Search

Introduction: Angiopoietin-2 (Ang-2) is a novel marker of coronary artery disease (CAD) and diabetes (DM). The aim was to evaluate Ang-2 as a potential new biomarker of non-ST elevation myocardial infarction (NSTEMI) in patients with or without type 2 DM (T2DM).Material and methods: This was a multi-center, prospective study that included 138 (males: 91/66%) consecutive patients hospitalized due to NSTEMI, T2DM, or different cardiac disorders. The subjects were divided into four study groups: group A: 28 patients with NSTEMI and T2DM; group B: 47 patients with NSTEMI without T2DM; group C: 31 patients with T2DM, without a history of CAD; group D: 32 patients as a control group. Patients with NSTEMI underwent urgent coronarography. Clinical characteristics including biomarkers (hs-CRP, hsTnT, NT-proBNP, VEGF, HbA1c), SYNTAX SCORE, type of intervention (PCI vs. CABG), and number of implanted stents were taken into account in the analysis.Results: Serum Ang-2 concentrations were significantly higher in patients with NSTEMI (group A: 1769 pg/ml; group B: 1757 pg/ml) and patients with T2DM (group C: 1993 pg/ml) as compared to the patients without CAD and without T2DM (group D: 866.8 pg/ml; p < 0.05). The prognostic accuracy of Ang-2 in NSTEMI diagnosis was determined with the area under the ROC curve (area under curve (AUC) = 0.63).Conclusions: Angiopoietin-2 serum concentration is elevated in the presence of NSTEMI in patients with and without T2DM and does not correspond to the degree of myocardial injury and hemodynamic status. Ang-2 remains elevated also in patients with T2DM without a history of CAD. [ABSTRACT FROM AUTHOR]

Optical coherence tomography (OCT) has opened new horizons for intravascular coronary imaging. It utilizes near-infrared light to provide a microscopic insight into the pathology of coronary arteries in vivo. Optical coherence tomography is also capable of identifying the chemical composition of atherosclerotic plaques and detecting traits of their vulnerability. At present it is the only tool to measure the thickness of the fibrous cap covering the lipid core of the atheroma, and thus it is an exceptional modality to detect plaques that are prone to rupture (thin fibrous cap atheromas). Moreover, it facilitates distinguishing between plaque rupture and plaque erosion as a cause of acute intracoronary thrombosis. Optical coherence tomography is applied to guide angioplasties of coronary lesions and to assess outcomes of percutaneous coronary interventions broadly. It identifies stent malapposition, dissections, and thrombosis with unprecedented precision. Furthermore, OCT helps to monitor vessel healing after stenting. It evaluates the coverage of stent struts by the neointima and detects in-stent neoatherosclerosis. With so much potential, new studies are warranted to determine OCT's clinical impact. The following review presents the technical background, basics of OCT image interpretation, and practical tips for adequate OCT imaging, and outlines its established and potential clinical application. [ABSTRACT FROM AUTHOR]

We investigated the response of insulin-like growth factor (IGFI), insulin-like growth factor binding protein-3 (IGFBP-3) and some hormones, i.e., testosterone (T), growth hormone (GH), cortisol (C), and insulin (I), to maximal exercise in road cyclists with and without diagnosed left ventricular hypertrophy. M- mode and two-dimensional Doppler echocardiography was performed in 30 professional male endurance athletes and a group of 14 healthy untrained subjects using a Hewlett-Packard Image Point HX ultrasound system with standard imaging transducers. Echocardiography and an incremental physical exercise test were performed during the competitive season. Venous blood samples were drawn before and immediately after the maximal cycling exercise test for determination of somatomedin and hormonal concentrations. The basal concentration of IGF-I was statistically higher (p < 0.05) in athletes with left ventricular muscle hypertrophy (LVH) when compared to athletes with a normal upper limit of the left ventricular wall (LVN) (p < 0.05) and to the control group (CG) (p < 0.01). The IGF-I level increased significantly at maximal intensity of incremental exercise in CG (p < 0.01), LVN (p < 0.05) and LVH (p < 0.05) compared to respective values at rest. Long-term endurance training induced an increase in resting (p < 0.01) and post- exercise (p < 0.05) IGF-I/IGFBP-3 ratio in athletes with LVH compared to LVN. The testosterone (T) level was lower in LVH at rest compared to LVN and CG groups (p < 0.05). These results indicate that resting serum IGF-I concentration were higher in trained subjects with LVH compared to athletes without LVH. Serum IGF-I/IGFBP-3 elevation at rest and after exercise might suggest that IGF-I act as a potent stimulant of left ventricular hypertrophy in chronically trained endurance athletes. [ABSTRACT FROM AUTHOR]

