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Background Exercise testing constitutes the usual tool for decision making in chest pain units. This policy implies logistical constrains. Our aim was to evaluate a new strategy, combining a clinical risk score and N-terminal pro–B-type natriuretic peptide (NT-proBNP), in patients presenting to the emergency department with chest pain, without ischemic electrocardiogram changes or troponin elevation. Methods A total of 320 patients were randomized to either usual management, involving exercise testing, or a new strategy combining a clinical risk score and NT-proBNP without exercise testing. In the usual management, discharge decision was guided by the result of exercise test. In the new strategy, those patients with low clinical risk score and NT-proBNP were directly discharged. The primary outcome was hospitalization at the index episode. Secondary outcomes were cardiac events at 1 year. Results A total of 110 patients (69%) were hospitalized using usual management in comparison with 90 (56%) in the new strategy ( P = .03). There were no differences in death or myocardial infarction (n = 11, 6.9% vs n=6, 3.8%, P = .3) or cardiac events (n = 38, 24% vs n=28, 18%, P = .2). Revascularizations at the index episode were more frequent under usual management (18% vs 8%, P = .01), although the new strategy was associated with higher rate of planned postdischarge revascularizations (0.6% vs 5%, P = .04). Conclusions A strategy combining clinical history and NT-proBNP is simpler and reduced initial emergency hospitalizations in patients with chest pain, in comparison with the usual strategy involving exercise testing. Larger studies to assess its impact on long-term hard end points are needed. (ClinicalTrials.govNCT00493844)

Recently, the theory that hyperinflammation is the body's primary response to potent stimulus has been challenged. Indeed, a deregulation of the immune system could be the cause of multiple organ failure. So far, clinicians have focused on the last steps of the inflammatory cascade. However, little attention has been paid to lymphocytes, which play an important role as strategists of the inflammatory response. Experimental evidence suggests a crucial role of T lymphocytes in the pathophysiology of atherosclerosis and acute myocardial infarction (AMI). In summary, from the bottom of an imaginary inverted pyramid, a few regulatory T-cells control the upper parts represented by the wide spectrum of the inflammatory cascade. In AMI, a loss of regulation of the inflammatory system occurs in patients with a decreased activity of regulatory T-cells. As a consequence, aggressive T-cells boost and anti-inflammatory T-cells drop. A pleiotropic proinflammatory imbalance with damaging effects in terms of left ventricular performance and patient outcome is the result of this uncontrolled immune response. It is needed to unravel the thread of the inflammatory cells to better understand the pathophysiology as well as to open innovative therapeutic options in AMI.

The objective of this study was to evaluate the simultaneous evolution of 5 cardiovascular magnetic resonance-derived myocardial viability indexes.We studied 72 patients with a first ST-elevation myocardial infarction and sustained TIMI 3 flow. In the first week and in the sixth month of the study, using cardiovascular magnetic resonance imaging, we determined wall thickening (WT) and the following viability indexes: wall thickness, WT with low-dose dobutamine, microvascular perfusion in first-pass imaging, microvascular obstruction in late-enhancement imaging, and transmural extent of necrosis.In 250 dysfunctional segments, the evolution outcomes for the viability indexes were as follows: (1) wall thickness thinned (8.6 +/- 2.9 versus 7.7 +/- 3 mm, P.001), (2) WT with low-dose dobutamine improved (1.5 +/- 1.9 versus 2.6 +/- 3 mm, P.001), (3) the number of segments showing abnormal microvascular perfusion in first-pass imaging decreased (22% versus 7%, P.001), (4) the number of segments showing microvascular obstruction in late-enhancement imaging decreased (14% versus 2%, P.001), and (5) the transmural extent of necrosis remained stable throughout follow-up (56% +/- 40% versus 54% +/- 39%, P = .3).After reperfused myocardial infarction, dynamic changes in wall thickness, contractile reserve, microvascular perfusion, and microvascular obstruction take place. These changes may affect their accuracy as viability indexes early after myocardial infarction. The transmural extent of necrosis does not vary, however.

