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Woven coronary artery is extremely rare. It is characterised by thin channels arising from the coronary artery and reanastamosis at the distal portion. A 62-year-old man was diagnosed of coronary artery disease. Coronary angiography showed 3-vessel coronary artery disease. The distal right coronary artery derived 3 twisting thin channels, and the inferior thin channel sprouted second-class thin channels, which then reanstomosed distally. He received off-pump coronary artery bypass. The present patient had woven coronary artery with a more complex configuration of thin channels different from the previously reported cases. (Folia Morphol 2013; 72, 3: 263–266)
A 57-year-old female patient with a family history of coronary artery disease admitted to our hospital for the coronary check-up. A coronary angiography was performed with ECG-gated 128 slice dual source computed tomography. Multidetector computed tomography (MDCT) showed, in addition to the normal coronary arteries, a persistent levoatrial cardinal vein (LCV) draining into vena cava superior. ECG-gated cardiac MDCT is a useful tool showing the origin, course, and drainage site of LCV. (Folia Morphol 2013; 72, 3: 274–277)
Angiotensin I-converting enzyme (ACE), which plays an important role in blood pressure regulation, and methylenetetrahydrofolate reductase (MTHFR) involved in homocysteine metabolism belong to a large group of polypeptides which may be po­tential risk factors for atherosclerosis and coronary artery disease (CAD). To assess whether polymorphisms of the genes encoding these peptides are associated with CAD in Silesian we conducted a study among 68 individuals suffering from CAD (in­cluding 52 cases after myocardial infarction), 51 subjects with positive family history of CAD and 111 controls. We analysed the distribution of genotypes and allele fre­quencies of the insertion/deletion (I/D) polymorphism in the ACE gene using PCR am­plification, and the C677^T polymorphism in the MTHFR gene using PCR-RFLP analysis. We found that D allele frequency was significantly higher in CAD patients (61%) than in controls (43%) (P = 0.001, OR = 2.06). The D allele carriers (DD + ID geno­types) were more frequent in the CAD patients (85%) compared to control group (65%) (P = 0.003, OR = 3.14), whereas the familial CAD risk group shows the highest frequency of the ID genotype (57% vs 43% in controls). In contrast, the MTHFR polymorphism does not seem to be associated with the disease. Our data indicate that in Silesian CAD patients the disease is strongly associated with carrier-state of the ACE D allele, but not with the C677->T transition in the MTHFR gene.
Bilirubin, an antioxidant in the blood, plays a role in protection from atherosclerosis. The level of bilirubin is highly correlated to the incidence of coronary artery disease (CAD). Unconjugated bilirubin is conjugated with glucuronic acid through the reaction of uridine 5′-diphosphate-glucuronosyl transferase 1A1 (UGT1A1). The interactions of CAD and the variations in the coding regions of the UGT1A1 gene have never been evaluated. The purpose of this study was to analyze the influence of the UGT1A1 variant on the incidence of CAD. There were 135 participants in this study: 61 in the experimental group, who had CAD, and 74 in the control group, who did not have CAD. The blood samples from all 135 participants were collected and assayed to clarify the relationship between bilirubin and CAD. The assay of the polymerase chain reaction and the sequence of the UGT1A1 gene were examined to find the gene’s polymorphisms. The bilirubin levels for the participants in the control group were significantly higher than for the patients in the CAD group. Although the concentration of bilirubin in the UGT1A1 variant was higher than the wild type for the patients in the CAD group, there was no significant difference in the polymorphism of UGT1A1 between the patients in the CAD group and the participants in the control group.
