V kazuistike opisujeme prípad 49-ročného muža od detstva morbídne obézneho (BMI 40 kg/m2), s artériovou hypertenziou (asi od 15 rokov, liečená od roku 2004), dyslipidémiou (od roku 2006), diabetes mellitus 2. typu (od roku 2006, na inzulinoterapii od roku 2008) a fajčením (do roku 2011, 20 cigariet denne). Liečba: 16 druhov liekov, 8 na hypertenziu, statín, liečba diabetu, aspirín, alopurinol. V roku 2010 (ako 45-ročný) hospitalizovaný na našej klinike pre dyspnoe a bolesti na hrudníku s hodnotou krvného tlaku 180/110 mm Hg (zistené srdcové zlyhávanie s ejekčnou frakciou ĽK 33 %, vo funkčnej triede NYHA II, echokardiograficky: ľavá predsieň: 46 mm, rozmer ľavej komory v diastole: 70 mm, interventrikulárne septum: 12 mm, hypokinéza septa, dopplerovská ultrasonografia artérií dolných končatín (kalcifikácie, difúzne aterosklerotické zmeny, neprítomná stenóza), CT koronárna angiografia (signifikantná stenóza ľavej koronárnej artérie). Zahájená liečba perorálny furosemid 40 mg denne. V máji roku 2011 hospitalizovaný pre akútny koronárny syndróm: akútny NSTEMI spodnej steny (koronarografia: 2-cievne postihnutie, realizovaná PKI, implantovaný DES – ramus circumflexus, paroxyzmus fibrilácie predsiení, funkčná trieda NYHA III, ľavokomorová ejekčná frakcia: 30 %, pľúcna hypertenzia). V roku 2012 realizovaná renálna denervácia pre rezistentnú hypertenziu, implantovaný karotický stent pre stenózu karotickej artérie, prítomná diabetická nefropatia (KDOQI 3. stupňa, GF 40 ml/min). V auguste roku 2014 hospitalizovaný na našej klinike pre pľúcny edém, kardiogénny šok, akútnu ischémiu pravého predkolenia pri periférnej embolizácii, prítomný atriálny flutter, zhoršenie renálnych parametrov, echokardiograficky: ľavá predsieň: 55 mm, rozmer ľavej komory: 75 mm, akinéza septa a zadnej steny, oklúzia artérií pravej dolnej končatiny (vzhľadom na vážny stav pacienta kontraindikovaná angiochirurgická intervencia, zvažovaná amputácia končatiny z vitálnej indikácie), pacient zomrel po 4 dňoch hospitalizácie na intenzívnej jednotke po neúspešnej liečbe. Kombinácia ochorení diabetes, hypertenzia a ischemická choroba srdca je častá a prognosticky vážna. Diabetes zvyšuje kardiovaskulárnu morbiditu a mortalitu, a preto by sme mali hľadať diabetes u všetkých kardiovaskulárnych pacientov., The case study describes a case of 49-year-old man with morbid obesity since childhood (BMI 40 kg/m2), arterial hypertension (approx. since aged 15, treated since 2004), dyslipidemia (since 2006), type 2 diabetes mellitus (since 2006, on insulin therapy since 2008) and smoking (until 2011, 20 cigarettes a day). Treatment: 16 types of medication, 8 for hypertension, statin, therapy for diabetes, aspirin, allopurinol. In 2010 (when aged 45) hospitalized in our clinic with dyspnoea and chest pain with a high pressure reading of 180/110 mm Hg (identified symptoms of heart failure with LV ejection fraction of 33 %, in NYHA II functional class, echocardiographically: left atrium: 46 mm, left ventricular chamber size in diastole: 70 mm, interventricular septum: 12 mm, septal hypokinesis, Doppler ultrasonography of lower limb arteries (calcification, diffuse atherosclerotic changes, absent stenosis), CT coronary angiography (significant stenosis of the left coronary artery). Treatment started with 40 mg oral dose of furosemide daily. In May 2011 he was hospitalized with an acute coronary syndrome: acute NSTEMI of the inferior wall (coronarography: 2-vascular problems, implemented PKI, implanted DES – ramus circumflexus, paroxysmal atrial fibrillation, NYHA III functional class, left ventricular ejection fraction: 30 %, pulmonary hypertension). In 2012 renal denervation for resistant hypertension was carried out, carotid stent implanted for stenosis of the carotid artery, presence of diabetic nephropathy (KDOQI stage 3, GF 40 ml/min). In August 2014 admitted to our clinic with pulmonary oedema, cardiogenic shock, acute ischemia of the right calf with peripheral embolisation, presence of atrial flutter, impairment of renal parameters, echocardiographically: left atrium: 55 mm, left ventricle size: 75 mm, akinesis of the septum and posterior wall, occlusion of the right leg arteries (given the patient‘s serious state angio-surgical intervention was contraindicated, vitally indicated leg amputation considered), the patient died after 4 days of hospitalization in an intensive care unit after unsuccessful treatment. A combination of diabetes, hypertension and ischemic heart disease is frequent and prognostically serious. Diabetes increases cardiovascular morbidity and mortality and therefore we should check for diabetes in all cardiovascular patients., and Miroslav Pernický, Juraj Papinčák, Adriana Reptová, Soňa Kiňová, Ján Murín
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
