Overview of coronary artery variants, aberrations and anomalies.

Coronary artery anomalies and variants are relatively uncommon congenital disorders of the coronary artery anatomy and constitute the second most common cause of sudden cardiac death in young competitive athletes. The rapid advancement of imaging techniques, including computed tomography, magnetic resonance imaging, intravascular ultrasound and optical coherence tomography, have provided us with a wealth of new information on the subject. Anomalous origin of a coronary artery from the contralateral sinus is the anomaly most frequently associated with sudden cardiac death, in particular if the anomalous coronary artery has a course between the aorta and the pulmonary artery. However, other coronary anomalies, like anomalous origin of the left coronary artery from the pulmonary artery, atresia of the left main stem and coronary fistulae, have also been implicated in cases of sudden cardiac death. Patients are usually asymptomatic, and in most of the cases, coronary anomalies are discovered incidentally during coronary angiography or on autopsy following sudden cardiac death. However, in some cases, symptoms like angina, syncope, heart failure and myocardial infarction may occur. The aims of this article are to present a brief overview of the diverse coronary variants and anomalies, focusing especially on anatomical features, clinical manifestations, risk of sudden cardiac death and pathophysiologic mechanism of symptoms, as well as to provide valuable information regarding diagnostic workup, follow-up, therapeutic choices and timing of surgical treatment.

Inadvertent cardiac phlebography.

We are reporting a case of a 80-year-old lady with effort angina who underwent coronary angiography through the right radial artery, using a dedicated radial multipurpose 5 French Optitorque Tiger catheter. The catheter was advanced into the left ventricle and a left ventriculogram was obtained, while the catheter appeared optimally placed at the centre of the ventricle and the pressure waveform was normal. A large posterior interventricular vein draining into the right atrium was opacified, presumably because the catheter's end hole inadvertently cannulated an endocardial opening of a small thebesian vein, with subsequent retrograde filling of the epicardial vein. Our case suggests that caution is needed when a dedicated radial catheter with both an end-hole and a side hole is used for a ventriculogram, as a normal left ventricular pressure waveform does not exclude malposition of the end-hole against the ventricular wall.

The role of sex and biochemical markers of inflammation in left ventricular remodelling, before and after surgery, in elderly patients with aortic valve stenosis.

INTRODUCTION: The aim of this study was to determine whether sex and biochemical markers of inflammation have a role in left ventricular (LV) remodelling after aortic valve replacement in elderly patients with aortic valve stenosis. METHODS: We studied 52 elderly patients with aortic valve stenosis (32 men, mean age 65 +/- 11 years and 20 women, mean age 68 +/- 9 years). Body surface area did not differ between men and women (1.81 +/- 0.15 versus 1.84 +/- 0.20, respectively). All patients underwent a complete echocardiographic examination for the determination of ejection fraction (EF), LV mass and mass index, peak and mean systolic pressure gradient, aortic valve area, early (E) and late (A) transmitral flow wave velocities and their ratio (E/A), tissue Doppler indexes of the mitral annulus (Sa, Ea, Aa), and the E/Ea ratio. In addition, levels of high sensitivity C-reactive protein (hsCRP), tumour necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) were measured from venous blood samples taken before, and 10 days, 3 months and 6 months after aortic valve replacement. RESULTS: LV mass decreased from 297 +/- 99.7 g before aortic valve replacement to 210 +/- 67 g 3 months after surgery and to 210 +/- 74 g 6 months after surgery (p<0.001). LV EF did not change significantly (p=0.836). Peak and mean systolic pressure gradients decreased, whereas aortic valve area increased after valve replacement (p<0.001). These changes were similar in men and women. In women Sa was greater (p=0.017) and the E/Ea ratio lower (p=0.025) than in men. The long-term changes in peak and mean pressure gradients, aortic valve area and LV mass after aortic valve replacement were well correlated with the long-term changes in hsCRP, TNF-alpha and MCP-1 in both men and women. CONCLUSIONS: LV remodelling is similar in elderly men and women with aortic valve disease who have similar body surface area. Although inflammatory markers are not correlated with echocardiographic parameters before aortic valve replacement, a strong correlation exists after operation. This correlation is similar in men and women.

Time course of C-reactive protein, tumour necrosis factor-alpha and monocyte chemoattractant protein-1 following the surgical treatment of patients with aortic valve stenosis.

INTRODUCTION: Patients with aortic valve stenosis show elevated levels of inflammatory markers in peripheral blood. The aim of this study was to investigate the time course of changes in these markers and to look for sex-related changes in their biological behaviour following aortic valve replacement. METHODS: We studied 52 patients (32 men, 20 women) who underwent aortic valve replacement and had no concomitant coronary artery disease. Men and women did not differ significantly with respect to age, body surface area, or body mass index. Levels of high sensitivity C-reactive protein (hsCRP), tumour necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) were measured from venous blood samples taken before, and 10 days, 3 months and 6 months after aortic valve replacement. RESULTS: Baseline hsCRP levels were 5.34 +/- 5.71 mg/dl and 7.64 +/- 7.46 mg/dl for men and women, respectively. Levels increased significantly at 10 d (49.11 +/- 32.15 and 51.63 +/- 34.3 mg/dl, p < 0.001), then reduced at 3 m (5.85 +/- 5.04 and 8.49 +/- 7.69 mg/dl, p < 0.001) and 6 m (3.41 +/- 0.83 and 7.84 +/- 7.32 mg/dl, p < 0.001). Women had higher levels than men at 6 m (p = 0.027). Levels of TNF-alpha reduced progressively, from 212.4 +/- 119.5 and 255.7 +/- 171.3 pg/ml at baseline, to 121.6 +/- 47.7 and 150.0 +/- 33.5 pg/ml at 10 d, 134.7 +/- 25.3 and 138.6 +/- 30.9 at 3 m, and 48.7 +/- 8.8 and 44.9 +/- 10.5 pg/ml at 6 m (p < 0.001). MCP-1 levels also reduced progressively, from 157 +/- 64.8 and 145.6 +/- 13.4 pg/ml at baseline, to 128.6 +/- 18.8 and 122.7 +/- 10.3 pg/ml at 10 d, 49.0 +/- 12.4 and 56.6 +/- 11.5 pg/ml at 3 m, and 29.1 +/- 6.4 and 30.6 +/- 7.3 pg/ml at 6 m (p < 0.001). The time course of the changes in these indexes was identical for men and women, except that 6 m hsCRP levels were significantly higher in women. CONCLUSIONS: After aortic valve replacement, hsCRP levels show an early increase followed by a decrease, whereas both TNF-alpha and MCP-1 are reduced progressively. The time course curve is identical in men and women, except that hsCRP levels are higher in women than in men 6 months after aortic valve replacement.