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Aspirin non-responsiveness has been described as having a normal closure time (CT) by platelet function analyzer (PFA)-100 assay despite confirmed treatment with aspirin. There is no standard definition of aspirin non-responsiveness by PFA-100, with a variety of cut-off values having been used. We proposed an alternative definition of aspirin non-responsiveness by PFA-100 assay.One hundred eighty-four patients with diagnosis of stable coronary artery disease or diabetes mellitus were included in the study. Blood samples were drawn before and after the 7 days of aspirin therapy. An individual was labelled as aspirin non-responder if his/her post-aspirin CT was not 2SD above his/her baseline CT, where SD was calculated from the baseline CTs of the study population. Aspirin non-responsiveness was also defined as having a normal post-aspirin CT (or =193 s) regardless of pre-aspirin CT.The baseline CT ranged 82-187 s (mean 129.1 +/- 27.5, median 128 s) in the study population. At the end of 1 week of aspirin administration, CT increased to a mean of 260.7 +/- 63.6 s (range 102-301). According to our definition, 28 (15.2%) of 184 patients were aspirin non-responders. Univariate analysis indicated that aspirin non-responsiveness was closely associated with gender (P = 0.012) diabetes (P = 0.006), smoking (P = 0.0496) and hypertension (P = 0.021). Multivariate analysis identified diabetes (P = 0.016) as the only significant independent predictor for the presence of aspirin non-responsiveness. Thirty-four of 184 patients (18.5%) classified as aspirin non-responders according to the second criteria. Seven patients with prolongation of post-aspirin CT more than 2SD were classified as aspirin non-responders by the second criteria. Only 1 patient without prolongation of CT more than 2SD was classified as aspirin responsive by the second criteria.Definition of aspirin non-responsiveness as post-aspirin CTsor =193 s might overestimate the prevalence of aspirin non-responsiveness. Nevertheless, definition of aspirin non-responsiveness by PFA-100 must be standardized and its utility as a predictor of cardiovascular events needs to be further investigated.

Platelets of diabetic patients have been reported to be less sensitive to aspirin. The aim of this study is to compare a medium (300 mg) and low (100 mg) dose of aspirin on platelet function in diabetic patients.We have included one hundred and two patients with type 2 diabetes mellitus. Platelet function was measured as closure time (CT) with the Platelet Function Analyzer (PFA)-100 before the administration of aspirin. Initially the patients were given 100 mg aspirin once daily for seven days, and then the measurements were repeated. If the CT exceeded the upper limit of 300 s, the study was terminated. If not, the patients continued the aspirin therapy with a dose of 300 mg daily for another seven days, and the CTs were measured again.After taking 100 mg aspirin, the CT significantly increased from 126+/-29 s to 256+/-66 s (p0.001). In 68 of 102 (67%) patients, the CT increased to 300 s. In the remaining 34 patients, the baseline CT was 113+/-29, and increased to 170+/-45 s after 100 mg aspirin (p0.001). In these patients, there was a further increase in the CT from 170+/-45 to 229+/-75 s following 300 mg aspirin (p0.001). On average, the CT was increased by 60% and 39% following ingestion of 100 and 300 mg aspirin, respectively. CT300 s were obtained in 15 (44%) of 34 patients after 300 mg aspirin.Although, a daily dose of 100 mg aspirin effectively inhibited platelet function in a majority of diabetics, a considerable proportion of patients showed a greater platelet inhibition with the use of 300 mg aspirin. The PFA-100 closure time may be used to separate those patients who require a higher dose of aspirin to achieve desired antiplatelet effect.

Electrocardiographically, the QT interval is shortened, ST segment is depressed, and T wave becomes negative in hypercalcemia. The use of diuretics in cases with hyperparathyroidism decreases the excretion of calcium, causes changes in bone-calcium turnover and parathyroid hormone activity, and forms hypercalcemia. A 67 year-old Turkish female patient in whom we electrocardiographically observed a J wave is presented as a hypercalcemic case with primary, hyperparathyroidism aggravated by the use of a thiazide diuretic.

