Janusz Kochanowski

Altered Gene Expression Pattern in Peripheral Blood Mononuclear Cells in Patients with Acute Myocardial Infarction

Background Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. Methods and Results Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4–6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease, without history of myocardial infarction. Gene expression analysis was performed with Affymetrix Human Gene 1.0 ST microarrays and GCS3000 TG system. Lists of genes showing altered expression levels (fold change >1.5, p<0.05) were submitted to Ingenuity Pathway Analysis. Gene lists from each group were examined for canonical pathways and molecular and cellular functions. Comparing acute phase of MI with the same patients after 6 months (stable phase) and with control group we found 24 genes with changed expression. In canonical analysis three pathways were highlighted: signaling of PPAR (peroxisome proliferator-activated receptor), IL-10 and IL-6 (interleukin 10 and 6). Conclusions In the acute phase of STEMI, dozens of genes from several pathways linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability show altered expression. Up-regulation of SOCS3 and FAM20 genes in the first days of myocardial infarction is observed in the vast majority of patients.

Does a blanking period after pulmonary vein isolation impact long-term results? Results after 55 months of follow-up.

BACKGROUND The aims of the study are 1) to assess antiarrhythmic prophylaxis efficacy during the first 2 months after radiofrequency ablation (ARF) due to AF; 2) to define risk factors for early AF recurrence (EAFR) after ARF; 3) to determine the long-term follow-up results and risk factors for late AF recurrence (LAFR). METHODS A total number of 210 consecutive patients who had undergone ARF due to AF were analyzed. Patients were randomized into three groups: Group 1 (G1), without any anti-arrhythmic drug (AAD); Group 2 (G2), with amiodarone or sotalol; Group 3 (G3), with last ineffective AAD. The study was designed to analyze two periods: short-term observation, the first 2 months after ARF; and at least 2 years of long-term follow-up. RESULTS After 2 months, clinical data were collected from 171 patients (123 males, mean age of 50.3 years; persistent AF in 19.8%; lone AF in 36.6%). Sinus rhythm (SR) was maintained in 84 (49.1%) patients; 35 (20.4%) patients presented with a single episode of AF, 39 (23%) patients experienced a reduction in number of AF episodes, and 13 (7.5%) patients showed no improvement. No predisposing factor for early recurrence was found. After a mean follow-up of 55 months, clinical data were collected in 137 patients, of which 47 (34%) maintained SR. Those more likely to sustain SR were: males (82.9% vs. 62.2%; p = 0.018), younger patients (44.8 ± 12.7 vs. 52.5 ± 9.9; p = 0.0001), patients with smaller left atrium diameter (4.05 ± ± 0.49 cm vs. 4.25 ± 0.51 cm; p = 0.04), and those without any AF recurrence during the first 2 months after ARF (78.7% vs. 35.6%; p < 0.0001). In the multivariable analysis, the independent risk factors for LAFR were hypertension (p < 0.001) and persistent AF (p = 0.014). CONCLUSIONS Antiarrhythmic prophylaxis does not affect the number of AF recurrences during the first 2 months after ablation. SR maintenance during a blanking period after AF ablation is a positive prognostic factor in long-term follow-up. Persistent AF and hypertension are independent risk factors for late AF recurrence after pulmonary vein isolation.

Simple markers can distinguish Takotsubo cardiomyopathy from ST segment elevation myocardial infarction

BACKGROUND Takotsubo cardiomyopathy (TTC) is a clinical condition mimicking acute myocardial infarction. A specific biomarker for TTC screening is required, but until now, no single biomarker has been established for the early diagnosis of TTC and differentiation from ST-segment elevation myocardial infarction (STEMI). In our study we focused on the simple markers that are available in every hospital. METHODS In 66 consecutive patients (pts) who were hospitalized with TTC and 66 pts with STEMI, cardiac biomarkers, such as NT-proBNP, TnI, CK and CKMB mass were determined during 12h from admission and compared with demographic, clinical and echocardiographic findings. RESULTS The concentration of NTproBNP was greater in pts with TTC than STEMI (4702pg/ml vs 2138pg/ml). The concentration of TnI and CKMB mass was greater in the STEMI group than in the TTC group (TnI: 2.1ng/ml and CK MB mass: 9.5ng/ml in pts with TTC vs TnI: 19ng/ml and CK MB mass: 73.3ng/ml in pts with STEMI). The NTproBNP/TnI ratio and NTproBNP/CKMB mass ratio were, respectively, 2235.2 and 678.2 in pts with TTC and 81.6 and 27.5 in pts with STEMI (p<0.001). Moreover, the NTproBNP/EF ratio was also statistically significant (110.4 in TTC group and 39.4 in STEMI group). CONCLUSIONS NTproBNP/TnI, NTproBNP/CKMB mass and NTproBNP/EF ratios can distinguish TTC from STEMI at an early stadium. The most accurate marker is the NTproBNP/TnI ratio.

