Imaging of all three coronary arteries by transthoracic echocardiography. an illustrated guide

BACKGROUND: Improvements in ultrasound technology has enabled direct, transthoracic visualization of long portions of coronary arteries : the left anterior descending (LAD), circumflex (Cx) and right coronary artery (RCA). Transthoracic measurements of coronary flow velocity were proved to be highly reproducible and correlated with invasive measurements. While clinical applications of transthoracic echocardiography (TTE) of principal coronary arteries are still very limited they will likely grow. The echocardiographers may therefore be interested to know the ultrasonic views, technique of examination and be aware where to look for coronary arteries and how to optimize the images. METHODS: A step-by-step approach to direct, transthoracic visualization of the LAD, Cx and RCA is presented. The technique of examination is discussed, correlations with basic coronary angiography views and heart anatomy are shown and extensively illustrated with photographs and movie-pictures. Hints concerning optimization of ultrasound images are presented and artifacts of imaging are discussed. CONCLUSIONS: Direct, transthoracic examination of the LAD, Cx and RCA in adults is possible and may become a useful adjunct to other methods of coronary artery examination but studies are needed to establish its role

Percutaneous transluminal angioplasty in patients with peripheral arterial disease does not affect circulating monocyte subpopulations

Monocytes are mononuclear cells characterized by distinct morphology and expression of CD14 and CD16 surface receptors. Classical, quiescent monocytes are positive for CD14 (lipopolysaccharide receptor) but do not express Fc gamma receptor III (CD16). Intermediate monocytes coexpress CD16 and CD14. Nonclassical monocytes with low expression of CD14 represent mature macrophage-like monocytes. Monocyte behavior in peripheral arterial disease (PAD) and during vessel wall directed treatment is not well defined. This observation study aimed at monitoring of acute changes in monocyte subpopulations during percutaneous transluminal angioplasty (PTA) in PAD patients. Patients with Rutherford 3 and 4 PAD with no signs of inflammatory process underwent PTA of iliac, femoral, or popliteal segments. Flow cytometry for CD14, CD16, HLA-DR, CD11b, CD11c, and CD45RA antigens allowed characterization of monocyte subpopulations in blood sampled before and after PTA (direct angioplasty catheter sampling). Patients were clinically followed up for 12 months. All 61 enrolled patients completed 12-month follow-up. Target vessel failure occurred in 12 patients. While absolute counts of monocyte were significantly lower after PTA, only subtle monocyte activation after PTA (CD45RA and β-integrins) occurred. None of the monocyte parameters correlated with long-term adverse clinical outcome. Changes in absolute monocyte counts and subtle changes towards an activation phenotype after PTA may reflect local cell adhesion phenomenon in patients with Rutherford 3 or 4 peripheral arterial disease

Nowy marker molekularny genu dla receptora endotelinowego typu A - brak zależności między polimorfizmem G1354C a chorobą miażdżycową tętnic u mężczyzn

Background. There is some evidence pointing toward endothelin system involvement in pathogenesis of atherosclerosis, manifested as coronary heart disease (CHD) and peripheral arterial occlusive disease (PAOD). Material and methods. In the study, 133 male patients - 46 with CHD (age 47.1 ± 4.12 years), 87 with PAOD (51.7 ± 5.31) and 87 healthy controls (46.35 ± 3.81) were genotyped by a polymerase chain reaction and restrictive fragments length polymorphism (PCR-RFLP) for a endothelin-A receptor (ENDRA) polymorphism. The allelic and genotype frequencies were compared between the groups using the χ2 test. Results. The novel single nucleotide polymorphism of the ENDRA gene (G1354C) was studied as a marker in CHD or PAOD. Genotype distribution in each of the groups did not deviate from the Hardy-Weinberg equilibrium. The allelic and genotype frequencies of the ENDRA gene did not differ between the groups. The allele G frequencies were 0.522 in CHD group, 0.506 in PAOD patients and 0.483 in controls. Conclusions. No genetic association between allelic variants of ENDRA and CHD or PAOD was found. It is unlikely that genetic variation at this ENDRA gene locus could contribute to the pathogenesis of arterial disease.Wstęp. Istnieją przesłanki wskazujące na udział układu endotelin w patogenezie miażdżycy objawiającej się klinicznie jako choroba wieńcowa (CHD) i choroba obwodowych naczyń tętniczych (PAOD). Materiał i metody. Badaniem objęto 133 chorych mężczyzn - 46 osób z CHD w wieku 47,1 ± 4,12 roku, 87 pacjentów z PAOD w wieku 51,7 ± 5,31 roku oraz grupę kontrolną 87 zdrowych mężczyzn w wieku 46,35 ± 3,81roku. Genotypowanie polimorfizmu genu dla receptora endotelinowego typu A (ENDRA) wykonano z zastosowaniem reakcji łańcuchowej polimerazy i polimorfizmu długości fragmentów restrykcyjnych (RFLP-PCR). Porównano częstości występowania alleli i genotypów pomiędzy grupami, posługując się testem χ2. Wyniki. Poszukiwano asocjacji genetycznej nowego polimorfizmu pojedynczego nukleotydu genu ENDRA (G1354) z występowaniem CHD i PAOD. We każdej z grup częstości występowania genotypów były zgodne z prawem Hardy’ego-Weinberga. Częstości alleliczne i genotypowe genu ENDRA nie różniły się istotnie w badanych grupach. Częstość występowania allelu G wynosiła 0,522 u osób z CHD; 0,506 u pacjentów z PAOD i 0,483 w grupie kontrolnej. Wnioski. Nie stwierdzono asocjacji genetycznej między wariantami allelicznymi ENDRA a CHD i PAOD. Zbadany wariant genetyczny genu dla receptora endoteliny nie wiąże się z ryzykiem miażdżycy tętnic