AimsTo compare primary percutaneous coronary intervention (pPCI) and fibrinolysis in very old patients with ST-segment elevation myocardial infarction (STEMI), in whom head-to-head comparisons between both strategies are scarce.Methods and resultsPatients ≥75 years old with STEMI <6 h were randomized to pPCI or fibrinolysis. The primary endpoint was a composite of all-cause mortality, re-infarction, or disabling stroke at 30 days. The trial was prematurely stopped due to slow recruitment after enroling 266 patients (134 allocated to pPCI and 132 to fibrinolysis). Both groups were well balanced in baseline characteristics. Mean age was 81 years. The primary endpoint was reached in 25 patients in the pPCI group (18.9%) and 34 (25.4%) in the fibrinolysis arm [odds ratio (OR), 0.69; 95% confidence interval (CI) 0.38–1.23; P = 0.21]. Similarly, non-significant reductions were found in death (13.6 vs. 17.2%, P = 0.43), re-infarction (5.3 vs. 8.2%, P = 0.35), or disabling stroke (0.8 vs. 3.0%, P = 0.18). Recurrent ischaemia was less common in pPCI-treated patients (0.8 vs. 9.7%, P< 0.001). No differences were found in major bleeds. A pooled analysis with the two previous reperfusion trials performed in older patients showed an advantage of pPCI over fibrinolysis in reducing death, re-infarction, or stroke at 30 days (OR, 0.64; 95% CI 0.45–0.91).ConclusionPrimary PCI seems to be the best reperfusion therapy for STEMI even for the oldest patients. Early contemporary fibrinolytic therapy may be a safe alternative to pPCI in the elderly when this is not available.Clinicaltrials.gov # NCT00257309.

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). ...

No abstract

No abstract

No abstract