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Coronary Artery Disease: HELP
Articles by Ales Linhart
Based on 14 articles published since 2008

Between 2008 and 2019, A. Linhart wrote the following 14 articles about Coronary Artery Disease.
+ Citations + Abstracts
1 Guideline 2013 ESC guidelines on the management of stable coronary artery disease: the Task Force on the management of stable coronary artery disease of the European Society of Cardiology. 2013

Anonymous3190768 / Montalescot, Gilles / Sechtem, Udo / Achenbach, Stephan / Andreotti, Felicita / Arden, Chris / Budaj, Andrzej / Bugiardini, Raffaele / Crea, Filippo / Cuisset, Thomas / Di Mario, Carlo / Ferreira, J Rafael / Gersh, Bernard J / Gitt, Anselm K / Hulot, Jean-Sebastien / Marx, Nikolaus / Opie, Lionel H / Pfisterer, Matthias / Prescott, Eva / Ruschitzka, Frank / Sabaté, Manel / Senior, Roxy / Taggart, David Paul / van der Wall, Ernst E / Vrints, Christiaan J M / Anonymous3200768 / Zamorano, Jose Luis / Achenbach, Stephan / Baumgartner, Helmut / Bax, Jeroen J / Bueno, Héctor / Dean, Veronica / Deaton, Christi / Erol, Cetin / Fagard, Robert / Ferrari, Roberto / Hasdai, David / Hoes, Arno W / Kirchhof, Paulus / Knuuti, Juhani / Kolh, Philippe / Lancellotti, Patrizio / Linhart, Ales / Nihoyannopoulos, Petros / Piepoli, Massimo F / Ponikowski, Piotr / Sirnes, Per Anton / Tamargo, Juan Luis / Tendera, Michal / Torbicki, Adam / Wijns, William / Windecker, Stephan / Anonymous3210768 / Knuuti, Juhani / Valgimigli, Marco / Bueno, Héctor / Claeys, Marc J / Donner-Banzhoff, Norbert / Erol, Cetin / Frank, Herbert / Funck-Brentano, Christian / Gaemperli, Oliver / Gonzalez-Juanatey, José R / Hamilos, Michalis / Hasdai, David / Husted, Steen / James, Stefan K / Kervinen, Kari / Kolh, Philippe / Kristensen, Steen Dalby / Lancellotti, Patrizio / Maggioni, Aldo Pietro / Piepoli, Massimo F / Pries, Axel R / Romeo, Francesco / Rydén, Lars / Simoons, Maarten L / Sirnes, Per Anton / Steg, Ph Gabriel / Timmis, Adam / Wijns, William / Windecker, Stephan / Yildirir, Aylin / Zamorano, Jose Luis. ·The disclosure forms of the authors and reviewers are available on the ESC website www.escardio.org/guidelines. ·Eur Heart J · Pubmed #23996286.

ABSTRACT: -- No abstract --

2 Review Prediction of coronary vessel involvement on the basis of atherosclerosis risk factor analysis. 2013

Kovarnik, T / Kral, A / Skalicka, H / Skalicka, L / Dostal, O / Kralik, L / Martasek, P / Aschermann, M / Horak, J / Linhart, A / Wahle, A / Sonka, M. ·Second Department of Internal Medicine, Charles University, Prague, Czech Republic. tkovarnik@yahoo.com ·Bratisl Lek Listy · Pubmed #23822628.

ABSTRACT: The prediction of coronary vessel involvement by means of noninvasive tests is one of the fundamental objectives of preventive cardiology. This review describes the current possibilities of coronary vessel involvement prediction by means of ultrasonographic examination of carotid arteries, analysis of polymorphisms in the genes encoding enzymes responsible for production of nitric oxide and carbon monoxide and assessment of levels of certain proinflammatory cytokines. In the presented work these noninvasive markers are correlated with the extent of coronary vessel involvement as assessed by coronary angiography, intravascular ultrasound and virtual histology (Fig. 5, Ref. 40).

