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The effects of vitamin D (Vit-D) deficiency and Vit-D treatment (VDT) on atrial fibrillation (AF) remain inconclusive. This study sought to determine the effects of VDT and nontreatment on AF risk in Vit-D-deficient patients without a previous history of AF. In this nested case-control study, 39,845 individuals with low 25-hydroxy-Vit-D ([25-OH]D) levels (20 ng/ml) were divided into group-A (untreated, levels ≤20 ng/ml), group-B (treated, levels 21 to 29 ng/ml), and group-C (treated, levels ≥30 ng/ml). The risk of AF was compared utilizing propensity score-weighted Cox proportional hazard models. Among the individuals receiving VDT for ≥6 months, the risk of AF was significantly lower in group-B (hazard ratio [HR] 0.89, 95% confidence interval [CI] 0.80 to 0.98, p = 0.03] and group-C (HR 0.84, 95% CI 0.73 to 0.0.95, p = 0.007] than in group-A. A subgroup analysis of men65 years showed individuals with hypertension had a significantly lower risk of AF in group-C than in group-B (HR 0.79, CI 0.65 to 0.94, p = 0.02) and group-A (HR 0.78, CI 0.64 to 0.96, p = 0.012). A similar result was found in men65 years with diabetes mellitus in group-C compared with group-B (HR 0.69, CI 0.51 to 0.93, p = 0.012) and group-A (HR 0.63, CI 0.47 to 0.84, p = 0.002). In what is, to best of our knowledge, the largest observational study to date of patients with Vit-D deficiency and no previous history of AF, (25-OH)D level of20 ng/ml with VDT for ≥6 months was associated with a significantly lower risk of AF. Additionally, men65 years with hypertension or diabetes mellitus had a further decrease in AF risk when the (25-OH)D levels were ≥30 ng/ml.

The effect of normalization of serum testosterone levels with testosterone replacement therapy (TRT) in patients with a history of myocardial infarction (MI) is unknown. The objective of this study was to determine the incidence of recurrent MI and all-cause mortality in subjects with a history of MI and low total testosterone (TT) with and without TRT. We retrospectively examined 1,470 men with documented low TT levels and previous MI, categorized into Gp1: TRT with normalization of TT levels (n = 755) Gp2: TRT without normalization of TT levels (n = 542), and Gp3: no TRT (n = 173). The association of TRT with all-cause mortality and recurrent MI was compared using propensity score-weighted Cox proportional hazard models. All-cause mortality was lower in Gp1 versus Gp2 (hazard ratio [HR] 0.76, confidence interval [CI] 0.64 to 0.90, p = 0.002), and Gp1 versus Gp3 (HR 0.76, CI 0.60 to 0.98, p = 0.031). There was no significant difference in the risk of death between Gp2 versus Gp3 (HR 0.97, CI 0.76 to 1.24, p = 0.81). Adjusted regression analyses showed no significant differences in the risk of recurrent MI between groups (Gp1 vs Gp3, HR 0.79, CI 0.12 to 5.27, p = 0.8; Gp1 vs Gp2 HR 1.10, CI 0.25 to 4.77, p = 0.90; Gp2 vs Gp3 HR 0.58, CI 0.08 to 4.06, p = 0.58). In conclusion, in a large observational cohort of male veterans with previous MI, normalization of TT levels with TRT was associated with decreased all-cause mortality compared with those with non-normalized TT levels and the untreated group. Furthermore, in this high-risk population, TRT was not associated with an increased risk of recurrent MI.

This study evaluated the incidence and type of acute myocardial infarction (AMI) in a consecutive population with increased troponin I (TnI). AMI has recently been redefined and subclassified. Incidence, demographic data, angiographic findings, and hospital mortality of patients with various AMI subtypes or an increased TnI in the absence of AMI have not been previously reported in a prospective study. Over a 3-month period, all patients admitted from an emergency room or from in-patient services with >1 TnI level >0.04 ng/ml were evaluated and subclassified in AMI subgroups. In-hospital or recent coronary angiograms were reviewed. In-hospital mortality was noted. Of 2,944 patients with serial TnI measurements, 728 had an increased TnI and 701 (23.8%) were evaluated. Two hundred sixteen (30.8% with increased TnI and 42.7% with "rule-out MI" on admission) met criteria for AMI. One hundred forty-three (20.4%) had type 1, 64 (9.1%) had type 2, whereas 461 (65.8%) did not meet criteria for AMI. On multivariate analysis, use of angiography, peak TnI level, hyperlipidemia, and illicit drug use were independently associated with the diagnosis of AMI. TnI of 0.28 ng/ml had a 70% sensitivity and specificity for AMI diagnosis. In conclusion, a minority admitted with increased TnI have AMI by the universal definition. Type 1 is the most common AMI and is associated with higher TnI values and these patients are more likely to undergo angiography. Type 2 AMI is often associated with illicit drug use.

