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Background Mortality in cyanotic patients with congenital heart diseases (CHD) is high, mainly due to cardiovascular complications. It is known that endothelial dysfunction, increased arterial stiffness, and impaired vascular function have negative influence on cardiovascular prognosis. The aim of the study was to assess parameters of arterial stiffness and vascular dysfunction in cyanotic patients with CHD as well as their potential relation to impaired blood oxygen saturation and polycythemia parameters typical for cyanosis. Methods A total of 36 CHD cyanotic patients (17 males) (42.3 ± 16.3 years) and 35 healthy individuals (16 males) (39.6 ± 10.4 years) were enrolled. Assessed parameters were intima media thickness and flow-mediated dilatation (FMD). Assessed parameters using applanation tonometry methods were aortic systolic pressure, aortic pulse pressure (AoPP), augmentation pressure (AP), augmentation index (AI), pulse pressure amplification (PPampl), and pulse wave velocity (PWV). Results AoPP (37.3 ± 11.1 mmHg vs. 29 ± 6.5 mmHg; p = 0.002), AP (10.1 ± 7.3 mmHg vs. 1.1 ± 3.9 mmHg; p = 0.00001), AI (24.7 ± 13.5% vs. 3.0 ± 13.6%; p = 0.00001), and PWV (7.4 ± 2.1 m/s vs. 6.3 ± 0.7 m/s; p = 0.003) were higher, and PPampl was lower (135.3 ± 16.1% vs. 160.4 ± 12.8%; p = 0.00001) in the studied group compared to controls and proved the presence of the increased stiffness of arteries. Impairment of FMD was observed (9.0 ± 5.6 vs. 10.9 ± 4.7; p = 0.04). No significant correlations were found between analyzed arterial parameters and biochemical ones characterizing cyanotic patients depicting rheological properties of blood. Conclusions Cyanotic patients with CHD are characterized by increased arterial stiffness estimated with pulse wave analysis parameters and by deteriorated arterial function expressed with worse vasodilatative response in comparison with healthy population. It may confirm relevance of those mechanisms in development of increased rate of cardiovascular events in this population. Association between oxygen saturation or polycythemia and arterial stiffening or vascular dysfunction was not found in these patients. [ABSTRACT FROM AUTHOR]

Background It has been demonstrated that postconditioning (postcon), brief episodes of ischemia during reperfusion period, in patients with ST-segment elevation myocardial infarction (STEMI) confers protection against ischemia–reperfusion injury and as a result, postcon might reduce infarct size. However, whether postcon may exert its beneficial effect on STEMI patients by reducing the occurrence of early malignant ventricular arrhythmias (VA) is still unknown. The aim of the study was to evaluate the influence of postcon on the presence of VA in early presenters with high-risk STEMI treated with primary coronary intervention (PCI). Methods Seventy-five STEMI patients treated with primary PCI within 6 h from symptoms onset were randomly assigned to postcon group ( n = 37) or conventional PCI group ( n = 38) in 1:1 ratio. Postcon was performed immediately after restoration of coronary flow as follows: the angioplasty balloon was inflated 4× 1 min with low-pressure inflations, each separated by 1 min of deflation. After that the patients were continuously monitored electrographically for 48 h. The end-point of the study was the occurrence of VA (ventricular fibrillation-VF, sustained ventricular tachycardia-sVT, non-sustained ventricular tachycardia-nsVT) within 48 h after the procedure. Results In the postcon group, the occurrence of VAs was significantly lower: VF-3, sVT-0, nsVT-15, i.e. (18 patients – 48.6%) in comparison to control group: VF-2, sVT-4, nsVT-23 (29 patients – 76.3%); p = 0.013. The occurrence of accelerated idioventricular rhythm varied insignificantly between both groups (postcon – 45.9% vs control – 34.2%; p = NS). Conclusions Postcon may reduce the occurrence of malignant VA in patients with STEMI treated with primary PCI. [ABSTRACT FROM AUTHOR]