3 Clinical Trial Plaque volume and plaque risk profile in diabetic vs. non-diabetic patients undergoing lipid-lowering therapy: a study based on 3D intravascular ultrasound and virtual histology. 2017

Kovarnik, Tomas / Chen, Zhi / Mintz, Gary S / Wahle, Andreas / Bayerova, Kristyna / Kral, Ales / Chval, Martin / Kopriva, Karel / Lopez, John / Sonka, Milan / Linhart, Ales. ·2nd Department of Medicine-Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, II. interni klinika VFN a 1. LF UK, U nemocnice 2, 128 08, Praha 2, Czech Republic. tomas.kovarnik@vfn.cz. · Department of Electrical & Computer Engineering and Iowa Institute for Biomedical Imaging, The University of Iowa, Iowa City, IA, USA. · Cardiovascular Research Foundation, New York, USA. · 2nd Department of Medicine-Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, II. interni klinika VFN a 1. LF UK, U nemocnice 2, 128 08, Praha 2, Czech Republic. · Institute for Research and Development of Education, Faculty of Education, Charles University in Prague, Prague, Czech Republic. · Cardiology Department, Na Homolce Hospital, Prague, Czech Republic. · Loyola University Stritch School of Medicine, Maywood, IL, USA. ·Cardiovasc Diabetol · Pubmed #29212544.

ABSTRACT: BACKGROUND: Coronary atherosclerosis progresses faster in patients with diabetes mellitus (DM) and causes higher morbidity and mortality in such patients compared to non-diabetics ones (non-DM). We quantify changes in plaque volume and plaque phenotype during lipid-lowering therapy in DM versus non-DM patients using advanced intracoronary imaging. METHODS: We analyzed data from 61 patients with stable angina pectoris included to the PREDICT trial searching for prediction of plaque changes during intensive lipid-lowering therapy (40 mg rosuvastatin daily). Geometrically correct, fully 3-D representation of the vascular wall surfaces and intravascular ultrasound virtual histology (IVUS-VH) defined tissue characterization was obtained via fusion of two-plane angiography and IVUS-VH. Frame-based indices of plaque morphology and virtual histology analyses were computed and averaged in 5 mm long baseline/follow-up registered vessel segments covering the entire length of the two sequential pullbacks (baseline, 1-year). We analyzed 698 5-mm-long segments and calculated the Liverpool active plaque score (LAPS). RESULTS: Despite reaching similar levels of LDL cholesterol (DM 2.12 ± 0.91 mmol/l, non-DM 1.8 ± 0.66 mmol/l, p = 0.21), DM patients experienced, compared to non-DM ones, higher progression of mean plaque area (0.47 ± 1.15 mm CONCLUSION: Based on detailed 3D analysis, we found advanced plaque phenotype and further atherosclerosis progression in DM patients despite the same reached levels of LDLc as in non-DM patients. Trial registration ClinicalTrials.gov identifier: NCT01773512.

4 Clinical Trial Reduced thrombin generation and soluble P-selectin after intravenous enoxaparin during PCI. 2011

Kvasnička, J / Horák, J / Zenáhlíková, Z / Kvasnička, Tomáš / Simek, S / Kovárník, T / Malíková, I / Linhart, A / Aschermann, M. ·Center for Thrombosis Research, General Teaching Hospital, Charles University, Karlovo n. 32, Prague, 121 11, Czech Republic. ·Cardiovasc Drugs Ther · Pubmed #21584633.

