Response of the QT-sensing, rate-adaptive ventricular pacemaker to mental stress.
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Aged↗
Biomedical subjects
M A Frais
Publications and source records attributed to M A Frais.
A comparison of desflurane and isoflurane in patients undergoing coronary artery surgery.
Animal studies indicate that desflurane and isoflurane have similar hemodynamic effects when administered in equipotent anesthetic concentrations. The authors compared desflurane and isoflurane, used as primary anesthetics for patients undergoing elective coronary artery bypass surgery whose left ventricular ejection fractions were greater than 0.34. After induction of anesthesia with thiopental (dose 180 +/- 45 mg [mean +/- standard deviation]) and fentanyl, 10 micrograms.kg-1, either desflurane or isoflurane was administered to maintain systolic blood pressure within 70-120% of, and heart rates less than 120% of, the patients' average preoperative values. If adjusting the end-tidal anesthetic concentration within the range of 0-2.0 MAC could not maintain these predefined hemodynamic limits, additional fentanyl or vasoactive drugs were used. Induction and maintenance of anesthesia was accompanied by a significant decrease in mean arterial pressure in both groups (desflurane 97 +/- 12 mmHg at control, decreasing to 71 +/- 5 mmHg during skin preparation; isoflurane 95 +/- 9 mmHg at control, 74 +/- 9 mmHg during skin preparation). One minute after sternotomy, mean arterial pressure in the isoflurane group had returned to control, 97 +/- 9 mmHg, which was significantly greater than in the desflurane group, 87 +/- 12 mmHg. Systolic arterial pressure was also significantly greater in the isoflurane group 1 min after intubation, during skin preparation, and 1 min after sternotomy. Otherwise, the hemodynamic effects of these volatile agents were similar. There were no differences between groups in the incidence of ECG changes indicative of myocardial ischemia prior to cardiopulmonary bypass, perioperative myocardial infarction, or perioperative mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Left and right ventricular diastolic function during acute pericardial tamponade.
The aim of the study was to determine the effect of acute pericardial tamponade on left (LV) and right ventricular (RV) intracavitary and transmural pressure-volume (P-V) relations and to assess the effect of changing blood volume during tamponade on LV and RV volumes. The experiments were done in 11 acutely instrumented anaesthetized dogs in which LV and RV volumes were determined by computed tomography (CT) (n = 5) and LV and RV diameters by sonomicrometry (n = 6). Pressures were measured in the pericardium (balloon transducer), in the aorta and in the ventricles. Incremental pericardial infusion (up to 180 ml) caused a progressive left and upward shift of the LV and the RV intracavitary P-V relationship. This shift was entirely due to increased pericardial pressure (PP). The induction of tamponade caused no change in the LV and RV transmural P-V relationship. During tamponade with ventricular filling pressures above 10-15 mmHg, blood volume expansion caused only minimal increase in LV and RV volumes. In conclusion, pericardial tamponade shifted the LV and the RV intracavitary diastolic P-V relation by increasing PP. However, there was no change in the transmural P-V relationship, indicating unchanged myocardial compliance. Volume loading caused only minimal increase in LV and RV volumes during tamponade.
Animals↗
Exercise-induced T wave normalization is not specific for myocardial ischemia detected by perfusion scintigraphy.
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Adult↗
The dependence of the time constant of left ventricular isovolumic relaxation (tau) on pericardial pressure.
The purpose of this study was to investigate the dependence of tau, the time constant of left ventricular (LV) isovolumic relaxation, on pericardial pressure and to compare values of tau as determined by the methods of previous investigators and by a standard exponential curve fit. All of the more recent methods involve an additional parameter--the pressure to which the exponential relaxation finally declines (PB, the pressure intercept in the method of Craig and Murgo and the asymptote in the exponential fits). An additional purpose of the study was to determine the relation of these parameters to pericardial pressure. In eight closed-chest anesthetized dogs, tau was calculated from intracavitary (Plv) and transmural LV pressure (Plv = Plv-Pper) by each method as pericardial (Pper) and LV end-diastolic pressure were changed by pericardial infusion and intravenous volume loading. The time constant determined by the method of Weiss et al was dependent on pericardial pressure; the time constants determined by the other methods were not. PB and the asymptotes were found to be similar and to increase almost equally with pericardial pressure. When pericardial pressure was zero, these values were approximately -20 mm Hg. Thus, both these parameters seem to indicate the same baseline pressure, a pressure that increases pari passu with pericardial pressure. Reported changes in the value of tau calculated from intracavitary LV pressure by the method of Weiss et al may reflect factors other than changes in LV diastolic function.
