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PubMed2002

MR imaging at rest early after myocardial infarction: detection of preserved function in regions with evidence for ischemic injury and non-transmural myocardial infarction.

Patients with subacute myocardial infarction were studied to detect regions of ischemic injury but with preserved myocardial function combining different MRI techniques. On a 1.5-T imaging system 27 patients were examined 7-14 days after acute myocardial infarction. The imaging protocol included T2-weighted fast spin-echo imaging, a cine fast low-angle shot (FLASH) 2D technique to determine regional function at rest, and a first pass as well as late contrast enhancement perfusion study injecting 0.1 mmol/kg Gd-DTPA. Preserved function was compared with the transmural extent of first-pass perfusion phenomena, increased T2 signal intensity (SI), and late contrast enhancement. Semi-quantitative first-pass perfusion parameters were correlated with quantitative myocardial wall thickening (MWT) and degree of coronary artery stenosis. Indicating ischemic injury increased T2 SI and late enhancement was present in 29 and 26% of segments. Preserved function was found predominantly in segments with non-transmural late enhancement (112 of 338 segments with late enhancement) and transmural increase of T2 SI (129 of 386 segments with increased T2 SI). A high-grade perfusion deficit was detected in 4% of all segments and regularly associated with markedly decreased systolic function. Correlation of first-pass perfusion parameters was observed with MWT (r=0.50-0.90, p<0.001) but not with the degree of coronary artery stenosis. Our data suggest that preserved function was detected in non-transmural myocardial infarction demonstrated by non-transmural late enhancement and increase of T2 SI.

Aged↗
PubMed1999

Surgical and medical management of patients with massive cerebellar infarctions: results of the German-Austrian Cerebellar Infarction Study.

Surgical intervention (ventricular drainage or decompressive craniotomy) may be necessary in patients with cerebellar infarction if mass effect develops. However, patient selection and timing of surgery remain controversial, and there are few data on clinical signs in the early course that are predictive for outcome. The clinical course and neuroradiological features of 84 patients (aged 22-78, mean 58.5 years) with massive cerebellar infarction confirmed by computed tomography were prospectively observed for 21 days after admission and at 3-month follow-up using a standardized protocol. Data were gathered from 1992 to 1996 in 17 centers. The patients were assigned to three treatment groups depending on the decision of the primary caretaker: 34 underwent craniotomy and evacuation, 14 received ventriculostomy, and 36 were treated medically. Treatment groups differed regarding the level of consciousness, signs of mass effect in computed tomography and signs of brainstem involvement. The overall risk for poor outcome depended on the level of consciousness after clinical deterioration (odds ratio = 2.8). Subgroup analysis of awake/drowsy or somnolent/stupor patients revealed no relationship to treatment. The vascular territory involved did not affect outcome. Surgical treatment for massive cerebellar infarctions was not found to be superior to medical treatment in awake/drowsy or somnolent/stupor patients. Half of all patients deteriorating to coma treated with ventricular drainage or decompressive craniotomy had a meaningful recovery. We were unable to compare surgical versus medical therapy in this subgroup due to lack of control group. This study supports the notion that the level of consciousness is the most powerful predictor of outcome, superior to any other clinical sign and treatment assignment. Deterioration of consciousness typically occurred between days 2 and 4, with a maximum on day 3.

Adult↗
PubMed1981

Serial plasma catecholamine response early in the course of clinical acute myocardial infarction: relationship to infarct extent and mortality.

Clinical and experimental evidence suggest that sympathoadrenal activation contributes to mortality in patients with ischemic heart disease. To determine the level of sympathoadrenal activation in the very early phase of acute myocardial infarction (AMI) and to determine if location of infarction (anterior versus inferior) was related to sympathoadrenal activation, we studied norepinephrine (NE) and epinephrine (E) within 4 hours after the onset of symptoms and prior to any rise in plasma creatine kinase (CK). Mean (+/- SE) initial (NE = 591 +/- 111 pg/ml and E = 73 +/- 19 pg/ml), peak (NE = 1356 +/- 178 and E +/- 1098 +/- 608) and average (NE = 815 +/- 142 and E = 252 +/- 68) plasma catecholamine concentrations were considerably above normal (NE = 228 +/- 10 and E = 34 +/- 2 pg/ml, n 60) and values were similar for inferior and anterior infarctions. During an 18-month follow-up, three patients died in whom the AMI mean NE and E and peak CK were higher than in the eight late survivors. Thus the three AMI patients with peak EP values greater than 1000 died, whereas the eight AMI patients with peak EP values less than 1000 survived (p less than 0.01). The magnitude of sympathoadrenal activation early in the course of clinical AMI appeared related to the extent of myocardial damage and late mortality.