ABSTRACT: PURPOSE: The objective of our study was to identify changes in the coagulation and serum concentration of soluble P-selectin (sP-sel) after i.v. bolus of 0.75 mg/kg enoxaparin in a group of 33 patients during PCI. METHODS AND RESULTS: As compared to baseline, i.v. enoxaparin increased anti -Xa activity and FIIa inhibition together with APTT and thrombin time tests within 20 min, that persisted for 60 min. At 6 h, the results of all tests had returned to baseline. In contrast, the level of prothrombin fragments (F1 + 2) decreased persistingly for a period of 6 h (baseline 1.19 ± 0.42 nmol/l, after 20 min 1.03 ± 0.46 nmol/l, after 60 min 1.06 ± 0.43 nmol/l, after 6 h 0.95 ± 0.40 nmol/l, p < 0.001 vs. baseline for all values). In addition, i.v. enoxaparin decreased serum sP-sel level (baseline 111.80 ± 37.05 ng/ml, after 20 min 87.80 ± 33.17 ng/ml, after 60 min 86.45 ± 29.15 ng/ml, after 6 h 92.24 ± 31.34 ng/ml, p < 0.001 vs. baseline value for all). sP-sel level mildly correlated with both F Xa inhibition (r = -0.275, p < 0.05) and F1 + 2 level (r = 0.274, p < 0.05). CONCLUSION: Intravenous enoxaparin induced target F Xa inhibition (>0.6 IU/ml) for 60 min in 82% of study patients. During the 6 h of monitoring, a decrease of thrombin generation (F1 + 2) and sP-selectin levels were observed.

5 Article Pathologic Intimal Thickening Plaque Phenotype: Not as Innocent as Previously Thought. A Serial 3D Intravascular Ultrasound Virtual Histology Study. 2017

Kovarnik, Tomas / Chen, Zhi / Wahle, Andreas / Zhang, Ling / Skalicka, Hana / Kral, Ales / Lopez, John J / Horak, Jan / Sonka, Milan / Linhart, Ales. ·2nd Department of Internal Medicine, Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Praha, Czech Republic. Electronic address: tomas.kovarnik@vfn.cz. · Department of Intravascular Imaging, Iowa Institute for Biomedical Imaging, The University of Iowa, Iowa City, United States. · 2nd Department of Internal Medicine, Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Praha, Czech Republic. · Department of Invasive Cardiology, Loyola University, Stritch School of Medicine, Maywood, Illinois, United States. ·Rev Esp Cardiol (Engl Ed) · Pubmed #27615562.

ABSTRACT: INTRODUCTION AND OBJECTIVES: Pathologic intimal thickening (PIT) has been considered a benign plaque phenotype. We report plaque phenotypic changes in a baseline/follow-up intravascular ultrasound-based virtual histology study. METHODS: A total of 61 patients with stable coronary artery disease were analyzed from the HEAVEN trial (89 patients randomized between routine statin therapy vs atorvastatin 80mg and ezetimibe 10mg) with serial intravascular ultrasound imaging of nonculprit vessels. We compared changes in 693 baseline and follow-up 5-mm long segments in a novel risk score, Liverpool Active Plaque Score (LAPS), plaque parameters, and plaque composition. RESULTS: The PIT showed the highest increase of risk score and, with fibrous plaque, also the LAPS. Necrotic core (NC) abutting to the lumen increased in PIT (22 ± 51.7; P = .0001) and in fibrous plaque (17.9 ± 42.6; P = .004) but decreased in thin cap fibroatheroma (TCFA) (⿿15.14 ± 52.2; P = .001). The PIT was the most likely of all nonthin cap fibroatheroma plaque types to transform into TCFA at follow-up (11% of all TCFA found during follow-up and 35.9% of newly-developed TCFA), but showed (together with fibrous plaque) the lowest stability during lipid-lowering therapy (24.7% of PIT remained PIT and 24.5% of fibrous plaque remained fibrous plaque). CONCLUSIONS: Over the 1-year follow-up, PIT was the most dynamic of the plaque phenotypes and was associated with an increase of risk score and LAPS (together with fibrous plaque), NC percentage (together with fibrous plaque) and NC abutting to the lumen, despite a small reduction of plaque volume during lipid-lowering therapy. The PIT was the main source for new TCFA segments.

