PubMed Health⌕ Search

Biomedical subjects

Torsten Toftegaard Nielsen

Publications and source records attributed to Torsten Toftegaard Nielsen.

At least 19 recordsLinked to original sources
PubMed2006

Adaptation of nonrevascularized human hibernating and chronically stunned myocardium to long-term chronic myocardial ischemia.

It is unknown whether human chronically ischemic dysfunctional myocardium degenerates over time or adapts to chronic ischemia. We studied whether perfusion, metabolism, and contractile function and reserve can be preserved in nonrevascularized human chronically stunned and hibernating myocardium. We studied 16 event-free, medically treated patients with ejection fractions of 31 +/- 2% and chronically stunned or hibernating myocardium in 56 +/- 5% of the left ventricle on technetium-99m sestamibi single-photon emission computed tomography/fluorine-18 fluorodeoxyglucose (FDG) positron emission tomography. Patients underwent repeat single-photon emission computed tomography, positron emission tomography, and tissue Doppler echocardiography at rest and during stress at follow-up after 25 +/- 4 months, and we investigated whether measurements of myocardial viability remained stable over time. Patients were stable with respect to New York Heart Association class and global left ventricular function (30 +/- 2%, p = 0.81). Wall motion score was unaltered in hibernating myocardium and chronically stunned regions, and a contractile reserve by tissue Doppler stress echocardiography was preserved. Overall, 74% of hibernating myocardium and chronically stunned regions retained their initial perfusion/metabolism pattern at follow-up. In hibernating myocardium, initial and follow-up sestamibi uptakes (53 +/- 1% and 53 +/- 2%, p = 0.85) and FDG uptakes (76 +/- 1% and 74 +/- 1%, p = 0.21) did not differ. In chronically stunned regions, sestamibi uptake displayed a minor decrease at follow-up (70 +/- 1% vs 67 +/- 1%, p <0.01) and FDG uptake remained constant (68 +/- 2% and 67 +/- 1%, p = 0.21). In conclusion, myocardial perfusion, FDG uptake, and contractile function in nonrevascularized chronically stunned and hibernating myocardium adapt to chronic ischemia in patients who are free of events. In chronically stunned regions, adaptation may be less complete than in hibernating myocardium.

Adaptation, Physiological↗
PubMed2006

Routine thrombectomy in percutaneous coronary intervention for acute ST-segment-elevation myocardial infarction: a randomized, controlled trial.

BACKGROUND: Distal embolization during primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction may result in reduced myocardial perfusion, infarct extension, and impaired prognosis. METHODS AND RESULTS: In a prospective randomized trial, we studied the effect of routine thrombectomy in 215 patients with ST-segment-elevation myocardial infarction lasting <12 hours undergoing primary PCI. Patients were randomized to thrombectomy pretreatment or standard PCI. The primary end point was myocardial salvage measured by sestamibi SPECT, calculated as the difference between area at risk and final infarct size determined after 30 days (percent). Secondary end points included final infarct size, ST-segment resolution, and troponin T release. Baseline variables, including ST-segment elevation and area at risk, were similar. Salvage was not statistically different in the thrombectomy and control groups (median, 13% [interquartile range, 9% to 21%] and 18% [interquartile range, 7% to 25%]; P=0.12), but 24 patients in the thrombectomy group and 12 patients in the control group did not have an early SPECT scan, mainly because of poor general or cardiac condition (P=0.04). In the thrombectomy group, final infarct size was increased (median, 15%; [interquartile range, 4% to 25%] versus 8% [interquartile range, 2% to 18%]; P=0.004). CONCLUSIONS: Thrombectomy performed as routine therapy in primary PCI for ST-elevation myocardial infarction does not increase myocardial salvage. The study suggests a possible deleterious effect of thrombectomy, resulting in an increased final infarct size, and does not support the use of thrombectomy in unselected primary PCI patients.

Aged↗
PubMed2006

Effects of levosimendan on myocardial infarct size and hemodynamics in a closed-chest porcine ischemia-reperfusion model.