Background: Recent studies, performed with the use of a commercially available diffusion weighted imaging (DWI) sequence, showed that they are sensitive to the increase of water content in the myocardium and may be used as an alternative to the standard T2-weighted sequences. The aim of this study was to compare two methods of myocardial edema imaging: DWI and T2-TIRM. Methods: The study included 91 acute and post STEMI patients. We applied a qualitative and quantitative image analysis. The qualitative analysis consisted of evaluation of the quality of blood suppression, presence of artifacts and occurrence of high signal (edema) areas. On the basis of edema detection in AMI and control (post STEMI) group, the sensitivity and specificity of TIRM and DWI were determined. Two contrast to noise ratios (CNR) were calculated: CNR1 - the contrast between edema and healthy myocardium and CNR2 - the contrast between edema and intraventricular blood pool. The area of edema was measured for both TIRM and DWI sequences and compared with the infarct size in LGE images. Results: Edema occurred more frequently in the DWI sequence. A major difference was observed in the inferior wall, where an edema-high signal was observed in 46% in T2-TIRM, whereas in the DWI sequence in 85%. An analysis of the image quality parameters showed that the use of DWI sequence allows complete blood signal suppression in the left ventricular cavity and reduces the occurrence of motion artifacts. However, it is connected with a higher incidence of magnetic susceptibility artifacts and image distortion. An analysis of the CNRs showed that CNR1 in T2-TIRM sequence depends on the infarct location and has the lowest value for the inferior wall. The area of edema measured on DWI images was significantly larger than in T2-TIRM. Conclusions: DWI is a new technique for edema detection in patients with acute myocardial infarction which may be recommended for the diagnosis of acute injuries, especially in patients with slow-flow artifacts in TIRM images. [ABSTRACT FROM AUTHOR]

Background: This study was conducted to determine the effect of left atrial structural remodeling on heart rhythm after radiofrequency ablation concomitant to mitral valve operation. Methods: Sixty-six consecutive patients with of atrial fibrillation (AF) and mitral valve disease underwent radiofrequency ablation and mitral valve operation. Heart rhythm was evaluated before and at 3, 6, and 12 months postoperatively. Biopsy specimens of the posterior wall of the left atrium were evaluated for the extent of fibrosis, myocyte diameter, intensity of inflammatory infiltrates, degree of myocytolysis, and capillary density. Results: Ten patients died and 1 patient was lost to follow-up. Heart rhythm at 12 months was used to divide the remaining 55 patients into two groups: group I, 34 with sinus rhythm; group II, 21 with AF. Paroxysmal AF preoperatively was more frequent among group I patients, and persistent/long-standing persistent AF in group II (p = 0.0006). Groups I and II differed significantly in myocyte diameter (17.9 ± 3.5 vs 20.3 ± 4.6 μm, p = 0.04), fibrosis percentage (38.7% ± 11.2% vs 47.6% ± 12.3%, p = 0.009), inflammatory infiltrates (p = 0.02), and preoperative left atrial diameter (5.03 ± 0.7 vs 5.5 ± 0.8 cm, p = 0.04). No differences were found in capillary density (797.9 ± 500.6 vs 946.0 ± 373.7/mm2, p = 0.3) and myocytolysis (p = 0.4). Multivariate analysis showed myocyte diameter (p = 0.047) and fibrosis (p = 0.014) were independent predictors for an AF persistence at 12 months. Conclusions: Left atrial structural remodeling strongly affects heart rhythm after concomitant radiofrequency ablation and mitral valve operation. [ABSTRACT FROM AUTHOR]