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Helicobacter pylori infection in coronary artery disease

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The role of inflammation in the pathogenesis and progression of coronary artery disease (CAD) has been increasingly discussed, but still remains unclear. Inflammatory changes in the vessel wall play an important role in the pathogenesis of atherosclerosis. Systemic inflammatory reaction can be detected by showing increased plasma levels of different proinflammatory cytokines and acute-phase proteins. Infectious agents have been linked to coronary heart disease on epidemiological and pathogenetic grounds. The prevalent condition and the exact mechanism of initiation of atherosclerotic vascular disease remain unclear. Nevertheless, many similarities exist between the processes of inflammation and atherogenesis, and the evidence is growing for the role of an active inflammation in the atherosclerosis in the coronary circulation and elsewhere. Although the seroepidemiological and eradication studies have suggested a causal relationship between Helicobacter pylori (Hp) infection and coronary heart disease; the issue is still controversial. The detection of Hp specific DNA in atheromatous plaque material from coronary arteries, but more important, the reduction in restenosis of coronary vessels after Hp eradication could be interpreted as an evidence for the involvement of a Hp infection in the progression of CAD induced by a local inflammatory process.
Nitric oxide (NO) is present in exhaled air in humans and its level may decrease in heart diseases. Nitrates are metabolized to NO. In the present study we prospectively investigated how coronary disease treated with oral nitrates and physical exercise influence the exhaled NO concentration (exNO). The study was performed in 44 patients with stable coronary artery disease (CAD) treated with oral nitrates (31 nonsmokers and 13 smokers) and 34 healthy volunteers (21 nonsmokers and 13 smokers). End-tidal concentration of exhaled NO was measured by the use of a chemiluminescence method. The Bruce protocol of an exercise test was performed in 21 coronary patients and 11 volunteers. NO was measured before and 2-5 min after the test. We found no significant differences in the exNO level between healthy controls and CAD patients as analyzed either for the whole groups or non-smoker and smoker subgroups (6.01 parts per billion (ppb) vs. 4.91 ppb; 7.02 ppb vs. 5.89 ppb; 3.62 ppb vs. 3.33 ppb, respectively). However, the coronary patients group, as a whole, had lower exNO after exercise (4.22 ppb vs. 3.84 ppb, P<0.01). The difference persisted after division of this group into non-smokers and smokers: 5.19 ppb vs. 4.79 ppb, P<0.05 and 3.63 ppb vs. 3.27 ppb, P<0.05, respectively). The level of exNO changed inappreciably after exercise in control subjects. We conclude that coronary disease and oral nitrates, in themselves, do not influence the exhaled NO concentration. Physical exercise, on the other side, lowers the exhaled NO level in coronary patients.
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Leukotrienes are lipid mediators produced via 5-lipooxygenase pathway of arachidonic acid. At least two cysteinyl-leukotrienes receptors are highly expressed in the heart, including the conduction system. Coronary angiography or angioplasty is accompanied by release of cysteinyl leukotrienes into coronary circulation and into urine. We tested the hypothesis that inhibition of leukotrienes biosynthesis would affect the conductance system function. In a double-blind placebo controlled study, patients with stable angina undergoing elective coronary catheterization or angioplasty were randomly assigned to 48 hrs treatment with a 5-lipoxgenase inhibitor (n=54) or placebo (n=49). ECG Holter recording was carried out for 24 hrs before and after the procedure and urinary leukotriene E4 measurements were done. Inhibition of 5-lipoxygenase caused 26% reduction of urinary leukotriene E4, associated with: 1) decrease in heart rate by about 7%, 2) enhanced heart rate variability; 3) protection against depressions in atrioventricular conductance and ventricular repolarization induced by the procedure. No effects on either arrhythmias, or ECG patterns of ischemia were noted. We conclude that pharmacological inhibition of 5-lipoxygenase, shortly before percutaneous coronary intervention, reveals specific actions of leukotrienes on the heart rhythm. Inhibitors of 5-lipoxygenase might be of interest as a novel class of cardiac drugs affecting the conductive system.
