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PubMed1986

[Changes in cerebral and central hemodynamics in response to hypotensive therapy of patients with essential hypertension and different types of circulation].

A study of indices of the cerebral and central hemodynamics in 122 patients with essential hypertension revealed differences in indices of the cerebral blood flow depending on the initial hemodynamic type. It was shown that the assessment of initial indices of the central hemodynamics makes it possible to achieve more favorable hemodynamic rearrangement, and an analysis of the cerebral hemodynamics--to foresee the inclusion of drugs correcting the cerebral blood flow in multimodality antihypertensive therapy.

Adrenergic beta-Antagonists↗
PubMed1988

[Clinical viewpoints of hemodynamics in cardiac arrhythmias and during anti-arrhythmia treatment].

1. Hemodynamics during cardiac arrhythmias: Cardiac syncopes can be caused by bradycardia (temporary asystole) or by tachycardia. However, tachycardia might be tolerated without causing such symptoms. The necessary compensatory mechanisms (as initiated from the heart, the circulatory system, and the metabolism) are incompletely understood in man. The tolerance of tachycardia depends on the underlying cardiac disease, heart rate, and duration of tachycardia, as well as on the efficiency of compensatory mechanisms. The aspects of tachycardia tolerance, presented here by hemodynamic analysis, include: atrial transport, ventricular tachycardia (arterial pressure, coronary flow, coronary reserve, extravascular resistance), syncopal ventricular tachycardia, supraventricular tachycardia, tachycardia in aortic valvular stenosis, the AFORMED phenomenon, arrhythmia effects on valvular heart disease, and perfusion of organic systems. 2. Hemodynamics during antiarrhythmic therapy: The cardiodepressive side effects inherent in virtually all antiarrhythmic (AA) drugs are complex, variable, and cannot be accurately differentiated as to their components by using conventional hemodynamic parameters. As a rule, this cardiodepression is effective only in cases of impaired myocardial function and/or increased vagal tone. These unwanted hemodynamic effects might influence LV-pump function directly (myocardium: negative inotrope) and indirectly (vasoactive, neurohumoral-reflectory: changes of pre and/or afterload, and of heart rate). The identification of the potentially participating negative inotropic action of the AA-induced cardiodepression, therefore, was accomplished using the elaborate method of analyzing the endsystolic pressure-volume relationship (conductance-catheter technique). The temporary balloon occlusion in the vena cava inferior was used to establish the equation of the isometric maxima. AA-induced alterations of the diastolic ventricular function used echocardiographic data for analysis.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

The acute hemodynamic response to pirbuterol at rest and exercise in patients with heart failure with observations on long-term response.

Rest and exercise hemodynamics with the beta agonist pirbuterol and a placebo preparation were studied in seven patients with severe chronic congestive heart failure. At rest, pirbuterol increased cardiac index (1.8 +/- 0.3 to 2.3 +/- 0.4 L/min/M2, p less than 0.01) and decreased systemic vascular resistance (1899 +/- 405 to 1419 +/- 257 dynes-sec-cm-5, p less than 0.01) without a significant change in heart rate, right atrial, pulmonary arterial, pulmonary arterial wedge, or systemic arterial pressures. Although there were slight increases in cardiac index at peak exercise with pirbuterol, neither total exercise time nor peak oxygen consumption were improved with this agent. No significant hemodynamic changes occurred with placebo at rest, nor was there improvement in exercise performance following placebo. Of three patients studied at six weeks, two showed total loss of hemodynamic effect of pirbuterol compared to the acute response. In conclusion, although acute rest hemodynamics improve with pirbuterol, the lack of improved acute exercise performance and the decrease in hemodynamic responsivity at six weeks appear to limit its usefulness in the treatment of heart failure.

Cardiotonic Agents↗
PubMed1988

Flosequinan induces hemodynamic improvement in heart failure complicating acute myocardial infarction.

