Assessment of coronary artery calcification using dual-source computed tomography in adult asymptomatic patients with type 1 diabetes mellitus.

BACKGROUND: Experience with dual-source computed tomography (DSCT) for detecting coronary artery calcification (CAC) in patients with type 1 diabetes is limited. MATERIAL/METHODS: A non-contrast DSCT scan was acquired in 46 type 1 diabetic patients. All scans were suitable for evaluating CAC expressed in Agatston-scores (effective radiation dose 0.66 [0.59-0.81] mSv; median [interquartile range]). RESULTS: In 21 patients Agatston scores were > or =1 (range 1-2353), while 25 patients had no detectable calcium deposits in the coronary arteries. Patients with vs. without CAC had higher age (52 [44-59] vs. 41 [38-48] yrs; p=0.0045), longer duration of diabetes (25.3 [23.4-36.3] vs. 23.3 [15.7-30.4] yrs; p=0.0238), greater waist circumference (88 [77-98] vs. 79 [75-87] cm; p=0.0147) and BMI (26.7 [24.5-28.4] vs. 22.6 [21.7-25.6] kg/m(2); p=0.0109). Moreover, patients with vs. without detectable CAC had higher serum LDL-cholesterol (3.35 [3.15-3.53] vs. 2.92 [2.62-3.33] mmol/l; p=0.0069) and serum uric acid values (236 [191-266] vs. 200 [170-219] micromol/l; p=0.0437). Hypertension was more frequent (p=0.0144) in patients with than without CAC. The 2 subgroups did not differ in long-term average HbA1c values (7.97 [7.30-8.56] vs. 8.06 [7.24-9.05]%; p=0.7491); however, estimated insulin sensitivity (estimated glucose disposal rate) was lower in patients with vs. without detectable CAC (7.43 [5.73-8.58] vs. 9.24 [8.22-10.72] mg/kg/min; p=0.0017). CONCLUSIONS: Non-invasive detection of CAC is feasible with a low dose DSCT scan. CAC in type 1 diabetic patients is associated with cardiovascular risk factors rather than with long-term glycemic control.

Analysis of platelet alpha2-adrenergic receptor activity in stable coronary artery disease patients on dual antiplatelet therapy.

Combined antiplatelet therapy reduces recurrent atherothrombotic events in stable coronary disease patients; however, high residual platelet reactivity measured ex vivo still raises concerns as a condition related to treatment failure. Alpha-2 adrenoceptor enhances platelet reactivity and might contribute to this phenomenon. For the present study, 121 stable angina patients on standard dual antiplatelet therapy (75 mg clopidogrel and 100 mg acetylsalicylic acid) were recruited. Born aggregometry was performed with adenosine diphosphate (ADP), collagen and epinephrine. To verify platelet adrenergic activity, potentiation by low-dose epinephrine and inhibition by selective alpha-2 receptor blocker atipamezole were determined. To assess the P2Y(12)-specific residual activity, cangrelor was used. Plasma norepinephrine, soluble CD40-ligand, high-sensitivity-C-reactive protein (hsCRP) - and in 24 subjects platelet P-selectin positivity were measured. Epinephrine - at very low concentration (10(-9)g/ml) - significantly potentiates (1.25 microM ADP: 26.5% vs. 43%; 5 microM ADP: 53% vs. 64.5%; collagen: 17% vs 42%, p < 0.001) while atipamezole inhibits ADP- and collagen-induced platelet aggregations (1.25 microM ADP: 26.5% vs. 23%; 5 microM ADP: 53% vs. 47%; collagen: 17% vs. 11%, p < 0.001). Patients with high adrenergic activity have significantly increased baseline ADP- and collagen-induced platelet aggregation. Based on cangrelor's efficacy, these patients have significantly more residual P2Y(12) activity as well. HsCRP and soluble CD40-ligand levels were similar. In conclusion, stable coronary heart disease patients with prominent adrenoceptor activity in vitro have significantly increased platelet aggregability and more functional P2Y(12) receptor, indicating poor inhibitory response to thienopyridines. Therefore, platelet adrenergic receptor represents a considerable, dynamic factor of high residual platelet reactivity and might contribute to cardiovascular events indicating failure of antiplatelet therapy.

Inverse correlation between coronary blood flow velocity and sICAM-1 level observed in ischemic heart disease patients.

Systemic factors and blood flow velocity related to atherosclerosis have been examined mainly separately or by in vitro studies. The aim of our study was to investigate the association between local coronary blood flow (corrected TIMI frame count, CTFC) and systemic atherosclerosis-related inflammatory parameters such as soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (Il-6), high sensitivity C-reactive protein (hsCRP) and von Willebrand factor (vWF) in humans. We enrolled the following groups of ischemic heart disease (IHD) patients: patients with coronary stenosis and stable (CAD, n = 96) or unstable angina (ACS, n = 27), patients with documented myocardial ischemia and normal coronary angiogram (NEG, n = 68). Patient groups showed only marginal differences in CTFC or sICAM-1 levels. In contrast, when IHD patients were studied individually, general positive correlation was found between CTFC and sICAM-1 level (r = 0.33; in NEG r = 0.25; in CAD r = 0.37; in ACS r = 0.61), being the strongest in ACS. The relation was independent from age, gender, BMI, smoking, hypertension, diabetes, previous myocardial infarction, family history of IHD, medication, hsCRP, IL-6 and vWF levels. (odds ratio, OR = 6.4; CI 95%: 2.43-16.84; p < 0.05). Nevertheless, correlation between CTFC and IL-6, hsCRP, vWF levels was not found. These results indicate inverse correlation between coronary blood flow and adhesion molecule production independently from conventional cardiovascular risk factors and inflammatory markers.

