S tudies have shown that human albumin undergoes a considerable reduction in its capacity to bind exogenous cobalt (Ischemia Modified Albumin (IMA); Ischemia Technologies, Denver, Colorado, USA), as measured by the albumin cobalt binding test, when exposed to an ischaemic insult. We have recently observed that plasma IMA levels increase soon after transient balloon inflation during percutaneous coronary intervention (PCI), even in the absence of considerable elevations of cardiac troponin. 1 Higher IMA levels have also been reported in patients with acute coronary syndrome attending the emergency department with recent-onset chest pain. 2 At present however, no data exist regarding the relationship between IMA and an accepted gold standard for myocardial ischaemia-that is, myocardial lactate extraction. 3 We therefore sought to assess whether increased IMA plasma levels documented in patients after PCI correlate with an increased production of lactate by the myocardium.
METHODSWe simultaneously measured coronary sinus and arterial lactate concentrations and plasma IMA levels before and after balloon inflation in 10 patients with chronic stable angina undergoing PCI to the proximal left anterior descending coronary artery. The study protocol was approved by the local ethics committee, and informed written consent was obtained from all patients before study entry. Patients with signs or symptoms of acute or chronic ischaemic conditions, including stroke, transient ischaemic attack, leg claudication or shock, were not included. Blood was drawn for detecting IMA and lactate: (1) immediately before PCI, using arterial and venous sheaths; (2) 1 min after the last balloon inflation (arterial and coronary sinus measurements); (3) 5 min after PCI (arterial and coronary sinus measurements); (4) 1 h after PCI (peripheral vein) for IMA; and (5) 6 h after PCI (peripheral vein) for IMA. For coronary sinus lactate sampling, a multi-purpose catheter was inserted via right femoral vein puncture and positioned in the coronary sinus just proximal to the great cardiac vein. The position was checked repeatedly by injections of small amounts of contrast medium. IMA was measured using the albumin cobalt binding test on the Roche Cobas MIRA PLUS instrument (Rotkreuz, Switzerland). 1 2 In our laboratory, the albumin cobalt binding test within-run duplicate percentage of coefficient of variation (CV%) of patient samples ranged from 0% to 6.5%, with an average of 1.9%. Lactate concentration was measured by an enzymatic kit (Boehringer Mannheim, Mannheim, Germany) with intraassay and interassay CVs of 3.7% and 4.8%, respectively. The analytical range for the study was 0.3-11.1 mmol/l. Net lactate extraction was calculated using the formula: (arterial lactate2sinus lactate)/arterial lactate 6100%, with the normal range being 10-60% and ischaemia developing with lactate extraction of (10%. 4 Non-parametric descriptive and comparative statistics for continuous variables were determined using Analyse-it v.1.62 (Analyse-it Software, Leeds, UK). ...
To examine changes in left ventricular (LV) mass and function (diastolic and systolic) after successful renal allograft transplantation (RT), we prospectively studied 30 patients (19 men, 11 women, aged 37 ± 13 years) by M-mode, two-dimensional and pulsed Doppler echocardiography at the time of surgery and 10 ± 1.8 months later. At the time of transplantation all patients had been undergoing dialysis (4 peritoneal dialysis, 26 hemodialysis) for 2.5 ± 3.2 years. A hematocrit of ≤30% was present in 26 patients. After RT the mean hematocrit increased from 26 ± 4 to 40 ± 7 (p < 0.01), whereas systolic, diastolic and mean blood pressure (BP) remained unchanged. The LV mass index (LVMI) decreased from 201 ± 56 to 171 ± 41 g/m2, (p < 0.01); LV diastolic diameter corrected by body surface area (LVDDI) decreased from 298 ± 38 to 279 ± 35 (p < 0.01) and the LV end-diastolic volume index (LVEDVI) from 72 ± 18 to 63 ± 15 (p < 0.01). There were no changes in LV fractional shortening or LV end systolic wall stress. Peak late transmitral velocity (A wave) decreased from 77 ± 16 to 68 ± 12 cm/s (p < 0.01) with no changes in other Doppler-derived indexes of diastolic function. No fistula patency influence on changes in LV mass and function was found. After RT, BP decreased in 21 patients from 150 ± 20 to 132 ± 15 (p < 0.001; group I) and increased in 9 patients from 130 ± 14 to 153 ± 16 (p < 0.05, group II). Patients in group I suffered a reduction in LVMI (p < 0.001), LV end-diastolic diameter (p < 0.05), LVDDI (p < 0.001); LV end-diastolic volume (p < 0.05); LVEDVI (p < 0.01); cardiac index (p < 0.05), and peak late transmitral velocity (p < 0.01), but no changes in group-II patients were observed. We concluded that BP is a major determining factor with regard to changes in LV hypertrophy and function following RT. LV mass and volumes can be expected to decrease after RT in patients with BP reduction.
Spontaneous self-terminating atrial fibrillation (AF) is one of the most common heart rhythm disorders, yet the regulatory molecular mechanisms underlying this syndrome are rather unclear. MicroRNA (miRNA) transcriptome and expression of candidate transcription factors (TFs) with potential roles in arrhythmogenesis, such as Pitx2, Tbx5, and myocardin (Myocd), were analyzed by microarray, qRT-PCR, and Western blotting in left atrial (LA) samples from pigs with transitory AF established by right atrial tachypacing. Induced ectopic tachyarrhythmia caused rapid and substantial miRNA remodeling associated with a marked downregulation of Pitx2, Tbx5, and Myocd expression in atrial myocardium. The downregulation of Pitx2, Tbx5, and Myocd was inversely correlated with upregulation of the corresponding targeting miRNAs (miR-21, miR-10a/10b, and miR-1, resp.) in the LA of paced animals. Through in vitro transient transfections of HL-1 atrial myocytes, we further showed that upregulation of miR-21 did result in downregulation of Pitx2 in cardiomyocyte background. The results suggest that immediate-early miRNA remodeling coupled with deregulation of TF expression underlies the onset of AF.
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