Introduction. Cardiac syndrome X (CSX) is defined by typical chest pain, ST segment depression on ECG and normal coronary angiography. Pathology of CSX may involve microvascular dysfunction related to inflammation and abnormal pain sensitivity. Kinins are labile peptides participating in vasodilation, inflammation and pain. Their effects are mediated by two receptors: B1 and B2. The aim of the study was to assess gene expression of kinin receptors in peripheral blood mononuclear cells (PBMC) from patients with CSX. Methods. The study was carried out in 34 patients with cardiac syndrome X, 13 with unstable angina and ten healthy subjects. Total mRNA was extracted from PBMC and the number of mRNA copies was assessed by quantitive reverse transcriptase polymerase chain reaction. Results and Conclusion. The study showed 7-fold higher transcriptional activity of B1R in CSX vs. control and 3.5 higher vs. UA. B2R expression was 2.5-fold higher in CSX group vs. control and UA, while in the letter two groups it was similar. Such disturbance in kinin signaling may participate in local vasoconstriction and may reflect disturbances in kinin signaling leading to nociceptive disturbances in these patients. [ABSTRACT FROM AUTHOR]

Abstract: Aim: To examine the effect of the beta1-selective beta-blocker nebivolol, administered as add-on therapy, on left ventricular function in 260 elderly patients (>65 years) with chronic heart failure (CHF). Methods: The principal inclusion criteria were (1) NYHA class II–IV CHF and (2) a left ventricular ejection fraction (LVEF) ≤35%. The primary end-point was the change in LVEF in response to nebivolol treatment for 8 months. Results: Baseline LVEF values in the two groups were as follows: nebivolol 25.41±7.09% and control 26.41±5.55%. LVEF improved significantly (p=0.027) more in the nebivolol group (6.51±9.15%) than in the control group (3.97±9.20%), the relative improvement (percentage increase in the initial value) being 35.70±57.62% in the nebivolol group and 19.19±40.96% (p=0.008) in the placebo group. Examination of different subgroups did not reveal any heterogeneity in the effects of nebivolol treatment vs. placebo treatment. There were no significant differences between the nebivolol and placebo groups as concerns the changes in clinical status, quality of life, or safety parameters. Conclusion: The findings of the ENECA study confirmed that nebivolol significantly improved cardiac function and proved to be safe and well tolerated in elderly patients with signs of CHF and an impaired LVEF. [Copyright &y& Elsevier]

We aimed to evaluate the clinical course and impact of the SARS-CoV-2 pandemic on the rate of diagnosis and therapy in the complete Polish population of patients (pts) with pulmonary arterial hypertension (PAH-1134) and CTEPH (570 pts) treated within the National Health Fund program and reported in the national BNP-PL database. Updated records of 1704 BNP-PL pts collected between March and December 2020 were analyzed with regard to incidence, clinical course and mortality associated with COVID-19. Clinical characteristics of the infected pts and COVID-19 decedents were analyzed. The rates of new diagnoses and treatment intensification in this period were studied and collated to the proper intervals of the previous year. The incidence of COVID-19 was 3.8% (n = 65) (PAH, 4.1%; CTEPH, 3.2%). COVID-19-related mortality was 28% (18/65 pts). Those who died were substantially older and had a more advanced functional WHO class and more cardiovascular comorbidities (comorbidity score, 4.0 ± 2.1 vs. 2.7 ± 1.8; p = 0.01). During the pandemic, annualized new diagnoses of PH diminished by 25-30% as compared to 2019. A relevant increase in total mortality was also observed among the PH pts (9.7% vs. 5.9% pre-pandemic, p = 0.006), whereas escalation of specific PAH/CTEPH therapies occurred less frequently (14.7% vs. 21.6% pre-pandemic). The COVID-19 pandemic has affected the diagnosis and treatment of PH by decreasing the number of new diagnoses, escalating therapy and enhancing overall mortality. Pulmonary hypertension is a risk factor for worsened course of COVID-19 and elevated mortality.

