The issue, whether the economic status at baseline in 1990 affected the development of coronary events, was investigated prospectively among participants of the Turkish Adult Risk Factor Study. Five ineome brackets had been delineated at baseline. However, since the number of paricipants in the highest bracket constituted no more than 5% of the sample, brackets 4 and S were combined, and analysis was canied out in 4 brackets. Information on the mode of death was obtained from first-degree relatives and/or the health personnel of the local health office; definite or suspect coronary heart disease (CHD) was diagnosed in survivors based on history, physical examination of the cardiovascular system and Minnesota coding of resting ECGs. Definition of CHD comprised fatal and nonfatal myocardial infa rction, stable angina and/or myocardial ischemia which had developed since the baseline survey. After having exclu ded participants with a CHD diagnosis at onset, a total of 237 deaths and 274 fatal and nonfatal CHD occurred in a mean 9.3 years' follow-up of 2648 men and women aged 20 years or over (mean age 41.6 [±5]). All-cause mortality was not found to be significantly associated with ineome brackets in a logistic regression analysis when controlled for age and gender or when three major risk factors were added to the model. Fatal and nonfatal CHD, adjusted for gender and age, exhibted a s ignificant excess in bracket 3 (p<0.047), and a significant reduction (p<0.044) in the highest bracket. Relative risk in these two ineome brackets were 1.27 and 0.77. Adding 3 major factors into the model, disclosed family ineome to be signifi cantly associated with coronary events (p<0.047) as a trend. The excess risk in bracket 3 was attenuated to nonsignificant levels and conversely RR in the highest bracket was further reduced to 0.7 (p

Abstract |Full Text PDF

Objective: Coronary interventional procedures are expected to induce soluble P (sP)-selectin , a cell adhesion molecule, release through the local injury on the coronary lesion. The ai m of this study was to evaluate the magnitude of sP-selectin secretioı1 in response to vascular injury after balloon angioplasty (PTCA) and its relationship with restenosis. Methods: The study group consis ted of 26 consecutive patients undergoing successful electi ve first PTCA. Patients suffering from any kind of infectious disease and systemic immunological illness or receiving an immune-modulating ınedication were excluded. Fifteen patients (age- and sex-matched) with normal coronaries served as controls. All procedures were performed with the same protocol. Plasma sP-selectin levels were measured before and immediately and 24 hours after the invasive procedure. ELISA method was used for the quantitative laboratory measurement of sPselectin. Results: sP-selectin levels before the in vas ive procedure were significantly higher when compared to control group and significantly increased 24 hours after PTCA (study group: serially 68±23 ng/ml , 63±2 1 ng/ml, and 133±20 ng/ml; control group 25±7ng/ml). There were no changes in sP-selectin levels immediately after the procedure. During the follow-up period, restenesis developed in 8 patients. The pre- and post 24 hour P-selectin levels were higher in patients who developed restenosis (for baseline values: 84±8 ng/ml vs 59±22 ng/ml, p=0,006;and for 24th hour values ı57±5 ng/ml vs ı20±13 ng/ml , p=O,OOı ) . Conclusion: 1. sP-selectin levels are increased in patients with coronary artery disease. 2. PTCA induces a significant rise in sP-selectin levels which may indicare a potential role of this mediator in the response of the vessel wall to PTCA injury. These findings suggest that PTCA triggers an inflammatory response leading to further sP-selectin secretion. 3. Patients in whom restenosis developed had higher levels of pre and post PTCA levels of P-selectin. There might be a relationship between the restenosis and P-selectin levels which is thought to be reflecting a triggering effect.