The N-terminal pro-brain natriuretic peptide as a marker of mitoxantrone-induced cardiotoxicity in multiple sclerosis patients.

BACKGROUND AND PURPOSE Mitoxantrone (MTX) has been shown to reduce progression of disability and number of clinical exacerbations in patients with progressive multiple sclerosis (MS). Prolonged administration of MTX, however, is limited by the risk of cardiotoxicity. Cardiac monitoring in MTX-treated patients includes usually measurement of left ventricular ejection fraction (LVEF) by means of echocardiography. The N-terminal pro-brain natriuretic peptide (NT-proBNP) represents a novel diagnostic tool in the assessment of heart failure. This study was aimed to evaluate the usefulness of NT-proBNP for early detection of MTX-induced cardiotoxicity in MS patients. MATERIALS AND METHODS We measured the NT-proBNP plasma levels in 45 MS patients who completed 24-month MTX therapy and in 37 MS patients of control group. RESULTS The median NT-proBNP plasma value was 15.12pg/mL. In 12 MTX-treated patients (27%), NT-proBNP plasma values were elevated, though this subgroup of patients neither clinical showed evidence of myocardial damage nor had the LVEF value <50%. In five patients with normal NT-proBNP, we observed LVEF decline >10%. We did not observe correlations between the NT-proBNP levels and patient age, MS duration, relapses index, Extended Disability Status Scale (EDSS), MTX single dose and the total cumulative dose of MTX. In 8 patients (22%) from control group, NT-proBNP plasma levels were also elevated. CONCLUSIONS The results of our study confirm that MTX therapy is safe for carefully selected and closely monitored MS patients. We believe that serial evaluation of NT-proBNP levels (before, during and after MTX therapy) can identify MS patients at high risk for MTX-induced cardiotoxicity.

Transesophageal Real Time Three‐Dimensional Echocardiography in Assessment of Partial Atrioventricular Septal Defect

We present a practical application of real time three‐dimensional transesophageal echocardiography in a 67‐year‐old male patient with congenital heart disease.

The oldest patient with takotsubo cardiomyopathy

Takotsubo cardiomyopathy (TTC) is a rare condition that affects mainly aging women. According to a retrospective review, patients with TTC accounted for approximately 2% of all the patients with suspected acute coronary syndrome (ACS). A few reports indicated that the average age of TTC patients was 68 years, although children or young adults may also be affected. In US and Europe, a number of contemporary TTC studies report that 90% of patients with TTC are women aged 65–70 years. Meta analysis showed that the age ranged from 10 to 89 years. [1] There was also one case study of a 90-year-old patient with TTC ― the oldest patient known so far. In that case, the patient died during the course of treatment from severe multi-organ failure. [2] In the present case report, we present a 98-years old woman with TTC admitted to our clinic. A 98-years old patient was admitted to our clinic because of significant chest pain and general weakness accompanied by hypotension that required catecholamine administration with ST-segment elevation in the anterolateral leads in ECG. The patient suffered from hypertension and third stage of chronic kidney disease. Urgent cardiac catheterization and ventriculography confirmed the absence of any critical coronary disease, but also the presence of a typical apical ballooning and midventricular hypokinesis. Troponin I (TnI) at admission was 5.555 ng/mL and creatine kinase soenzyme MB (CK-MB) mass was 14.5 ng/mL. Inflammatory parameters were not elevated, whereas N-terminal pro brain natriuretic peptide (NT-proBNP) concentration was markedly elevated, at 18,623 pg/mL. NT-proBNP/TnI ratio was 3352.48 on the first day and even higher after 24 h, at 7113.36. This markers profile is characteristic of TTC. There is a relatively small increase in creatine kinase and troponin concentrations in relation to the extent of wall motion abnormalities. BNP is always elevated in patients with TTC and is higher than in patients with ST-segment elevation myocardial infarction. Some researchers suggest that TTC can be distinguished from ACS on the basis of the characteristic profile of cardiac markers consisting of a sudden increase in the concentration of NT-proBNP in the first few days when there is only a small increase in markers of myocardial necrosis (the ratio of NT-pro BNP/troponin). [3]

