Robert Kaliszczak

Association of C34T AMPD1 gene polymorphism with features of metabolic syndrome in patients with coronary artery disease or heart failure.

Objective. The common C34T polymorphism in the AMP deaminase‐1 (AMPD1) gene results in an inactive enzyme in homozygotes for the mutated T allele. Some studies have shown an association of T allele with longer survival in heart failure (HF) and/or coronary artery disease (CAD). The aim of this study was to assess genotype–phenotype correlations in such patients, with emphasis on components of the metabolic syndrome. Methods. Ninety‐seven patients with CAD without HF (CAD+ HF–) and 104 with HF (HF+) were genotyped by PCR‐RFLP. The genetic control group comprised 200 newborns. Results. No significant differences were found in the frequency of AMPD1 genotypes between the groups. In the CAD+ HF– group, the carriers of T allele compared to CC homozygotes had significantly lower values of waist circumference (89.5±8.5 versus 97.7±11.2 cm; p = 0.00029), waist/hip ratio (p = 0.0059) and BMI (p = 0.045). There was no diabetes or fasting glycaemia ⩾126 mg/dL in T carriers, while these features were present in 25 % of CC homozygotes (p = 0.0024). In the HF+ group, a tendency towards a lower prevalence of diabetes (20 % versus 41 %; p = 0.068) and significantly lower systolic blood pressure (p = 0.048) were observed in T allele carriers. Conclusions. C34T AMPD1 polymorphism may be associated with reduced frequency of obesity in CAD patients and of hyperglycaemia and diabetes in both CAD and HF patients. Morphometric parameters associated with adipose tissue distribution and parameters of glucose metabolism should be analysed as potential confounders in further studies on the role of polymorphisms of AMPD1 and other genes associated with AMP and adenosine metabolism in cardiovascular disease.

Effect of Immunosuppressive Therapy on Proteinogram in Rats.

Background It has been observed that the use of immunosuppressive drugs in patients after transplantation of vascularized organs may be associated with changes in the concentration of certain fractions of plasma proteins. The concentration of these proteins was correlated with an increased risk of occurrence of stage 3 chronic kidney disease (CKD). This article examines the effect of the most commonly used immunosuppressive drugs on the concentration of plasma proteins in Wistar rats. Material/methods The study involved 36 rats grouped according to the immunosuppressive regimen used (tacrolimus, mycophenolate mofetil, cyclosporine A, rapamycin, and prednisone). The rats in all study groups were treated with a 3-drug protocol for 6 months. The treatment dose was adjusted based on available data in the literature. No drugs were administered to the control group. The rats were sacrificed and blood samples collected to determine the concentration of plasma proteins using electrophoresis technique. Results Statistically significant differences were observed between protein concentrations within the studied groups. The differences related to the proteins with masses of 195 kDa, 170 kDa, 103 kDa, and 58 kDa. Conclusions (1) Immunosuppressive drugs caused changes in the proteinogram of plasma proteins. (2) The strongest effect on rat plasma proteins was exerted by a regimen based on rapamycin. Intermediate, weak, and weakest effects were observed in regimens based on cyclosporine A, tacrolimus, and mycophenolate mofetil, respectively.

Multiple cardiovascular complications in a patient with missed small apical myocardial infarction caused by a coronary artery thrombus of uncertain origin

An 82 year-old hypertensive male with no concomitant diseases was admitted because of missed myocardial infarction (MI), 3 days after chest pain onset. On admission, the patient was pain free with stable haemodynamics and normal physical examination. The ECG (Fig. 1) showed atrial fibrillation (AF) and ischaemic changes with its resolution at follow-up. During coronarography (Fig. 2), the presence of a thrombus in the apical part of the left anterior descending (LAD) artery, atherosclerotic plaques with lack of culprit lesion clearly connected to the thrombus, and insignificant myocardial bridging (MB) were demonstrated. The patient was followed conservatively. Troponin and CK-MB elevation with decreasing consecutive values was observed. Transthoracic echocardiography (TTE) delineated left atrial (LA) enlargement, akinesia limited to the left ventricular apex with preserved global ejection fraction of 60% as well as a recent, partially movable, apical left ventricular mural thrombus (LVMT) (Fig. 3A). Warfarin therapy was introduced. On day 2, he developed acute ischaemic stroke (AIS). Carotid artery disease was excluded. On day 6, a systolic murmur demonstrated by echocardiography as an apical ventricular septal rupture (VSR) with left-to-right shunt and a thrombus partially occluding the defect which was smaller and less movable was diagnosed (Fig. 3B). The cardiothoracic surgeon recommended delaying surgical treatment. The patient’s haemodynamic status worsened gradually with signs of exclusive right ventricular failure. An intra-aortic balloon pump was not used due to lack of patient co-operation. On day 18, the family requested that he be discharged home where he finally died. It is most likely that atherosclerotic plaque was involved in the thrombus formation and coronary occlusion, although an AF related embolism is quite possible. These hypotheses could not be verified because there was no culprit lesion and no LA thrombus confirmation. Less probably, MB could have given rise to coronary thrombosis with subsequent MI. Finally, tako-tsubo cardiomyopathy, coronary vasospasm or MB can be a primary cause of apical akinesia, blood stagnation, LVMT development and secondary coronary embolism. LVMT and VSR are strongly associated with extensive anterior MI. In this case it was small and limited to the apex, but proximal LAD occlusion with downstream thrombus migration is possible. Moreover, we speculate that ST elevation in inferior leads might be related to dominant LAD and that ST depression in precordial leads might be a reciprocal change. A coincidence of LVMT and VSR has rarely been documented. Moreover, we observed the partial occlusion of the defect by the thrombus which might delay its recognition and slow the natural evolution. The most probable explanation for AIS is embolisation related to recent LVMT or AF.