Acute Disease↗
PubMed1987

Serum lipids and lipoproteins after myocardial infarction: associations with cardiovascular mortality and experience in the Aspirin Myocardial Infarction Study.

Serum cholesterol and triglyceride levels were measured at baseline in 4021 men and 503 women (myocardial infarction survivors) participating in the Aspirin Myocardial Infarction Study (AMIS). A cohort of participants (1824 men and 226 women) had, in addition, a determination of high-density lipoprotein (HDL) cholesterol and an estimate of low-density lipoprotein (LDL) cholesterol. In comparison with values obtained for normal Americans by the Lipid Research Clinics Prevalence Study Group, AMIS participants had higher serum cholesterol, higher serum triglyceride, higher LDL cholesterol, and lower HDL cholesterol levels. These values were the most disparate in the women and younger men. The serum total cholesterol, the ratio of LDL to HDL cholesterol, and the serum triglyceride level were significantly related (p less than 0.05) to the 3-year cardiovascular mortality rate for men less than 55 years of age (univariate relationships). For men older than 55 years, these relationships were not statistically significant. After adjustment for multiple risk factors, serum cholesterol and the ratio of LDL to HDL cholesterol remained significant risk factors for cardiovascular death and the combined incidence of cardiovascular death or nonfatal myocardial infarction in men less than age 55 years.

Adult↗
PubMed1978

Hemodynamic pattern resembling pericardial constriction after acute inferior myocardial infarction with right ventricular infarction.

Two patients with acute inferior myocardial infarction complicated by cardiogenic shock are presented. Cardiac catheterization 2 and 7 days after infarction, respectively, revealed a hemodynamic pattern resembling constrictive pericarditis. Right coronary occlusion proximal to the right ventricular marginal branches was present in both patients. Resolution of the constrictive hemodynamic pattern was demonstrated in the one survivor at repeat catheterization 7 weeks after infarction. The mechanism for constrictive hemodynamics in these patients is unclear.

Acute Disease↗
PubMed1984

Peri-infarction zone at risk during the first 5 days after an acute transmural myocardial infarction: electrocardiographic evidence.

An atrial pacing test was performed daily during the initial 5 days after a first myocardial infarction (MI) in 33 patients in Killip class I or II, to assess the presence of areas at risk of ischemia. Pacing caused a transient ST-segment shift of 1 mm or more in 26 patients (79%) (positive test, Group I) in the first 3.6 +/- 1.1 days after infarction, whereas no ST-segment change developed during pacing in 7 patients (negative test, Group II). Pacing-induced electrocardiographic changes were always localized in the leads involved by the MI. Right and left ventricular filling pressures were higher in Group I than in Group II (8 +/- 4 vs 5 +/- 3 mm Hg, p less than 0.05, and 16 +/- 7 vs 12 +/- 7 mm Hg, p less than 0.02, respectively). Both groups had similar increases in peak enzyme values and a similar mortality rate (2 of 26 vs 1 of 7 at an average follow-up of 16 months). The reinfarction rate was higher in Group II (3 of 7 vs 1 of 26). In 7 patients similar to the 33 patients studied, metabolic studies revealed lactate abnormalities during pacing in 4 of the 6 patients with positive test results and unchanged metabolism in the patient with a negative test result. Thus a jeopardized peri-infarction area appears to exist in most patients soon after an uncomplicated MI. Its presence is often associated with silent heart failure, but it is probably unrelated to peak enzyme increase or to prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Myocardial infarct size threshold for two-dimensional echocardiographic detection: sensitivity of systolic wall thickening and endocardial motion abnormalities in small versus large infarcts.