Transoesophageal real-time three-dimensional echocardiography in assessing large multiperforated atrial septal aneurysm

A 51-year-old woman presented with a 2 year history of declining exercise capacity and irregular palpitations. Clinical examination revealed sinus rhythm at 86 b.p.m., and blood pressure of 112/70 mmHg, without pedal oedema. Initial transthoracic echocardiography (TTE) revealed moderate right ventricular (RV) enlargement with moderate tricuspid regurgitation and mild pulmonary hypertension (estimated PASP 40 mmHg). There was interventricular septal flattening in diastole due to RV volume overload. Transoesophageal two-dimensional echocardiography (2D TEE) demonstrated multiperforated atrial septal aneurysm (ASD II-atrial septal defects type II) …

Dislocation of Amplatzer Septal Occluder Device after Closure of Secundum Atrial Septal Defect

Atrial septal defect transcatheter occlusion techniques have become an alternative to surgical procedures. With the increasing use of this new technology, several complications have been identified. The authors present the case of a patient who was admitted to the hospital for primary percutaneous closure of a secundum atrial septal defect. On routine follow-up examination 24 hours after implantation, transthoracic echocardiography revealed a partial dislocation of the occluder into the right atrium. The patient was referred for cardiosurgical treatment. Strict selection criteria and the choice of the device may help reduce the incidence of complications such as dislocation of the occluder into the right atrium following the percutaneous device closure of an atrial septal defect.

Coronary spasm secondary to hypocalcaemia and hypomagnesaemia

A 43-year-old man was admitted to the Endocrinology Department because of hypocalcaemia and hypomagnesaemia developed after surgical treatment of hyperparathyroidism. There was no history of coronary heart disease and hypercholesterolemia before admission, only moderate hypertension. At about 2 pm the patient experienced sudden chest pain radiating to the jaw and upper limbs. Electrocardiogram revealed temporary horizontal ST-segment elevation in II, III and aVF leads (Fig. 1). The patient was referred to the Cardiology Department and coroangiography was performed. There were neither atherosclerotic changes nor contraction of coronary arteries during angiography (Fig. 2A–C). Laboratory test made shortly after the onset of pain revealed severe ionised hypocalcaemia — 0.69 mmol/L (1.13–1.29 mmol/L) and hypomagnesaemia — 0.52 mmol/L (0.7–1.0 mmol/L). Troponin I level was within the normal range — 0.039 ng/mL (0.0–0.056 ng/mL) but a slight elevation of creatine kinase-MB mass was present — 4.6 ng/mL (0.0–3.6 ng/mL). The chest pain ceased following intravenous administration of calcium and magnesium. Two-dimensional transthoracic echocardiography showed normal left ventricular size and function with ejection fraction of 57%, mild left ventricular hypertrophy and mild mitral and tricuspid regurgitation (Fig. 3). Although coronary spasm secondary to hypocalcaemia is a very rare facet of angina, failing to consider it in differential diagnoses in all cases of variant angina might pose a grave threat to the patient’s life.

Purulent pericarditis in patient with esophageal cancer presenting with cardiac tamponade.

A 39-year-old patient with no relevant history of cardiovascular disease presented after syncope, with rest dyspnea and no chest pain. A few months earlier, the patient had undergone palliative stent implantation in the distal part of the esophagus due to inoperable esophageal cancer. On admission, physical examination of the patient revealed the following: cachexia with severe dehydration, arterial hypotension (90/50 mm Hg), tachycardia (heart rate 115 beats/min), tachypnea (36 breaths/min), body temperature of 37°C (98.6°F), distended neck veins, no pulmonary congestion, mild hepatomegaly, and decreased heart sounds. The initial electrocardiogram (ECG) showed persistent diffuse concave-upward ST-segment elevation that was not confined to any arterial territory (Figure 1). The baseline serum troponin I level was not elevated. Bedside transthoracic echocardiography (TTE) demonstrated a considerable (about 5 cm) amount of heterogeneous fluid in the pericardium with numerous non-regular, mobile fibrin clots creating thin intrapericardial bands (Figure 2a). In addition, TTE showed various signs indicating cardiac tamponade (near total diastolic collapse of the right ventricle and the right atrium; excess buildup of fluid in the vena cava, known as inferior vena cava [IVC] plethora; the absence of normal inspiratory IVC collapse; and respiratory variations in tricuspid and transmitral flow on Doppler echocardiography) (Figures 2b–d). Emergency pericardio-