We assessed the effect of impaired myocardial blush after primary coronary intervention (PCI) on left ventricular remodeling in patients with ST-segment elevation myocardial infarction (STEMI). The study population consisted of 145 patients with first anterior STEMI that was treated successfully (Thrombolysis In Myocardial Infarction grade 3 flow) with PCI. Left ventricular remodeling was defined as an increase of ≥20% in end-diastolic volume based on repeated echocardiographic measurements in patients. The study population was divided into 2 groups according to the presence (myocardial blush grade [MBG] 2 to 3, n = 86) or absence (MBG 0 to 1, n = 59) of myocardial reperfusion. Left ventricular remodeling appeared in 21% of the entire study group. Poor myocardial blush after PCI was associated with an increased rate of remodeling compared with good myocardial reperfusion (32% vs 14%, hazard ratio 2.308, 95% confidence interval [CI] 1.21 to 4.39, p=0.014). Symptoms of heart failure were observed significantly more often in patients with MBG 0 to 1 (35.6% vs 18.6%, p = 0.032) than in patients with MBG 2 to 3. In multivariate analysis, only age (odds ratio 0.96, 95% CI 0.92 to 0.99, p = 0.02) and MBG 0 to 1 (odds ratio 3.15, 95% CI 1.35 to 7.31, p = 0.008) were associated with left ventricular dilation. In conclusion, impaired microvascular reperfusion is associated with left ventricular remodeling and development of congestive heart failure in patients with anterior STEMI that is treated with primary coronary angioplasty. [Copyright &y& Elsevier]

Abstract: We investigated correlation between mitral valve morphology and first heart sound (S1) and opening snap (OS) amplitude. The analysis revealed negative correlation between the OS amplitude and the area of calcification and the mitral orifice area. We also found negative correlation between the S1 intensity and the area of calcification. [Copyright &y& Elsevier]

An abstract of the paper "Detection of myocardial oedema with the use of diffusion-weighted imaging in acute myocardial infarction," by Anna Kociemba and colleagues, from the 2011 SCMR/Euro CMR Joint Scientific Sessions, held in Nice, France, from February 3-6, 2011, is presented.

Abstract: Objectives: To evaluate influence of Bone Marrow Stem Cells (BMSC) intracoronary infusion on exercise capacity, pulmonary function, heart rate recovery and SAECG in patients with AMI of anterior wall, compared to control group – from baseline in the acute phase during 12months follow up. Methods: Forty five patients were randomized 2:1 to BMSC group (n =31 pts) or to control group (n =14 pts). BMSC were administered into infarct related artery (IRA) at 4–6day after primary PCI. Patients were followed up with cardiopulmonary exercise testing. The QRS duration, QT and QTc interval were measured and signal averaged ECGs (SAECG) were performed to evaluate late potentials. Results: There were no significant differences between both groups neither at peak VO2 (190.7±7.4 at baseline; 24.2±5.2 at 6months; 22.2±7.4ml/kg/min at 12months vs 18.4±8.2 at baseline; 22.0±7.2 at 6months; 21.8±6.2ml/kg/min at 12months; BMSC vs control group respectively; p =ns), nor VO2 at anaerobic threshold, nor in VE/VCO2 slope, RER, and systolic blood pressure at peak exercise at baseline and any time point of follow-up. There were no significant differences between groups concerning HR peak, HRR1 and HRR2 at any time point and also QRS, QT parameters, and SAEKG. There were no significant differences between both groups at any time point (baseline, 6 and 12months) concerning FVC, FEV1 and FVC/FEV1 and % of their normal values. Conclusions: We did not find that BMSC therapy in patients with anterior wall myocardial infarction influences exercise capacity. We did not confirm it''s potential proarrhythmogenic influence as assessed with SAECG and standard ECG analysis. [Copyright &y& Elsevier]