V současné době je věnována familiární hypercholesterolemii (FH) po letech opět zvýšená pozornost. Je tomu tak především proto, že se toto geneticky podmíněné onemocnění stává cílem velmi účinných nových hypolipidemik, PCSK-9 inhibitorů, lomitapidu a mipomersenu. Předložené sdělení se zabývá popisem 2 souborů nemocných (vždy ve své době z největších na světě), před 50 lety a nyní. I když přímé statistické srovnání není možné, lze přeci jen najít v klinickém obrazu FH jisté vývojové změny. Faktem však je, že základní charakteristika FH se zásadně nezměnila. V biochemickém obrazu dominuje těžká izolovaná hypercholesterolemie s hodnotami celkového cholesterolu 9–10 mmol/l, s hodnotami LDL-cholesterolu 7–8 mmol/l a s normálními hodnotami triglyceridů. Je zajímavé, že právě triglyceridy se při srovnání s dobou před 50 lety významně zvyšují a dosahují hraničních hodnot. Hladiny HDL-cholesterolu jsou normální. Manifestace ICHS ve věku od 40 let u mužů a od 50 let u žen není výjimkou (ojediněle se vyskytují i případy infarktu myokardu již ve 3. dekádě života). Klasickou klinickou manifestací FH je xantomatóza. Pravděpodobně v důsledku časné detekce nemocných s FH a účinné agresivní léčby se se šlachovými xantomy, s xanthelasma palpebrarum a arcus lipoides setkáváme méně často než před desítkami let. Obezita, diabetes mellitus (DM) ani hypertenze nepatří mezi typické klinické příznaky FH., Currently, the familial hypercholesterolemia (FH) rises the interest. The reason is that this genetic disorder is targeted by newly emerged and highly effective hypolipidemic agents, PCSK-9 inhibitors, lomitapid and mipomersen. Present paper discusses 2 patient study groups, before 50 years and nowadays. Although direct statistical analysis is impossible some changes in clinical features of FH might be found over the course of the time. In fact, the basic FH characteristic has not changed dramatically. Severe isolated hypercholesterolemia with total cholesterol 9–10 mmol/l, LDL-cholesterol 7–8 mmol/l and normal values of triglycerides dominates in laboratory analysis. Interestingly, the values of triglycerides increase and almost reach the pathological range in comparison to the values from the period 50 years ago. The values of HDL-cholesterol are normal. Manifestation of CHD in male patients over 40 years of age and in female patients over 50 years of age is not exceptional (rarely occur cases of myocardial infarction in third decade of age). Typical clinical manifestation of FH is xanthomatosis. The early detection and aggressive treatment in FH patients cause that xanthoma tendinosum, xanthelesma and arcus lipoides are less frequent as decades ago. Obesity, diabetes mellitus (DM) and hypertension do not belong to typical clinical sign of FH., and Richard Češka, Michal Vrablík, Tereza Altschmiedová, Martina Prusíková, Zuzana Urbanová, Josef Šobra
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
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
Ateroskleróza je difuzní onemocnění, které může vést k tvorbě nestabilního aterosklerotického plátu, jehož ruptura ohrožuje pacienta rozvojem akutní ischemické příhody. Typickou prezentaci takové nestability představuje aterosklerotický plát s mobilní komponentou. Pacienti s takovým plátem jsou ve vysokém riziku vzniku akutní ischemické příhody. V současné literatuře existuje mnoho prací zabývajících se problematikou mobilních plátů v oblasti karotického řečiště a hrudní aorty. Zcela však chybí data týkající se výskytu mobilních plátů v oblasti tepenného řečiště dolních končetin. V tomto článku prezentujeme vzácný případ kardiovaskulárně rizikového pacienta s generalizovanou aterosklerózou, u kterého byl zachycen mobilní aterosklerotický plát s vysokým embolizačním potenciálem v oblasti a. femoralis communis, jenž byl úspěšně odstraněn endarterektomií. Na příkladu této kazuistiky jsou následně diskutovány možnosti a limitace současných zobrazovacích metod v detekci mobilních plátů periferních tepen i volba optimálního terapeutického postupu. Klíčová slova: akutní končetinová ischemie – ateroskleróza – embolie – endarterektomie – mobilní plát – nestabilní plát – trombóza – vaskulární sonografie, Atherosclerosis is a diffuse disease which may lead to the development of unstable atherosclerotic plaque. Its rupture can result in acute ischemic event. The atherosclerotic plaques with a mobile component are typical presentations of such instability and patients with these plaques are at high risk of acute ischemic events. In the current literature, substantial data regarding the mobile atherosclerotic plaques in carotid arteries and thoracic aorta is published. However there are almost no data concerning the mobile plaques in the peripheral arteries of the lower limbs. We present a rare case of a patient with generalized atherosclerosis, in whom an asymptomatic mobile atherosclerotic plaque in the common femoral artery with a high embolic potential was diagnosed. This plaque was successfully removed by femoral endarterectomy. On the basis of this case, we review the possibilities and limitations of the current imaging methods in detection of mobile plaques in the peripheral arteries. Moreover optimal therapeutic approaches in such patients are discussed. Key words: acute limb ischemia – atherosclerosis – embolism – endarterectomy – mobile plaque – thrombosis – unstable plaque – vascular sonography, and Daniel Rob, David Ručka, Miroslav Chochola, Debora Karetová, Jan Hrubý, Eliška Kusová, Jean Claude Lubanda