This study evaluated the ability of 2-dimensional echocardiography to detect myocardial infarcts of varying sizes. Echocardiography was performed in 29 closed-chest, conscious dogs 2 days after circumflex coronary artery occlusion, and the ultrasonic recordings were analyzed for regional abnormalities in either wall thickening or endocardial motion. Acute myocardial infarct (AMI) size and extent were assessed by morphologic examination. In 5 dogs, coronary occlusion failed to produce AMI; in these dogs wall thickening analysis showed no abnormalities (100% specificity), and endocardial motion analysis yielded 1 false-positive result (80% specificity). In 24 dogs an AMI developed; infarcts larger than 18% of left ventricular mass uniformly resulted in echocardiographically detectable contraction abnormalities. When the AMI was small (1 to 6% of left ventricular mass) and primarily subendocardial, the sensitivity of echocardiography was poor: Only 3 of 10 of the dogs with a small AMI had abnormalities by wall thickening, and only 1 of 10 by endocardial motion. Thus, in this canine model of AMI, 2-dimensional echocardiography was insensitive to small, subendocardial AMI. If this is so in humans as well, it is a potential limitation of the clinical use of echocardiography in the detection of AMI.

Animals↗
PubMed1987

Hemodynamic profile of patients with acute myocardial infarction at risk of infarct expansion.

To identify patients at risk of cardiac expansion during hospital stay for a first acute myocardial infarction (AMI), 41 patients underwent right-sided cardiac catheterization soon after admission and serial 2-dimensional echocardiography on days 1, 3 or 4 and between days 7 and 10. Infarct expansion was recognized by echocardiography in 11 patients (27%), most often on the second recording (day 3 or 4). Age, sex, time from onset of pain to catheterization, peak levels of creatine kinase and creatine kinase-MB isoenzyme, heart rate, mean pulmonary artery wedge pressure and left ventricular stroke work index were similar in the 2 groups. Patients in whom infarct expansion developed had a higher incidence of previous systemic hypertension (73% vs 27%, p less than 0.01) and anterior AMI (91% vs 30%, p less than 0.001) and a higher mortality rate at 1 year (73 vs 7%, p less than 0.001) than those who did not. They also had higher systolic (139 +/- 24 vs 126 +/- 18 mm Hg, p less than 0.05) and diastolic (91 +/- 14 vs 75 +/- 13 mm Hg, p less than 0.001) arterial pressures, lower stroke volume index (31 +/- 10 vs 40 +/- 10 ml/m2, p less than 0.01) and much higher systemic vascular resistance (SVR) values (1,713 +/- 380 vs 1,253 +/- 264 dynes s cm-5, p less than 0.0001). In the subgroups of patients with anterior AMI, differences were significant for diastolic arterial pressure, stroke volume index, SVR and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Prediction of preserved flow to the infarct area based on admission electrocardiogram in anterior wall acute myocardial infarction.

To determine whether preserved flow to the infarct area could be predicted from the admission electrocardiogram and to define the effect of preserved flow on the late results after reperfusion, 20 anterior myocardial infarction patients who were successfully reperfused were studied. Patients were divided into 3 groups: (1) no-flow group (8 patients), with an occluded infarct-related artery and no easily visible collaterals; (2) intact collateral group (6 patients); and (3) subtotal obstruction group (6 patients). From the admission electrocardiogram, the sum of ST-segment elevation (sigma ST), the sum of R-wave amplitude (sigma R) in leads V1 through V6 and the ratio of these (sigma R/sigma ST) were measured. There was no significant difference in sigma R among the 3 groups. The no-flow group had significantly lower sigma R/sigma ST and higher sigma ST than the intact collateral group or subtotal obstruction group. All patients (6 of 6) with subtotal obstruction and all except 1 patient (5 of 6) with intact collateral showed sigma R/sigma ST greater than 2.5 or sigma ST less than 2.0 mV. All patients (8 of 8) with no flow showed sigma R/sigma ST less than or equal to 2.5 and all except 1 patient with no flow (7 of 8) showed sigma ST greater than or equal to 2.0 mV. The regional wall motion was assessed by the radial method at 4 weeks. The mean percentage systolic shortening in the anterior and apical regions was significantly correlated with sigma R/sigma ST (r = 0.75, p less than 0.001) and sigma ST (r = -0.65, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effects of early captopril administration on infarct expansion, left ventricular remodeling and exercise capacity after acute myocardial infarction.

