Matrix metalloproteinases (MMPs) are endopeptidases participating in physiological processes of the brain, maintaining the blood–brain barrier integrity and playing a critical role in cerebral ischemia. In the acute phase of stroke activity, the expression of MMPs increase and is associated with adverse effects, but in the post-stroke phase, MMPs contribute to the process of healing by remodeling tissue lesions. The imbalance between MMPs and their inhibitors results in excessive fibrosis associated with the enhanced risk of atrial fibrillation (AF), which is the main cause of cardioembolic strokes. MMPs activity disturbances were observed in the development of hypertension, diabetes, heart failure and vascular disease enclosed in CHA₂DS₂VASc score, the scale commonly used to evaluate the risk of thromboembolic complications risk in AF patients. MMPs involved in hemorrhagic complications of stroke and activated by reperfusion therapy may also worsen the stroke outcome. In the present review, we briefly summarize the role of MMPs in the ischemic stroke with particular consideration of the cardioembolic stroke and its complications. Moreover, we discuss the genetic background, regulation pathways, clinical risk factors and impact of MMPs on the clinical outcome.

In patients with end stage renal disease (ESRD), left ventricular (LV) hypertrophy with impaired LV function, which is called uremic cardiomyopathy (UC) is often observed. The UC historically has been considered a contraindication for kidney transplantation (KTx). Currently, moderate LV dysfunction does not exclude the possibility of KTx. The amelioration of uremia after KTx improved cardiac function in patients with LV dysfunction. There is a little information on the function of the left atrium (LA) after the KTx procedure. There are no studies evaluating (LA) changes in patients with UC after KTx and determining the possibility of inhibiting the occurrence of LA unfavourable changes (remodelling) and even a possible LA recovery process (reverse remodelling) as a result of a successful KTx. The aim of the study was to assess the LA reverse remodelling in patients with ESRD undergoing KTx. The study group consisted of 42 patients, aged 43.3 ± 12.6 followed for 36 months after a deceased donor KTx. The patients were studied at five time points: 1, 3, 6, 12 and 36 months after KTx. In all patients transthoracic echocardiography was performed in order to assess the following LA planimetric parameters: LAmax, LAmin, LAwaveP. LAshortmax, LAshortmin, LAshortwaveP, LAlongmax, LAlongmin, LAlongwaveP, LAcircmax and LAareamax, volumentric parameters: LA volume (LAV), LA volume index (LAVI), and hemodynamic indices: LA ejection fraction (LAEF), LA active emptying fraction (LAAE), LA passive emptying fraction (LAPE), LA index of expansion (LAIE) and LA fractional shortening (LAFS). The LAVI values were 34.63 ± 10.34 ml/m2, 32.24 ± 9.59 ml/m2 (p < 0,001), 31.36 ± 9.20 ml/m2 (p < 0,001), 28.29 ± 8.32 ml/m2 (p < 0,001) and 27.57 ± 8.40 ml/m2 (p < 0,001), after: 1, 3, 6, 12 and 36 months after KTx, respectively. The reduction of the LA size was accompanied by gradual LA contractility improvement, which was manifested as an increase of the LA hemodynamic indices such as LAEF, LAAE, LAIE, LAFS and a decrease of LAPE. LA remodelling secondary to atrial uraemic cardiomyopathy is an example of complex cardiomyopathy with elements characteristic of both congestive and infiltrative cardiomyopathy. Early LAVI reduction post KTx mostly depends on changed haemodynamic conditions, whereas the main reason for further decrease of LAVI values is related to resolution of uraemic toxaemia.

Background: Paraoxonase1 (PON1), an enzyme connected to high density lipoproteins (HDL) particles, plays an important role in protecting arteries against atherosclerosis. The serum activity and concentration of PON1 depends on several genetic polymorphisms as well as environmental factors. Materials and methods: Investigated population consisted of 71 patients aged 43–76 years with confirmed coronary heart disease (CHD). Established risk factors of CHD such as hypertension, elevated total cholesterol and LDL cholesterol (LDL-C), low HDL cholesterol (HDL-C), diabetes mellitus, obesity, smoking and premature CHD in family history were assessed. PON1 genotype for −108C/T promotor region was determined by polymerase chain reaction-restriction fragments length polymorphism (PCR–RFLP) method. Paraoxonase activity towards paraoxon and arylesterase activity towards phenyl acetate were measured spectrophotometrically. Results: Significant correlations between diabetes mellitus and paraoxonase activity (R = −0.264, p = 0.026) and between the premature coronary heart disease in family history and PON1 activity (R = −0.293, p = 0.013) were found. In multivariate analysis, PON1 paraoxonase activity was independently of confounding factors associated with diabetes (OR = 0.985; p = 0.024) and premature CHD in family history (OR = 0.983; p = 0.027). PON1 activity towards aryl acetate positively correlated with HDL-C level (R = 0.255, p = 0.032). In patients treated with statins, PON1 paraoxonase activity was significantly (p = 0.033) higher than in patients without treatment. Conclusions: In diabetic patients with CHD, paraoxonase activity is lower than in normoglycemic patients despite similar lipid profiles. Diabetes and positive family history in patients with overt CHD are associated with the serum PON1 activity, which might be an additional factor helpful in evaluating cardiovascular risk in this group of patients.

