Safety of balloon pre-dilatation in the treatment of severe carotid artery stenosis.

AIM: To assess early outcome of predilatation prior stenting of severe carotid artery stenosis and to evaluate early major adverse cardiovascular and cerebral events (MACCE). PATIENTS AND METHODS: The study group consisted of 265 consecutive patients (200 males, 65 female, mean age 66.7 ± 8.6 years) in whom 275 percutaneous transluminal angioplasty (PTA) procedures of carotid arteries were performed. Staged carotid stenting was performed in patients with bilateral carotid stenosis. Neuroprotection with a distal protection device was used in all cases. The patients were divided into two groups: direct carotid stent implantation without previous pre-dilation was performed in 233 patients (direct stenting group) and predilatation was performed in 42 patients (predilatation group). Early events were recorded and analyzed subsequently. RESULTS: We treated 275 carotid stenoses and the stent was implanted in all patients. Ten patients (3.7%) were treated by staged carotid artery stenting (CAS) due to bilateral carotid artery disease. The technical success rate was 97.1%. During 1-month follow-up, the prevalence of primary endpoint was 2.18%. The prevalence of MACCE at 30 days was higher in the predilatation group (2.4% vs. 2.1%; p = 0.924). Also periprocedural rate of hypotension was higher in predilatation group (7.1% vs. 1.7%; p = 0.04). CONCLUSIONS: Balloon predilatation prior to stenting can be performed to treat severe carotid artery stenosis with acceptable periprocedural complication rate.

Elevated uric acid and functional mitral regurgitation in dilated cardiomyopathy.

BACKGROUND: Recent findings suggest that there is a close relationship between chronic heart failure and uric acid. AIMS: The aim of the study was to assess whether increased uric acid levels in patients with dilated cardiomyopathy might correlate with the degree of functional mitral regurgitation (MR). MATERIALS AND METHODS: Sixty two consecutive patients diagnosed with dilated cardiomyopathy were included in the study. The patients were classified according to severity of functional MR into two groups: mild-moderate functional MR (ERO < 0.2 cm2) and severe functional MR. RESULTS: The patients with severe functional MR had significantly higher serum uric acid levels compared to patients without severe functional MR (6.34 ± 1.61 mg/dL vs 5.43 ± 1.17 mg/dL respectively, p = 0.012). Furthermore, tenting area, an important predictor of functional MR severity, was moderately correlated with the serum uric acid levels (r = 0.351, p = 0.005). It was also shown that the serum uric acid concentrations were inversely correlated with left ventricular (LV) ejection fraction, and positively correlated with LV volumes. There was also a significant relation between the serum uric acid and left atrial volumes and also brain natriuretic peptide (BNP) levels. CONCLUSIONS: In conclusion, this study demonstrates that elevated serum uric acid levels in patients with dilated cardiomyopathy are correlated with the severity of functional MR and echocardiographic volume indices.

Two brothers with a 7.0 kb gene deletion associated with isolated growth hormone deficiency type 1A.

Familial growth hormone deficiency type 1A is an autosomal recessive disease, caused by various homogenous deletions of both alleles of growth hormone gene 1 (hGH1). The hGH1 gene deletion is an event occurring between the 5' and the 3' flanking regions by unequal recombination, which causes a deletion in the hGH1 gene, mostly of 6.7 kb and rarely 7.6 or 7.0 kb in size. Two brothers diagnosed with GH deficiency syndrome were sent to our hospital for further evaluation. DNA samples of the probands and controls were amplified by PCR; restriction endonuclease analysis was done with Sma I enzyme and the patterns were evaluated. Gel electrophoresis results showed that the two brothers had a 7.0 kb deletion. These are the third and fourth cases reported with a 7.0 kb deletion. Both patients responded well to replacement therapy and did not develop antibodies against rGH. No other relatives presented with macro deletions in the hGH1 gene.

A Turkish family with 6.7 Kb deletion associated with isolated growth hormone deficiency type 1A.

Familial growth hormone deficiency type 1A is an autosomal recessive disease caused by homogenous deletions of both alleles of growth hormone gene 1 (hGH1) in various patterns. The hGH1 gene deletion is an event that probably occurs between the 5' and 3' flanking regions by unequal recombination, and results in deletion of the hGH1 gene in different patterns. Deletions are mostly 6.7 kb and rarely 7.0 kb, 7.6 kb and 45 kb in size. A four-year-old girl diagnosed with growth hormone deficiency syndrome was send to us for further evaluation. DNA samples of the patient, her parents and controls were amplified by polymerase chain reaction (PCR); furthermore, restriction endonuclease analysis was done with Sma I enzyme and the patterns were evaluated. Our gel electrophoresis results show that the gene deletion pattern of the patient represents a homogenous 6.7 kb deletion, while her parents had a heterogeneous 6.7 kb deletion pattern.