6 Article Cystatin C Is Associated with the Extent and Characteristics of Coronary Atherosclerosis in Patients with Preserved Renal Function. 2016

Král, A / Kovárník, T / Vaníčková, Z / Skalická, H / Horák, J / Bayerová, K / Chen, Z / Wahle, A / Zhang, L / Kopřiva, K / Benáková, H / Sonka, M / Linhart, A. ·2nd Department of Medicine - Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. · Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine, Charles University and General University Hospital in Prague, Czech Republic. · Iowa Institute for Biomedical Imaging, Department of Electrical & Computer Engineering, The University of Iowa, Iowa City, IA, USA. · Cardiology Department of Homolka Hospital, Prague, Czech Republic. ·Folia Biol (Praha) · Pubmed #28189145.

ABSTRACT: Cystatin C (CysC), an endogenous inhibitor of cysteine proteases and a sensitive and accurate marker of renal function, is associated with the severity of coronary atherosclerosis assessed by angiography and future cardiovascular events according to previous studies. We aimed to evaluate the association between CysC levels and coronary plaque volume, composition and phenotype assessed by intravascular ultrasound and intravascular ultrasound-derived virtual histology in patients with preserved renal function. Forty-four patients with angiographically documented coronary artery disease and complete intravascular imaging were included in the study. Patients were categorized into tertiles by CysC levels. Subjects in the high CysC tertile had significantly higher mean plaque burden (48.0 % ± 6.9 vs. 42.8 % ± 7.4, P = 0.029), lower mean lumen area (8.1 mm2 ± 1.7 vs. 9.9 mm2 ± 3.1, P = 0.044) and a higher number of 5-mm vessel segments with minimum lumen area < 4 mm2 (17.9 ± 18.9 vs. 6.8 ± 11.7, P = 0.021) compared to patients in the lower tertiles. In addition, CysC levels demonstrated significant positive correlation with the mean plaque burden (r = 0.35, P = 0.021). Neither relative, nor absolute plaque components differed significantly according to CysC tertiles. The Liverpool Active Plaque Score was significantly higher in the high CysC tertile patients (0.91 ± 1.0 vs. 0.18 ± 0.92, P = 0.02). In conclusion, our study demonstrated a significant association of increased CysC levels with more advanced coronary artery disease and higher risk plaque phenotype in patients with preserved renal function.

7 Article Non-invasive endothelial function assessment using digital reactive hyperaemia correlates with three-dimensional intravascular ultrasound and virtual histology-derived plaque volume and plaque phenotype. 2016

Kovarnik, Tomas / Jerabek, Stepan / Chen, Zhi / Wahle, Andreas / Zhang, Ling / Dostalova, Gabriela / Skalicka, Hana / Kral, Ales / Horak, Jan / Sonka, Milan / Linhart, Ales. ·2nd Department of Medicine, Department of Cardiovascular Medicine, 1st Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Czech Republic. tomas.kovarnik@vfn.cz. ·Kardiol Pol · Pubmed #27160175.

ABSTRACT: BACKGROUND AND AIM: To study relationships between endothelial dysfunction (ED) and coronary atherosclerosis derived from intravascular ultrasound (IVUS) and virtual histology (VH). METHODS: Endothelial dysfunction was examined by EndoPAT system (Itamar Medical) in 56 patients who underwent IVUS and VH (Volcano corp.). Reactive hyperaemia index (RHI) < 2 was used for definition of ED. IVUS sequences were divided into 5 mm-long non-overlapping and adjacent vessel segments. Plaque phenotype was determined for each frame and 5 mm vessel segment was labeled according to highest frame score (from 0 for "no lesion" to 5 for "thin cap fibroatheroma; TCFA"). RESULTS: IVUS-VH data were collected from 41 patients suitable for three-dimensional analysis. Patients with ED exhibited larger plaque burden than those without ED (0.46 ± 0.08 vs. 0.39 ± 0.07, p = 0.014), smaller lumen area (8.59 ± 2.19 vs. 11.90 ± 3.50, p = 0.016), higher plaque risk score (2.82 ± 1.18 vs. 1.84 ± 0.90, p = 0.012), and higher number of TCFA frames (0.36 ± 0.22 vs. 0.22 ± 0.16, p = 0.038). Relative amounts of fibrous tissue correlated positively with RHI (p = 0.034, r = 0.33). The numbers of fibroatheromas and calcified plaques correlated with RHI inversely (r = -0.34, p = 0.031 and r = -0.32, p = 0.044, respectively). CONCLUSIONS: Endothelial dysfunction correlates with severity and phenotype of coronary lesions and can contribute to non-invasive detection of individuals with higher risk of cardiovascular events.

8 Article Arterial stiffening contributes to impairment of cerebrovascular reactivity in patients with coronary artery disease without carotid stenosis. 2015

Rucka, D / Marek, J / Rucklova, Z / Lubanda, J-C / Havranek, S / Skvaril, J / Varejka, P / Chochola, M / Karetova, D / Korinek, J / Linhart, A. ·Second Department of Internal Medicine - Cardiology and Angiology, General University Hospital, First School of Medicine, Charles University, Prague, Czech Republic. jkorinek@email.cz. ·Physiol Res · Pubmed #25536320.

ABSTRACT: Impaired cerebrovascular reactivity (CVR), an important risk factor for future stroke, is affected by a presence carotid stenosis. However, in some cases CVR can be impaired in the absence of carotid stenosis due to several poorly characterized mechanisms. We hypothesized that arterial stiffening as observed in coronary heart disease (CHD) could be associated with alteration in CVR in CHD patients without carotid stenosis. The study population consisted of patients referred for coronary angiography without significant carotid stenosis (<50 %). CVR was evaluated by breath holding index (BHI) measured with transcranial color code duplex ultrasound. Arterial stiffness was assessed by pulse wave velocity (PWV) measured by the oscillometric method. The extent of coronary atherosclerosis was quantified by Gensini score (GS). Out of 186 subjects, sixty-two patients fulfilled the inclusion and exclusion criteria. BHI decreased with increasing PWV (r = -0.47, p<0.001). Decrease in BHI was significantly inversely associated with GS (r = -0.61, p<0.001). GS was associated with PWV (p<0.001). In conclusion, impaired CVR was associated with increased arterial stiffening in CHD patients in the absence of significant carotid stenosis. Thus, we speculate that increased arterial stiffness may at least partially contribute to the pathophysiology of CVR alteration in coronary artery disease.

9 Article Darapladib for preventing ischemic events in stable coronary heart disease. 2014

Anonymous4340789 / White, Harvey D / Held, Claes / Stewart, Ralph / Tarka, Elizabeth / Brown, Rebekkah / Davies, Richard Y / Budaj, Andrzej / Harrington, Robert A / Steg, P Gabriel / Ardissino, Diego / Armstrong, Paul W / Avezum, Alvaro / Aylward, Philip E / Bryce, Alfonso / Chen, Hong / Chen, Ming-Fong / Corbalan, Ramon / Dalby, Anthony J / Danchin, Nicolas / De Winter, Robbert J / Denchev, Stefan / Diaz, Rafael / Elisaf, Moses / Flather, Marcus D / Goudev, Assen R / Granger, Christopher B / Grinfeld, Liliana / Hochman, Judith S / Husted, Steen / Kim, Hyo-Soo / Koenig, Wolfgang / Linhart, Ales / Lonn, Eva / López-Sendón, José / Manolis, Athanasios J / Mohler, Emile R / Nicolau, José C / Pais, Prem / Parkhomenko, Alexander / Pedersen, Terje R / Pella, Daniel / Ramos-Corrales, Marco A / Ruda, Mikhail / Sereg, Mátyás / Siddique, Saulat / Sinnaeve, Peter / Smith, Peter / Sritara, Piyamitr / Swart, Henk P / Sy, Rody G / Teramoto, Tamio / Tse, Hung-Fat / Watson, David / Weaver, W Douglas / Weiss, Robert / Viigimaa, Margus / Vinereanu, Dragos / Zhu, Junren / Cannon, Christopher P / Wallentin, Lars. · ·N Engl J Med · Pubmed #24678955.