Introduction: Paravalvular leak (PVL) may complicate cardiac valve replacement surgery. Radical treatment is required if a PVL produces heart failure (HF) symptoms or severe hemolysis. Even though transcatheter PVL closure (TPVLC) has become a valid alternative to reoperation, a number of anatomical conditions may prove technically challenging for transvascular access. We intended to verify the utility of transapical access in such settings., Methods: We report a prospective series of 7 patients with mitral PVLs who underwent transapical TPVLC. The Heart Team made the choice of treatment and Amplatzer Vascular Plug III devices were used off-label as occluders., Results: Transapical TPVLC enabled excellent sealing of mitral PVL in 6 cases. This resulted in HF symptom reduction and decreased NT-proBNP plasma concentration. No procedure-related complications occurred., Conclusions: Transapical access seems to be an efficient and safe alternative for transvascular approach for mitral TPVLC, but further technical development is still needed.

Objectives: To evaluate the transcatheter paravalvular leak closure (TPVLC) aptitude to reduce manifestations of heart failure caused by aortic paravalvular leak (PVL)., Background: TPVLC is a valuable alternative to reoperation. While technical feasibility of the method is well established, data on long-term clinical outcome are less abundant., Methods: We launched a prospective registry of patients with clinically significant aortic PVL. They were scheduled for TPVLC with Amplatzer vascular plug (AVP) II and III devices serving as occluders. The efficacy and safety were monitored at 6-month follow-up exam., Results: The occluder deployment reached a success rate of nearly 90%. Following the procedure, we recorded significant improvement both in terms of patient functional capacity and echocardiographic determinants of left ventricular performance. Simultaneously, NT-proBNP plasma concentration and hemolysis markers decreased. Only local complications related to puncture site occurred., Conclusions: Heart failure caused by aortic PVL can be safely and efficiently treated with TPVLC using AVP II and III devices as occluders.

The objective of the study was to investigate whether a blood pressure increase during static exercises might affect the left ventricular function and whether a possible pressure overload might decrease cardio-respiratory adaptation to aerobic exercise in power lifting athletes. Nine resistance-trained athletes and ten age-matched untrained men participated in high intensity isometric exercise performed during the Valsalva maneuver and in an incremental arm cranking test. All subjects underwent echocardiographic evaluation. The combine effect of exercise and increased intrathoracic pressure due to the Valsalva maneuver was a significant increase in systolic blood pressure in the athletes compared with controls. Echocardiography demonstrated significant differences in left ventricular mass and left ventricular mass index; both being higher in the athletes than in controls. The intraventricular septum diameter and left ventricular posterior wall thickness were significantly greater and the myocardial performance index was lower in the athletes compared with controls, indicating a better left ventricular function in the athletes. A cumulative effect of mechanical compression of peripheral blood vessels by contracting muscles and intrathoracic pressure increase during the Valsalva maneuver did not compromise myocardial contractility and cardiorespiratory adaptation to incremental arm exercise in power lifting athletes.

Background and Aim of the Study: Severe aortic stenosis (AS) with preserved systolic function may coexist with 'low flow' and a lower stroke volume (SV). As the mechanisms of this phenomenon are not fully understood, the study aim was to assess the cardiac and vascular mechanisms of 'low-flow' severe AS with a preserved left ventricular ejection fraction (LVEF)., Methods: Forty-four consecutive patients (mean age 69.7 +/- 7.6 years) with severe degenerative AS [mean effective orifice area (EOA) 0.7 +/- 0.3 cm2] and preserved LVEF (> 50%) were enrolled into the study, and allocated to two groups depending on their stroke volume index (SVI) (< 35 and > or = 35 ml/m2, respectively). The clinical data, N-terminal pro-brain natriuretic peptide (NT-proBNP) serum levels and ultrasound assessment of LV geometry and function [stroke work (SW), relative wall thickness (RWT)], AS severity, indices of systemic arterial hemodynamics [systemic arterial compliance (SAC), systemic vascular resistance (SVR)] and remodeling [flow-mediated dilatation (FMD), pulse wave velocity (PWV)], as well as valvuloarterial impedance (Z(va)) were analyzed for all study patients., Results: Twenty-four patients (56%; 13 females, 11 males) had low-flow LV output, and 20 (44%; four females, 16 males) had a normal LV output. The mean NT-proBNP serum levels were comparable between the study groups. An analysis of LV remodeling and function revealed a lower LV end-diastolic volume (LVEDV; 85.5 +/- 24.1 versus 160.4 +/- 60.9 ml, p = 0.001), LV end-systolic volume (LVESV; 40.3 +/- 18.5 versus 66.8 +/- 44.2 ml, p = 0.03), LV mass index (LVMI; 150.1 +/- 53.4 versus 183.7 +/- 57.5 g/m2, p = 0.07) and SW (95.6 +/- 23.7 versus 183.2 +/- 50.6 mmHg x ml, p < 0.0001) in the group with SVI < 35 ml/m2. The average RWT was higher in the group with SVI < 35 ml/m2 (48.7 +/- 14.8 versus 40.0 +/- 7.5, p = 0.04). The indices of systemic arterial hemodynamics were significantly different between the groups: the SAC was lower, and the SVR and Z(va) were higher, in patients with SVI < 35 ml/m2 while FMD values were significantly greater in patients with SVI < 35 ml/m2 (11.85 +/- 6.4 versus 7.29 +/- 6.3%, p = 0.035). However, the brachial artery diameter (BAd) was smaller in the latter group, and no differences were found in the FMD x BAd index values. The PWV values were comparable in both study groups., Conclusion: The low-flow phenomenon in severe AS with preserved LVEF is related to smaller LV dimensions, LV concentric hypertrophy, and an increased systemic arterial afterload without differences in plasma NT-proBNP levels. 'Paradoxically' higher values of FMD observed in this population may be associated with a higher proportion of females and a smaller BAd.