INTRODUCTION: Levosimendan is a positive inotropic drug with vasodilator action and proposed myocardioprotective properties. In a canine model, levosimendan increased coronary collateral flow and reduced myocardial infarct size (IS). We investigated the effect of levosimendan on IS and hemodynamics in the closed-chest porcine ischemia-reperfusion model, which is devoid of coronary collaterals. METHODS: Infusion with levosimendan (0.2 microg/kg/min following a bolus of 24 microg/kg) or saline was initiated 30 min prior to ischemia in anaesthetized pigs (n = 10 in both groups). Balloon occlusion of the left anterior descending coronary artery for 45 min was followed by 2 1/2 h of reperfusion. Hemodynamics were monitored with a Swan-Ganz catheter and a left ventricular pressure micromanometer. Left ventricular systolic and diastolic function was estimated by dP/dt(max) and tau, respectively. Myocardial area at risk (AAR) and IS were assessed in vivo by myocardial perfusion imaging (MPI) and ex vivo by histopathology (fluorescein staining for AAR, tetrazolium staining for IS). RESULTS: Prior to ischemia, levosimendan improved left ventricular systolic and diastolic function with coincident preload and afterload reduction. Cardiac output increased by 10 +/- 4% (p = 0.04), dP/dt(max) by 15 +/- 5% (p = 0.01). Pulmonary capillary wedge pressure decreased by 18 +/- 3% (p = 0.04), tau by 11 +/- 2% (p = 0.001), and mean arterial pressure by 11 +/- 2% (p < 0.001). A similar trend was observed during ischemia-reperfusion. The ratio of IS/AAR was not reduced by levosimendan compared to saline as evaluated by histopathology (76 +/- 4% vs. 64 +/- 7%, p = 0.12) and by MPI (94 +/- 2% vs. 87 +/- 5%, p = 0.14). CONCLUSION: Levosimendan improves hemodynamics but does not reduce IS in an ischemia-reperfusion model without coronary collaterals.

Animals↗
PubMed2006

Sestamibi single photon emission computed tomography immediately after primary percutaneous coronary intervention identifies patients at risk for large infarcts.

BACKGROUND: Primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction results in TIMI 3 flow in most patients. However, despite TIMI 3 flow, some patients do not achieve adequate tissue perfusion and have large infarctions. Techniques that, in the acute setting, could identify these patients at increased risk would potentially enable specific interventions to enhance perfusion. The object of the present study was to test whether corrected TIMI frame count (CTFC), myocardial blush grade (MBG), ST-segment resolution, and myocardial perfusion imaging (MPI) can identify those patients who, despite successful treatment with primary PCI for ST-elevation myocardial infarction, are at risk for large infarcts. METHODS: In 61 patients with TIMI 3 flow after primary PCI, CTFC, MBG, ST-segment resolution, and quantitative MPI by technetium Tc 99m sestamibi single photon emission computed tomography were estimated immediately after primary PCI. Infarct size was assessed by peak lactate dehydrogenase (LDH) and by MPI after 3 months. RESULTS: Infarct size by MPI was 12% (4, 23), and peak LDH was 1410 U/L (870, 2220); these measures correlated (rho = 0.80, P < .001). The acute perfusion defect predicted infarct size using either method (MPI rho = 0.88, P < .001; LDH rho = 0.77, P < .001); ST-segment residual correlated weakly to infarct size, whereas CTFC and MBG did not. In multivariate analysis, the acute perfusion defect was the only significant predictor of infarct size. CONCLUSION: Myocardial perfusion imaging performed immediately after successful PCI can identify patients at increased risk for large infarcts due to impaired tissue perfusion. Acute MPI might serve as a tool for early identification of patients, who, despite epicardial TIMI 3 flow, have inadequate tissue level perfusion.

Aged↗
PubMed2006

Coronary artery bypass grafting within the first year after treatment of large acute myocardial infarctions with angioplasty or fibrinolysis.

OBJECTIVES: To calculate the incidence and analyse and outcome after coronary artery bypass grafting (CABG) within the first year after randomisation of 1,572 patients with acute myocardial infarctions with ST-segment elevation (STEMI) to either percutaneous coronary intervention (PCI) or fibrinolysis. DESIGN: The study includes 131 patients: 108 male and 23 female with a mean age 62 years. RESULTS: The total 30-day mortality after CABG was 4.6% (7.5% in the PCI group and 2.6% in the fibrinolysis group). The 30-day mortality was 9.8% after CABG within the first 30-days and 1.3% after CABG within 31-365 days. The patients who were operated early had a reduced EF to 43% as compared to 50% in patients who were not operated or patients having CABG after 30-days (p=0.002). CONCLUSION: CABG was performed within the first year after STEMI in 10% of patients randomised to fibrinolysis and in 6.7% of patients randomised to PCI. Patients having CABG within the first 30-days after treatment of STEMI had an increased mortality of 9.8%.