There is stili controversy about early and Iate results of sequenital use of internal thoracic artery (ITA) in coronary artery bypass (CAB) operations. In thi s study, we report on a series of 430 consecutive patients who had undergone CAB operations between 1986 and 1998, with the use of at least one sequential IT A graft. The patients, 379 men and 51 women had a mean age of 56,4 years (range 29 to 80 years). Both ITA grafts were usedin 227 (52,8%). A total of 1744 (mean 4,05 per patient) distal coronary anastomoses were performed. 1172 of which (mean 2,72) were arterial and 980 of which (mean 2,28) were sequential ITA anastomoses. Thirty-day mortality was ı ,8% (n=8 patients). Perioperative myocardial infaretion occurred in 12 patients (2,8%) and 5 of them (1,2%) were confined to the sequential IT A grafted area. Follow-up ranged from ı month to 13 years (mean 63±37 ,7 months) for 372 patients (86,5%). Nine patients died during follow-up period. According to Kaplan-Me ier method, 5 and 10 year survival rate was 95,6% and 93,4% respectively. Coronary angiography was performed in 64 patients (17,2%) after a mean of 33 months ( ıO day to ı o year). In 31 of these patients angiography was performed due to returo of symptoms. Overall patency ra te of sequential IT A anastomoses was 9 ı , 7 % (1 11/1 21 ). Two patients underwent repeat CAB operations Sequential use of IT A grafts w as not associated w ith the increased perioperative mortality and morbidity and has the potential to improve the long-term results of CAB surgery because of excellent patency ra tes of sequential IT A anastomoses.

Biventricular pacing has been suggested as an effective therapeutic method in patients with advanced congestive heart fa ilure (CHF) and intraventricular conduction delay. We aimed to evaluate effects on cardiac perforinance and elinical status of biventricular pacing in patients with CHF and intraventricular conduction delay. Patients with advanced CHF (NYHA class III-IV) and intraventricular conduction delay were selected for biventricular pacemaker implantation. NYHA classification, exercise test with Naughton protocol, quality of life score and echocardiographic measurements (left ventricular dimensions, ejection fraction, dP/dt, diastolic fill ing time, the duration of mitral regu rgitation and QRS-aortic ejection interval) before implantation and at the end of the follow-up were compared. The long-term effects (lı±8 months) of biventricular pacing were evaluated in 23 patients. When basa! and at the end of the foll ow-up values were compared, mean NYHA class (3,6±0,5 1 2,6±l, ı , p=O,OOO ı ), mean exercise capacity (1,9±1 ,4 1 3,5±2,2 MET, p= O,OO ı ) and mean quality of life score (65±15 1 42±28, p= 0,00 ı) w ere improved. The mean LV dP/dt Türk Kardiyol Dem Arş I.UUI; LY: (484±150 1 744±312 mmHg/see, p= 0,007), mean ejection fraction (%25±8 1 %32±8, p= 0,004), mean diastolic filling time (324±111 1 402±78 msec, p= 0,004) increased and, mean QRS duration (175±24 1 149±16 msec, p= 0,0001), mean QRS-aortic ejection interval (163±36 1 135±34 msec, p= 0,005), mean LV end-systolic diameter (62±8 1 56±8 mm, p= 0,02) decreased by permanent biventricular pacing. Permanent biventricu lar pacing is a treatment method that may improve cardiac performance and elinical status in patients with advanced CHF and intraventricular conduction delay.

Regular exercise may indirectly benefit the heart by favorably modifying lipid and lipoprote in levels. Exercise training can decrease total blood cholesterol, serum triglycerides and, low density lipoprotein (LDL) cholesterol and can increase antiatherogenic high density lipoprotein (HDL) cholesterol. Aerobic exercise not only quantitatively induces changes in lipoprotein concentrations but also induces favorable changes in lipoprotein subclasses. Exercise causes a shift from atherogenic LDL phenotype B to LDL phenotype A and increases cardioprotective HDLı cholesterol concentrations. Exercise training al so improves apo A 1, apo A 1 apo B ratio and lipoprotein (a) levels significantly. The mechanisms by which exercise may improve the lipid profile remain uncertain. However, exerciseinduced lipolytic enzyme activity that promotes the degradation of triglyceride-rich lipoproteins appears to be a factor.

A patient who received a dual chamber implantable cardioverter defibri llator due to long QT syndrome presented with frequent shocks. High dual chamber pacing rate was found to be responsible for triggering frequent premature ventricular beats which initiated polymorphic ventricular tachycardia. Possible mechanisms were discussed.