In a I O-year follow-up of the original co h ort of the Turkish Adult Risk Factor Study, plasma lipids were determined by the e n zyınat ic method with a Reflotron apparatus in 1862 subjects (mean age 50.6 ±14), and trends were studied after stratifying for sex and age groups. In addition, serum Iipoproteins and apolipoproteins AI and B were determined in 2416 participants comprising the original and new cohorts, the latter by (Behring) turbidimetry. Randam plasma samples were validated in a reference Jaboratory. Af ter age-standardization, mean concentrations of total cholesterol (TC) were not significantly changed in the ı 990s whereas those of triglyceride rose by 4 and 12.8 mg/dJ in men and women, respectively. The presence of high ratios of apo B/apo AI (0.92 and 0.82) in men and women represented an adverse setting of coronary risk. Data of the survey allawed to estimate the presence of 800.000 Turks in whom lipid-towering drugs were being adınİnistered - mostly not in secondary but primary prevention. Strong correlations were noted in univariare analysis between triglycerides and apo B and (inversely) HDL-cholesterol levels in both genders. Among the apparently healthy population at baseline, TC/HDLC ratio proved to be the only significant independent predictor of future fatal and nonfatal coronary heart disease, in a logistic regression model comprising ll risk parameters. Relative risk of 1.295 signified an associated 68% excess coronary risk between a ratio of - for example - 4 and 6. In conclusion, over the past 10 years, an annual increase by 1 mg/dl in plasma triglyceride levels constituted the principal change in plasma lipids among Turks. A prospective evaluation for the prediction of fatal and nonfatal CHD, showed the TC/HDL-C ratio to be the best independent lipid marker which thus should draw special consideration in the risk assessment of Turkish adults.

In a 1 O-year follow-up of the co h ort of the Turkish Adult Risk Factor Study, blood pressure (BP) was measured in 1895 subjects (mean age 50.6 ±14), and trends were studied after stratifying for sex and age groups. Criteria for the diagnosis of coronary heart disease (CHD) and death from CHD canformed to those previously described. When age was kept constant, overall net mean BP of the sample population rose by 4.4/2.7 mmHg in men and 6.4/4.2 mmHg in women over 10 years. The prevalence of hypertension, defined as being on antihypertensive medication, or displaying a blood pressuı·e ~ 140 and/or ~90 mmHg, in the total cohort of 2455 participants, was 40% in men and 51.6% in women, indicating the existence of 11.5 million hypertensive Turkish adults. Forty-five % of them were estimated to be under drug treatment and that hypertension control was achieved only in 42% of themas defined by keeping BP at normal or mildly hypertensive !eve! s. Waist circumference again had the strongest correlation between systolic or diastolic pressure in both genders, followed by body weight. Logistic regression analysis for death from CHD ata lO-year follow-up among participants free of CHD at baseline revealed systolic BP to be significant independent predictor in both genders such that each inerement of 10 mmHg was associated with 59% excess coronary mortality. For nonfatal CHD, systolic BP had an independent impact only in men and at borderline significance, and diastolic BP carried a borderline significance solely in women. A high pulse pressure or a low diastolic pressure were shown for the first time among Turks to predict coronary events, at least in men.

Coınprehensive ca rdiac eval uations are recoınınended for all doxorubicin-treated patients to detect subclinical cardiac failure. In this study we exaınined the prolongation of con-ected QT interval (QTc) in doxorubicin treated rabbits. Male New Zealand rabbits (n=24) were randomised into two groups. Group A (n=l2) was given doxorubicin (2ıng/kg once a week) and Group B (n=l2) was given saline during 10 weeks. QTc intervals were ıneas ured in every two weeks from ex tre ınity leads for each aniınaL At the end of the study cardiac saınples were examined histologically and each animal was given a histopathological score between O and 4 according to degree of cardiomyopathy. Histopathological scores were 3 for one rabbit and 4 for the remaining 1 1 rabbits in Group A and were O for all the rabbits in Group B. QTc intervals at the beginn ing and at the end of the study were 248.5± 17 .7 msec. and 298.8±13.7 msec. consecutively (p=0.012) in Group A, 243.8±17.6 msec. and 245.4±17.8 msec. consecutively (p>0.05) in Group B. Prolongation of QTc was statistically significant at the end of the 4th week (262.3±17.9 msec.) when compared with the basa! value in Group A (p<.05). As a result, prolongation of QTc, a measure of myocardial repolarization may reflect injury to myocardial cells and is an easy and inexpensive method that can be used in the detection of subclinical cardiomyopathy in doxorubicin treated patients.