Angioplasty, Balloon, Coronary↗
PubMed2006

L-glutamate and glutamine improve haemodynamic function and restore myocardial glycogen content during postischaemic reperfusion: A radioactive tracer study in the rat isolated heart.

1. L-Glutamate and glutamine have been suggested to have cardioprotective effects. However, the issue is controversial and the metabolic mechanisms underlying a beneficial effect are not well understood. 2. In the present study we investigated the effects of L-glutamate and glutamine on haemodynamic recovery, the rate of de novo glycogen synthesis and myocardial glucose uptake during postischaemic reperfusion. 3. Hearts from male Wistar rats (250-300 g) were divided into three groups as follows: (i) control (n = 12); (ii) L-glutamate (n = 12); and (iii) glutamine (n = 12). Hearts were mounted in a Langendorff preparation and perfused with oxygenated Krebs'-Henseleit solution at 80 mmHg and 37C. Global ischaemia for 20 min was followed by 15 min reperfusion, during which L-glutamate (50 mmol/L) or glutamine (20 mmol/L) were administered. Left ventricular developed pressure (LVDP), de novo synthesis of glycogen using [14C]-glucose and myocardial glucose uptake using D-[2-3H]-glucose were measured. 4. L-Glutamate and glutamine increased postischaemic LVDP (P < 0.01 vs control hearts for both). L-Glutamate and glutamine increased de novo glycogen synthesis by 78% (P < 0.001) and 55% (P < 0.01), respectively. At the end of reperfusion, total myocardial glycogen content was increased by both L-glutamate and glutamine (5.7 +/- 0.3 and 6.2 +/- 0.7 micromol/g wet weight, respectively; P < 0.05 and 0.01, respectively) compared with that in control hearts (3.6 +/- 0.4 micromol/g wet weight). Neither L-glutamate nor glutamine affected myocardial glucose uptake during reperfusion. 5. Improved postischaemic haemodynamic recovery after L-glutamate and glutamine supplementation during reperfusion is associated with increased de novo glycogen synthesis, suggesting a favourable modulation of intracellular myocardial carbohydrate metabolism.

Animals↗
PubMed2006

Acute haemodynamic effects of erythropoietin alone and in combination with dopamine in a porcine model.

BACKGROUND: Previous studies in rodents from different kinds of shock models and isolated vessel models indicate that erythropoietin (EPO) has haemodynamic effects through interaction with sympathetic stimuli. This has relevance to the recently described non-haematopoietic effects of EPO, e.g. tissue protective effects. Studies describing the acute effects on integrated physiological haemodynamic variables in larger animal models are scarce though. AIM: To examine the acute effects of EPO on standard physiological haemodynamic parameters as well as a possible synergistic effect of a sympathetic agonist (dopamine) and EPO on these parameters. RESULTS AND DESIGN: A porcine model was applied. Invasive haemodynamic variables were recorded at baseline, during 2 h after EPO injection and with addition of dopamine. Significant changes were only seen with addition of dopamine. Thus cardiac output increased only significantly in control group (21% versus 4%, P<0.05), and accordingly a decline in systemic vascular resistance was only seen in the control group (19% versus 5%, P< 0.05) with addition of dopamine. Pulmonary vascular resistance increased in EPO group (42% versus unchanged, P<0.05). There was a trend towards increase in left ventricular contractility as measured by slope of the pressure-volume relation (E(max)) in EPO group with addition of dopamine. CONCLUSION: Erythropoietin has small but significant haemodynamic effects on the response to a sympathetic agonist in the present minimal invasive porcine model.

Animals↗
PubMed2005

A phase of increased ST elevation during coronary occlusion following ischemic preconditioning.