In a double-blind study, 99 patients (82 men, age range 40 to 75 years) with acute myocardial infarction (AMI) were randomly assigned to receive captopril or placebo. Treatment began within 24 hours of admission. Serial echocardiographic measurements of endocardial segment lengths and left ventricular (LV) volumes, and ejection fractions were obtained. The 2 groups were matched at baseline except for an excess of previous AMI in the placebo group (13 of 50 vs 2 of 49 patients, p = 0.002). The increase in anterior segment length, from baseline to 2 months, was significantly less in the captopril than in the placebo group (2.8 +/- 1.6 vs 10.4 +/- 2.4mm, 95% confidence interval [CI] -13.5 to -1.7, p = 0.01). The increase in posterior segment length was also less in the captopril group, but the difference was not significant (3.2 +/- 1.2 vs 7.0 +/- 1.8mm, 95% CI -8.0 to 0.5, p = 0.08). Fewer patients in the captopril group demonstrated increases in segment length greater than 2 standard deviations of the measurement error (14 of 70 [20%] vs 29 of 72 [40%] patients, p = 0.009). In patients with anterior AMI, the infarct-containing anterior segment length increased by 4.5 +/- 2.3 mm in the captopril versus 12.4 +/- 3.1 mm in the placebo group (95% CI -15.7 to -0.2, p = 0.046), and fewer patients in the captopril group demonstrated infarct expansion (6 of 20 [30%] vs 13 of 21 [62%] patients, p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Relation of left ventricular volume and function over one year after acute myocardial infarction to infarct size determined by technetium-99m sestamibi.

Twenty patients with a first acute myocardial infarction (AMI) (15 anterior, 5 inferior) who received successful reperfusion therapy underwent tomographic imaging with technetium-99m (Tc-99m) sestamibi and radionuclide ventriculography at discharge, 6 weeks, and 1 year after AMI. Patency of the infarct-related artery after reperfusion (thrombolysis, 8 patients; coronary angioplasty, 12 patients) was confirmed by angiogrpahy in all patients. Tc-99m sestamibi perfusion defect at discharge (a measure of infarct size) was quantitated using previous methods and expressed as a percentage of the left ventricle (28 +/- 19%, range 0 to 59%). This perfusion defect size correlated closely with ejection fraction at discharge (r = -0.87), 6 weeks (r = -0.81) and at 1 year (r = -0.78, all p less than 0.0001). Perfusion defect size at discharge also correlated closely with end-systolic volume index at discharge (r = 0.71, p less than 0.0005), 6 weeks (r = 0.63, p less than 0.005) and at 1 year (r = 0.76, p less than 0.0001). Perfusion defect size at discharge did not correlate significantly with end-diastolic volume index at discharge or at 6 weeks, but did correlate at 1 year (r = 0.66, p less than 0.005). There was no significant group change in end-systolic or end-diastolic volume indexes from discharge to 1 year later, although 7 patients had definite individual changes in end-diastolic volume index (3 increased and 4 decreased). There was no relation between defect size and late changes in end-systolic volume index, but there was a weak correlation between defect size and late changes in end-diastolic volume index (r = 0.42, p = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Association of patency of the infarct-related coronary artery with plasma levels of plasminogen activator inhibitor activity in acute myocardial infarction.

