Objectives: Several studies have shown an association between elevated serum uric acid (SUA) levels and coronary heart disease and cardiovascular mortality. We investigated the relationship between SUA levels and the patency of saphenous vein grafts (SVG) after coronary artery bypass graft (CABG) surgery.
Study design: The study included 192 patients (152 men, 40 women) who underwent elective coronary angiography after a mean of 5.6 years following CABG surgery, which involved the use of at least one SVG. The patients were divided into two groups depending on the extent of SVG patency. Stenosis of 50% or greater within the SVG was accepted as hemodynamically significant. Serum uric acid levels were determined with the enzymatic colorimetric method.
Results: Ninety patients (71 men, 19 women; mean age 62±8 years) were found to have patent SVG. Stenotic SVGs were detected in 102 patients (81 men, 21 women; mean age 62±10 years). The time interval between surgery and angiography was significantly longer in the stenotic group (p<0.001). Compared to patients without SVG disease, the mean SUA level was significantly higher in patients with SVG disease (4.9±1.2 mg/dl vs 5.8±1.4 mg/dl; p=0.02). Serum uric acid levels were similar in patients having stenosis in a single vein graft or multiple vein grafts (p=0.224). In multiple regression analysis, SVG disease was independently associated with SUA (p<0.001), diabetes mellitus (p=0.028), and smoking (p=0.039).
Conclusion: Our results show that there is a significant association between increased SUA levels and SVG disease in patients undergoing CABG, which may justify the need for early screening for hyperuricemia and antiuricemic treatment.

Marfan syndrome primarily involves the musculoskeletal, cardiovascular, and ocular systems. Isometric exercises such as weight lifting lead to significant stress along the aortic wall and predispose patients to dissection and rupture. A 30-year-old male patient presented with a complaint of back pain. He had a history of two operations for recurrent inguinal hernia. His father and elder brother died on separate occasions following loss of consciousness after weight lifting. He also had a brother who had undergone an emergency operation for De Bakey type I acute aortic dissection after presentation with acute back pain following weight lifting. The patient was 180 cm tall, had elongated limbs and arachnodactyly. On auscultation, there was a diastolic murmur of 1-2/6 over the aortic area. A chest roentgenogram demonstrated mild cardiomegaly and mediastinal widening. Transthoracic echocardiography showed moderate aortic insufficiency with dilatation of the aortic root and ascending aorta. He was diagnosed as having Marfan syndrome and underwent complete replacement with a composite aortic valve-ascending aortic conduit. Histologic sections of the ascending aortic wall showed medial cystic and myxoid degeneration and loss of nuclei in the media. Von Gieson staining showed elastic fragmentation and loss of elastic lamellae. Screening of other family members showed Marfan syndrome in his sister and in one of his nephews. His other two brothers had Marfanoid habitus without findings of systemic involvement.

Little is known about the management of coronary thrombosis in myeloproliferative disease. The occurrence of myocardial infarction in myeloproliferative disease is mostly attributed to coronary thrombosis due to hyperviscosity and thrombocytosis. We presented three cases of acute myocardial infarction associated with polycythemia vera in one patient (male, age 33 years) and essential thrombocytosis in two patients (male, ages 36 and 46 years). None of the patients had diabetes mellitus, hypertension, hyperlipidemia, or a positive family history. One patient with early presentation received thrombolytic therapy, and all the patients were treated with aspirin, beta-blocker, angiotensin 2 receptor blocker, statin, lowmolecular- weight heparin, parenteral nitrate, and clopidogrel for acute coronary syndrome, and hydroxyurea for essential thrombocytosis. Control angiographies showed patent coronary arteries in all the cases.

Right ventricular outflow tract tachycardias comprise a subgroup of idiopathic ventricular tachycardias that occur in the absence of structural heart disease. Twelve-lead surface electrocardiography shows a left bundle branch block morphology and an inferiorly-oriented frontal axis during tachycardia. Non-sustained nature of arrhythmia and structure of the outflow tract makes catheter ablation of focal arrhythmia origin difficult. Herein, we presented ablation of right ventricular outflow tract tachycardia in a 32-year-old male patient using a new, simplified technique, described by Saleem et al., for three-dimensional mapping of the outflow tract. The patient was admitted with tachycardia of left bundle branch block with inferior axis morphology. In this technique, a spiral multipolar catheter was positioned in the right ventricular outflow tract and served as a guide for mapping and ablation. The patient was asymptomatic in the first and third months of the procedure.

Obstructive sleep apnea syndrome (OSAS) refers to recurring episodes of upper respiratory track obstruction and frequent decreases in arterial oxygen saturation due to repetitive occlusions of the posterior pharynx during sleep. Its prevalence in adult population is 4% in men and 2% in women. The most important causes of morbidity and mortality in affected patients are traffic accidents and cardiovascular complications including systemic arterial hypertension, coronary artery disease, congestive heart failure, and cardiac arrhythmias. The initial phases of apnea are associated with a transient increase in the parasympathetic activity resulting in bradyarrhythmias, followed by tachycardias due to increased sympathetic activity and arousal after the end of apnea episodes. The most frequent arrhythmia in OSAS is cyclic variation of heart rate. Most of the arrhythmias seen in OSAS are secondary to OSAS and disappear with OSAS treatment, without any electrophysiological conduction system abnormalities.

The output of publications in cardiovascular medicine during 2007 originating from Turkey’s institutions was evaluated based on data of the Web of Science. After exclusion of meeting abstracts and letters to the editor, articles in fulltext appearing in source publications of Science Citation Index CD Edition alone were included. A weighted credit system was used for items published jointly with a foreign or noncardiological discipline. Turkey’s publications rose to 187 articles and her share of world publication remained at 10.0 per mille. Four-fifths of the output originated from adult cardiology. The median impact factor of periodicals in which these articles were published remained stable as in the previous year, with 1.51 (interquartile range 0.99- 2.23). The number of papers published in journals with an impact factor 3.5 or over rose to 17. In the 4-year period of 2004-07, 501 papers were published in adult cardiology, 111 in cardiovascular surgery, and 32 in pediatric cardiology. While Turkey Yüksek Ihtisas Hospital, Siyami Ersek Cardiovascular Surgery Center, Gülhane Military Medical Academy, and Başkent University formed the four leading centers generating the cardiovascular publications, the established medical faculties persisted to fail to exhibit a performance commensurate with their past. Unless new reforms are put in place, short-to-mid-term future will continue to cause disappointment about these institutions.

Ekim 2007 tarihli 7.sayıda yayınlanan İntrakardiyak tümörü andıran mitral anülüs kalsifikasyonu başlıklı yazı için değerlendirme yazısıdır