The association between intravascular ultrasound (IVUS) signs of plaque instability and plasma levels of biomarkers was determined in patients with unstable angina and non-ST–segment elevation ...myocardial infarction (UA/NSTEMI).
Fifty-two patients underwent coronary angiography and IVUS 8 ± 5 hours after the onset of chest pain. IVUS analysis included plaque morphology, disruption, thrombi and eccentricity, lumen, external elastic membrane, and plaque plus media areas of culprit lesion and reference segments and arterial remodeling. Plasma levels of the thrombin activation system (thrombin-antithrombin complex TAT, tissue factor pathway inhibitor TFPI, and prothrombin fragments 1+2 F1+2) and plasmin activation system (tissue and urokinase-type plasminogen activator t-PA and u-PA, plasminogen activator inhibitor-1 PAI-1, and D-dimer) were measured with enzyme-linked immunosorbent assay kits before angiography.
Elevated levels of TAT (7.2 ± 6.0 μg/L), F1+2 (1.8 ± 1.0 nmol/L), TFPI (179.1 ± 131.0 ng/mL), PAI-1 (95.4 ± 54.6 ng/mL), t-PA (10.6 ± 8.8 ng/mL), and u-PA (2.6 ± 0.9 ng/mL) were found in patients with UA/NSTEMI. The serum levels of D-dimer (40.0 ± 39.5 ng/mL) remained in reference range. Expansive and constrictive remodeling were found in 18 (35%) and 12 (23%) patients, respectively. Expansive remodeling of the culprit lesion was associated with significantly higher plasma levels of PAI-1 (121.6 ± 55.0 vs 87.7 ± 61.5 and 77.4 ± 42.8 ng/ml, P = .039), and u-PA (3.0 ± 1.2 vs 2.2 ± 0.5 and 2.5 ± 0.7 ng/mL, P = .026) as compared with constrictive and neutral remodeling. Increased plasma levels of u-PA were associated with plaque rupture (3.0 ± 0.7 vs 2.5 ± 0.9 ng/mL, P = .062). Plasma levels of PAI-1 and u-PA correlated positively with plaque plus media (P = .0297 and P = .0093) and external elastic membrane areas (P = .010 and P = .0002).
Elevated levels of biomarkers of plasmin activation system are associated with signs of plaque instability of culprit lesion in UA/NSTEMI and might therefore serve as non-invasive determinants of the population that is at high risk for subsequent adverse events.
Inadvertent Duplicate Publication Laggner, Anton N.; Kaik, Gerhard; Lenz, Kurt ...
British medical journal (Clinical research ed.),
02/1985, Letnik:
290, Številka:
6467
Journal Article
A new preparation of nifedipine for sublingual application in hypertensive urgencies was investigated in a prospective study. Patients admitted to the Emergency Department with a persistent elevation ...of systolic blood pressure (SBP) greater than 190 mmHg and/or a diastolic blood pressure (DBP) greater than 100 mmHg received nifedipine 10 mg sublingual with a sprayer. A second dose was administrated fifteen minutes later if an adequate response defined as a stable reduction of SBP below 180 mmHg and DBP below 100 mmHg had not occurred. Of 30 patients, 21 (70%) responded to the first nifedipine application, 7 responded to the second dose, and 2 nonresponders had to be treated with urapidil. Overall mean SBP was 206 +/- 19 mmHg and mean DBP was 113 +/- 15 mmHg before treatment, and a significant antihypertensive effect was noted within fifteen minutes after nifedipine spray (p < 0.05). The maximum antihypertensive effect was for SBP in sixty minutes (146 +/- 19 mmHg) and for DBP after one hundred twenty minutes (78 +/- 18 mmHg). The average reduction in SBP was 29% and in DBP 31%. In first-dose responders (n = 21) a significant antihypertensive effect was noted within fifteen minutes. SBP declined from 205 +/- 21 to a minimum of 142 +/- 15 mmHg (22.3%) after sixty minutes and DBP from 113 +/- 13 to a minimum of 77 +/- 11 mmHg (22.2%) after one hundred twenty minutes. In second-dose responders (n = 7) a significant antihypertensive effect was noted within thirty minutes.
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