Numerous association studies have been involved in studying the angiotensinogen (AGT) variants, AG T plasma levels and relations to cardiovascular diseases, such as hypertension, myocardial infarction, coronary heart disease. To investigate a role of AGT G(-6)A and M235T genetic variants for chronic heart failure (CHF) and advanced atherosclerosis (AA), a total of 240 patients with CHF and 200 patients with AA of the Czech origin were evaluated for the study. The study shows the role of polymorphism AGT G(-6)A in genetic background among advanced atherosclerosis patients and chronic heart failure patients (Pg=0.001). This difference was also observed in comparison of AA patients with subgroup of CHF with dilated cardiomyopathy (Pg=0.02; Pa=0.009), and ischemic heart disease (Pg=0.007). The greatest difference between triple-vessel disease and chronic heart failure groups was observed in freque ncy of GT haplotype (P<0.001) and GGMT associated genotype (P <0.001). Retrospectively, we found the same trend when the subgroups of CHF were compared to AA group (AA vs. IHD with CHF P<0.001; AA vs. DCM P<0.001). These results suggest AGT genetic variants as a risk factor for chronic heart failure compared to advanced atherosclerosis disease without heart failure, with a strong difference between IHD patients and chronic heart failure patients with ischemic heart disease, especially in haplotypes and associated genotypes., M. Pávková Goldbergová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfus ion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts ( P<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts ( P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts., I. Mourouzis ... [et al.]., and Obsahuje seznam literatury
Lipoprotein(a) [Lp(a)] comprises of an LDL particle and apolipoprotein(a) [apo(a)] and its elevated levels are considered a risk factor for atherosclerosis. The aim of our study was to find out whether elevated Lp(a) levels are associated with increased risk of atherosclerosis in patients with multiple other risk factors. We further tested the association of three polymorphisms of the apo(a) gene promoter with Lp(a) levels. No significant correlation was detected between Lp(a) levels and lipid and clinical parameters tested. The study demonstrated a significantly (p=0.0219) elevated Lp(a) level (mean 28±35 mg/dl, median 0.14) in patients with coronary heart disease (CHD). In a group with premature CHD the correlation was not significant anymore. There was a significant correlation between polymorphic loci of the promoter region of apo(a) gene and Lp(a) levels (+93C>T, p=0.0166, STR, p<0.0001). Our study suggests that elevated Lp(a) level is an independent risk factor of CHD in carriers of other important CHD risk factors. Observed association of sequence variants of the promoter of apo(a) gene with Lp(a) levels is caused in part due to linkage to a restricted range of apo(a) gene length isoforms., L. Zlatohlávek, K, Zídková, M. Vrablík, T. Haas, M. Prusíková, H. Svobodová, R. Češka., and Obsahuje bibliografii a bibliografické odkazy
Cieľom kohortového kontrolovaného experimentu bolo preukázať vplyv biofeedbackovej metodiky (HRV biofeedback) na anxietu, depresiu, nezameranú hostilitu, časovú tieseň, vnímanie stresu, vnímanie sociálnej opory, kvalitu života a variabilitu srdcovej frekvencie (HRV). Zrovnocenený súbor (N = 66) bol získaný štatistickým vyvážením skupín pacientov absolvujúcich kúpeľnú liečbu podľa veku, pohlavia, society, farmakoterapie, kardiorehabilitačných procedúr a časového obdobia absolvovania kúpeľnej liečby po konzultácii s lekárom. Experimentálnej skupine (N = 39) bola poskytnutá štandardná kardiorehabilitácia a HRV biofeedback. Kontrolnej skupine (N = 27) sa poskytla len štandardná liečebná kardiorehabilitácia. Výsledky boli spracované parametrickou štatistikou s možnosťou zrovnocenenia vstupných údajov merania, analýzu kovariancie a viacnásobnou hierarchickou regresnou analýzou. Preukázal sa signifikantne pozitívny vplyv absolvovania HRV biofeedbacku na všetky sledované biopsychosociálne oblasti osobnosti pacientov. Pozitívny efekt sa potvrdil aj zmenami HRV v sede, v stoji, v ľahu, ale predovšetkým pri mentálnej záťaži. Dosiahnuté výsledky podnietili implementáciu tejto metódy do štandardných kardiorehabilitačných intervencií FNsP L. Pasteura v Košiciach.
Ischemická choroba srdeční ICHS je nejčastějším závažným onemocněním postihujícím obyvatelstvo vyspělých zemí. ICHS způsobuje nejen vysokou nemocnost, ale i vysokou invaliditu a je příčinou 40 % všech úmrtí ve vyspělých zemích. ICHS je klinický projev aterosklerózy koronárních tepen. Usazující se aterosklerotické pláty v koronárním řečišti jsou příčinou sníženého průtoku krve v myokardu. Srdeční sval trpí nedokrevností - ischemií. Klinickým projevem ischemie myokardu je bolest na hrudi - angina pectoris. V současnosti je jednou z mnoha chirurgických metod léčení ICHS i transmyokardiální laserová revaskularizace TMLR. Principem této metody je pomocí ekvivalentních laserových impulsů vytvořit v oblasti levé síně kanálky, jež by obnovily přísun krve do postižené srdeční tkáně., Jaroslav Huynh., and Obsahuje seznam literatury
a1_Ischemic preconditioning (I-PC) induced by brief episodes of ischemia and reperfusion (I/R) protects the heart against sustained I/R. Although activation of mitochondrial K ATP channels (mitoK ATP) interacting with reactive oxygen species (ROS) has been proposed as a key event in this process, their role in the antiarrhythmic effect is not clear. This study was designed: 1) to investigate the involvement of mito K ATP opening in the effect of I-PC (1 cycle of I/R, 5 min each) on ventricular arrhythmias during test ischemia (TI, 30-min LAD coronary artery occlusion) in Langendorff-perfused rat hearts and subsequent postischemic contractile dysfunction, and 2) to characterize potential mechanisms of protection confer red by I-PC and pharmacological PC induced by mito K ATP opener diazoxide (DZX), with particular regards to the modulation of ROS generation. Lipid peroxidation (an indicator of increased ROS production) was determined by measurement of myocardial concentration of conjugated dienes (CD) and thiobarbituric acid reactive substances (TBARS) in non-ischemic controls, non-preconditi oned and preconditioned hearts exposed to TI, I-PC alone, as well as after pretreatment with DZX, mito K ATP blocker 5-hydroxydecanoate (5-HD) and antioxidant N-acetylcysteine (NAC)., a2_Total number of ventricular premature beats (VPB) that occurred in the control hearts (518±71) was significantly (P<0.05) reduced by I-PC (195±40), NAC (290±56) and DZX (168±22). I-PC and NAC suppressed an increase in CD and TBARS caused by ischemia indicating lower production of ROS. On the other hand, I-PC and DZX themselves moderately enhanced ROS generation, prior to TI. Bracketing of I-PC with 5-HD suppressed both, ROS production during PC and its cardioprotective effect. In conclusion, potential mechanisms of protection conferred by mito K ATP opening in the rat heart might involve a temporal increase in ROS production in the preconditioning phase triggering changes in the pro/antioxidant balance in the myocardium and attenuating ROS production during subsequent prolonged ischemia., J. Matejíková ... [et al.]., and Obsahuje seznam literatury