Although the pressure gradient between the normal and stenotic vascular regions is known to be most important factor for collateral vessel development, factors which are responsible for vari ations among patients with ischemic heart disease are not well known. Likewise, it is stili not clear whether diabetes mellitus (DM) has any effect on coronary collateral development. Coronary angiography, the most commonly used technique for studying collateral ci rculation, may not be accu rate in assessing col lateral c irculation because most collaterals are situated intramurally or too smail to visualize angiographically. Intracoronary pressuı·e ınea sureınent is a new technique to provide accurate and quantitative in formation about the collateral circulation. We therefore sought the effects of DM on coronary collateral vessels in patients with CAD by using intracoronary pressure ıneasureınent technique. Methods: Study population consisted of 40 patients (20 diabetic) with chronic ischeıni c heart disease referred to angiography laboratory due to their ischemic syınptoıns verifed prev iously with at least one non- invasive test. All of the patients had singlevessel disease with more than 70% narrowing and underwent PTCA and/or s tent iınplantation procedure for this vesseİ. After angiography, fibereptic pressure ınonitoring guide-wire (Pressure wireRadi) was advanced to the stenosis to be dilated. The same wire was used as guide wire for angioplasty catheter. During coınplete occlusion with balloon inflation, distal pressure was recorded as coronary wedge pressure (CWP). As a more va luable p ara ın ete r , collateral flow index (CFI) was determined by the ratio of siınultaneously ıneasured CWP (mmHg) to aortic pressure (Pa, mmHg, obtained from the guiding catheter) (CFI: CWP/Pa). Results: Pressure measurements were performed on 20 diabetic and 20 non-diabctic patients. The mean value of CWP was I 8. 1 ± 8.6 mmHg in the diabetic group and 26.8 ± 9.6 mmHg in the non-diabctic group (p<0.05). The ınean value of CFI was also significantly higher in the non-diabctic group (0.1 7 ± 0.08 in diabetic group and 0.25 + 0.09 in nondiabctic group, p<0.05) In conclusion, it was deınons trated that coronary collateral vessel development is impaired in diabetic patients compared with nondiabetic patients.

It was the purpose of our study to assess the validity of EuroSCORE in our patient population. Between March 1999 and September 2000, information on risk factors and mortality was collected for 625 consecutive adult patients undergoing heart surgery with cardiopulmonary bypass. EuroSCORE was used for risk stratification. Mean age ± standard deviation was 58.6 ± 10.8 and 28.5% of the patients were female. The ineidence of common risk factors were as follows: diabetes mellitus (17 .6%), hypertension (38.7%), chronic airway disease (8.2%), recent myocardial infaretion (3 1.4% ), chronic renal failure ( 1.7%), extracardiac arteriopathy (5.9%), reduced left ventricular ejection fraction (35.7%), previous cardiac surgery (2.7%), and non-elective operation (4.3%). Regarding epidemiology, isolated CABG accounted for 82% of adult cardiac surgery. The patients with 2 or Jess points were allocated to low risk group, with 3 to 5 points to moderate risk group, and with 6 or more to high risk group. Expected and observed mortality rates for each group were obtained. Expected and observed mortality rates for low (n = 253), moderate (n = 249), and high risk (n = 123) groups were, 1.2 ±0.8 vs O; 3.9 ± 0.8 vs 0.8 ± 0.9;_ and 8.4 ± 3.2 vs 3.2 ± 0.2, respectively. Overall, the expected and observed mortality rates were 3.7 ± 3.1 vs 0.96±9.8. There was no overlap between the 95% cofidence intervals of observed and expected mortality in all three groups (p