Animals↗
Dramatic electrocardiographic T-wave changes associated with gastric dilatation.
A case report is presented of a 54-year old female patient with a history of acute-onset sharp retrosternal chest pain. Clinical examination was unremarkable, but the 12-lead ECG showed anterior T-wave inversion and the chest x-ray film showed gaseous dilatation of the stomach. The patient's symptoms and electrocardiographic abnormalities resolved immediately after gastric decompression. Further investigations revealed no evidence of coronary artery disease. This case report documents marked T-wave changes and atypical chest pain with gastric dilatation. The possible causes of the ECG changes and chest pain are discussed.
Acute Disease↗
The effect of oxygen on respiration and sleep in patients with congestive heart failure.
STUDY OBJECTIVE: To determine the effect of supplemental oxygen on Cheyne-Stokes respiration, nocturnal oxygen saturation (SaO2), and sleep in male patients with severe, stable congestive heart failure. DESIGN: Randomized, single-blind, placebo-controlled crossover study. SETTING: Patients referred from outpatient cardiology clinics of two teaching hospitals. PATIENTS: Sequential sample of nine outpatients with severe, stable congestive heart failure. INTERVENTIONS: For each patient, sleep studies (after an adaptation night) from two consecutive randomized nights were compared; one study was done while the patient breathed compressed air and the other while the patient breathed oxygen (O2). Compressed air and oxygen were both administered through nasal cannulae at 2 to 3 L/min. MEASUREMENTS AND MAIN RESULTS: Cheyne-Stokes respiration, defined as periodic breathing with apnea or hypopnea, was found in all patients. Low-flow oxygen significantly reduced the duration of Cheyne-Stokes respiration (50.7% +/- 12.0% to 24.2% +/- 5.4% total sleep time), mainly during stage 1 NREM (non-rapid eye movement) sleep (21.3% +/- 7.1% to 6.7% +/- 2.3% total sleep time) with no significant change during stage 2 sleep, slow-wave sleep, or REM (rapid eye movement) sleep. Although patients had normal SaO2 (96.0% +/- 1.7%) while awake, severe sleep hypoxemia was common; breathing oxygen reduced the amount of time that SaO2 was less than 90% from 22.3% +/- 8.0% to 2.41% +/- 1.93% of total sleep time. Sleep, disrupted to a variable extent in all patients, improved with oxygen therapy: There was an increase in total sleep time from 275.3 min +/- 36.6 to 324.6 min +/- 23.3; a reduction in the proportion of stage 1 sleep (27.6% +/- 5.8% total sleep time to 15.2% +/- 2.6% total sleep time); and a reduction in the number of arousals (30.4/h +/- 8.0 to 13.8/h +/- 1.9). The apnea-hypopnea index was reduced from 30.0 +/- 4.7 to 18.9 +/- 2.4 with oxygen breathing. CONCLUSION: In severe, stable congestive heart failure, nocturnal oxygen therapy reduces Cheyne-Stokes respiration, corrects hypoxemia, and consolidates sleep by reducing arousals caused by the hyperpneic phase of Cheyne-Stokes respiration. Correction of nocturnal hypoxemia and sleep disruption may improve the clinical status of these patients.
Adult↗
Respiration and abnormal sleep in patients with congestive heart failure.
We investigated the interaction between respiration and sleep in ten male outpatients with severe, stable, maximally treated congestive heart failure (CHF). Cheyne-Stokes respiration (CSR), defined as periodic breathing with apnea or hypopnea, was found in all patients with a mean duration of 120 +/- 87 minutes [50.2 +/- 34.4 percent total sleep time (TST)]. The CSR was found predominantly during stage 1 (20.6 +/- 6.7 percent TST) and stage 2 (25.8 +/- 6 percent TST) NREM sleep and occurred rarely during slow wave sleep (SWS) (1.6 +/- 1 percent TST) and REM sleep (1.6 +/- 0.5 percent TST). All apneas and hypopneas were central. Despite normal awake arterial oxygenation (SaO2) (96.1 +/- 1.6 percent), significant, severe hypoxemia was found during sleep in seven patients with SaO2 less than 90 percent for 9 to 59 percent TST (mean +/- SD, 23 +/- 23 percent TST), and this was significantly related to the duration of CSR (r = 0.66, p less than 0.05). The mean minimum SaO2 for sleep stage was lowest during stage 1 (82.1 percent +/- 2.6 percent) and stage 2 (78.9 percent +/- 2.8 percent) NREM sleep, intermediate during REM sleep (84.5 percent +/- 1.8 percent) and highest during SWS (87.6 percent +/- 2.7 percent). Sleep was disrupted to a variable extent in all patients with a short mean TST (287 +/- 106 minutes), a high proportion of stage 1 sleep (26 +/- 19 percent TST), virtual absence of SWS (5 +/- 7 percent TST) which was found in only four patients, and a high number of sleep stage changes (30 +/- 27/hour) and arousals (28 +/- 25/hour). Arousals occurred predominantly during stage 1 (17 +/- 20/hour) and stage 2 (10 +/- 7/hour) NREM sleep and the majority immediately followed the hyperpneic phase of CSR. The amount of CSR (percent TST) was inversely related to the length of TST (r = -0.73, p less than 0.05), and directly related to the number of sleep stage changes (r = 0.79, p less than 0.01) and the number of arousals (r = 0.66, p less than 0.05). We conclude that in severe, stable CHF, CSR occurs predominantly during light sleep, that despite normal awake arterial oxygen saturation, significant hypoxemia may develop during sleep due to CSR, and that sleep is unstable and disrupted due to frequent arousals caused by the hyperpneic phase of CSR. These sequelae of CSR may be important determinants of the clinical status and outcome of patients with severe CHF.
Adult↗
Comparative effects of atenolol and cicloprolol on cardiac performance in coronary heart disease.
Cicloprolol is a new cardioselective beta-blocking agent with partial agonist activity (intrinsic sympathomimetic activity, ISA). Its haemodynamic profile was compared with that of atenolol (cardioselective; no ISA) in a comparative dose-response study of 24 ischaemic patients with diminished cardiac reserve. Following a stable control period, equivalent intravenous (i.v.) beta-blocking boluses of atenolol (1, 1, 2, and 4 mg) or cicloprolol (0.025, 0.025, 0.05, and 0.1 mg/kg) were randomly administered and haemodynamics and left ventricular ejection fraction were determined at rest and during bicycle exercise. At rest, atenolol reduced heart rate (HR) and cardiac index; diastolic blood pressure (DBP), systemic vascular resistance index (SVRI), and pulmonary artery occluded pressure (PAOP) increased without change in mean arterial pressure (MAP). Cicloprolol increased left ventricular ejection fraction, reduced its end-diastolic volume, and tended to reduce filling pressure without change in other variables. During exercise, atenolol reduced ejection fraction and increased SVRI; in contrast, cicloprolol did not significantly alter these parameters. Attenuation of exercise tachycardia and cardiac index increase was similar after each agent. Thus, the cardiac performance assessed from left ventricular stroke index or ejection fraction/filling pressure relationships was less depressed after cicloprolol as compared with atenolol. The relevance of such haemodynamic differences to exercise ability or quality of life during sustained therapy warrants examination.
Adrenergic beta-Antagonists↗
Hemodynamic comparison of dopexamine hydrochloride and dopamine in ischemic left ventricular dysfunction.
The hemodynamic dose-response effects of intravenous dopexamine hydrochloride (0.5 to 2.0 micrograms/kg/min) have been compared with dopamine (2.5 to 10 micrograms/kg/min) in 12 patients with ischemic left ventricular dysfunction in an open randomized crossover study. Both drugs increased cardiac output and decreased systemic vascular resistance. Dopexamine hydrochloride appeared to increase heart rate more than dopamine although this did not reach statistical significance. Dopexamine hydrochloride produced small increases in systolic and decreases in diastolic blood pressure, whereas dopamine had a biphasic effect resulting in a decrease in mean blood pressure at low doses and an increase at the highest dose studied. With increasing dosage, there was a trend toward more vasodilator activity with dopexamine hydrochloride than with dopamine. Dopexamine hydrochloride produced fewer adverse effects than dopamine.
Adult↗
Left ventricular external constraint: relationship between pericardial, pleural and esophageal pressures during positive end-expiratory pressure and volume loading in dogs.
Left ventricular (LV) diastolic filling is limited by the constraining effects exerted by the pericardium (PE) and the lung/chest wall. The aim of the present study was to assess the validity of various estimates of external cardiac constraint, compared to pericardial surface pressure (Ppe) measured lateral to the LV myocardium. In nine anesthetized dogs we measured Ppe, pleural surface pressure (Ppt) (lateral to the pericardium) and esophageal pressure (Pes) under conditions of volume loading and positive end-expiratory pressure (PEEP). We measured Ppe and Ppl with flat, liquid-containing silastic rubber balloons and Pes with an air-containing cylindrical balloon. After instrumentation, the chest was resealed and continuous suction (-5 mm Hg, 1 mm Hg = 0.133 kPa) was maintained. Volume loading with incremental intravenous infusions of saline was used to increase LV end-diastolic pressure to 20-25 mm Hg. PEEP of 0, 10 and 20 mm Hg were applied at baseline and after each increment of volume loading. At low volume, increases in PEEP caused simultaneous increases in LV end-diastolic pressure (P less than 0.01) and in Ppe (P less than 0.0001) but a reduction in transmural LV pressure (P less than 0.0005). Ppl and Pes both increased with PEEP (P less than 0.001 and P less than 0.01, respectively). However, Ppe always exceeded Ppl, while Pes remained at only approximately 1/3 Ppl throughout. Volume loading caused a significant increase in Ppe (P less than 0.0001) and a smaller, but significant increase in Ppl (P less than 0.05). Pes remained unchanged during volume loading. Thus external cardiac constraint increased markedly during volume loading and PEEP as evidenced by a marked elevation of Ppe. Both Ppl and Pes markedly underestimated this increase. Therefore, calculation of transmural LV pressure by subtracting pleural or esophageal pressure from intracavitary pressure can lead to overestimation of LV preload. The decrease in cardiac output during PEEP occurs secondary to decreased preload, i.e. decreased transmural pressure and end-diastolic dimension. Analysis of performance using cardiac function curves does not suggest a change in contractility with PEEP.
Animals↗
Haemodynamic dose-response actions of cicloprolol in left ventricular dysfunction due to ischaemic heart disease.
Cicloprolol is a cardioselective beta-1 partial agonist; its haemodynamic and radionuclide (nuclear stethoscope) effects were determined in 22 patients with impaired left ventricular function due to coronary artery disease. Following a 20 min stable control period, the effects of four doses of cicloprolol (0.025, 0.025, 0.05 and 0.1 mg/kg at 10 min intervals) were measured at rest 5-10 min after each intravenous injection. The effects of the cumulative 0.2 mg/kg dosage were assessed during supine bicycle exercise and compared with a control exercise period. At rest there were significant increases in systolic arterial without change in mean blood pressure. The heart rate and cardiac index were unchanged. There was a significant increase in left ventricular ejection fraction with a reduction in filling pressure and volume. Patients with resting heart rate below 75 beats/min and with ejection fraction greater than 35% showed the greatest improvement. During supine bicycle exercise, ejection fraction was increased compared to control (31 +/- 2 to 36 +/- 2; P less than 0.01), cardiac volume reduced and exercise tachycardia attenuated. These data suggest that cicloprolol may be of value where beta-blockade is considered in the presence of underlying left ventricular dysfunction due to ischaemic heart disease.
Adrenergic beta-Antagonists↗
Comparative hemodynamic dose-response effects of five slow calcium channel-blocking agents in coronary artery disease.
A prospective, randomized study compared the hemodynamic effects of equivalent doses of five slow calcium channel blockers (verapamil, diltiazem, nicardipine, nisoldipine, and amlodipine) in 50 patients with ischemia. After a stable control period, dose-response curves were constructed for each drug with hemodynamics measured 10 minutes after intravenous boluses. Each drug reduced mean systemic arterial pressure (P less than 0.01) and systemic vascular resistance index (P less than 0.01). The heart rate increased after nicardipine, nisoldipine, and amlodipine (P less than 0.01) but was unchanged after verapamil and reduced after diltiazem (P less than 0.01). The left ventricular filling pressure increased after amlodipine (P less than 0.05) and verapamil (P less than 0.01) but was unchanged with the other compounds. Cardiac index increased substantially after the dihydropyridines (P less than 0.01), with little change after verapamil or diltiazem. Cardiac double product fell only after verapamil and diltiazem. These studies provide quantitation of the comparative actions of acute intravenous calcium channel blockade in coronary disease.
Amlodipine↗
Immediate effects of bumetanide on systemic haemodynamics and left ventricular volume in acute and chronic heart failure.
1 The haemodynamic and radionuclide effects of i.v. bumetanide (25 micrograms kg-1) were prospectively studied in 24 patients with angiographically documented coronary artery disease and either acute exercise-induced (Group I, n = 12) or chronic (Group II, n = 12) heart failure. 2 Bumetanide at rest increased systemic arterial blood pressure and vascular resistance index; cardiac index and pulmonary artery occluded pressure (PAOP) were reduced at an unchanged heart rate in all patients. The left ventricular ejection fraction fell in patients with normal resting left ventricular filling pressure without change in those with chronic heart failure. The cardiac volumes were unchanged in either group. 3 During constant-load supine bicycle exercise, there were similar effects on systemic arterial pressures, vascular resistance index and PAOP; however the cardiac index was maintained at a reduced left ventricular filling pressure and unchanged ejection fraction and volumes. 4 These data demonstrate immediate mild pressor and vasoconstrictor actions of bumetanide which appear independent of the state of cardiac function; they suggest that any immediate improvement in patient symptomatology following bumetanide may be consequent on the reduction in PAOP; short-term reductions in volume may not occur.
Acute Disease↗
Pharmacokinetic, haemodynamic and radionuclide studies with nicardipine in coronary artery disease.
Pharmacokinetic, haemodynamic and radionuclide studies explored the acute pharmacokinetic and pharmacodynamic actions of nicardipine in patients with coronary heart disease. Nicardipine infusion resulted in dose-related reductions in systolic and diastolic blood pressure and an increased heart rate. Pharmacodynamic activity was evident between 12 and 24 min following 5 and 10 mg i.v. nicardipine but by 3-6 min following the higher doses of 15 and 20 mg; hypotensive activity persisted for up to 2 h. Post-infusion nicardipine concentrations declined biexponentially; however the limited data precluded formal compartmental analysis. Plasma clearance ranged from 5-12 ml/min/kg, and appeared lower than previously reported volunteer data. The haemodynamic actions of nicardipine (10 mg infusion over 10 min) in 6 patients undergoing diagnostic catheterization were reductions in systolic, diastolic and mean systemic arterial pressure and systemic vascular resistance index. Heart rate and stroke volume index increased, and there was a small but statistically significant increase in pulmonary artery occluded pressure. Radionuclide parameters were measured in 20 patients with stable angina, at rest and during supine bicycle exercise, before and 3-5 min after nicardipine 10 mg intravenously. The left ventricular ejection fraction increased by 4% at rest but not during exercise. The left ventricular rest and exercise ejection and filling rates both increased with a concurrently reduced left ventricular ejection time. There was a highly significant inverse relationship between baseline exercise ejection fraction and the response to nicardipine; ejection fraction increased with low initial values but was either unchanged or fell with higher initial values.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Differences in haemodynamic response to beta-blocking drugs between stable coronary artery disease and acute myocardial infarction.