ABSTRACT: BACKGROUND: Elevated lipoprotein-associated phospholipase A2 activity promotes the development of vulnerable atherosclerotic plaques, and elevated plasma levels of this enzyme are associated with an increased risk of coronary events. Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A2. METHODS: In a double-blind trial, we randomly assigned 15,828 patients with stable coronary heart disease to receive either once-daily darapladib (at a dose of 160 mg) or placebo. The primary end point was a composite of cardiovascular death, myocardial infarction, or stroke. Secondary end points included the components of the primary end point as well as major coronary events (death from coronary heart disease, myocardial infarction, or urgent coronary revascularization for myocardial ischemia) and total coronary events (death from coronary heart disease, myocardial infarction, hospitalization for unstable angina, or any coronary revascularization). RESULTS: During a median follow-up period of 3.7 years, the primary end point occurred in 769 of 7924 patients (9.7%) in the darapladib group and 819 of 7904 patients (10.4%) in the placebo group (hazard ratio in the darapladib group, 0.94; 95% confidence interval [CI], 0.85 to 1.03; P=0.20). There were also no significant between-group differences in the rates of the individual components of the primary end point or in all-cause mortality. Darapladib, as compared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95% CI, 0.84 to 0.98; P=0.02). CONCLUSIONS: In patients with stable coronary heart disease, darapladib did not significantly reduce the risk of the primary composite end point of cardiovascular death, myocardial infarction, or stroke. (Funded by GlaxoSmithKline; STABILITY ClinicalTrials.gov number, NCT00799903.).

10 Article The prediction of coronary artery disease based on non-invasive examinations and heme oxygenase 1 polymorphism versus virtual histology. 2013

Kovarnik, Tomas / Kral, Ales / Skalicka, Hana / Mintz, Gary S / Kralik, Lubomir / Chval, Martin / Horak, Jan / Skalicka, Lenka / Sonka, Milan / Wahle, Andreas / Downe, Richard W / Uhrova, Jana / Benakova, Hana / Cernohousova, Lenka / Martasek, Pavel / Belohlavek, Jan / Aschermann, Michael / Linhart, Ales. ·2nd Department of Medicine - Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, II. interni klinika, U nemocnice 2, Prague, 12808 Czech Republic. tomas.kovarnik@vfn.cz ·J Invasive Cardiol · Pubmed #23293173.

ABSTRACT: OBJECTIVE: Prediction of coronary atherosclerosis in patients with stable angina based on non-invasive examinations. METHODS: Pro-inflammatory markers, heme oxygenase-1 (HO-1) polymorphism, lipid levels, Framingham risk score (FRS), and carotid ultrasound were analyzed and compared to grayscale and virtual histology intravascular ultrasound (VH-IVUS). RESULTS: A total of 101 patients were included, and genetic analysis was performed on 81 patients (80.2%). The HO-1 risk polymorphism was more frequent in patients post-myocardial infarction (61.3% vs 32%; P=.0097), or with diabetes (68.4% vs 35.5%; P=.011) or a higher FRS (21.5 vs 15.7; P=.014). Plaques in patients with the HO-1 risk polymorphism contained less fibro-fatty tissue (17.1% vs 23.2%; P=.005) and more necrotic core (NC; 17.1% vs 12.7%; P=.02) and calcification (10.2% vs 5.7%; P=.035) compared to patients without the HO-1 risk polymorphism. Carotid intima media thickness (P=.05) and carotid bulb plaque (P=.008) predicted plaque burden. The level of Apo A inversely correlated with NC (P=.047; r = -0.27) and was lower in patients with VH-thin-cap fibroatheroma (VH-TCFA; 1.19 mmol/L vs 1.3 mmol/L; P=.04). FRS correlated with NC (P=.007; r = 0.2), with angiographic disease severity (P=.032; r = 0.21) and was higher in patients with VH-TCFA (9.1 vs 7.8; P=.03). CONCLUSION: Carotid ultrasound and HO-1 polymorphism improve coronary atherosclerosis prediction.

11 Article Virtual histology evaluation of atherosclerosis regression during atorvastatin and ezetimibe administration: HEAVEN study. 2012

Kovarnik, Tomas / Mintz, Gary S / Skalicka, Hana / Kral, Ales / Horak, Jan / Skulec, Roman / Uhrova, Jana / Martasek, Pavel / Downe, Richard W / Wahle, Andreas / Sonka, Milan / Mrazek, Vratislav / Aschermann, Michael / Linhart, Ales. ·2nd Department of Medicine, First Faculty of Medicine, Charles University in Prague, Prague, Czech Republic. tomas.kovarnik@vfn.cz ·Circ J · Pubmed #22076422.

ABSTRACT: BACKGROUND: There is no study focusing on changes in coronary atherosclerosis during dual lipid-lowering therapy with statin and ezetimibe. METHODS AND RESULTS: Eighty-nine patients with stable angina randomized in a 1:1 ratio to Group A (aggressive therapy: atorvastatin 80mg, ezetimibe 10mg) and Group S (standard therapy) were analyzed. Treatment period was 12 months. Coronary arteries were examined by intravascular ultrasound and virtual histology. We found a decrease in the percent atheroma volume (PAV) (-0.4%) in Group A compared with an increase (+1.4%) in Group S (P=0.014) and this was accompanied by an increased frequency of combined atherosclerosis regression (increased lumen volume+decreased PAV) in group A (40.5%) compared with group S (14.9%) (P=0.007). The target low-density lipoprotein cholesterol level <2mmol/L, presence of at least 4 of 5 atherosclerotic risk factors, and decreased level of vascular cellular adhesive molecule were independent predictors of plaque regression. There were no significant differences in plaque composition between the 2 groups over the study duration. However, during analysis of the 2 groups together, fibrous and fibro-fatty tissues decreased and dense calcification and necrotic core increased during follow-up. CONCLUSIONS: Dual lipid-lowering therapy starts atherosclerosis regression, but does not lead to significant changes in plaque composition. The continuous shift in plaque from fibro and fibro-fatty to necrotic with calcification was present in both groups.

12 Article Genetic variants in haem oxygenase-1 and endothelial nitric oxide synthase influence the extent and evolution of coronary artery atherosclerosis. 2011

Král, A / Kovárník, T / Králík, L / Skalická, H / Horák, J / Mintz, G S / Uhrová, J / Sonka, M / Wahle, A / Downe, R / Aschermann, M / Martásek, P / Linhart, A. ·Second Department of Medicine-Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Prague, Czech Republic. ales.kral@vfn.cz ·Folia Biol (Praha) · Pubmed #22123460.

ABSTRACT: The genetic basis for atherosclerosis development and progression is poorly characterized. We aimed to assess the relationship between endothelial nitric oxide synthase (ENOS) 894 G/T, haem oxygenase-1 (HO1) dinucleotide-length promoter polymorphisms and coronary artery atherosclerotic invol vement and its changes during statin therapy. Coronary angiography, intravascular ultrasound (IVUS), IVUS-derived virtual histology (VH) and genetic polymorphism analysis were performed at study entry. Patients were randomized 1:1 to standard or aggressive hypolipidaemic treatment, and a follow-up evaluation was performed after twelve months. Plaque magnitude was significantly higher in carriers of HO1 risk variants when compared with carriers of the protective variants (< 25 GT repeats). Similarly, the total coronary atherosclerotic burden was significantly greater in HO1 risk variant carriers than in HO1 protective variant carriers. Both parameters did not differ with respect to the ENOS genotype. A higher prevalence of thin-cap fibroatheroma (TCFA) in HO1 risk variant carriers was observed, compared with the HO1 protective variant carriers. The prevalence of TCFA was not influenced by the ENOS genotype. Baseline plaque composition did not differ significantly with respect to both polymorphisms. Significant interactions between plaque composition changes and ENOS and HO1 genotypes were observed during statin treatment. In conclusion, the protective HO1 promoter polymorphism correlates with a lower coronary artery plaque burden, whereas the protective ENOS 894 G/T polymorphism seems to favourably influence changes of coronary artery plaque composition during statin therapy, but has no significant correlation to the magnitude of coronary atherosclerosis.