The aim of this study was to define the utility of the combined measurement of troponin I, myoglobin, C-reactive protein, fibrinogen, and homocysteine to predict risk in non-ST elevation acute coronary syndromes.Troponin I, myoglobin, high-sensitivity C-reactive protein, fibrinogen, and homocysteine were measured in 557 consecutive patients admitted to our institution for non-ST elevation acute coronary syndrome. The risk for major events (death or nonfatal myocardial infarction) at first month and at first year follow-up was analyzed.In a multivariate model adjusting for baseline characteristics and electrocardiographic changes, the only biomarkers related to major events at first month were C-reactive protein (P = .007) and myoglobin (P = .02), and at first year troponin I (P = .02), C-reactive protein (P = .03), and homocysteine (P = .04). The rate of major events depending on the number (0-5) of elevated biomarkers were at first month: 4.1%, 3.7%, 5.7%, 6.1%, 6.5%, and 30.8% (P.0001), and at first year: 8.2%, 11.1%, 12.3%, 16.2%, 23.7%, and 50% (P.0001). A simple score including the number of elevated biomarkers showed an adjusted risk of major events of 1.6 [1.3-1.9] at first month and of 1.4 [1.2-1.7] at first year.Markers of myocardial damage, inflammation, and homocysteine analyzed separately provide prognostic information. The number of elevated biomarkers is an independent risk predictor of major events.

Background Resting ST-segment elevation on Q leads after an acute myocardial infarction has been related to a greater infarct size. Otherwise, the relation between exercise-induced ST-segment elevation and myocardial viability is controversial. We investigated the relation between ST-segment elevation on Q leads at rest and during exercise and regional dysfunction and its evolution, contractile reserve, left ventricular dilation, and coronary patency. Methods and Results Exercise testing and cardiac catheterization were performed at the first week after infarction in 51 patients. The study group was divided according to the existence (in 2 or more Q leads; n=36) or not (n = 15) of resting ST-segment elevation and according to the existence (n = 28) or not (n = 23) of exercise-induced ST-segment elevation. Left ventricular end-diastolic and end-systolic volumes (mL/m 2 ), regional wall motion (SD/chord), contractile reserve (wall motion percentage improvement with low-dose dobutamine), and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 35 patients; systolic recovery (wall motion percentage improvement), left ventricular volumes, and coronary patency were again evaluated. Patients with resting ST-segment elevation showed poorer wall motion (2.1 ± 0.8 SD/chord vs 1.2 ± 1 SD/chord, P = .002), lesser contractile reserve (17% [0% to 39%] vs 41% [4% to 92%], P = .04), greater end-systolic volume (32 ± 15 mL/m 2 vs 23 ± 11 mL/m 2 , P = .04), and higher percentage of occlusion (36% vs 7%, P = .04) than did patients without ST-segment elevation. Likewise, patients with exercise-induced ST-segment elevation showed lesser contractile reserve (8% [0% to 40%] vs 35% [12% to 86%], P = .03) than did patients without exercise-induced ST-segment elevation. The only independent predictors of contractile reserve were wall motion P = .01) and the absence of exercise-induced ST-segment elevation (OR 5.7, CI 4.9 to 6.5, P = .02). There were no significant differences between patients with and those without ST-segment elevation (at rest or during exercise) in systolic recovery or left ventricular volumes at the sixth month. Conclusions ST-segment elevation on Q leads at rest is related to a poorer systolic function (more severe regional dysfunction, greater end-systolic volume, and less response to dobutamine). ST-segment elevation during exercise is independently related to a lesser contractile reserve. ST-segment elevation (at rest or during exercise) is not related to the evolution of volumes or regional dysfunction during the first 6 months after infarction. (Am Heart J 1999;137:1107-15.)