Atherosclerosis is regarded as a combination of two major separate diseases: atherosis and sclerosis. Sclerotic component depends on deterioration of elastic properties of the aortic wall and is called aortic stiffness. The most valuable, non-invasive method of aortic stiffness assessment is echocardiography, which allows to calculate the aortic stiffness index (ASI). ASI is an independent predictor of all-cause and cardiovascular mortality in different groups of patients. The main aim of study was the assessment of the aortic reverse remodeling in patients with end-stage renal disease (ESRD) after renal transplantation (RT). Study group involved 42 patients aged 43.3 ± 12.6 years, including 19 women aged 49.9 ± 10.9 years and 23 men aged 41.5 ± 12.91 years, who have undergone RT from non-related renal transplant donors, The study protocol has been consisted of 5 stages: 1 week after RT, 3 months after RT, 6 months after RT, 1 year after RT and 3 years after RT. The echocardiographic examination was performed and measurements of Aomax, Aomin were done. On the base of obtained parameters ASI, aortic distensibility (AD) and aortic strain (AS) were calculated according to adequate formulas. The improvement of indices characterizing the elastic properties of aorta were noted. These changes attained the statistically significant level only at the end of the observation. ASI just after RT was equal – 4.65 ± 1.58, three months after RT – 4.54 ± 1.49, six months after RT – 4.59 ± 1.61, one year after RT – 4.35 ± 1.21 and three years after RT – 3.35 ± 1.29, while AD reached respectively – 6.55 ± 3.76 cm2/dyn−110−6 just after RT, − 6.38 ± 3.42 cm2/dyn−110−6 three months after RT, − 6.53 ± 3.60 cm2/dyn−110−6 six months after RT, − 6.48 ± 2.79 cm2/dyn−110−6 one year after RT and – 8.03 ± 3.95 cm2/dyn−110−6 three years after RT. Noted AS values were equal – 6.61 ± 4.05%, just after RT, − 6.40 ± 3.58% three months after RT, − 6.56 ± 3.76%, six months after RT, − 6.45 ± 2.80% one year after RT, − 8.01 ± 3.97%. and three years after RT. The exact analysis of parameters concerning aortic function showed that to achieve ASI, AD and AS improvement, long time was needed, because the most significant changes of these indices were observed only between 1 year and 3 years after RT. There is a relationship between renal transplantation and improvement of the aortic elastic properties. The recovery of the renal function allows to initiate the reparative processes leading to at least partial restitution of the structure and features of the aorta, which is called reverse remodelling. Improvement of aortic wall elastic properties after renal transplantation is a continuous and prolonged process.

Background:The aim of this study was to evaluate whether –108C/T polymorphism of the paraoxonase 1 (PON1) gene and the plasma enzyme activity are risk factors for adverse cardiac events after coronary artery bypass grafting (CABG). Material andMeth...

Serum paraoxonase 1 (PON1), an enzyme associated with high – density lipoproteins (HDL) particles, inhibits the oxidation of serum lipoproteins and cell membranes. PON1 activity is lower in patients with atherosclerosis and in inflammatory diseases. The systemic inflammatory response provoked during cardiopulmonary bypass grafting may contribute to the development of postoperative complications. The aim of the present study was to estimate the dynamic changes in paraoxonase 1 (PON1) activity towards paraoxon and phenyl acetate during and after coronary artery surgery. Twenty six patients with coronary heart disease undergoing coronary artery bypass grafting (CABG) were enrolled into the study. Venous blood samples were obtained preoperatively, after aortic clumping, after the end of operation, at 6, 18, 30 and 48 h after operation. Paraoxonase activity was measured spectrophotometrically in 50 mM glycine/NaOH buffer (pH 10.5) containing 1.0 mM paraoxon, and 1.0 mM CaCl2. Arylesterase activity was measured in 20 mM TrisCl buffer (pH 8.0) containing 1 mM phenyl acetate and 1 mM CaCl2. PON1 activity toward paraoxon and phenyl acetate significantly decreased after aorta cross clumping and increased directly after operation. PON1 activity towards paraoxon in preoperative period and PON1 activity towards phenyl acetate in seventh stage of experiment tended to inversely correlate with the occurrence of postoperative complications. The paraoxonase 1 plasma activity is markedly reduced during CABG surgery.