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In the pathophysiology of acute coronary syndrome (ACS) plaque vulnerability is much more iınportant than plaque size and stenosis severity. Plaque vulnerability is the consequence of inflammatory activity within the plaque. Rupture-prone vulnerable plaques are characterized by 1) a soft lipid core occupying at least 50% of the plaque v o l uın e, 2) a thin fibrous cap with reduced collagen content, 3) a high density of monocytes/macrophages , lyınphocytes, ınast cells, 4) low density of smooth muscle cells, 5) a high t issue facto1 content. Inflaınmatory cells (macrophages) produce specific metalloproteinases that degrade collagen within the fibrous cap. Macrophages and lyın phocytes also secrete cytokines that are cytotoxic for smooth muscle cells and activated macrophages can also induce smooth muscle cell apotos is by direct eel! contact. The result is a decrease in the number of smooth muscle cells and decreased collagen synthesis. The plaques with large soft lipid pool and a thin fibrous cap cannot resist local mechanical stresses and easily rupture with subsequent superimposed thrombosis and results in ACS. What causes inflammation in the atherosclerotic plaque? Where does the inflammatory stinıul us coıne from? At the present, the exact mechanism is not known; however, it is fair to state that oxidised LDL, oxidative stresses, low grade chronic infections and autoimmune respanses have a role in plaque activation. The evidence that in flaınmation is an essential feature of vulnerable plaque has !ed to intensive search for ischemic markers of plaque inflammation. High-sensitive -C reactive protein (hs CRP) has been found to have a strong correlation in the risk of a future acute cardiac event.

The rupture of a vulnerable atherosclerotic plaque usually underlies acute coronary syndroınes. Early identification of such a plaque is essential for the prevention from subsequent elinical events. The methods for identifying vulnerable plaques should demonstrate both the intdnsic features- leading to rupture i.e. increased lipid content, thin fıbrous cap and increased inflammatory activity and, systemic tendeney for the plaque progression. Therefore, these methods for the detection of vulnerable plaques can be classified into two groups: l.Locally identifying methods, 2.Systeınic markers Türk Kardiyol Dem Arş 2001; 29: 330-333 Most of the locally identi fy ing methods are invasive. Intravascular ultrasound and coronary angioscopy are the leading methods. Electron beam computed tomography (EBCT) which calculates the vascular calcification score, magnetic resonance imaging (MRI) techniques which help in characterization of the plaque structure and thermographic methods d em a n s ır a tin g the increased vascular heat production due to i n fl a mın ato ry activity are other promising ın ethods. Systemic markers which reflect the increased and ongo ing inflaınmatory activity ineJude C-reactive protein, serum aın ilo id A, interleukin 6, activated protein C res istance and seropositivity for chlamydia pneumonia. The best approach should probably be the evaluation of the information obtained from locally identifying methods in the light of systemic markers and risk factors.

Acute coronary syndromes results mainly from rupture of a vulnerable atherosclerotic plaque. Regular exercising, quit to smoke, lipid lowering agents, angiatensin converting enzyme inhibitors have been shown to reduce the ineidence of acute coronary syndromes presumably through plaque stablization. The evidence supporting plaque stablization by these agents and the mechanisms by which these agents stablize plaques are discussed in this rev iew.

Cor triatriatum is characterised with a membranous diaphragm which divides the left atrium into two chambers, the proximal chamber accepts the pulmonary veins and the distal one communicates with left ventricle via mitral valve. The size of the orifice between chambers is the main determinant of physiologic abnormalities and elinical syınptoms. Herein, we report two cases of cor triatriatuın . The first case was a 7-year-old boy who was admitted to our hospital with failure to thrive and palpitation. Echocardiography showed obstructive type of cor triat riatuın. Cardiac catheterization revealed elevated p ulın o n ary artery and pulmonary capillary wedge pressures. The meınbrane was removed surgically. The second case was a 1-year-old boy with syın pt oms of heart failure. Echocardiography showed perimembranous VSD and a nonobstructive membranous diaphragm which div ided the left atrium into two chambers. Cardiac catheterization revealed moderate left-to-right shunt and mild pulmonary hypertension. The patient underwent surgical procedure for VSD closure and even though it was not an obstructive one, the membrane of cor triatriatum was removed. Both patients are is well after operation. This report illustrates the wide symptoınato l ogy of cor triatriatum.

Coronary stenting with stent-grafts have been reported to be a safe and quick treatment option for coronary artery aneurysms although long-term results in large patient groups are not available. We report a case of saccular aneurysm of proximal lefı anterior descending artery (LAD) associated with anterior myocardial infaretion in the absence of any significant stenosis. The aneurysm was successfully obliterated by using a polytetrafluoroethylene-coated coronary artery stent. However, the patient presented with anterior reinfarction two months after stent implantation. Coronary angiography demonstrated sustained occlusion of the coronary aneurysm and severe focal stenosis at the proximal edge of the stent, involving the ostium of LAD. The patient underwent coronary bypass surgery, and he is stili asymptomatic 3 months after the operation.