To examine the fibrinolytic capacity in patients with acute myocardial infarction (AMI), baseline levels of plasma plasminogen activator inhibitor (PAI) activity and tissue-type plasminogen activator (t-PA) antigen were measured in 47 patients with Q-wave AMI who underwent emergent coronary angiography 3.0 +/- 0.2 hours after the symptom onset. They received intracoronary injection of urokinase if their infarct-related arteries were occluded. They were classified into 3 groups according to the patency of the infarct-related artery before and after thrombolytic therapy: the patent group (13 patients), the recanalized group (23 patients) and the occluded group (11 patients). The mean level of plasma PAI activity (IU/ml) was higher in patients with AMI as a whole than in the control group (12.8 +/- 1.6 vs 5.4 +/- 0.5, p less than 0.01). The level was lower in the patent group (3.0 +/- 1.1) and higher in the recanalized (18.6 +/- 2.2) and occluded (10.8 +/- 2.5) groups than in the control group (each p less than 0.01). The level was lower in the occluded than in the recanalized group (p less than 0.01) and 62% of the patients in the occluded group had levels within range of the control group. The mean level of plasma t-PA antigen (ng/ml) was higher in patients with AMI as a whole than in the control group (10.3 +/- 0.8 vs 5.8 +/- 0.3, p less than 0.01). There was no difference in the level among the 3 groups with AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Myocardial infarct artery patency and reocclusion rates after treatment with duteplase at the dose used in the International Study of Infarct Survival-3. Burroughs Wellcome Study Group.

Duteplase, 98% double-chain recombinant tissue-type plasminogen activator, was administered intravenously in 488 patients with acute myocardial infarction in a multicenter, open, safety and patency study. Duteplase dosing was based on body weight. Duteplase was administered as a bolus of 0.04 MIU/kg of thrombolytic activity followed by 0.36 MIU/kg over 1 hour and 0.067 MIU/kg/hour for 3 additional hours. The patency rate of the infarct-related artery at 90 minutes was 69% (330 of 478). The reocclusion rate at 3 to 48 hours was 6% (18 of 301). Reinfarction occurred in 7.6% of patients (37 of 488), but 12 reinfarctions occurred after coronary angioplasty. Serious bleeding occurred in 7.6% of patients (37 of 488), predominantly at the catheterization entry site. There were 3 instances of central nervous system bleeding, 1 fatal. Fibrinogen levels declined to 83% of baseline at 24 hours. Weight-based dosing may explain the low incidence of serious bleeding in this study. The in-hospital mortality was 6.6% (32 of 488). This study documents that the dose of duteplase used in the International Study of Infarct Survival-3 results in a 90-minute coronary artery patency rate and safety profile comparable to those reported in published studies on the approved dose of alteplase.

Coronary Angiography↗
PubMed1993

Frequency and significance of right ventricular dysfunction during inferior wall left ventricular myocardial infarction treated with thrombolytic therapy (results from the thrombolysis in myocardial infarction [TIMI] II trial). The TIMI Research Group.

To determine the effect of thrombolytic therapy on the frequency of right ventricular (RV) dysfunction, and whether RV dysfunction is a risk factor for morbidity and mortality after discharge from the hospital, 1,110 patients in the Thrombolysis in Myocardial Infarction (TIMI) II trial with acute inferior wall left ventricular myocardial infarction were studied. RV dysfunction was defined as an RV wall motion abnormality on equilibrium radionuclide ventriculography performed a mean of 9 days after admission to the hospital. Fifty-eight patients (5%) had RV dysfunction. Baseline clinical characteristics among patients with and without RV dysfunction were similar. However, patients with RV dysfunction had a lower mean left ventricular ejection fraction (51.2 +/- 1.2% vs 55.5 +/- 0.3%; p < 0.001) and a greater frequency of in-hospital complications. Angiographic data from patients undergoing protocol catheterization 18 to 48 hours after hospital admission show that the infarct-related artery was more likely to be occluded in those with RV dysfunction (48% [15 of 31] vs 14% [68 of 495]; p < 0.001). There was no difference in the frequency of multivessel disease between the 2 groups. In patients with RV dysfunction in whom radionuclide ventriculography was repeated 6 weeks after hospital discharge, RV wall motion abnormalities persisted in only 18% (8 of 45). Mortality in the year after discharge was 3.5% (2 of 58) among patients with RV dysfunction compared with 1.7% (18 of 1,052; p = NS) among those without RV dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1994

Comparison of continuous ST-segment recovery analysis with methods using static electrocardiograms for noninvasive patency assessment during acute myocardial infarction. Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) 7 Study Group.

