anxiety has not been studied in normal subjects. METHODS AND RESULTS: P(max), P(min) and P(d) were measured in 726 physically and mentally healthy young male volunteers, aged 21.23 +/- 1.25 years (range 20-26). The Spielberger State-Trait Anxiety Inventory (STAI) was scored concomitantly. Blinded intra- and interobserver reproducibility of the P wave duration and P(d) measurement were evaluated, and comparison revealed a Pearson correlation coefficient of 0.87 and 0.89 for the P wave duration, and 0.93 and 0.90 for P(d), respectively (p < 0.001). P(max) and P(d) were significantly correlated with the state anxiety (STAI-1) subscale (r = 0.662, p < 0.001, and r = 0.540, p < 0.001, respectively) and the trait anxiety (STAI-2) subscale (r = 0.583, p < 0.001, and r = 0.479, p < 0.001, respectively). P(min) did not show any significant correlation with anxiety. Across 3 variables included in a multiple linear regression analysis, STAI-1 and STAI-2 were the significant independent determinants of P(max) and P(d). Beta coefficients indicated that the contribution of STAI-1 to P(max) (66.3 and 33.7%) and P(d) (65 and 35%) was much greater than that of STAI-2. CONCLUSIONS: STAI-1 and STAI-2 are associated with an increase in P(max) and P(d). The association of P(d) resulted from an augmentation of P(max). This is the first study to show the relation between P(max), P(d) and anxiety.

The role of angiotensin converting enzyme genotype in coronary artery ectasia.

Coronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE.