Acute Coronary Syndrome Presenting during On- and Off-Hours: Is There a Difference in a Tertiary Cardiovascular Center?

Background and Objectives: ACS presents an acute manifestation of coronary artery disease and its treatment is based on timely interventional diagnostics and PCI. It has been known that the treatment and the outcomes are not the same for all the patients with ACS during the working day, depending on the availability of the procedures and staff. The aim of the study was to explore the differences in clinical characteristics and outcomes in patients admitted for ACS during on- and off-hours. Materials and Methods: The retrospective study included 1873 consecutive ACS patients admitted to a tertiary, university hospital that underwent coronary angiography and intervention. On-hours were defined from Monday to Friday from 07:30 h to 14:30 h, while the rest was considered off-hours. Results: There were more males in the off-hours group (on-hours 475 (56%) vs. off-hours 635 (62%); p = 0.011), while previous MI was more frequent in the on-hours group (on 250 (30%) vs. off 148 (14%); p < 0.001). NSTEMI was more frequent during on-hours (on 164 (19%) vs. off 55 (5%); p < 0.001), while STEMI was more frequent during off-hours (on 585 (69%) vs. off 952 (93%); p < 0.001). Patients admitted during on-hours had more multivessel disease (MVD) (on 485 (57%) vs. off 489 (48%); p = 0.006), as well as multivessel PCI (on 187 (22%) vs. off 171 (16%); p = 0.002), while radial access was preferred in off-hours patients (on 692 (82%) vs. off 883 (86%); p = 0.004). Left main PCI was performed with similar frequency in both groups (on 37 (4%) vs. off 35 (3%); p = 0.203). Death occurred with similar frequency in both groups (on 17 (2.0%) vs. off 26 (2.54%); p = 0.404), while major adverse cardio-cerebral events (MACCEs) were more frequent in the on-hours group (on 105 (12.4%) vs. off 70 (6.8%); p = 0.039) probably due to the more frequent repeated PCI (on 49 (5.8%) vs. off 27 (2.6%); p = 0.035). Conclusions: Patients admitted for ACS during working hours in a tertiary hospital present with more complex CAD, have more demanding interventions, and experience more MACCEs during follow-up mostly due to myocardial infarctions and repeated procedures.

Early Selective C-Reactive Protein Apheresis in a Patient with Acute ST Segment Elevation Myocardial Reinfarction.

The patient was admitted for urgent coronary angiography following an acute anterior ST segment elevation myocardial reinfarction (STEMI) caused by acute stent thrombosis. A stent had been implanted 10 days prior to the reinfarction for an acute anterior STEMI. However, the patient had stopped taking ticagrelor post-discharge. Primary percutaneous coronary intervention of the left anterior descending artery was performed. Subsequently, due to a high C-reactive protein (CRP) level, 3 CRP apheresis sessions were performed, with the first session starting 12 h after the onset of symptoms. A significant drop in CRP was noted after each apheresis. The post-procedural course was uneventful.

Cloning and expression profiling of muscle regulator ANKRD2 in domestic chicken Gallus gallus.

Striated muscle signaling protein and transcriptional regulator ANKRD2 participates in myogenesis, myogenic differentiation, muscle adaptation and stress response. It is preferentially expressed in slow, oxidative fibers of mammalian skeletal muscle. In this study, we report on characterization of chicken ANKRD2. The chicken ANKRD2 coding region contains 1002 bp and encodes a 334-amino acid protein which shares approximately 58% identity with human and mouse orthologs, mostly in the conserved region of ankyrin repeats. Comprehensive analysis of the ANKRD2 gene and protein expression in adult chicken demonstrated its predominant expression in red muscles of thigh and drumstick, compared to white muscle. It was not detected in heart and white pectoral muscle. Uneven expression of ANKRD2 in chicken skeletal muscles, observed by immunohistochemistry, was attributed to its selective expression in slow, oxidative, type I and fast, oxidative-glycolytic, type IIA myofibers. Association of chicken ANKRD2 with phenotypic differences between red and white muscles points to its potential role in the process of myofiber-type specification. In addition to expression in slow oxidative myofibers, as demonstrated for mammalian protein, chicken ANKRD2 was also detected in fast fibers with mixed oxidative and glycolytic metabolism. This finding suggests that ANKRD2 is responsive to metabolic differences between types of avian myofibers and orientates future studies towards investigation of its role in molecular mechanisms of myofiber-type-specific gene expression.

Differential expression and localization of Ankrd2 isoforms in human skeletal and cardiac muscles.

Four human Ankrd2 transcripts, reported in the Ensembl database, code for distinct protein isoforms (360, 333, 327 and 300 aa), and so far, their existence, specific expression and localization patterns have not been studied in detail. Ankrd2 is preferentially expressed in the slow fibers of skeletal muscle. It is found in both the nuclei and the cytoplasm of skeletal muscle cells, and its localization is prone to change during differentiation and upon stress. Ankrd2 has also been detected in the heart, in ventricular cardiomyocytes and in the intercalated disks (ICDs). The main objective of this study was to distinguish between the Ankrd2 isoforms and to determine the contribution of each one to the general profile of Ankrd2 expression in striated muscles. We demonstrated that the known expression and localization pattern of Ankrd2 in striated muscle can be attributed to the isoform of 333 aa which is dominant in both tissues, while the designated cardiac and canonical isoform of 360 aa was less expressed in both tissues. The 360 aa isoform has a distinct nuclear localization in human skeletal muscle, as well as in primary myoblasts and myotubes. In contrast to the isoform of 333 aa, it was not preferentially expressed in slow fibers and not localized to the ICDs of human cardiomyocytes. Regulation of the expression of both isoforms is achieved at the transcriptional level. Our results set the stage for investigation of the specific functions and interactions of the Ankrd2 isoforms in healthy and diseased human striated muscles.

Neutrophil elastase gene polymorphisms: modulators of response to therapy in childhood bronchiectasis?

BACKGROUND: The aim of this study was to investigate polymorphisms in the promoter region of the neutrophil elastase (ELANE) gene as potential modulators of the therapeutic response in children with idiopathic bronchiectasis. METHODS: The study included 48 children between 5 and 17 years old who were diagnosed with idiopathic bronchiectasis based on high-resolution computed tomography of the thorax. In all patients therapy included administration of antibiotics, anti-inflammatory drugs, expectorants, and postural drainage. Response to therapy was evaluated by the change in FeNO levels before and after administration of therapy. The ELANE promoter region polymorphisms were analyzed by PCR-direct DNA sequencing. RESULTS: According to the predicted activity of ELANE genotypes, subjects were divided into two groups: low/intermediate activity (n = 18) and high activity (n = 30). Subjects in the group with high-activity genotype had higher initial FeNO levels and this difference was statistically significant (t = 2.906; p = 0.006). The difference between FeNO levels before and after therapy was also statistically significantly higher in children with high-activity genotype (t = 3.329; p = 0.002). Statistically significant correlation was observed between the change in FeNO levels and ELANE genotypes (r = 0.350; p = 0.015). CONCLUSION: Children with high-activity genotype had higher initial FeNO levels and showed better response to therapy than children with low/intermediate-activity genotypes.

The imPAct of Trimetazidine on MicrOcirculation after Stenting for stable coronary artery disease (PATMOS study).

Background: Myocardial ischemia is caused by epicardial coronary artery stenosis or atherosclerotic disease affecting microcirculation. Trimetazidine (TMZ), promotes glucose oxidation which optimizes cellular energy processes in ischemic conditions. Small studies demonstrated protective effects of TMZ in terms of reducing myocardial injury after percutaneous coronary intervention (PCI), its effect on microcirculation using contemporary investigative methods has not been studied. The aim of the study was to examine effects of trimetazidine, given before elective PCI, on microcirculation using invasively measured index of microcirculatory resistance (IMR). Methods: This was prospective, single blinded, randomized study performed in a single university hospital. It included consecutive patients with an indication for PCI of a single, de novo, native coronary artery lesion. Patients were randomly assigned to receive either TMZ plus standard therapy (TMZ group) or just standard therapy. Coronary physiology indices fractional flow reserve (FFR), coronary flow reserve (CFR) and index of microcirculatory resistance (IMR) were measured before and after PCI using coronary pressure wire. Results: We randomized 71 patients with similar clinical characteristics and risk profile, previous medications and coronary angiograms. Patientshad similar values of Pd/Pa, FFR and CFR prior to PCI procedure. After PCI, FFR values were higher in TMZ group, while IMR values were lower in this group respectively (FFR TMZ + 0.89 ± 0.05 vs. TMZ - 0.85 ± 0.06, p = 0.007; CFR TMZ + 2.1 ± 0.8 vs. TMZ- 2.3 ± 1.3, p = 0.469; IMR TMZ + 18 ± 9 vs. TMZ- 24 ± 12, p = 0.028). In two-way repeated measures ANOVA PCI was associated with change in FFR values (TMZ p = 0.050; PCI p < 0.001; p for interaction 0.577) and TMZ with change in IMR values (TMZ p = 0.034, PCI p = 0.129, p for interaction 0.344). Conclusion: Adding trimetazidine on top of medical treatment prior to elective PCI reduces microvascular dysfunction by lowering postprocedural IMR values when compared to standard therapy alone.

Antitumor activity of natural pigment violacein against osteosarcoma and rhabdomyosarcoma cell lines.

PURPOSE: Sarcomas are rare and heterogenic tumors with unclear etiology. They develop in bone and connective tissue, mainly in pediatric patients. To increase efficacy of current therapeutic options, natural products showing selective toxicity to tumor cells are extensively investigated. Here, we evaluated antitumor activity of bacterial pigment violacein in osteosarcoma (OS) and rhabdomyosarcoma (RMS) cell lines. METHODS: The toxicity of violacein was assessed in vitro and in vivo, using MTT assay and FET test. The effect of violacein on cell migration was monitored by wound healing assay, cell death by flow cytometry, uptake of violacein by fluorescence microscopy, generation of reactive oxygen species (ROS) by DCFH-DA assay and lipid peroxidation by TBARS assay. RESULTS: Violacein IC50 values for OS and RMS cells were in a range from 0.35 to 0.88 µM. Its selectivity toward malignant phenotype was confirmed on non-cancer V79-4 cells, and it was safe in vivo, for zebrafish embryos in doses up to 1 µM. Violacein induced apoptosis and affected the migratory potential of OS and RMS cells. It was found on the surfaces of tested cells. Regarding the mechanism of action, violacein acted on OS and RMS cells independently of oxidative signaling, as judged by no increase in intracellular ROS generation and no lipid peroxidation. CONCLUSION: Our study provided further evidence that reinforces the potential of violacein as an anticancer agent and candidate to consider for improvement of the effectiveness of traditional OS and RMS therapies.

Feasibility of semi-quantitative assessment of left ventricular contractile reserve in dilated cardiomyopathy.

BACKGROUND: We and others have shown previously that left ventricular (LV) contractile reserve assessed quantitatively by high-dose dobutamine stress-echocardiography (DSE) has prognostic implications in patients with dilated cardiomyopathy. PURPOSE: To assess the feasibility of semi-quantitative assessment of LV contractile reserve by differently skilled operators in patients with dilated cardiomyopathy. METHODS: High-dose DSE was performed in 63 consecutive patients, mean age 50 ± 10 years and ejection fraction (EF) 19 ± 8%. LVEF was calculated 1) using Simpson's biplane formula, and 2) semi-quantitatively (5% increments) by novice and experienced echocardiographers, and by a DSE expert. Patients were considered to have preserved LV contractile reserve if LVEF dobutamine-induced change was ≥5%. RESULTS: Twenty-seven (45.8%) patients died during the 5-year follow-up. The feasibility of the assessment was 89%, 94%, and 98% for novice and experienced readers and DSE expert, respectively. Kaplan-Meier analysis showed that LV contractile reserve assessed semi-quantitatively by DSE expert and experienced reader achieved the best prognostic separation (log rank 19.63 and 18.99, respectively, p < 0.001 for both), followed by quantitative assessment (log rank 9.76, p = 0.0018) and assessment by novice reader (log rank 8.76, p = 0.012). Areas under the curves were similar for quantitative and semi-quantitative assessment of LV contractile reserve. CONCLUSIONS: Our data indicate that semi-quantitative assessment of LV contractile reserve is feasible by differently skilled operators.

The stress responsive gene ankrd1a is dynamically regulated during skeletal muscle development and upregulated following cardiac injury in border zone cardiomyocytes in adult zebrafish.

Ankyrin repeat domain 1 (ANKRD1) is a functionally pleiotropic protein found in the nuclei and sarcomeres of cardiac and skeletal muscles, with a proposed role in linking myofibrilar stress and transcriptional regulation. Rapid upregulation of its expression in response to both physiological and pathological stress supports the involvement of ANKRD1 in muscle tissue adaptation and remodeling. However, the exact role of ANKRD1 remains poorly understood. To begin to investigate its function at higher resolution, we have generated and characterized a TgBAC(ankrd1a:EGFP) zebrafish line. This reporter line displays transgene expression in slow skeletal muscle fibers during development and exercise responsiveness in adult cardiac muscle. To better understand the role of Ankrd1a in pathological conditions in adult zebrafish, we assessed ankrd1a expression after cardiac ventricle cryoinjury and observed localized upregulation in cardiomyocytes in the border zone. We show that this expression in injured hearts is recapitulated by the TgBAC(ankrd1a:EGFP) reporter. Our results identify novel expression domains of ankrd1a and suggest an important role for Ankrd1a in the early stress response and regeneration of cardiac tissue. This new reporter line will help decipher the role of Ankrd1a in striated muscle stress response, including after cardiac injury.

Repair of hammock mitral valve with hypoplastic posterior leaflet in an adult.

BACKGROUND AND AIM OF THE STUDY: Congenital hammock mitral valves are rarely discovered in adulthood. The case is presented of a 29-year-old woman in NYHA functional class III and with markedly depressed left ventricular (LV) function, who underwent surgery for severe mitral regurgitation. METHODS AND RESULTS: Preoperative transthoracic echocardiography showed grade 3+/4 mitral regurgitation due to restricted leaflet motion, and an almost immobile posterior leaflet due to the attachment of fibrotic chordae high on the posterior LV wall. At surgery, limited motion of both leaflets and partial agenesis of the posterior leaflet were found. The valve was repaired by resecting the posterior leaflet defect, mobilizing the papillary muscle, and then widening the posterior leaflet. Postoperative echocardiography revealed no further mitral regurgitation, and the valve remained competent despite a postoperative episode of cardiac decompensation. CONCLUSION: Hammock mitral valve repair is a highly challenging procedure, particularly in patients presenting with LV dilatation. The greatest degree of leaflet mobility must be restored in order to prevent tethering. Thus, it is strongly recommended that the posterior leaflet is systematically widened, even in the presence of an apparently large leaflet surface.

Comparison of valve annuloplasty and replacement for ischemic mitral valve incompetence.

OBJECTIVE: Mitral incompetence is a chronic sequela of myocardial infarction. It is caused by apical displacement and tethering of the mitral valve leaflets after myocardial infarction, resulting in incomplete coaptation. The consensus is for mitral valve surgery in the presence of significant ischemic mitral regurgitation (IMR). Previously, the only option was mitral valve replacement (MVR) with a mechanical or tissue valve. The suboptimal results obtained prompted the development of several methods of mitral valve repair. Today, the most commonly used repair is undersized annuloplasty. METHODS: We conducted a retrospective nonrandomized study of all patients who underwent operation for coronary artery disease and IMR between 2000 and 2006. The surgeon chose the surgical method used for the mitral valve procedure. The most commonly used procedures were restrictive mitral valve annuloplasty (MVP) and MVR with a mechanical prosthesis. We collected all pertinent preoperative, intraoperative, and early-postoperative data. We followed up with phone interviews of the patients and their relatives and with complete clinical and echocardiography examinations. RESULTS: We carried out operations on 138 patients during the study period (MVR, 52 patients; MVP, 86 patients). The 2 groups had comparable demographic data and risk factors. The 2 groups were significantly different with respect to mean (+/-SD) New York Heart Association (NYHA) class (MVP, 2.72 +/- 0.62; MVR, 2.48 +/- 0.70; P < .01) and ejection fraction (MVP, 29.01% +/- 11.00%; MVR, 35.87% +/- 11.00%; P

Characterization of zebrafish (Danio rerio) muscle ankyrin repeat proteins reveals their conserved response to endurance exercise.