Continuous ST-segment recovery analysis and 5 static methods using ST-segment comparison between a pre- and post-treatment electrocardiogram were compared for their ability to predict infarct-related artery patency in 82 patients with acute myocardial infarction who underwent angiography a median of 124 minutes after onset of thrombolytic treatment. Accuracy at the moment of angiography was 85% (95% confidence interval [CI] 77% to 93%) for the continuous method, and 68% (CI 57% to 78%), 78% (CI 69% to 87%), 83% (CI 74% to 91%), 82% (CI 73% to 90%), and 80% (CI 71% to 89%) for the static methods. At the moment of angiography the most accurate static method and the continuous method agreed in patency assessment in 90% of the patients (CI 84% to 97%). Agreement was reduced to 83% (CI 75% to 91%) of patients when a patency assessment was performed earlier at 90 minutes after treatment onset, and was only 77% (CI 68% to 86%), at 60 minutes. Early disagreement was mainly seen when the continuous ST recording showed ST recovery from a delayed peak ST elevation after the pretreatment static electrocardiogram or when dynamic ST changes suggesting cyclic reperfusion occurred. Continuous ST-segment recovery analysis appears to be as accurate as the most accurate static methods. Continuously updated reference points appear to give important additional information when ST recovery follows a delayed peak ST elevation or when re-elevation occurs, suggesting cyclic flow changes. Such findings appear to affect about half of patients with acute myocardial infarction treated with intravenous thrombolysis, particularly early after administration of therapy.

Aged↗
PubMed1992

Factors which provoke post-infarction depression: results from the post-infarction late potential study (PILP).

Symptoms of depression in the majority of patients immediately following acute myocardial infarctions (AMI) resolve rapidly; they are an adjustment reaction. However, in a group of 552 male patients there were 80 (14.5%) patients with persistent major depressive symptoms during a finite period after AMI. Infarction size was assessed by maximum creatine kinase levels, the QRS-complex and the occurrence of late potentials. These measures did not correlate with the degree of depressed moods in these groups. An arrhythmic event in the early hospitalization phase, a recurrent infarction, dyspnoea, and persistent angina pectoris before the AMI were significantly related to more profound degrees of depression. Patients who reported serious life-events in the last 2 yr before AMI, or who suffered from exhaustion and fatigue in the prehospital phase were subject to significantly higher levels of depression. A prodromal phase prior to hospitalization free of bodily symptoms and the use of denial were related to low levels of depression. The logistic regression model incorporating all univariate significant variables revealed that symptoms of exhaustion and fatigue prior to AMI had the strongest independent correlation with post AMI depression.

Activities of Daily Living↗
PubMed1989

Clinical correlates of acute right ventricular infarction in acute inferior myocardial infarction.

Right ventricular infarction was diagnosed on the basis of ST-segment elevation greater than or equal to 1 mm in at least one right precordial lead (V3R-V6R) in 20 of 50 patients with first acute inferior myocardial infarction. Seventy five percent of these had ST elevation in 2 or more right precordial leads. Giddiness and hiccups were more common amongst such patients (P less than 0.05). Signs of right ventricular dysfunction-raised jugular venous pressure (65%), Kussmaull's sign (45%), hypotension (without cardiogenic shock, 40%) and right-sided third sound (25%) in the absence of clinical left ventricular failure, were noted in 65% of such patients. Eleven patients had 2 or more of the above signs. ST elevation in 2 or more right precordial leads was found in 10 of these 11 patients. A more complicated course in the hospital characterised by bradyarrhythmias, hypotension and cardiogenic shock, combined with a greater mortality was seen in such patients. We conclude that the bedside diagnosis of haemodynamically significant right ventricular infarction can be made on the basis of a combination of clinical signs and ST elevation in 2 or more right precordial leads, even in units not equipped for bedside haemodynamic monitoring, echocardiography and radionuclide studies. This should lead to a better identification and management of such patients.

Acute Disease↗
PubMed1989

Acute right ventricular infarction without infero-posterior left ventricular infarction.

Two cases of acute right ventricular infarction associated with acute extensive anterior myocardial infarction in the absence of inferior and/or posterior left ventricular infarction are presented. Such a combination is likely to occur from acute occlusion of the left anterior descending artery in the face of severe narrowing of the infundibular (conus) artery rather than from acute occlusion of the right coronary artery.

Aged↗