Pregnancy-associated plasma protein A and proform eosinophilic major basic protein in the detection of different types of coronary artery disease.

Kryptor system was proven to be a rapid, standard method for pregnancy-associated plasma protein A and proform eosinophilic major basic protein (PAPP-A/proMBP) complex detection in coronary artery disease (CAD). No age and/or gender differences in 51 controls and 110 stable coronary artery disease (SCAD) patients were found. SCAD patients did not differ from controls and no difference in PAPP-A/proMBP levels with regards to the number of affected vessels was found. In 21 unstable angina pectoris (UAP), in 35 without and 66 with ST elevation acute myocardial infarctions (NSTEMI, STEMI respectively) patients PAPP-A/proMBP levels were increased (P=0.004 and P<0.0005, respectively). PAPP-A/proMBP levels did not correlate with cardiac troponin I (cTnI) in STEMI and NSTEMI patients. PAPP-A/ proMBP increase was more frequent than cTnI (P=0.036) within the early phase of STEMI. In NSTEMI patients PAPP-A/proMBP positivity was present in 50% of cTnI negative cases. Receiver operating characteristic (ROC) analysis revealed the highest diagnostic accuracy of PAPP-A/proMBP (0.919) in STEMI cTnI positive cases. The highest specificity/sensitivity PAPP-A/proMBP levels for particular acute coronary syndrome (ACS) types were 10.65-14.75 mIU/l. Combination of PAPP-A/proMBP with cTnI increases their diagnostic efficacy within the early phase of ACS. Our results suggest that PAPP-A/proMBP complex is involved in processes preceding vulnerable plaque development in ACS.

[Deferral of coronary intervention based on measurement of myocardial fractional flow reserve]. / Osud nemocných po odlození koronární intervence na základe merení frakcní prutokové rezervy myokardu.

BACKGROUND: Myocardial fractional flow reserve (FFR) is a useful method in assessment of functional significance of coronary stenosis. Deferral of intervention of angiographically intermediate lesion based on FFR measurement is safe in selected patient population as previously described. The aim of the study was to assess mid-term results after deferring coronary intervention of intermediate lesion in a non-selected patient population with no respect to the extent of coronary artery disease and to the results of stress tests if performed. METHODS: A coronary intervention of angiographically intermediate lesion (40 - 70% according to QCA) was deferred in a group of 50 consecutive patients (33 men, mean age 60.8 +/- 10.2 y.) on the basis of FFR > or = 0.75 (mean FFR 0.89 +/- 0.06). FFR was measured in 62 lesions (mean stenosis diameter 55 +/- 7%, left anterior descending 34 lesions, circumflex artery 13 lesions, right coronary artery 15 lesions). One-vessel disease was presented in 14 pts (28%), 36 pts (72%) presented with multivessel disease (two-vessel disease in 27 pts - 54% and three-vessel disease in 9 pts - 18%). Stress test was positive in 15 pts, in 1 pts. negative, and in 3 pts. non-diagnostic. All-cause mortality, cardiac mortality, non-fatal myocardial infarction (MI) and ischemia driven target vessel revascularization (TLR) were recorded during follow-up. Severity of angina pectoris (CCS classification) and a need for antianginal treatment (beta-blockers, nitrates, calcium channel blockers) at the baseline and at the end of clinical follow-up was recorded. RESULTS: Follow-up was completed in 49 patients (98%). Mean time of follow-up is 15.4 +/- 2 months (range 12 - 22 months, median 15 months), two patients died (4 %)--one from colon cancer, the other patient died from lung cancer, there was not any cardiac death recorded, two patients (4%) had target vessel revascularization. Estimated 22 months event-free (all-cause death, MI, TLR) survival was (mean +/- SEM) 86 +/- 7%. There was a significant difference in symptom severity--mean grade of angina pectoris at baseline was 1.8 +/- 1.3, at follow-up 1.1 +/- 1.0 (p < 0.05). There was not difference in use of antianginal drugs was same at baseline and at follow-up (1.7 +/- 0.8 vs. 1.7 +/- 0.7). Thirty-five patients (71%) were treated by statins. CONCLUSIONS: Deferring of coronary interventions of intermediate stenosis based on FFR measurement is safe in a mid-term follow-up. Despite of the same intensity of antianginal treatment there was a significant decrease in symptom severity.