UNLABELLED: ATP-sensitive potassium channels are opened during the course of ischemic preconditioning (IP). As experimental data suggest that opening of sarcolemmal ATP-sensitive potassium channels underlie ST elevation during myocardial ischemia, one would expect to observe increased ST elevation during ischemia following IP. However, clinical studies have reported IP to attenuate ST elevation during repeated brief coronary occlusions. The objective of this study was to characterize the temporal course of ST elevation during coronary occlusion following IP. Twenty-eight closed-chest pigs were subject to catheter-based left anterior descending coronary artery occlusion/ reperfusion for 45/120 minutes. Thirteen animals were preconditioned by two occlusion/reperfusion cycles of 10/30 minutes. Fifteen pigs served as controls. The electrocardiographic ST vector magnitude was continuously monitored. IP reduced the infarct size normalized for area at risk (IP 9.6 +/- 15.8%; control 71.2 +/- 14.7%; p < 0.001). IP increased the time between coronary artery occlusion and appearance of significant rise in ST vector magnitude from 51 +/- 17 to 94 +/- 33 seconds (p < 0.01). IP reduced the rise in ST vector magnitude after 120 seconds of occlusion from 202 +/- 85 microV to 68 +/- 28 microV (p < 0.001) and increased the rise in ST vector magnitude after 600 seconds from 265 +/- 106 microV to 427 +/- 232 microV (p < 0.001). CONCLUSION: Ischemic preconditioning reduced and delayed early ST elevation during subsequent coronary artery occlusion, but increased late ST elevation. Thus, ischemic preconditioning causes a dynamic and critically time-dependent biphasic pattern of ST elevation during repeated coronary occlusions.

Animals↗
PubMed2005

Potential significance of spontaneous and interventional ST-changes in patients transferred for primary percutaneous coronary intervention: observations from the ST-MONitoring in Acute Myocardial Infarction study (The MONAMI study).

AIMS: In patients with ST-elevation myocardial infarction (STEMI) scheduled for primary percutaneous coronary intervention (primary PCI), acute risk-assessment may be valuable for tailoring of adjunctive therapy at the time of coronary intervention. The present study was designed to quantify pre-, per-, and post-interventional ST-changes, to evaluate whether a pre-specified continuous ST-monitoring classification provides potential prognostic information in the pre- and per-interventional phase, and to compare post-interventional ST-resolution parameters derived from continuous ST-monitoring and snapshot ECGs, respectively. METHODS AND RESULTS: In 92 STEMI patients, continuous ST-monitoring was initiated in the pre-hospital phase and continued during and 90 min following PCI. Patients were divided into three groups: (A) patients achieving spontaneous ST-resolution before PCI; (B) patients with preserved ST-elevation immediately before PCI and with no increase in ST-elevation during PCI; and (C) patients with preserved ST-elevation immediately before PCI and with increase in ST-elevation during PCI. Groups A (n=22), B (n=43), and C (n=27) differed in peak level of troponin-T (1.4, 4.7, and 7.2 microg/L, P<0.001), creatinine kinase MB isoenzyme (35, 150, and 325 microg/L, P<0.001), and N-terminal pro-brain natriuretic peptide (Nt-pro-BNP) (183, 175, and 269 pmol/L, P=0.084) during admission, and left ventricular ejection fraction evaluated within 2 h of PCI (0.53, 0.48, and 0.45, P=0.047) and after 3 months (0.58, 0.54, and 0.45, P<0.001). Groups B and C also differed in time from first balloon inflation to > or =70% resolution of ST-elevation (14 vs. 42 min, P=0.002), whereas no differences were observed in traditional 90 min ST-resolution analysis or angiographically assessed parameters. CONCLUSION: STEMI patients transferred for primary PCI are heterogeneous with respect to pre- and per-interventional ST-changes, and a pre-specified ST-monitoring classification seems useful for stratification of patients at time of PCI into groups with low, intermediate, and high risk profile. Furthermore, post-interventional ST-monitoring indicates that traditional 90 min ST-resolution analysis may have limited value in the era of primary PCI.

Aged↗
PubMed2005

Simple risk stratification at admission to identify patients with reduced mortality from primary angioplasty.

BACKGROUND: Randomized trials comparing fibrinolysis with primary angioplasty for acute ST-elevation myocardial infarction have demonstrated a beneficial effect of primary angioplasty on the combined end point of death, reinfarction, and disabling stroke but not on all-cause death. Identifying a patient group with reduced mortality from an invasive strategy would be important for early triage. The Thrombolysis in Myocardial Infarction (TIMI) risk score is a simple validated integer score that makes it possible to identify high-risk patients on admission to hospital. We hypothesized that a high-risk group might have a reduced mortality with an invasive strategy. METHODS AND RESULTS: We classified 1527 patients from the Danish Multicenter Randomized Study on Fibrinolytic Therapy Versus Acute Coronary Angioplasty in Acute Myocardial Infarction (DANAMI-2) trial with information for all variables necessary for calculating the TIMI risk score as low risk (TIMI risk score, 0 to 4) or high risk (TIMI risk score > or =5) and investigated the effect of primary angioplasty versus fibrinolysis on mortality and morbidity in the 2 groups. Follow-up was 3 years. We classified 1134 patients as low risk and 393 as high risk. There was a significant interaction between risk status and effect of primary angioplasty (P=0.008). In the low-risk group, there was no difference in mortality (primary angioplasty, 8.0%; fibrinolysis, 5.6%; P=0.11); in the high-risk group, there was a significant reduction in mortality with primary angioplasty (25.3% versus 36.2%; P=0.02). CONCLUSIONS: Risk stratification at admission based on the TIMI risk score identifies a group of high-risk patients who have a significantly reduced mortality with an invasive strategy of primary angioplasty.

Aged↗
PubMed2005

Reduction of treatment delay in patients with ST-elevation myocardial infarction: impact of pre-hospital diagnosis and direct referral to primary percutanous coronary intervention.

AIMS: The majority of patients with ST-elevation myocardial infarction (STEMI) are admitted to local hospitals without primary percutaneous coronary intervention (primary PCI) facilities. Acute transferral to an interventional centre is necessary to treat these patients with primary PCI. The present study assessed the reduction in treatment delay achieved by pre-hospital diagnosis and referral directly to an interventional centre. METHODS AND RESULTS: Two local hospitals without primary PCI facilities were serving the study region. Pre-hospital diagnoses were established with the use of telemedicine, by ambulance physicians, or by general practitioners. Primary PCI was accepted as the preferred reperfusion therapy in patients with STEMI. From 31 October 2002 to 31 January 2004 all patients transported by ambulance and transferred for primary PCI were registered. Patients with STEMI were divided into three groups: (A) patients diagnosed at a local hospital (n = 55), (B) patients diagnosed pre-hospitally and admitted to a local hospital (n = 85), and (C) patients diagnosed pre-hospitally and referred directly to the interventional centre (n = 21). When comparing group A with group B and C, no difference was found in age, sex, infarct location, or distance from the scene of event to the interventional centre, whereas the median time from ambulance call to first balloon inflation was 41 min shorter in group B compared with group A (P<0.001) and 81 min shorter in group C compared with group A (P<0.001). CONCLUSION: In a cohort of patients scheduled for admission to a local hospital and subsequent transferral to an interventional centre for primary PCI, those diagnosed pre-hospitally had shorter treatment delay compared with those diagnosed in hospital, both in the setting of initial admission to a local hospital, and to an even larger extent in the setting of referral directly to the interventional centre.

Aged↗
PubMed2005

Suppressed phospholamban levels differentiate irreversibly dysfunctional from hibernating myocardium in humans.

OBJECTIVES: We studied whether dysfunction of human hibernating (HIB) and irreversibly dysfunctional myocardium (IRDM) are associated with altered levels of the sarcoplasmatic reticulum calcium handling proteins Ca2+-ATPase (SERCA2a) and its inhibitor phospholamban (PLB). DESIGN: In 12 patients myocardial biopsies were taken during bypass surgery and analysed for contents of these proteins. We classified regions as control, HIB, or IRDM based on echocardiographic studies before and 6 months after surgery. RESULTS: SERCA2a content (mean+/-SEM) was similar to control in HIB and IRDM (2.6 +/- 1.7, 3.8 +/- 2.0, and 3.4 +/- 1.9 units/g non-collagen protein (NCP), p = 0.40). PLB content was similar to control in HIB (2.6 +/- 0.4 and 3.5 +/- 0.5 units/microg NCP) but reduced in IRDM (0.9 +/- 0.2 units/microg NCP, p < 0.05). SERCA2a:PLB ratio, an indicator of SERCA2a activity, did not differ between control and HIB (1.2 +/- 0.3 and 1.4 +/- 0.4 units/microg NCP) but was increased in IRDM (5.1 +/- 1.7 units/microg NCP, p < 0.05). CONCLUSIONS: Inappropriate SERCA2a activity due to suppressed PLB levels may represent a maladaptive mechanism in chronic ischemic myocardium being causally linked to irreversibility of left ventricular dysfunction.