Muscle proteins with ankyrin repeats (MARPs) ANKRD1 and ANKRD2 are titin-associated proteins with a putative role as transcriptional co-regulators in striated muscle, involved in the cellular response to mechanical, oxidative and metabolic stress. Since many aspects of the biology of MARPs, particularly exact mechanisms of their action, in striated muscle are still elusive, research in this field will benefit from novel animal model system. Here we investigated the MARPs found in zebrafish for protein structure, evolutionary conservation, spatiotemporal expression profiles and response to increased muscle activity. Ankrd1 and Ankrd2 show overall moderate conservation at the protein level, more pronounced in the region of ankyrin repeats, motifs indispensable for their function. The two zebrafish genes, ankrd1a and ankrd1b, counterparts of mammalian ANKRD1/Ankrd1, have different expression profiles during first seven days of development. Mild increase of ankrd1a transcript levels was detected at 72 hpf (1.74±0.24 fold increase relative to 24 hpf time point), while ankrd1b expression was markedly upregulated from 24 hpf onward and peaked at 72 hpf (92.18±36.95 fold increase relative to 24 hpf time point). Spatially, they exhibited non-overlapping expression patterns during skeletal muscle development in trunk (ankrd1a) and tail (ankrd1b) somites. Expression of ankrd2 was barely detectable. Zebrafish MARPs, expressed at a relatively low level in adult striated muscle, were found to be responsive to endurance exercise training consisting of two bouts of 3 hours of forced swimming daily, for five consecutive days. Three hours after the last exercise bout, ankrd1a expression increased in cardiac muscle (6.19±5.05 fold change), while ankrd1b and ankrd2 were upregulated in skeletal muscle (1.97±1.05 and 1.84±0.58 fold change, respectively). This study provides the foundation to establish zebrafish as a novel in vivo model for further investigation of MARPs function in striated muscle.

Stomatin-like protein 2 overexpression in papillary thyroid carcinoma is significantly associated with high-risk clinicopathological parameters and BRAFV600E mutation.

Stomatin-like protein 2 (SLP-2), a member of the stomatin protein family, has emerged as a potential molecular hallmark of tumor progression in several human malignancies. The aim of this study was to analyze SLP-2 expression pattern in benign and malignant thyroid tumors (n = 210) and to examine its relationship with clinicopathological parameters and BRAFV600E mutation in thyroid cancer. SLP-2 immunohistochemical expression was not detected in benign adenomas and was absent/weak in follicular and anaplastic carcinomas. High expression levels of SLP-2, found only in papillary thyroid carcinoma (PTC), particularly in the classical variant, were significantly associated with adverse clinicopathological parameters: lymph node metastasis (p = 0.002), extrathyroid invasion (p < 0.001), pT status (p < 0.001), and advanced tumor stage (p = 0.001). Additional genotyping of PTC cases for the BRAFV600E mutation revealed for the first time a close relation between SLP-2 overexpression and the presence of BRAF mutation (p = 0.02) with high positive rates of lymph node metastasis (70%) and extrathyroid invasion (80%) in these cases. The significant association of SLP-2 overexpression with unfavorable clinicopathological characteristics and BRAFV600E mutation indicates that SLP-2 may have a role in aggressiveness of BRAF-mutated PTC and that SLP-2 evaluation could be clinically useful in identification of high-risk PTC patients.

Effect of Elective Bentall Procedure on Left Ventricular Systolic Function and Functional Status: Long-Term Follow-Up in 90 patients.

Because there are so few data on the long-term effects on left ventricular systolic function and functional status in patients who electively undergo Bentall procedures, we established a retrospective study group of 90 consecutive patients. This group consisted of 71 male and 19 female patients (mean age, 54 ± 10 yr) who had undergone the Bentall procedure to correct aortic valve disease and aneurysm of the ascending aorta, from 1997 through 2003 in a single tertiary-care center. We monitored these patients for a mean period of 117 ± 41 months for death, left ventricular ejection fraction and volume indices, and functional capacity as determined by New York Heart Association (NYHA) class. There were no operative deaths. The survival rate was 73.3% during follow-up. There were 10 cardiac and 13 noncardiac deaths, and 1 death of unknown cause. Echocardiography was performed before the index procedure and again after 117 ± 41 months. In surviving patients, statistically significant improvement in left ventricular ejection fraction, in comparison with preoperative values (0.49 ± 0.11 vs 0.41 ± 0.11; P <0.0001), was noted at follow-up. Similarly, we observed statistically significant reductions in left ventricular end-systolic (39.24 ± 28.7 vs 48.77 ± 28.62 mL/m(2)) and end-diastolic volumes (54.63 ± 6.97 vs 59.17 ± 8.92 mL/m(2); both P <0.0001). Most patients (53/66 [80.3%]) progressed from a higher to a lower NYHA class during the follow-up period. The Bentall procedure significantly improved long-term left ventricular systolic function and functional status in surviving patients who underwent operation on a nonemergency basis.