The hemodynamic effects of a single dose of flosequinan, a new balanced vasodilator, were studied in twelve patients with severe acute onset heart failure complicating acute myocardial infarction. Flosequinan was added to conventional therapy within 3.8 +/- 0.5 days of the infarction, in the form of a single oral dose of 100 mg in ten of the patients. In the remaining two, reinfarction developed on the sixth day and they received flosequinan immediately thereafter. Hemodynamic monitoring was performed for four hours after the administration, without any other drug being given. Flosequinan produced hemodynamic improvement in all patients. The effect peaked at one to two hours and remained at this level at four hours. Pulmonary capillary wedge pressure decreased from 27.4 +/- 5.0 to 16.5 +/- 2.9 mm Hg and cardiac output increased from 3.5 +/- 0.3 to 4.1 +/- 0.4 l/min (p less than 0.001 for both). Pulmonary arterial and right atrial pressures and systemic and pulmonary vascular resistances were also significantly reduced. Heart rate was not significantly altered (from 84.0 +/- 4.5 to 87.4 +/- 4.6). Mean systemic arterial pressure was slightly reduced. Administration of flosequinan was not associated with any adverse effects and the hemodynamic effect was not related to the pre-treatment serum sodium concentration. We concluded that flosequinan can produce acute hemodynamic improvement in patients with heart failure, complicating acute myocardial infarction. The drug is well tolerated.

Adult↗
PubMed1988

Endotoxin shock in newborn dogs: serial hemodynamic studies.

Using a newly modified dye dilution method for cardiac output determination, we successfully performed frequent serial hemodynamic measurements in newborn dogs to characterize hemodynamic changes in endotoxin shock in neonates. Sixty-seven mongrel newborn dogs (2 to 20 days old, 300 to 1500 gm) were divided into four groups: group 1 (2 to 20 days old, 300 to 1500 gm) received normal saline solution, group 2 (2 to 10 days old, 300 to 800 gm) received 1.5 mg/kg of Escherichia coli lipopolysaccharide (LPS), group 3 (2 to 10 days old, 300 to 800 gm) received 10 mg/kg of LPS, and group 4 (11 to 20 days old, 801 to 1500 gm) received 10 mg/kg of LPS. Cardiac output, heart rate, mean arterial pressure, systemic vascular resistance, and minute work were measured serially after endotoxin administration for 4 hours. Despite extensive manipulation, these measurements were stable in controls throughout the length of the study. Endotoxin, administered at two different doses of 1.5 mg/kg and 10 mg/kg, had profound effects on hemodynamic responses. These effects included a significant dose-related fall in cardiac output, minimal changes in heart rate, and a marked rise in systemic vascular resistance. The hemodynamic changes reported in this study lend additional support to the hypothesis that maturational factors are involved in the hemodynamic response to LPS.

Animals↗
PubMed1987

Hemodynamic long-term results after medical and surgical therapy of hypertrophic cardiomyopathies.

The therapeutic effectiveness of propranolol, verapamil and surgery (transaortal subvalvular myectomy) in hypertrophic cardiomyopathy was assessed in 100 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 12 patients with hypertrophic non-obstructive cardiomyopathy (HNCM) by means of exercise tests with hemodynamic measurements. The effects of propranolol were assessed in 13 HOCM patients, of verapamil in 68 HOCM patients and 12 HNCM patients, and of surgery in 31 HOCM patients after a mean of 3 to 9 months. Of the 68 verapamil-treated patients, 23 were reexamined once more after a mean of 38 months. Ten of the 31 surgically treated patients were reexamined after a mean of 52 months. In the studies performed within the first year of medical treatment or after surgery, verapamil was clinically and hemodynamically superior to propranolol, but not as effective as surgical treatment. Functional limitation according to the NYHA classification improved after propranolol in 31% of the patients, after verapamil in 41%, and after surgery in 94% of the cases. Improvements by more than one NYHA class were observed exclusively after surgical treatment. Maximal exercise capacity was, on average, not changed after propranolol, but increased after verapamil and, more substantially, after surgery. These different responses to treatment could be attributed to hemodynamic changes, especially concerning heart rate, stroke volume, cardiac output, arterio-venous oxygen difference and pulmonary artery pressure. In the case of verapamil, the beneficial hemodynamic effects occurred independently of the site of intraventricular obstruction in HOCM (subvalvular or midventricular), but seemed to be superior in HOCM as compared to HNCM. The late reexaminations, an average of 38 months after beginning verapamil treatment and 52 months after surgery, demonstrated that the initial salutary clinical and hemodynamic effects of verapamil were not maintained during long-term follow-up in the majority of patients, whereas they persisted or even intensified during long-term observation after surgery.

Adolescent↗
PubMed1987

[Hemodynamic studies on the action kinetics of phenoxybenzamine in healthy persons and hypertensive patients].

The hemodynamic profile of the pre- and postsynaptic alpha-receptor blocker phenoxybenzamine (POB) was investigated by a non-invasive technique in healthy subjects and in patients with essential hypertension. At a dose of 0.03 mg POB/kg body weight no hemodynamic changes were detected. POB at a dose of 0.07 mg/kg resulted in an initial transient rise in systemic vascular resistance and mean arterial pressure and a fall in heart rate without changes in stroke volume or cardiac index. 6 h after administration of 0.13 mg POB/kg a transient fall in peripheral vascular resistance and mean arterial pressure with an increase in heart rate and cardiac index was observed. A rise of orthostatic index, however, occurred within 1 h after administration of POB and reached its maximum after 4 h. 8 h after POB no hemodynamic changes were detectable. In patients with essential hypertension a similar fall in systemic vascular resistance and mean arterial pressure was observed after 0.13 mg POB/kg body weight. No change in heart rate occurred and the hemodynamic effects were significant already 3 h after administration of POB and persisted up to 8 h after POB administration. In contrast to healthy subjects, patients with essential hypertension showed no significant changes in the orthostatic index after POB. These hemodynamic findings point to a previously unexpected rapidly reversible functional alpha-receptor blockade by POB.

Adult↗
PubMedDate not supplied

Effect of hydrocortisone on the hemodynamics and serum CK and MBCK enzymes in acute myocardial infarct in dogs.

The effects of hydrocortisone on the hemodynamics and plasma creatine kinase (CK) in dogs with acute myocardial infarction were investigated. Acute myocardial infarction was produced by ligating the anterior descending branch of the left coronary artery and the effects on hemodynamics and plasma CK were observed for two hours. Complete coronary ligation produced a decrease in the cardiac index and left ventricular work index following two hours of coronary ligation. Other hemodynamic parameters (systemic and pulmonary arterial pressure, left ventricular pressure, right atrial pressure, pulmonary arterial wedge pressure, systemic and pulmonary vascular resistance, heart rate, cardiac effort) were essentially unaffected. There was a tendency for an increase in (dp/dt)/IIP but the increase was not significant. In hydrocortisone treated dogs, all the hemodynamic parameters were unaffected except the cardiac index which decreased significantly. Partial coronary ligation produced an increase in the systemic and pulmonary vascular resistance and a decrease in the cardiac index. The other hemodynamic parameters were unaffected. Plasma CK and MBCK increased significantly in dogs with partial or complete ligation of coronary artery. The serum CK was more in partially ligated than in complete coronary ligated dogs. Although hydrocortisone pretreatment decreased the rise of plasma CK it did not change the rise in MBCK observed in coronary ligated dogs without hydrocortisone treatment. These results indicate that hydrocortisone prevents, although not completely, the deleterious effects of ischemia on the plasma CK but has no effect on the increase in plasma MBCK and decrease in the cardiac index.

Animals↗
PubMed1987

Hemodynamics of protamine administration. Comparison of right atrial, left atrial, and aortic injections.

Protamine administration for heparin reversal after cardiopulmonary bypass on occasion is associated with mild to severe hemodynamic deterioration. The route of administration may modify these reactions. A prospective randomized study was done in 68 patients undergoing isolated coronary artery bypass grafting. The route of protamine administration was randomized in a balanced fashion between right atrium, left atrium, and aorta. The preoperative and operative characteristics of the three groups were similar. Hemodynamic measurements were recorded before cannulation, after removal of the venous drainage catheter, and 1 minute, 5 minutes, and 10 minutes after protamine administration. Hypotension occurred in 11 patients with no significant difference among the three groups. The hypotension was immediate in three patients in whom route of administration was the aorta. The overall hemodynamic changes observed for the three treatment groups were not significantly different. An analysis for type II error indicated that it was unlikely that an important difference had been missed. We conclude that the route of administration does not affect the hemodynamic changes associated with protamine administration. We did not observe a case of severe hemodynamic deterioration, so that we cannot assess the effect of route of administration on the severity of an anaphylactic reaction.

Aorta↗
PubMedDate not supplied

[Typologic characteristics of central hemodynamics in the monkey in reclining and upright positions].

By tetrapolar rheography central hemodynamics was investigated in 74 rhesus monkeys in the reclining and orthostatic position. The basic hemodynamic parameters were examined in relation to the entire sample, to the groups with a higher or lower blood pressure (BPmean), and to four states of central circulation in orthostatic animals. The typological circulatory differences in the orthostatic state were shown to be determined by qualitatively different hemodynamic mechanisms responsible for BPmean. The hemodynamic characteristics in the reclining and orthostatic position were found to be reciprocally related. It is recommended to take into consideration the typological differences of hemodynamics that can modify cardiovascular responses to various effects.

Animals↗
PubMed1986

Clinical application of monitoring techniques: hemodynamic monitoring.

In the diagnosis of myocardial ischemia continuous hemodynamic monitoring may contribute to detection of transient ischemia, to definition of location and to elimination of its pathogenesis, and to characterization of hemodynamic response to ischemia. It can be helpful in investigating the significance of negligible, non specific and/or short-lasting electrocardiographic changes accompanying typical anginal symptoms. Simultaneous right ventricular and left ventricular pressure monitoring gives information regarding biventricular interaction during episodes of transient ischemia: an early left ventricular dysfunction, with or without a late right ventricular impairment, a selective right dysfunction, and a simultaneous left ventricular and right ventricular impairment all represent the hemodynamic patterns associated with left, right and biventricular ischemia respectively. Monitoring of hemodynamic parameters related to myocardial oxygen consumption and the study of their changes preceding the onset of ischemia during both spontaneous and provoked episodes of ischemia, may help in identifying whether functional or organic factors or both are involved in the pathogenesis of transient ischemia in individual patients. Two principal hemodynamic patterns appear to be associated with transient ischemia: a) left ventricular and/or right ventricular impairment, usually beginning shortly before the onset of electrocardiographic changes, followed by a rapid recovery and often an overshooting, b) a sudden and sustained increase in systolic pressure and heart rate, simultaneous with the onset of ST-T changes. In both cases, the 'excitatory' pattern appears to be unrelated to pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1985

Hemodynamic and clinical assessment after therapy for acute deep vein thrombosis. A prospective study.

This prospective study was undertaken in 153 patients who had sustained DVT of various extents and had been treated with streptokinase or heparin. Its aim was (1) to assess hemodynamic changes occurring in the deep venous system over a 2 year period, and (2) to correlate these hemodynamic changes with the clinical features that subsequently developed. Foot volumetry, a noninvasive, objective, and accurate technique, was used to measure hemodynamic changes. Within 2 years of DVT, there was severe hemodynamic impairment (equivalent to that seen in established postphlebitic limbs) in a fifth of the limbs with calf vein DVT, and in half of the limbs with more extensive proximal DVT. Symptoms were worse after major DVT. Even when successful, thrombolytic therapy does not prevent hemodynamic deterioration. The results appear to be no better than for a group of patients who, with the same degree of thrombosis, received heparin therapy.

Female↗
PubMed1985

[Effects of intravenous diltiazem in acute myocardial infarction: hemodynamic evaluation].

The acute hemodynamic effects of intravenous Diltiazem were studied in 20 pts. with acute myocardial infarction, admitted to Coronary Care Unit within 24 hours from onset of Symptoms--19 men, 1 woman, aged from 46 to 83 years, 14 with anterior myocardial infarction, 6 with inferior myocardial infarction. All, but one, where at the time of their admission to CCU in first Forrester's hemodynamic subset (CI greater than 2.2 L/min/m2, WP less than 18 mmHg); in the last patient WP was 21 mmHg, CI 2.6 L/min/m2. Hemodynamic measurements were performed before (no drugs with hemodynamic effects were allowed during 4-6 hours before the study protocol) and after the administration of Diltiazem, 0,3 mg/kg i.v. administered in 2 min. (bolus) in 12 patients, Group A. In 8 pts--Group B--the bolus was followed by continuous infusion of Diltiazem at the rate of 5 mcg/Kg/min for three hours. The hemodynamic measurements were repeated: in Group A 2-5-30-60-120 min. after the end of the bolus; in the Group B at the same time as Group A, at the end of infusion (180 min) and 60 min after the end of infusion. Diltiazem induced no significant changes of HR, CVP, WP, CI, LVSWI and Triple product, in both groups of pts., at any time. Systolic and diastolic blood pressure decreased significantly (P less than 0.01) only 2 min. after Diltiazem administration (Group A: SBP 125.0 +/- 15.8----114.0 +/- 16.0 mmHg, DBP 85.4 +/- 6.5----76.6 +/- 10.5 mmHg; Group B: SBP 123.0 +/- 20.0----113.0 +/- 11.0 mmHg, DBP 78.1 +/- 7.0----75.0 +/- 4.9 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1979

[State of general and renal hemodynamics in acute myocardial infarct].

The results of studying central and renal hemodynamics in 49 patients with a different course of myocardial infarction in the acute period (1st, 3rd, and 10th day) are analysed. It was established that on the 1st day the cardiac output decreases considerably in circulatory insufficiency and hardly changes in an uncomplicated course of the disease. The stroke output of the heart reduces significantly in all forms of the course of myocardial infarction. At an increase of total peripheral resistance is observed in myocardial infarction, particularly in circulatory insufficiency. A significant increase in the central hemodynamics indices is noted at the end of the acute period. On analysing the dependence of central and renal hemodynamics, the authors conclude that local mechanisms are involved in the changes in renal hemodynamics in addition to its dependence on the disorders of central hemodynamics.

Acute Disease↗
PubMed1983

Central hemodynamics of beta-adrenoceptor blocking drugs: beta 1 selectivity versus intrinsic sympathomimetic activity.

It was the purpose of the present study to assess the hemodynamic effects of adrenergic beta-receptor blocking drugs possessing intrinsic sympathomimetic activity (ISA) and/or beta 1 selectivity, both at rest and during exercise. The hemodynamic effects of seven different beta-blockers (propranolol, atenolol, acebutolol, ICI 72,222, ICI 89,406, and pindolol) were studied at rest in patients with ischemic heart disease. Heart rate (HR), cardiac output (CO), arterial blood pressure (BP), and pulmonary artery pressure (PP) were determined. At rest, it was possible to subdivide the various beta-blockers into three main groups according to the degree of ISA. One group without ISA, including propranolol and atenolol, reduced CO by 25% and HR by 15%. A second group with moderate ISA, represented by practolol, acebutolol and ICI 72,222, reduced CO only by 15% and HR by 10%. A third group with pronounced ISA, represented by pindolol and ICI 89,406, did not change CO and HR significantly. All three groups consisted of drugs both with and without beta 1 selectivity. During exercise, pindolol and propranolol reduced CO, HR, and BP to the same extent. In conclusion, the central hemodynamic response to beta-blockers at rest is determined by the degree of ISA, whereas beta 1 selectivity does not modify the central hemodynamic response to beta-blockade. However, the hemodynamic differences between adrenergic beta-blocking drugs with and without ISA disappear in situations with increased sympathetic drive, such as exercise.

Adrenergic beta-Antagonists↗
PubMed1982

[Hemodynamics of congestive cardiomyopathy].

202 patients with congestive cardiomyopathy have been classified according to their hemodynamic, angiographic, echocardiographic and scintigraphic findings: 72 patients were in the late stage (LS), 103 patients in an early stage (ES) and 17 patients showed a latent form of the disease. 48% of the hemodynamic ES were found to be clinically in stage IV NYHA and 53% of ES fell in class III. 40% of the patients with LS showed a stationary clinical course whereas 46% could improve their classification by one grade. The mortality in hemodynamic LS was 46% within an interval of 18 +/- 14 months after the diagnosis. In ES 64% showed a stable clinical course, where a 22% were deteriorating. Mortality in this group was 10%. Sensitivity and specificity of echocardiography (93 vs 80%) and radionuclide methods (80 vs 71%) were quite good in the late stage whereas in ES specificity was only 71% vs 80%. There was a discrepancy between the degree of myocardial impairment and clinical symptoms in the late stage whereas in the early stage there was no correlation between exercise capacity and LV-hemodynamics. Non-invasive methods allow the hemodynamic evaluation of the disease; invasive methods are required for clarification of diagnosis or establishing prognosis.

Adult↗
PubMed1983

[8-hour hemodynamic study of 2 sustained-release nitrate derivatives. Comparative double-blind study against placebo].

The aim of this study was to evaluate the duration of the hemodynamic effects of a new slow release preparation of isosorbide dinitrate and to compare its action with placebo and a slow release nitroglycerin preparation whose hemodynamic efficacity has already been demonstrated. The study was undertaken in 30 patients admitted to the intensive care unit during the acute phase of myocardial infarction complicated by left ventricular failure less than 12 hours after the onset of the chest pain. The patient population was uniform: 24 males, 6 females, mean age 61 years. Fifteen patients had anterior infarcts and 15 posterior infarcts. The drugs were administered double blind in a randomised fashion to 3 groups of 10 patients, the initial clinical and hemodynamic characteristics of which were comparable: 10 patients received placebo (placebo group); 10 patients received slow release nitroglycerin in a 7,5 mg gelule (NTG group) and 10 patients received 40 mg slow release isosorbide dinitrate (ISDN group). The following parameters were compared: heart rate, right atrial pressure, pulmonary artery and capillary pressures, systemic arterial pressure, cardiac index and systemic and pulmonary arterial resistances. These parameters were measured before therapy, half an hour, one hour and every two hours up to the 8th hour after drug administration. All patients were in moderate left ventricular failure with an initial mean capillary pressure of 18 mmHg +/- 1,3 mmHg. In the placebo group, none of the parameters studied changed significantly during the study. Pulmonary artery pressure fell significantly by 11 p. cent in the NTG group and 7,5 p. cent in the ISDN group. Mean pulmonary capillary pressure fell progressively in both treatment groups; the change was significant compared to the placebo group from the first hour for the ISDN group, and from the second hour for the NTG group. The fall remained significant at the 8th hour for the ISDN group but not in the NTG group. Cardiac index, systemic blood pressure, systemic and pulmonary arterial resistances did not change significantly. The cardiac index remained stable in the 30 patients, but with a number of individual variations depending on initial mean pulmonary capillary pressure and the importance of its fall after nitrate administration. The authors conclude that the hemodynamic effects of slow release NTG and ISDN in the acute phase of myocardial infarction complicated by moderate left ventricular failure are comparable. Pulmonary capillary pressure was the hemodynamic parameter which underwent the greatest variation in the two treatment groups. Its fall was more prolonged in the ISDN than in the NTG group.

Administration, Oral↗
PubMed1983

[Angina pectoris with normal coronary arteries: clinical, hemodynamic and metabolic study].

Sixty patients without organic heart disease presenting with chest pain suggestive of angina pectoris and angiographically normal coronary arteries underwent clinical, hemodynamic and metabolic investigation. The study of myocardial lactate metabolism during atrial pacing (168 +/- 14 bpm) allowed identification of two groups: --40 patients with a normal coefficient of lactate extraction (K greater than or equal to 9 per cent); --20 patients with a pathologically low coefficient of lactate extraction (K less than 9 per cent) reflecting myocardial ischemia. In the first group, chest pain was often atypical (75 per cent of cases). Hemodynamic investigation showed minor abnormalities of the left ventricle in 48 per cent of cases. The diagnosis of angina was rejected in these patients. In the second group, the majority of patients developed chest pain (85 per cent of cases) at the maximal heart rate with significant ST depression (80 per cent of cases). The chest pain was typical of angina pectoris in 50 per cent of cases. Hemodynamic and angiographic investigation of the left ventricle was completely normal in nearly all cases. Only these patients with clinical, electrocardiographic and metabolic signs of myocardial ischemia can be considered as having angina with normal coronary arteries. Although studies of myocardial lactate metabolism and other signs of myocardial ischemia distinguish clearly between these two groups of patients, the coronary hemodynamics were similar. Resting coronary flow, its increase for the same myocardial oxygen demands and coronary resistances were comparable in both groups, and not significantly different from the values obtained in a control group of patients without coronary artery disease or chest pain. These results confirm that about 30 per cent of patients investigated for chest pain suggestive of angina pectoris who have angiographically normal coronary arteries, develop signs of myocardial ischemia during atrial pacing. The physiopathological explanation remains unclear as coronary hemodynamics have been found to be normal.

Adult↗