Analysis of Variance↗
PubMed2005

Lack of cardioprotection from metabolic support with glutamine or glutamate in a porcine coronary occlusion model.

OBJECTIVE: Previous experimental studies indicate that glutamine or glutamate may provide cardioprotection by improving the oxidative metabolism in myocardial ischemia. We investigated the effect of glutamine or glutamate, given during reperfusion, on resulting infarct size and hemodynamic recovery. DESIGN: A porcine coronary occlusion model was applied. Infusions were initiated 15 min before reperfusion and supplemented with intracoronary bolus doses at reperfusion. The primary outcome measure was infarct size in relation to area at risk determined by a standard tissue staining procedure. Secondary outcome measures were the hemodynamic variables. RESULTS: The infarct sizes as a proportion of the area at risk (mean+/-SD) were: control group, 0.64 +/- 0.19 (n = 9); glutamine group, 0.87 +/- 0.07 (p < 0.05 vs control group) (n = 8); glutamate group, 0.72 +/- 0.11 (n = 9). Glutamine increased systemic vascular resistance, while glutamate preserved cardiac output during infusion. CONCLUSION: Substrate supplementation with the anaplerotic precursors glutamine and glutamate is ineffective as adjunctive therapy for severe myocardial ischemia. Beneficial effects documented in less complex experimental systems could not be transferred to a more pathophysiological relevant model.

Analysis of Variance↗
PubMed2005

Effects of KATP channel modulation on myocardial glycogen content, lactate, and amino acids in nonischemic and ischemic rat hearts.

ATP-sensitive potassium (KATP) channels are involved in the mechanisms underlying ischemic preconditioning. KATP channels open during ischemia, presumably secondary to intracellular metabolic alterations. The direct effects of KATP channel modulation on myocardial metabolism have not been studied. The aim of the present study was to investigate whether a KATP opener (diazoxide) and blocker (glibenclamide) modulates myocardial glycogen, lactate, and amino acid content before, during, and after ischemia. In isolated perfused rat hearts, we investigated the effect of diazoxide (30 microM) and glibenclamide (10 microM) administered 15 minutes before ischemia on myocardial glycogen, lactate, and amino acid content before, during, and after ischemia. Diazoxide increased left-ventricular developed pressure during reperfusion (P < 0.05) and decreased myocardial glycogen depletion (P < 0.05) and lactate accumulation (P < 0.05) during ischemia compared with the control group. Glibenclamide decreased myocardial glycogen content (P < 0.05) and increased myocardial lactate (P < 0.05) and alanine (P < 0.05) content before ischemia and reduced myocardial glycogen content after ischemia (P < 0.05) compared with control. KATP channel activation by diazoxide modulates myocardial metabolism. These findings suggest that activation of KATP channels protects against ischemia-reperfusion injury by a mechanism that involves decreased energy depletion.

Alanine↗
PubMed2004

Mortality rates in patients with ST-elevation vs. non-ST-elevation acute myocardial infarction: observations from an unselected cohort.

AIMS: Acute myocardial infarction (AMI) is categorized, according to the presenting electrocardiogram, into non-ST-elevation myocardial infarction (non-STEMI), ST-elevation myocardial infarction (STEMI), or bundle branch block myocardial infarction (BBBMI). Data on the prognostic significance of these categories mainly originate from voluntary based registries or large-scale clinical trials and may be hampered by selection and information bias. The aim of this historical cohort study was to evaluate the prognostic significance of different categories of AMI in an unselected cohort. METHODS AND RESULTS: From 1 November 1999 to 31 October 2001, patient records were reviewed from all admissions to hospitals serving a study region with 139,000 inhabitants. An Endpoint Committee determined whether patients fulfilled the European Society of Cardiology criteria of AMI. A total of 654 patients with AMI were identified. The proportion having non-STEMI, STEMI, and BBBMI was 54, 39 and 6%, and the associated 1 year mortality was 31, 21, and 55%, respectively (log rank 54, P<0.001). The more favourable outcome observed in patients with STEMI remained significant according to multivariable analysis (P=0.044). CONCLUSION: In an unselected cohort of patients admitted with AMI, the mortality was considerably higher than expected from voluntary-based registries and large-scale clinical trials. The most favourable outcome is observed in patients with STEMI.

Aged↗