Angiographic studies support an association between troponin elevation, intracoronary thrombus, and presumed embolization, but previous studies have indicated that only 20% to 25% of patients with positive troponin levels had angiographic evidence of intracoronary thrombus compared with 5% of patients who were troponin negative. 1–3 Although there already exists an association, 75% to 80% of patients with increased troponin levels had no evidence of intracoronary thrombus. It has been previously shown that the angiographic morphology of the culprit lesion in unstable angina pectoris (UAP) or non–Q-wave acute myocardial infarction (AMI) is characteristic, with 50% to 70% of patients having an acute coronary or complex lesion, which is the angiographic correlate of a disrupted or fi ssured atherosclerotic plaque and/or the presence or intracoronary thrombus. 4,5 This lesion is uncommon in culprit lesions from patients presenting with symptoms of stable angina. Therefore, it was hypothesized that this lesion classifi cation system might represent a more sensitive method for examining the association between elevated troponin and the presence of intracoronary thrombus.

3:864–871. 7. Vandenberg BF, Weiss RM, Kinzey J, Acker M, Stark CA, Stanford W, Burns TL, Marcus ML, Kerber RE. Comparison of left atrial volume by two-dimensional echocardiography and cine-computed tomography. Am J Cardiol 1995;75:754–757. 8. Rodevand O, Bjornerheim R, Ljosland M, Maehle J, Smith HJ, Ihlen H. Left atrial volumes assessed by threeand two-dimensional echocardiography compared to MRI estimates. Internat J Card Imag 1999;15:397–410. 9. Patel VV, Ren J-F, Marchlinski FE. A comparison of left atrial size by transthoracic two-dimensional guided M-mode echocardiography and magnetic endocardial catheter mapping. PACE 2002;25:14–17. 10. Gepstein L, Hayam G, Ben-Hain SA. A novel method for nonfluoroscopic catheter-based electroanatomic mapping of the heart. Circulation 1997;95:1611– 1622. 11. Gepstein L, Evans SJ. Electroanatomical mapping of the heart: basic concepts and implications for the treatment of cardiac arrhythmias. PACE 1998;21:1268– 1278. 12. Pappone C, Oreto G, Lamberti F, Vicedomini G, Loricchio ML, Shpun S, Rillo M, Calabro MP, Conversano A, Ben-Haim SA, Cappato R, Chierchia S. Catheter ablation of paroxysmal atrial fibrillation using a 3D mapping system. Circulation 1997;96:2715–2721. 13. Brockenbrough EC, Braunwald E. A new technique for left ventricular angiocardiography and transseptal left heart catheterization. Am J Cardiol 1960; 6:1062–1068. 14. Wahr D, Yin SW, Schiller NB. Left ventricular volumes determined by two-dimensional echocardiography in a normal adult population. J Am Coll Cardiol 1983;1:863–868. 15. Sanfilippo AJ, Abascal VM, Sheehan M, Oertel LB, Harrigan P, Hughes RA, Weyman AE. Atrial enlargement as a consequence of atrial fibrillation: a prospective echocardiographic study. Circulation 1990;82:792–797.

The predictors of troponin release after percutaneous coronary intervention were prospectively assessed in 405 consecutive patients. Troponin release occurred frequently (27%) and was associated with complications during the procedure, including sapheneous vein graft interventions, multistent use, glycoprotein IIb/IIIa use, and a history of hypercholesterolemia.

Glycoprotein (GP) IIb/IIIa receptor blockers have been shown to reduce adverse events in randomized clinical trials. 1‐ 4 Not only will these agents reduce platelet aggregation but, as activated platelets facilitate thrombin formation, these agents should also possess effects on reducing thrombin generation.5 Experimental and in vivo studies indicate that abciximab alone or in combination with standard-dose intravenous heparin decrease thrombin generation and fibrin formation. 6‐8 Furthermore, in a thrombin generation assay triggered by tissue factor, Reverter et al 9 found that c7E 3Fab (abciximab) through both GP Ilb/IIIa blockade and a v b3 blockade (vitronectin receptor) inhibited tissue factor-induced thrombin generation. 9 On the other hand, the small molecule inhibitors of the GP IIb/IIIa receptor are specific for this receptor alone and do not interact with the vitronectin receptor. Their effects in vivo on thrombin generation in human subjects have not been well studied. In this paper, we compared these antithrombin effects of tirofiban and heparin compared with abciximab and heparin on the activated clotting time (ACT), prothrombin fragment F1.2, and GP IIb/IIIa platelet receptor occupancy using a standardized protocol.