In the old and newly recruited cohorts of the Turkish Adult Risk Factor Srudy consisting of 2350 men and ıvomen (n1ean age 52±12 years). body mass index (BM/). ıvaisr circwnference and waist-to -lıip rario (WHR) were assessed cross-secrionally and prospectively. Coronary lı e art disease (CHD) ıva s diagnosed based 0n elinical jindings and Minnesota coding of resring electmcardiograms. Ar standardized age. meanıvaist circumferellce and BM/ inmen ıvere 90.7 cm and 27.3 kglm2. respectively. and inıvomen 90.8 ile 29.1 kglm2. respectiı•ely.lt is esiimared rlıar 10.5millioll adıı/ts (22 .6% ofmell and 61% of women) in Turkey may be designated ro lıa ve abdomina/ obesity. Fol/oıving difference inmagnitude or ratio oj variab/es e.xisted across tlıe /ıiglıest and fowest quintifes ojwaist circumference: 22 mg/d! in apofipoprotein (apo) B. 3.5-fold to 2-fo/d in C-reactive protein (CRP). 2 to 2.4-jofd in fasring senun ilmtfin concentrations. Furtlıermore. diabetes was morefrequent by 2.2-fold in men and by 4.8-jofd in women across rlıese quintifes. In a fogisric regression cmalysis over a 4-year jolfow-up. waist circumference significantly tHediered nonfatal and/orfatal CHD risk in men. and among men and women combined. independent of9 otlıer salie/If risk factors, imparting 35% excess risk for eaclı inerement of 12 cm (= 1 SD) ofıvaist circumfe rence. ltı tlıe presence of tlıe lauer. BM/ failed to contribute to CHD prediction. lt ı va s concluded that abc/om ina/ obesity in Turkish adults not only mbstantially elevatec/ tlıe con centratimıs of im porta//( cardiovascu/ar risk jactors suc/ı as serum apo B. ilısu/in. CRP. and tlı e prevalence oj type ll diabetes. but alsa COIIfribwed independently to cardiovascular morbidity and mortality. particularly among men. Tlı e ''curve" betıveen CHD risk and tlıe stated a tlıerogenic riskjactors suggested that Turkishmen witlı a ıvaisi circumference of96 cm slıou ld be considered m the "action level" . These findings should guide future public heart health policies.

This Jtudy was conducted in /0 centres to evaluate tire efficacy and safety of micronizedfenofibirare il ı cı coft.ort of Tu rkish dyslipidemic patients. Ir was an open study wirlıour a control group. 98 patients (53% were women). were selecred and 72 patients between tlıe age group of 18 to 75 years (54±10.5). wir/ı rype Ila (n=25). rype /Ib (n=43) and rype IV (n=4) dyslipide111ia. ıvere l'olwrtarily included in the study. After ar leasr a 4-ıveek waslı-ow period wirlr a srandardised die ı. 200 mg once-daily dose ofmicronisedfenofibrate was given to parienis w!rose dyslipidemia was proven by laborarory test s. Efficacy and safety parameren were assessed at the begimıing and at tlıe 4tlı. 6tlı and 12tlı ıveeks of treamıelll in 72 patients wlıo completed tlıe study according to tlıe protocol. hı comparison to the baseline values, patiellts witlı type Ila dyslipidemia slıowed a decrease of /8.5% in total clı o/este ro/ (TC) /eve/. and 27.4% inlow density lipoprotein clıo lesterol (LDL-C) /eve/ and 32.6% (49.6% as median value) in triglyceride (TC) !eve/ and an increase of 19.7% inlıiglı density lipoprotein clıolestero/ (HDL-C) !evet after 12-week treatment. All tlıe ParialiO/ıs in Flı e lipid va/ues were coiiSidered statistically significant (p

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Primary pulmonary lıype rlemion ( PPH) isa disease wir/ı a poor prognosis w il h 110 effective treatment. Sildenafil. a se/ecrive phosp/ıodiesterasf!;-5 enzy11ıe inhibilor. awses ptt!monary vasodilatalion by increasing eyetic guanosine monoplıosplı ate /eve/s. In order lo investigcue 1/ıe effecl and safely of slıorl-temı orallı iglı-dose sildenafil treatment on hemodynamic pammeters in patienls wilh PPH. 8 parients were given sildelıafil ata dose of 200 mg/day (50 mg q.i .d) for 3 days. Righr m ıd le.flhearl catlıeterizaıion was performed be.fore lrea/ment and 1 h oıır af/er the lm'f dose of si/denafil. No significant change in mean systemic arterial blood pressııre (90±9 mmHg. pre-treatmetl/; 88±7 mmHg. post-lreatment; p=0./25) was obserl'ed wilh a sigtıificant decrease inmeatı pulmonary artery pressure (60±1/mmHg. pre-treaunellf; 54±14mmHg. post-tremment; p=0.008). No s ide effect reqııiring withdrawa/ oj si/denafil was observed. Wlıen palients were eva/uated indiviclııally. tlıe decrease inmean pulmonary artery pressure ıvas over 20% in 2 patients. benveen 5 and /0% in 2 patiellfs and belo ıv 5% in 4 patienls. Thus. sildena.fil treatmeni decreased meatı pu/monary artery pressure by a selective vasodilatory effect on pttlmonary vascu/ar bed in patients ıvitlı PPH. Nonetheless. this effect is variable among patients.