In recent decades a significant raise in the incidence of myocardial infarction among young women has been recorded. It is presumed that, apart from the classical risk factors, other reasons exist for premature atherosclerosis in young women, related to the homeostasis of gonadal hormones. The aim of the study was to analyze the levels of gonadal hormones (estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone, testosterone and dehydroepiandrosterone) measured in the luteal phase, in 65 normally menstruating women post myocardial infarction (MI) and to investigate a possible relationship between the hormone profile and selected coronary artery disease (CAD) risk factors. The levels of gonadal hormones: estradiol, progesterone, follicle-stimulating hormone, luteinizing hormone, testosterone and dehydroepiandrosterone were measured in the luteal phase. All examined women had normal mean levels of gonadal hormones. In the post MI patients leading a sedentary life style, a significantly lower mean progesterone concentration was observed (16.29 ± 9.11 versus 29.43 ± 21.14 nmol/l, p = 0.05) and significantly higher mean testosterone concentration (2.34 ± 0.98 versus 1.76 ± 1.09 nmol/l, p = 0.05) when compared to patients from the same group, but leading a more active life. In obese post MI women (BMI ≥ 30 kg/m2) a lower mean concentration of progesterone was detected (18.02 ± 8.12 versus 26.16 ± 14.72 nmol/l, p = 0.05), than in slimmer patients from the same group. In post MI women with a positive family history for CAD, a significantly higher mean concentration of testosterone was detected (2.31 ± 1.22 versus 1.67 ± 0.74 nmol/l, p = 0.05) than in patients with no family history. The results suggest a correlation between levels of gonadal hormones and classical CAD risk factors.
Congenital anomalies of systemic veins are usually asymptomatic and found incidentally during ultrasonography, computed tomography (CT) or magnetic resonance examinations performed for other clinical indications. Persistent left superior vena cava (PLSVC) with absent right superior vena cava (RSVC) is the congenital aberration in the thoracic venous system which occurs in only 0.09% to 0.13% of patients who have congenital heart defects. In this paper, we present the extremely rare case of a 72-year-old male with PLSVC associated with an absence of RSVC, referred for coronary CT angiography. Multidetector CT angiography is a powerful tool for the detection of venous anomalies, which is essential before invasive procedures such as the implantation of pacemakers. (Folia Morphol 2013; 71, 3: 271–273)
The phenotypes of CAD related to arterial hypertension co-occurrence were analysed in 174 male patients and 117 control men for the associations with the polymorphisms of the MTHFR gene (677C>T and 1298A>C) and the PON1 gene (-108C>T) in relation to age at diagnosis (less or equal and more than 50 years). We noted the increased frequency of the three MTHFR genotypes: CC/AC, CT/AA and CC/CC in the CAD group (65.5%) in comparison to the control group (45.3%), corresponding to the 2.3-fold increased risk of CAD for men with these genotypes (95%CI (1.4-3.7); p=0.0005). The higher increase in risk of CAD was noted for the younger men (OR=3.6; 95%CI(1.6-8.3); p=0.002) and lower for the older (OR=1.8; 95%CI(1.0-3.4); p=0.03). In the normotensive men the greater impact on CAD risk had the homozygous genotypes; the 2.3-fold higher risk was associated with MTHFR CC/AC, CC/CC and TT/AA genotypes (95%CI(1.2-4.4); p=0.01). After adjustment for age, the association between CAD and MTHFR was significant only for the younger normotensive men (OR=2.8; 95%CI (1.0-8.0); p=0.04). Additionally, we found that the younger part of the control group was characterized by higher frequency of the low expression PON1 -108T allele and PON1 -108TT genotype (0.54 and 31.9% respectively) in comparison to the older men (0.41 and 17.1% respectively; p=0.03).
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Why study sympathetic nervous system?

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Cardiovascular diseases are the most frequent causes of morbidity and mortality around the world. However, during last decades, an improvement was made in diagnosis and therapy of cardiovascular diseases, there was still a need for better understanding of their pathophysiology. Among neurohormonal systems, SNS plays a central role in cardiovascular regulation in both health and disease. Involvement of SNS in pathogenesis of hypertension, coronary artery disease or heart failure is well known and proved. Methods such as microneurography, direct catecholamine measurements, heart rate variability or baroreflex sensitivity assessment allowed studying sympathetic activity and its influence on cardiovascular disorders. Although introduced into scientific practice methods of SNS evaluation are not commonly used in the clinic. However, two of the methods: analysis of heart rate variability (HRV) and baroreflex sensitivity (BRS) were recommended as the diagnostic tools and can be found in clinical guidelines as basic assessment methods.
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