Heart rate variability during and after chemotherapy with anthracycline in patients with breast cancer

INTRODUCTION Breast cancer is one of the most common types of cancer. Fortunately, the survival rate of breast cancer patients is quite high. However, cardiotoxicity after breast cancer treatment is a potentially life-threatening complication. Cardiac function can be assessed with echocardiography and biological markers [1]. However, there are few studies on heart rate variability (HRV) in patients with cancer, especially breast cancer, assessed with 24-h Holter electrocardiography (ECG). To our knowledge, no study has assessed HRV parameters immediately after chemotherapy infusion cessation. Low HRV has been shown to be a risk factor for cardiovascular diseases and a marker for all-cause mortality [2]. The present study aimed to assess early HRV changes during chemotherapy, assessed with 24-h Holter ECG in breast cancer patients.

The paradox of the first cycle of chemotherapy—transient improvement of contractility and diastolic function after the first cycle of anthracycline-based chemotherapy: a prospective clinical trial

Aims Breast cancer is the most common cancer among women, and anthracyclines are the most commonly administered drugs for these patients. Cardiotoxicity is one of the complications, which limits the success of this therapy. Very few studies have evaluated anthracycline toxicities within the first few hours after the first infusion, and the majority of published studies were performed in animal models. The present study aimed to evaluate changes in echocardiographic parameters in women with breast cancer 24 hours after receiving the first dose of an anthracycline. Materials and Methods and Results The present study included 75 chemotherapy-naive female patients without heart failure, who were diagnosed with breast cancer and were scheduled to undergo anthracycline-based chemotherapy (epirubicin and doxorubicin). During their visits to the Heart Center, the patients underwent detail echocardiographic examination, including assessment of systolic and diastolic function and longitudinal strain. There were no differences in baseline echocardiographic parameters between patients with and those without cardiotoxicity. Cardiotoxicity was observed during follow-up in 14 patients (18.7%). Improvements in left ventricular ejection fraction and global longitudinal strain were observed at 24 hours after administration of the cytotoxic agent in the subgroup of patients without further cardiotoxicity. The changes were transient and the assessment of left ventricular ejection fraction after completion of chemotherapy revealed similar values to those before the treatment. Conclusions The findings of our study suggest that transient improvement in contractility and systolic and diastolic function might occur 24 hours after anthracycline administration, especially in patients who do not develop cardiotoxicity.

Pseudo-allergic symptoms as a rare manifestation of an ascending aortic aneurysm.

A 79-year-old man was admitted early in the morning to the emergency department (ED) due to oedema of the lips, tongue and dyspnoea. The symptoms awoke the patient from sleep in a supine position. On admission, heart rate was irregular about 80/min, blood pressure 150/80 mm Hg, respiratory rate 23/min, and temperature 36.8°C. Abnormal findings included visible, painless swelling of the lower part of the face, lips, mucous membranes of the mouth and throat, tongue and hoarseness. No itching was present. There were no obvious respiratory or cardiovascular abnormalities on physical examination. Medical history revealed ischaemic heart disease and myocardial infarct of the inferior wall 12 years ago and persistent atrial fibrillation. Aortic dilatation had been found on echocardiography ten years ago without follow up since that time. There was no history of exposure to chemicals or allergies but due to the swelling of the lips and tongue of unknown cause, the patient had twice attended the emergency department (in 2004 and 2005). The last episode of similar symptoms had occurred a year earlier during a long train trip and the symptoms subsided spontaneously. First line therapy at ED included oxygen mask and semi-supine position with some relief of symptoms. Chest X-ray (Fig. 1) detected the enlargement of the mediastinal shadow on the right side. Echocardiography revealed the extension of ascending aorta to the diameter of 56–57 mm at the height of 5 cm above the aortic valve (Figs. 2, 3). Acute superior vena cava syndrome (SVCS) was diagnosed based on the medical history and clinical picture, confirmed by echocardiography. The patient did not agree to further diagnostics and potential surgical intervention. Symptoms and signs of vena cava obstruction regressed within 4 hours of the observation. The patient left the ED in a stable general condition, without symptoms reported on admission. Currently, thrombosis caused by the presence of an intravascular device is the most common cause of nonmalignant SVCS. In most cases, thrombotic complications are revealed within 100 days from device introduction. The second major cause of SVCS is ascending aorta abnormality. The length of superior vena cava varies between 6 cm and 8 cm. It runs along the right edge of the sternum and then forms an arch whose concave margin is adjacent to the ascending aorta. The distension of aortic diameter is mainly due to degenerative changes of the aortic wall. The significantly dilated aorta (> 55 mm) may compress superior vena cava. In the case described above, swelling of the facial soft tissues was the main symptom and had to be differentiated from an allergic reaction which is present in 40% of patients admitted to ED with vasomotor response and urticaria. Demographic changes with increasing numbers of older patients will result in the more frequent occurrence of similar cases, and a differential diagnosis of obscure oedema located in the upper part of the body should involve the exclusion of an ascending aortic aneurysm as a possible cause.