[Assessment of speed of an anti-platelet effect after two different doses of acetylsalicylic acid by flocculation]. / Stanovení rychlosti nástupu úcinku protidestickového vlivu dvou ruzných dávek kyseliny acetylsalicylové agregometrickou metodou.

UNLABELLED: Acetylsalicylic acid inhibits aggregation of blood platelets through affecting arachidon acid metabolism--a precursor of thromboxan which is a strong platelet aggregation inhibitor. A standard method for measurement of aggregation activity blockade (in percents) of platelet rich plasma is turbidimetric aggregomethry based on spectrophotometric principle. According to results of recent studies administration of acetylsalicylic acid is one of the basic pillars of prevention of thrombotic complications in atherosclerotic arterial disease. Acetylsalicylic acid doses differ from study to study. An aim of our work was to measure speed of two different doses of acetylsalicylic acid. RESULTS: Level of aggregation activity blockade in samples of platelet rich plasma was measured by aggregometry in 26 healthy volunteers after administration of four inductors of thrombocyte aggregation (arachidon acid, adenosindiphosphate, collagen, and ristocetin). The samples were taken before administration and 120, 240, and 360 minutes after single peroral administration of 100 or 400 mg of acetylsalicylic acid. Samples of plasma were analysed immediately after sampling. Before drug administration there was no aggregation activity in 27.7% of the sample after arachidon acid administration, 28.3% after ADP administration, 21.5% after collagen administration and 25.3% after ristocetin administration. After administration of 400 mg of acetylsalicylic acid and administration of arachidon acid as an inductor 89.9% of the aggregation activity of the sample was blocked after 120 minutes, 89.6% after 240 minutes, and 90.6% after 360 minutes. After administration of adenosindiphosphate as an inductor 71.7% of the aggregation activity of the sample was blocked after 120 minutes, 68.3% after 240 minutes, and 69.9% after 360 minutes. And, after administration of ristocetin as an inductor 64% of the aggregation activity of the sample was blocked after 120 minutes, 66.4% after 240 minutes, and 54% after 360 minutes. Blockade of aggregation activity after collagen administration was not statistically significant. After administration of 100 mg of acetylsalicylic acid and administration of arachidon acid 83.8% of the aggregation activity of the sample was blocked after 120 minutes, 89.2% after 240 minutes, and 89.6% after 360 minutes. After adenosindiphosphate administration statistically significant blockade of aggregation activity was achieved after 360 minutes in the 56.7% of the sample. Also after collagen administration 42.5% of aggregation activity of the sample was blocked significantly after 360 minutes while ristocetin has not proved to influence aggregation in a statistically significant manner. CONCLUSION: Both doses of acetylsalicylic acid influenced aggregation activity of platelets in a statistically significant manner as soon as after 120 minutes following their peroral administration. However, they had different ability to influence platelets response to alternative ways of activation--by adenosindiphosphate, collagen, and ristocetin. 400 mg dose blocked these ways while 100 mg dose was efficient in blocking these ways after 360 minutes and in case of ristocetin--an inductor used to monitor platelet adhesion ability--100 mg dose has not led to statistically significant blockade at all.

Tissue factor, tissue factor pathway inhibitor and cytoadhesive molecules in patients with an acute coronary syndrome.