Theoretically the increased sympathoadrenal activity following acute myocardial infarction might augment the haemodynamic impact of beta-adrenoceptor blockade. To evaluate this question 32 haemodynamic studies were performed to compare the effects of equivalent beta-blocking doses of propranolol (8 mg i.v.) and pindolol (0.8 mg i.v.) in patients with a recent acute myocardial infarction (A.M.I.) or stable coronary artery disease (and a presumptive low sympathetic state). In stable coronary artery disease there were clear differences between the haemodynamic impact of propranolol and pindolol. Propranolol decreased both heart rate (delta HR -7 beat/min) and cardiac index (delta CI -0.4 l/min/m2), with an increased pulmonary artery occluded pressure (delta PAOP +4 mmHg) and systemic vascular resistance index (delta SVRI +358 dyn X s X cm-5 m2). However an equivalent beta-blocking dose of pindolol increased PAOP (delta PAOP +3 mmHg) leaving other variables unchanged. These differential actions of propranolol and pindolol have previously been ascribed to the intrinsic sympathomimetic activity (I.S.A.) of pindolol maintaining cardiac pumping function in a low sympathetic state. In contrast following myocardial infarction, both drugs reduced cardiac index to a significantly greater extent compared with stable coronary artery disease (delta CI propranolol -0.81/min/m2; pindolol -0.4 l/min/m2; p less than 0.05); propranolol also reduced the systemic arterial blood pressure (delta systolic -10 mmHg; delta mean -5 mmHg; p less than 0.05). The haemodynamic relevance of the I.S.A. of pindolol appeared attenuated following A.M.I. These data are compatible with experimental evidence of sympathetic nervous activation following coronary occlusion; the resulting hyperadrenergic state appears to condition an augmented haemodynamic response to beta-blocking drugs irrespective of their ancillary pharmacological properties.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic beta-Antagonists↗
A haemodynamic study of the effects of combined slow-calcium channel blockade (nisoldipine) and beta-blockade (metoprolol) in coronary heart disease.
The interaction of a new slow-calcium blocker (nisoldipine) and the beta-blocker metoprolol was evaluated in 16 patients with stable angina. Haemodynamic parameters were determined in a control rest and exercise period. Patients were then randomised equally to nisoldipine (4-8 micrograms/kg) or metoprolol (10 mg) and the haemodynamics of monotherapy assessed; finally the second drug was administered and the effects of combination determined. At rest nisoldipine reduced systemic blood pressure and vascular resistance (P less than 0.01); heart rate, cardiac and stroke volume indices increased (P less than 0.01) at an unchanged pulmonary artery occluded pressure. Metoprolol alone reduced heart rate (P less than 0.05) and increased the pulmonary artery occluded pressure (P less than 0.05). Combination therapy reduced systemic blood pressure and vascular resistance (P less than 0.01); cardiac index and pulmonary artery occluded pressure increased (P less than 0.01) at an unchanged heart rate. The effect of combination was influenced by the order of administration; an improvement in cardiac performance was particularly evident when nisoldipine was added to metoprolol. The interaction during dynamic exercise was similar to that at rest. Thus these data indicated the haemodynamic safety of concurrent nisoldipine/metoprolol therapy; the addition of nisoldipine to metoprolol appeared to offset in part the cardiodepressant properties of beta-blockade.
Adult↗
Assessment of pericardial constraint: the relation between right ventricular filling pressure and pericardial pressure measured after pericardiocentesis.
Experimental studies have shown that right ventricular filling pressure (that is, intracavitary diastolic pressure) approximates pericardial surface pressure but, in many patients after removal of pericardial effusion, right ventricular filling pressure has been found to markedly exceed pericardial pressure recorded by an open catheter. The aim of this study was to determine whether this apparent contradiction was related to the technique of pericardial pressure measurement. Nine patients with chronic pericardial effusion were studied and, although these pressures diverged to varying degrees in individual patients, the previous observation was confirmed in that, although initially similar, right ventricular filling pressure and pericardial pressure (measured by means of an open catheter) tended to diverge during removal of the effusate; when the evacuation was as complete as possible pericardial pressure was 2.1 +/- 1.0 (mean +/- SE), while right ventricular filling pressure was 8.7 +/- 1.7 mm Hg (p less than 0.01). In six open chest, anesthetized, volume-loaded dogs with pericardial effusion (50 ml), right ventricular filling pressure and pericardial pressures measured with both open catheter and flat balloon were all equal. With decreasing volume of pericardial fluid, right ventricular filling pressure and pericardial pressure (by catheter) diverged as had been observed in patients. However, pericardial pressure (balloon) continued to be equal to right ventricular filling pressure. (With 0 ml in the pericardium, right ventricular filling pressure = 12.9 +/- 0.9 mm Hg, pericardial pressure [catheter] = 1.4 +/- 1.9 mm Hg and pericardial pressure [balloon] = 12.4 +/- 1.5 mm Hg.) Thus, these observations support the use of right ventricular filling pressure as an estimate of pericardial constraint in patients.
Adult↗