Objectives: Arterial hypertension and its complications are associated with an increased morbidity and mortality in patients after aortic coarctation (CoA) repair. It is debatable whether early surgery can prevent it. Residual stenosis of descending aorta (AoD) and stiffness in the precoarctation region supposedly lead to hypertension. The aim of this study was to evaluate aortic pulse-wave parameters in adult patients after CoA repair and to determine the influence of residual stenosis and age at operation on their values., Methods: Eighty-five patients underwent CoA repair (53 males; aged 34.6±10.3 years, age at operation: 10.9±8.2 years). The control group consisted of 30 individuals (18 males; aged 33.6±8.2 years). Augmentation pressure (AP), augmentation index (AI), aortic pulse pressure (APP), and pulse-wave velocity (PWV) were measured with applanation tonometry method., Results: Normotensive patients after CoA repair (47/55%) had higher values of AP (7.3±4.6 vs. 4.4±3.6 mmHg; P=0.002), AI (18.6±10.4 vs. 13.5±4.3%; P=0.03), APP (39.6±8.8 vs. 35.1±9.8; P=0.00001), and PWV (6.8±1.2 vs. 5.4±0.9 m/s; P=0.003) than controls. Forty-six patients presented signs of recoarctation. No significant differences in the systolic blood pressure and diastolic blood pressure, AI and PWV were found between AoD(+) and AoD(-) but AoD(+) had significantly higher APP (46.7±13.8 vs. 38.3±6.9; P=0.001) and AP (10.5±6.9 vs. 7.5±4.1; P=0.02). Significant correlations were found between current age and APP, AP, and AI. No significant correlations were found between central parameters and the age at operation., Conclusion: Normotensive patients after CoA repair have elevated central parameters, related to the residual AoD gradient, regardless of the age at operation. Even early repair cannot prevent progressive vascular impairment in CoA.

Introduction: Cardiac syndrome X (CSX) is characterized by anginal pain with ECG suggestive of ischaemia and normal coronary arteries at angiography. Pathology of CSX involves microvascular dysfunction and is possibly linked with metabolic syndrome. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an enzyme involved in glycolysis. The GAPDH gene is a "housekeeping" gene and is used for normalization in quantitative gene expression assays. The aim of the study was to evaluate GAPDH gene expression in CSX., Material and Methods: The study was performed in 35 CSX patients and 10 control subjects. mRNA was extracted from peripheral blood mononuclears and the mRNA was assessed by QRT-PCR., Results: GAPDH gene expression was enhanced in CSX patients vs. controls (93022 ±23837 copies/μg vs. 1067 ±240 copies/μg respectively; p < 0.001). Moreover, transcriptional activity of the GAPDH gene was heterogeneous within the CSX group., Conclusions: GAPDH gene expression is markedly enhanced in CSX, which reflects carbohydrate metabolism disturbances and makes the GAPDH gene unsuitable as an endogenous control in patients with CSX.