Abstract: Background: Myocardial reperfusion in acute myocardial infarction may fail despite successful recanalization of the infarct-related artery. The purpose of this study was to assess the impact of myocardial reperfusion on clinical outcome and left ventricular (LV) function. Methods: The clinical significance of myocardial blush grade (MBG)–angiographic marker of myocardial reperfusion, in 104 patients (age 62±13 years) with first anterior myocardial infarction, successfully (TIMI 3) treated with primary angioplasty was analysed. Echocardiography was performed at baseline and after 6 months. Mortality and major cardiovascular event (MACE) rates were analysed 30 days and 1 year after acute myocardial infarction. Patients were divided into two groups according to presence (group 1, MBG 2–3, n =64) or absence of myocardial blush (group 2, MBG 0–1, n =40). Results: One-year mortality was significantly higher in group 2 in comparison to group 1 (22.5% vs 6.25%, HR: 3.6, 95% CI: 1.187–10.9, p =0.0175). The rate of MACE was significantly lower in patients with MBG 2–3, both after 1 and 12 months (9.4% vs 30%, p =0.008 and 20.3% vs 60%, p <0.001, respectively). At baseline, both global and regional contractile function were significantly better in group 1 than in group 2 (ejection fraction (EF) 47.4±8.8% vs 43.3±7.9%, p =0.04 and wall motion score index (WMSI) 1.64±0.4 vs 1.87±0.3, p =0.001, respectively). Similarly, at 6 months follow-up, LV function was better in group 1 as compared with group 2 (EF 54.9±14.5% vs 46±13.2%, p =0.005 and WMSI 1.43±0.4 vs 1.76±0.46, p =0.001, respectively). Conclusions: Impaired microvascular reperfusion in patients with anterior myocardial infarction is associated with poor prognosis and worse early and late left ventricular function. [Copyright &y& Elsevier]

Cardiac pseudoneoplasms are rare and benign. According to World Health Organization, they are classified as tumor-like lesions. We report two patients with recurrent ventricular tachycardia (VT) in whom magnetic resonance imaging revealed a pathological mass occupying a large part of the left ventricle. The localization of both tumors precluded the possibility of resection; thus, only surgical biopsy was performed. After deducting the prospect of malignancy of the tumors, we treated both patients with amiodarone and implantation of a cardioverter–defibrillator [implanted cardioverter/defibrillator (ICD)]. VT is one of many probable symptoms indicating a tumor within the heart; therefore, treatment with an ICD should only be considered after a more thorough diagnosis. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Cardiovascular events are the main cause of premature death after successful repair of aortic coarctation (CoA). The aim of this study was to assess the selected biochemical markers of atherosclerosis in normotensive CoA repaired patients and to establish its relation to ultrasound indexes of vascular pathology. Methods: 62 patients after CoA repair (37 males, age: 34.1±1.4yrs) and 20 control individuals (10 males, age: 34.8±2.2yrs) were enrolled in the study. The serum markers: asymmetric dimethylarginine (ADMA), nitrites/nitrates (NOx), high-sensitivity C-reactive protein (hsCRP), and following vascular parameters: flow-mediated dilatation (FMD), intima-media thickness (IMT) and pulse wave velocity (PWV) were analyzed. Results: 33 CoA repaired patients were normotensive, and compared to controls, they presented higher serum ADMA concentrations (0.59±0.04umol/l vs. 0.46±0.03umol/l, p=0.035). An analysis of the vascular parameters revealed decreased FMD (4.75±0.5%), NMD (11.86±0.8%) and increased PWV (6.90±0.2m/s) values in the normotensive patients as compared with the control group (FMD: 8.6±0.9%, p<0.001, NMD: 20.94±1.7%, p<0.001; PWV: 5.49±0.2, p=0.023). There were no differences in the serum levels of NOx, hsCRP as well as IMT values between normotensive patients and the control group. A multivariate regression analysis revealed that serum ADMA level was a factor independently associated with the FMD value (r=−0.334; p=0.031) in normotensive CoA repaired group. Conclusions: Early biochemical and vascular indices of atherosclerosis such as increased serum ADMA concentration as well as impaired vasodilatation and increased arterial stiffness are observed in patients after CoA repair. Serum ADMA is a strong predictor of endothelial dysfunction in patients with CoA repair. [Copyright &y& Elsevier]