13 Article Levels of circulating biomarkers at rest and after exercise in coronary artery disease patients. 2010

Danzig, V / Míková, B / Kuchynka, P / Benáková, H / Zima, T / Kittnar, O / Skrha, J / Linhart, A / Kalousová, M. ·Second Department of Medicine, First Faculty of Medicine, General University Hospital, Charles University, Prague, Czech Republic. ·Physiol Res · Pubmed #19681661.

ABSTRACT: As traditional risk factors are unable to fully explain the pathogenesis of coronary artery disease (CAD), novel mechanisms became a target of many investigations. Our aim was to study the response of selected markers to physical exercise. High-sensitive C-reactive protein (hs-CRP), matrix metalloproteinases 2 and 9 (MMP-2, MMP-9), advanced oxidation protein products (AOPP), soluble receptor for advanced glycation end-products (sRAGE), pregnancy-associated plasma protein A (PAPP-A), E-selectin, vascular endothelial growth factor (VEGF) and B-type natriuretic peptide (BNP) levels were measured in serum of 21 CAD patients and in 22 healthy controls at rest and after exercise bicycle stress test performed up to the maximal tolerated effort. At rest, hs-CRP, AOPP, MMP-9 and BNP were significantly elevated in the CAD patients as compared with controls. In contrast, P-selectin was significantly lower in CAD patients and a tendency to lower levels of sRAGE was noted. After exercise MMP-9 and BNP, increased significantly in both groups. In conclusions, CAD patients have elevated hs-CRP, AOPP, MMP-9 and BNP--novel markers related to cardiovascular risk or left ventricular overload. MMP-9 and BNP increase significantly with exercise in both healthy individuals and CAD patients.

14 Article Intravascular ultrasound assessment of coronary artery involvement in Fabry disease. 2008

Kovarnik, T / Mintz, G S / Karetova, D / Horak, J / Bultas, J / Skulec, R / Skalicka, H / Aschermann, M / Elleder, M / Linhart, A. ·Second Department of Internal Medicine, First Faculty of Medicine, Charles University, Prague, Czech Republic. tkovarnik@yahoo.com ·J Inherit Metab Dis · Pubmed #18998239.

ABSTRACT: AIM: We used intravascular ultrasound (IVUS) to characterize coronary artery involvement in patients with Fabry disease (FD). METHODS: Nine FD patients (5 women) were matched to 10 control patients (5 women) chosen from our IVUS database. Standard volumetric IVUS analyses were performed along with assessment of plaque echodensity. RESULTS: Plaques in FD patients were diffuse and hypoechogenic compared with more focal and more echogenic lesions in control patients. Echogenicity of plaques was significantly lower in FD patients (median 30.7 +/- 12.9 vs 55.9 +/- 15.7, p = 0.0052, mean 37.2 +/- 15.6 vs 66.2 +/- 13.3, p = 0.0014). Diffusiveness was assessed as differences between mean and median plaque burden versus the plaque burden in each of the analysed cross-sections. These differences were lower in FD vs controls (5.8 +/- 4.8 vs 8.7 +/- 6.6, p < 0.001 for mean, and 5.8 +/- 4.9 vs 8.8 +/- 7.3, p < 0.001 for median) indicating a more diffuse involvement. The occurrence of lipid cores was significantly higher in FD patients than in controls (2.4 +/- 1.5 vs 1.0 +/- 0.94, p = 0.02). CONCLUSION: IVUS showed diffuse hypoechogenic plaques in patients with FD. The explanation may be higher lipid content in plaques and accumulation of glycosphingolipid in smooth-muscle and endothelial cells.