Background: The ventricular late potential (VLP) detected using the technique of signal average electrocardiography (SAECG) interacts with several factors, primarily time. Method: In this study, we examined the interaction, over time, of VLP with the initial ischemic burden and enzyme levels in acute myocardial infarction. Patients diagnosed as having acute myocardial infarction were included in the study. On the first day, the patients underwent enzyme analysis and electrocardiography (ECG) follow-up every 6 hours. A 24-hour ambulatory ECG was performed on the seventh day in order to determine the ischemic burden. SAECG findings (TQRS, RMS, LAS were obtained on the seventh day, in the first and third months. The study was continued with the patients who did not require angioplasty as decided with angiographic evaluation in the first month. Results: The study included 30 patients with acute myocardial infarction (mean age 51 ± 12, 28 males and 2 females). The initial mean CK-MB levels and the mean ischemic burden were 98 ± 31 U/L and 44 ± 96 minutes. The TQRS (ms), LAS (ms), and RMS (μV) values (mean ± SD) obtained at day 7, month 1, and month 3 are 97 ± 12, 96 ± 9, 103 ± 11, P = 0.01; 31 ± 10, 31 ± 11, 32 ± 10, P = 0.46; 43 ± 28, 41 ± 26, 33 ± 25, P = 0.01, respectively. We observed that the TQRS and RMS values changed significantly with time, but these levels of significance disappeared when adjusted for the initial ischemic burden and CK-MB levels (P = 0.06; P = 0.53). The VLP frequency was 33% at day 7 and 23% at month 3. Unlike the CK-MB level, the initial ischemic burden was significantly different between the patients with and without VLP at month 3 (150.85 ± 149.28, 12.34 ± 26.48, P = 0.001). When tested together with age and gender, it was found that the high initial ischemic burden increased the possibility of VLP (OR: 24, Cl: 2.09–279.52, P = 0.01) at month 3. Conclusion: SAECG findings in patients with myocardial infarction changed with time; however, this change occurred depending on the initial ischemic burden and CK-MB levels. Of these, only the initial ischemic burden, especially in high levels, was a determinant for the presence of VLP in the late period of myocardial infarction. A.N.E. 2002;7(3):242–246

Two-dimensional color Doppler tissue imaging (CDTI) has so far been used, in general, to evaluate ventricular function. In this study, the left atrial appendage (LAA) tissue velocity was measured by CDTI. LAA function in 38 patients with mitral stenosis in sinus rhythm (SR) and 19 healthy subjects undergoing transesophageal echocardiography were examined by CDTI. Systolic tissue appendage velocity (SaV, m/s) was measured at the tip of the LAA in the basal short-axis view. LAA emptying (LAAEV) and filling (LAAFV) velocities (m/s) were also recorded 1 cm below the orifice of the appendage. LAA ejection fraction was also measured. In addition, two-dimensional imaging was used to determine the presence of thrombus and/or spontaneous echo contrast (SEC). Patients with mitral stenosis in SR had significantly decreased LAAEV, LAAFV, SaV, and LAA ejection fraction compared to controls (0.34 +/- 0.15 vs 0.72 +/- 0.17, 0.37 +/- 0.13 vs 0.63 +/- 0.19, 0.050 +/- 0.015 vs 0.071 +/- 0.093, and 39 +/- 14% vs 69 +/- 13%, respectively, P < 0.001, P < 0.001, P < 0.001, and P < 0.001). Among the patients with mitral stenosis in SR, 10 patients had SEC and one had LAA thrombus. Compared with patients without SEC, patients with SEC had decreased LAAEV, LAAFV, SaV, and LAA ejection fraction (0.24 +/- 0.05 vs 0.37 +/- 0.16, 0.29 +/- 0.05 vs 0.39 +/- 0.14, 0.039 +/- 0.087 vs 0.055 +/- 0.015, and 28 +/- 14% vs 43 +/- 12%, respectively, P = 0.01, P = 0.02, P = 0.01, and P = 0.006). In conclusion, these results suggest that the LAA dysfunction may occur in patients with mitral stenosis in SR and CDTI can successfully be used for the quantification of contraction at the tip of the LAA.

Aim : The purpose of this study was to document treatment profiles in 850 patients surviving acute myocardial infarction at 17 academic hospitals in Turkey. Methods and results : Pharmacological management data of acute myocardial infarction survivors were collected and divided into three categories: drugs which patients received before hospitalization, during the hospitalization, and at hospital discharge. Data regarding medical history, complications during hospitalization, MI extent (Q wave or non-Q wave), infarct location and diagnostic and revascularization procedures were also recorded. This study is based on the 850 patients who met the diagnostic criteria for initial acute MI in the period examined. Among 850 patients with myocardial infarction enrolled 408 (48%) received thrombolytic therapy. The median time interval from symptom onset to initiation of thrombolytic therapy was 196 min. The most commonly used thrombolytic agent was streptokinase (93%). Thrombolytic recipients were younger, and presented sooner after onset of symptoms. Among patients receiving thrombolytic therapy, concomitant pharmacotherapy included aspirin (95%), intravenous heparin (93%), intravenous nitroglycerin (91%), oral beta-blockers (44%), calcium channel antagonists (13%), and angiotensin converting enzyme inhibitors (41%). The lipid lowering therapy was only used in 4% of all patients, and was given to 18% of patients with hyperlipidemia. Conclusion : Current usage rates of thrombolytic therapy in Turkey are lower than expected, but when compared with previous reports it increased. Although adjunctive treatment with intravenous heparin and intravenous nitroglycerin is usually used, beta-blockers appear to be underused and calcium channel blockers appear to be overused. The lipid reducing therapies were infrequently prescribed.