Need for prophylactic application of verapamil in transradial coronary procedures: a randomized trial. The VITRIOL (is Verapamil In TransRadial Interventions OmittabLe?) trial.

BACKGROUND: Verapamil is traditionally applied prophylactically in transradial procedures to prevent radial artery spasm. However, verapamil may have side effects and is contraindicated in some clinical settings. METHODS AND RESULTS: During an investigator-initiated, randomized, double-blind trial, we evaluated the need for preventive verapamil administration. After vascular access was established, patients received either 5 mg verapamil (n=297) or placebo (n=294). We compared the rate of access site conversions as primary end point using a superiority margin of 5%. Occurrence of code breaks (composite of conversions and unplanned use of verapamil), overall verapamil use, procedural and fluoroscopic times, contrast volume, and subjective pain were investigated as secondary end points. The rate of access site conversions was not different in the 2 arms (placebo 1.7% versus verapamil 0.7%, P=0.28, difference 1.0%, 95% CI for the difference -1.1% to 3.3%). Proportion of code breaks was similar in the 2 groups (3.4% versus 1.3%, P=0.11), whereas overall verapamil use was markedly lower in the placebo arm (2.0% versus 100%, P<0.0001). Procedural time (median [IQR] 16.0 minutes [9.0 to 30.0 minutes] versus 17.0 minutes [10.0 to 31.0 minutes], P=0.37), fluoroscopic time (4.4 minutes [2.1 to 9.6 minutes] versus 4.8 minutes [2.4 to 10.7 minutes], P=0.28), contrast volume (72.5 mL [48.0 to 146.0 mL] versus 75.5 mL [47.0 to 156.5 mL], P=0.74), and pain score (P for trend=0.12) were comparable in the 2 groups. CONCLUSIONS: The preventive use of verapamil may be unnecessary for transradial procedures. The omission of prophylactic verapamil may not only reduce the rate of potential complications related to the drug but also allow the safe extension of the transradial method to those with contraindications to verapamil. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01402427.

Diagnostic value of the left atrial electrical potentials detected by body surface potential mapping in the prediction of coronary artery disease.

BACKGROUND: The electrocardiographic diagnosis of significant coronary artery stenosis (CAD) is often based on the investigation of the left ventricular repolarization changes during exercise ECG stress test (EST). Our aim was to prove that the electric activity of the left atrium can indicate the ischemic damage of the left ventricle, and furthermore, it is able to indicate CAD without exercise. METHODS AND RESULTS: Patients with chest complaints but without evidence of acute coronary syndrome were investigated by EST and body surface potential mapping (BSPM, 63 leads). CAD was proven in 45 cases (32 men, years 40-76) and excluded in 50 cases (35 men, years 38-72) with coronary angiography. Left atrial electric potentials (EP-LA) before and after 0.08 mg sublingual nitroglycerine administration differed significantly (p<0.001) in the two groups. According to Fischer linear discriminant analysis, this difference in % (EP-LA(d%)) was the best separating parameter: below limit of -14.17% (CAD prevalence was considered) this parameter predicted CAD with 93% sensitivity, 100% specificity, >10 positive and 0.05 negative likelihood ratio (weighted for prevalence). The EST predicted CAD with 71% sensitivity, 78% specificity, 2.43 positive and 0.28 negative likelihood ratios. CONCLUSION: The electrical activity changes of the left atrium seemed to be suitable to predict CAD as an EST-alternative resting method.

Very late drug-eluting stent thrombosis after nonsteroidal anti-inflammatory drug treatment despite dual antiplatelet therapy.

BACKGROUND: Drug-eluting coronary stent implantation emerged as a safe and effective therapeutic approach by preventing coronary restenosis and reducing the need for further revascularization. However, in contrast to bare metal stents, recent data suggest a unique underlying pathology, namely late coronary stent thrombosis and delayed endothelial healing. OBJECTIVE: To report a case of very late coronary stent thrombosis (834 days after implantation) requiring repeat urgent target-vessel revascularization. Importantly, six days before the acute coronary event, combined nonsteroidal anti-inflammatory drug therapy was initiated. RESULTS: Although a dual antiplatelet regimen was continuously maintained, aggregation measurements indicated only partial antiplatelet effect, which returned to the expected range when nonsteroidal anti-inflammatory drugs were omitted. CONCLUSIONS: The observation indicates that, even 834 days after drug-eluting stent implantation, effective combined antiplatelet therapy might be crucial in certain individuals and the possible impact of drug interactions should not be underestimated. Further efforts should focus on the challenging task of identifying patients or medical situations with prolonged, increased risk of stent thrombosis.