The aim of our study was to examine the role of a new, simple protocol of intracoronary adenosine administration performed during primary angioplasty on the immediate angiographic results and clinical course. A prospective, single-center, randomized, placebo-controlled trial of 70 consecutive patients (64 ± 14 years, 54 men) with acute myocardial infarction with ST-segment elevation undergoing primary percutaneous coronary intervention (PCI) was conducted. Patients were randomized to 2 groups. Group 1 (n = 35) received intracoronary adenosine (1 to 2 mg) with a hand injection through the guiding catheter 2 times: immediately after crossing the lesion of the infarct-related artery with guidewire and then after the first balloon inflation. Group 2 (n = 35) received placebo. The baseline clinical and angiographic characteristics of the 2 groups were similar. Percutaneous coronary intervention resulted in Thrombolysis In Myocardial Infarction grade 3 flow after PCI in 32 patients (91.4%) in the adenosine group and 27 patients (77.1%) in the placebo group (p = 0.059). Myocardial blush grade 3 was observed at the end of PCI in 23 patients (65.7%) in the adenosine group and 13 (37.1%) in the placebo group (p <0.05). Resolution of ST-segment elevation (>50%) was more frequently observed in the adenosine than in the placebo group: 27 (77%) versus 15 (43%), respectively (p <0.01). In conclusion, intracoronary adenosine administration improved the angiographic and electrocardiographic results in patients with acute myocardial infarction with ST-segment elevation undergoing PCI. Adenosine administration seemed to be associated with a more favorable clinical course. [ABSTRACT FROM AUTHOR]

Apoptosis is recognized as a mechanism of cell loss in the setting of acute myocardial infarction (AMI). Whether it contributes to myocyte elimination late after AMI has not yet been confirmed. We attempted to identify the features of apoptosis in myocytes that survived AMI. A search for ongoing apoptosis was performed in samples obtained from 38 human hearts: group I (n = 10), noncardiac death (control); and group II (n = 28), left ventricular aneurysm (in 20 patients, the samples were collected during aneurysmectomy and from 8 at autopsy). The morphometric evaluation included the degree of cellular hypertrophy, density of the capillary network, extent of myocytolysis, and features of apoptosis. Immunohistochemistry for caspase-3 and Bcl-2 was used as a prerequisite for transmission electron microscopy. Slides showing the strongest reaction for caspase-3 and negative for Bcl-2 were selected for transmission electron microscopy. CD-34 immunohistochemistry was used to quantify the capillary density. A significant reduction in capillary density was observed compared to the control group (1,085.6 ± 205.0/mm2 vs 2,968.7 ± 457.3/mm2; p <0.001). Myocytes that survived the acute phase of AMI were significantly hypertrophied (24.5 ± 4.7 μm vs 14.5 ± 1.6 μm; p <0.001) and showed a moderate to severe degree of myocytolysis. The average intensity score of the immunohistochemistry reactions for caspase-3 was 8.2 ± 3.8. Using transmission electron microscopy, apoptotic bodies were found in caspase-3–positive samples. In conclusion, the expression of caspase-3 and the presence of apoptotic bodies confirmed apoptosis as a common pathway of cardiomyocyte death in the setting of a limited blood supply after AMI. [Copyright &y& Elsevier]

It has been demonstrated that high blood vascular endothelial growth factor (VEGF) levels in patients with myocardial infarction decrease rapidly after reperfusion, possibly in response to heparin administration. We measured serum VEGF concentration before and after heparin infusion in 105 patients with ST-elevation acute myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PCI). Serum VEGF concentration in patients with STEMI was significantly higher than in healthy controls. After PCI, the concentration of VEGF decreased by approximately 70%, with the greatest decrease seen in patients with the highest initial VEGF levels. To determine whether heparin could decrease VEGF concentration by sequestering VEGF in the endothelium, a fixed dose of recombinant VEGF was incubated for 40 minutes with EA.hy926 endothelial cells in vitro. Recovery of VEGF from medium after culture was decreased by up to 15% with increasing doses of heparin. Concentration of VEGF did not change in the absence of heparin and/or endothelial cells. In conclusion, these results suggest that a rapid decrease in blood VEGF after PCI may be related to the administration of heparin, which binds simultaneously to VEGF and endothelial cells. [Copyright &y& Elsevier]