Simultaneous hybrid carotid stenting and coronary bypass surgery versus concomitant open carotid and coronary bypass surgery: a pilot, feasibility study.

OBJECTIVES: Concomitant carotid and cardiac surgery carries an increased perioperative morbidity and mortality risk. Whether the hybrid procedure of carotid artery stenting (CAS) and coronary bypass surgery decreases the risk of stroke and other complications is still unknown. The aim of this study was to assess early outcomes after simultaneous hybrid CAS and coronary bypass grafting versus open concomitant carotid and coronary bypass surgery. METHODS: We included 20 patients in this study. According to the protocol, all the patients were divided into two groups: Group 1 (10 patients) with hybrid CAS and coronary bypass surgery and Group 2 (10 patients) with concomitant carotid and coronary surgery. Different preoperative, intraoperative and postoperative variables were compared. The primary end point was combined incidence of stroke and death 30 days after surgery or during initial hospitalization. The secondary end points were myocardial infarction, atrial fibrillation, blood loss and need for blood transfusion and duration of intensive care unit and hospital stay. RESULTS: Groups 1 and 2 were similar in preoperative characteristics including age (65.3 ± 6.8 vs 70.7 ± 7.0, P = 0.191) New York Heart Association class (2.3 ± 0.5 vs 1.8 ± 0.7, P = 0.218), EuroSCORE (2.8 ± 2.0 vs 3.6 ± 2.3, P = 0.547), the degree of carotid stenosis (79 ± 12 vs 87 ± 13%, P = 0.224) and average left ventricular ejection fraction (44.3 ± 12.4 vs 43.4 ± 13.3%, P = 0.896). Also, the groups did not differ in intraoperative variables with an exception of extracorporeal circulation time (65.7 ± 14.1 vs 90.0 + 17.4 min, P = 0.023), which was significantly shorter in Group 1. Although rare, and without significant difference, primary end point occurred only in Group 2 (1 stroke and 1 death, 20%). There was no difference in the duration of mechanical ventilation, need for transfusion and duration of intensive care unit and hospital stay between the two groups. CONCLUSIONS: Although limited by a small sample size, our results show that the hybrid procedure of carotid stenting and coronary surgery might be a good therapeutic option but further extended studies are needed to assess its real value.

[Moderate ischemic mitral regurgitation: to operate or to ignore?].

INTRODUCTION: Moderate ischemic mitral regurgitation (MR) is characterized by significant, symptomatic multivessel coronary disease and mitral regurgitation 2-3+. CASE OUTLINE: A 60-year-old patient was admitted at the Cardiovascular Institute "Dedinje" due to the symptoms of unstable angina pectoris. He survived a myocardial infarction (inferoposterolateral localization) 8 years ago. On admission echocardiogram revealed regional disturbances of the left ventricle wall with ejection fraction of 25% and mitral regurgitation 2+. The patient underwent a triple coronary bypass with surgical correction of mitral regurgitation. Postoperative course was normal. CONCLUSION: Several authors are against surgical correction of MR in moderate ischemic MR due to several reasons: revascularization of ischemic areas will improve regional wall motion and correct MR, while mitral valve surgery adds significantly to the operative risk of coronary surgery. Other authors, however, favour combined operation emphasizing that in many patients coronary surgery alone will not correct a moderate ischemic MR. Today there is no consensus whether to operate the moderate ischemic MR or to ignore it. Some novel studies underscore significant predictors of a long-term survival of these patients: NYHA (New York Heart Association) class and left ventricle ejection fraction. In that respect a combined operation should be recommended in patients with heart failure and NYHA class III and IV.

Mitral stenosis in patient undergoing vascular surgery: prediction of perioperative hemodynamics by dobutamine stress-echocardiography.

Patient was admitted for endarterectomy of the left internal carotid artery. Echocardiography showed mitral stenosis with mitral valve area of 1.4 cm2. Since the patient's functional capacity could not be determined due to left-sided hemiplegia, it was decided to perform high-dose dobutamine stress-echocardiography in order to assess the patient's hemodynamics during stress. Gradients over mitral valve increased from 32/10 mmHg at baseline to 43/16 mmHg at 40 mcg/kg/min dobutamine infusion. Preoperative and 24 hour perioperative hemodynamic variables were monitored by Swan-Ganz catheter, and their values did not change significantly as compared to baseline. Postoperative course was uneventful, and the patient was discharged on the fifth postoperative day.