Arrhymogenic right ventricular dysplasia (ARVD) is afamilıal. progressive heartmuscle disease. lt is clıaracterized by fatty infiltration of the right ventricle. w/ı i c lı frequently results in life threatening cardiac arrlıytlımias. lt is one oj the importaııt causes of sudden cardiac eleatlı in tlıe young. Familial inlıerimnce of the disease is well known. Tlıe most CO/ll/liOn partem of inlıeritance is alliosomai dominam. A recessive syndromic form oj ARVD associateclıvitlı woolly /ıair and pa/mopla111ar keratodemıcı. refen·ed as Naxos disease, has also been reported. According to o11r knowledge. ıve noıv prese1ıt tlıefirsl ARVD cases oj two jamilies witlı an aııtosomal recessive non-syndromic form of t/ıe disease. Botlı of these families origin(l(e ji'om Rize . Alljanıi/y members cons ideredfor tlıe study wıderwent elinical examination. 12-/ead e/ectrocardiograplıy (ECC). 24 lı !-lo/ter elecrmcardiograplıy and eclıocardiograplıy. Magnetic resonance imaging ıvas done in all a.ffecteclfamily members. The diagnosis of ARVD was done according to intemational/y established diagnostic criteriafor ARVD. Our initialmolecular s1udies e.rc/11(/ed the known ARVD !oc i on clıromosomes 1. 2. 3. 10. 14 and 17. TlıiJ resnit provides evi de nce for furt/ıer genetic lıeterogeneity of tlıe disease. A.ffected members of these families w il/ be c/inically followed-up and tlıese jwure sflldies ıvill give mo re insights into rhe progression and prognosis of recessive fonns oj ARVD.

Aim: Mitral regurgitation in milral valve prolapse (MVP) has a different character, and it is of high importance to assess the severity of regurgitation accurately in these patients. To our knowledge, this is the first study comparing the echocardiographic nıethods in assessing the severity of mitral regurgitation (MR) due to MVP. Metlıods: Forty-seven patients with MVP having at least moderate mitral insufficiency established by Doppler echocardiographic methods were studied. Quantitative Doppler was usedas the reference method and regurgitarı fraction (RF) caleulated. Severe MR was diagnosed if RF was 50%. Doppler flow mapping was us ed to de termine regurgitan jet area (JNLAA),flow eonvergence (EROA-PISA) and Vena Canıraeta width (VCW). Systolie pulmonary verıousflow reversal (SPVFR) and E wave veloeity were alsa obtained. Results: Presenee of severe MR (n=28) was sigrıifıeantly eorrelated to EROA-PISA (r=0.85, p

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A tweutyeiglıt year old ma/e patient first preselli ed in !995 w !ten !te was 21 years old w it/ı symptoms of !temoptysis and dyspnea. T!te diagnosis of primary pulmonary !typertension was m ade after excluding ot/ter etiologies of pulmonary arterial !typertemion.T!te pat i em w/to !tad a history of familial primary pulmonary lıyperlension was tremed wit!t ca/ci um c/ıamıel blackers and warfarin for 2 years. Because of tlı e increase in t!te patient's symptoms t!te tlı erap/ıy was clıanged to intravenous prostacyc/in. Wit!t this t!teraplıy tlıe symptoms of tlıe patient recovered and lıis survival was prolonged. However. most of tlı e side e.ffects and complications related to iutravenous prostacycline infiısionwere also seen. After recieving prostacyc/infor 5 years. t!te symptoms started agailı. We decided to add endot/ıelin receptar mıtagonists(bosentan) and/or plıop/ıodiesterase in!tibitors(sidenafi/) to t!te treatmelli reg inıeu. We are reporting tftis case to s ftm·e our experience with long temı epoprosteuol treatment. Au overview of the modem treatment of primary pulmouary lypertension is also given.

Anomalous origin of the right or left coronary ar tery from the aorta is reported 0.5%-1.5% of patients wıdergoing coronary angiograplıy. Tiiccar E. and Eliımı A.just reported coronary artery abnormalities in adult Turkish populaıion. They analysed 5000 coronary angiograms. Twemy-five (0.5%) coronary arteries witlı anomalous origins werejound. We are preseniing an extremely ra re riglıt coronary origilı abnormality. In this case riglıt coronary ar tery ariginates from left amerior deseeneling coronary artery. According to prevailing opinion. coronary segment s ıvitlı an anomalotts course are no more vulnarable to obstmctive disease than normal segments in tlı e same individual. Coronary artery anomalies identified during cardiac cat/ıerization. only 10.1% lıad another congenitallıeart deject. Coronary ar tery anomalies are very important because coronary ar tery mıomalies rank secondasa cardiovascular ca use oj sudden deattı in tlıe young. belıind hypertrophic cardiomyopathy.

Twiddler's syndrome is characterized by coilinıg of the pacemaker lead due to the rotation of the pacem ak er generator on it s long axis. "Reel syndrome" is another form of Twiddler's syndrome. It occurs due to the rotation oftlıe pacemaker generator on i ts vertical axis witlı subsequent coi/ing of tlıe pacemaker generator on i ts vertical axis witlı subseqııent coiling of the pace1uaker leads around the pul se generator. In this report wedeseribed a patient w it/ı a two-clıamber pacemaker who presented w ith sudden onset abdominal pulsatian and subsequently diagnosed as Reel syndrome. Pacenıaker interrogatioıı slıowed effective atrial and ineffective ventricu/ar pacing. On chest X-ray. atrial lead was straightened. ventricular lead was in the vena cava

Cardiac invo/vemellt in Becker Muscular Dystroplıy. inc!tıding dilaıed cardiomyopatlıy, mi/d to moderate degree mitral regurgitaıion, cardiac condııc tion system abnormalities and various arrlıytlıymias, is one of the leading problems during the progression oj tlıe disease ( 1 ,2). But, complete atrioventricular b/ock associated wit!ı Becker Muscular Dystroplıy wlıich necessitates permaneni pacemaker implantation isa ra re condition. We reported a patiellf witlı Becker Muscular Dystroplıy which complicated complete atrioventricular block and dilated cardiomyopathy.