The tissue factor plays a crucial role in initiating blood coagulation after plaque rupture in patients with acute coronary syndrome. It is abundant in atherosclerotic plaques. Moreover, P-selectin, some cytokines, endotoxin and immune complexes can stimulate monocytes and induce the tissue factor expression on their surface. The aim of the study was to compare plasma levels of the tissue factor, tissue factor pathway inhibitor, P-selectin, E-selectin and ICAM-1 in patients with acute myocardial infarction, unstable angina pectoris, stable coronary artery disease and normal control subjects. In addition, plasma levels of the tissue factor, tissue factor pathway inhibitor, P-selectin, E-selectin and ICAM-1 were measured in the blood withdrawn from the coronary sinus in a subgroup of patients with unstable angina pectoris and stable coronary artery disease in which the difference between concentrations in the coronary sinus and systemic blood was calculated. A significant increase in tissue factor pathway inhibitor plasma levels was detected in patients with acute myocardial infarction (373.3+/-135.1 ng/ml, p<0.01) and unstable angina pectoris (119.6+/-86.9 ng/ml, p<0.05) in contrast to the patients with stable coronary artery disease (46.3+/-37.5 ng/ml) and normal subjects (45.1+/-14.3 ng/ml). The plasma levels of tissue factor pathway inhibitor were significantly increased both in the coronary sinus and systemic blood in the patients with unstable angina pectoris. There was only a non-significant trend to higher plasma levels of the tissue factor in patients with acute myocardial infarction and unstable angina pectoris as compared to the patients with stable coronary artery disease and normal subjects, the values being 129.1+/-30.2 pg/ml, 130.5+/-57.8 pg/ml, 120.2+/-45.1 pg/ml and 124.9+/-31.8 pg/ml, respectively. Plasma levels of soluble P-selectin was only slightly, but non-significantly higher in patients with unstable angina pectoris and stable coronary artery disease (184.2+/-85.4 ng/ml and 201.6+/-67.9 ng/ml, respectively) than in patients with the acute myocardial infarction (157.4+/-88.4 ng/ml) or normal subjects (151.4+/-47.1 ng/ml). The difference in plasma levels of soluble ICAM-1 between the blood withdrawn from the coronary sinus and systemic circulation correlated significantly with the corresponding difference in plasma levels of soluble P-selectin and E-selectin. In conclusion, the tissue factor and the tissue factor pathway inhibitor play a crucial role in the initiation of arterial thrombosis. The tissue factor pathway inhibitor levels are increased both in the systemic blood and in the coronary sinus of patients with the acute coronary syndrome.

[Angiographically marginally significant coronary stenoses--postponement of intervention based on measurement of myocardial fractional flow reserve]. / Angiograficky hranicne významné koronární stenózy--odlození intervence na základe merení frakcní prutokové rezervy myokardu.

INTRODUCTION: When evaluating angiographically marginal coronary stenoses (i.e. 40-70% reduction of the diameter of the arterial lumen) it is under certain conditions difficult to decide on their actual functional impact. Assessment of the fractional flow reserve (FFR) is a simple method based on assessment of intracoronary pressures during pharmacologically induced hyperaemia. For the severity of stenosis according to previous studies the liminal values is FFR lower than 0.75; furthermore it was proved that intervention of angiographically marginal stenoses with FFR values of 0.75 or more can be safely postponed. OBJECTIVE: Test the safety of FFR examination and take in a group of patients with marginally severe stenosis further steps according to results of FFR assessment. MATERIAL AND METHODS: During the period from January to Juky 2000 FFR assessments were made in a total of 34 patients (11 women, 23 men, mean age 62 +/- 12 years) who suffered from marginal stenosis of some coronary vessel. The FFR examination took place under pharmacologically induced hyperaemia after intracoronary adenosine administration. RESULTS: Measurements were made in a total of 41 stenoses. Only in two a value lower than 0.75 was found. In these patients coronary intervention was implemented; intervention was also made in two patients on account of technical problems and inconsistent results of FFR measurements. A FFR value of 0.75 or less was found in 37 stenoses (90%) and intervention was therefore postponed. Examination and the immediate subsequent course were without complications. CONCLUSION: According to initial experience FFR examination is a safe, simple and easily reproducible method. Based on the results of assessment and knowledge of the accomplished studies in the group of marginally significant stenoses in a great proportion of patients coronary intervention was postponed.