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PubMed1987

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator.

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1992

Salicylate reduces ventricular dysfunction and arrhythmias during reperfusion in isolated rat hearts.

Recent studies have shown the ability of salicylic acid (SA) to trap hydroxyl radicals (OH.) generated during reperfusion in ischemic myocardium. Since OH. is implicated in the pathogenesis of reperfusion injury, we examined the effect of SA on reperfusion-induced arrhythmias and postischemic ventricular dysfunction. Isolated rat hearts perfused by the Langendorff technique were preperfused with Krebs-Henseleit buffer containing SA for 10 min. Hearts were then made ischemic for 30 min, followed by 30 min of reperfusion. In a separate group, SA was administered only at the onset of reperfusion. The left ventricular contractile functions, left ventricular developed pressure (LVDP) and its first derivative (LV dP/dt), coronary flow (CF), and creatine kinase (CK) release were determined before and after ischemia. Epicardial electrocardiogram (ECG) was also recorded to analyze the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF). SA improved LVDP, LV dp/dt, and CF recovery and reduced CK release compared to the control group. The incidence of VT and VF during reperfusion was also significantly reduced by SA. Analysis of tissue thiobarbituric acid-reactive products indicates that SA decreased oxidative stress during reperfusion. In conclusion, these results suggest that SA reduces myocardial reperfusion injury and attenuates ventricular arrhythmias by trapping OH. radicals upon reperfusion in isolated rat hearts.

Animals↗
PubMed1990

Nitrous oxide does not exacerbate pulmonary hypertension or ventricular dysfunction in patients with mitral valvular disease.

Using the rapid-response thermistor pulmonary artery catheter and transoesophageal echocardiography, this study examined the effects of 100 per cent oxygen, 70 per cent nitrous oxide/30 per cent oxygen, and 70 per cent nitrogen/30 per cent oxygen on the pulmonary circulation and ventricular function in ten patients with pulmonary hypertension. In comparison with baseline measurements, nitrous oxide administration resulted in small but statistically significant (P less than 0.05) changes in mean arterial pressure (76 +/- 14 to 67 +/- 12), mean pulmonary arterial pressure (37 +/- 14 to 33 +/- 13 mmHg), and cardiac output (3.7 +/- 1.4 to 3.2 +/- 1.1 L.min-1). Seventy per cent nitrogen resulted in no significant changes from baseline. The repeat 100 per cent oxygen measurements were nearly identical to the nitrous oxide measurements. It is concluded that nitrous oxide does not exacerbate pulmonary hypertension or ventricular dysfunction during high-dose fentanyl anaesthesia in patients with mitral valvular disease.

Adult↗
PubMed1979

Atrial pacing induced left ventricular dysfunction: reversibility after aortocoronary bypass surgery.

Three patients with angina pectoris were studied before and after aortocoronary bypass surgery. Angiographic studies were performed with and without atrial pacing. Preoperative atrial pacing in all three patients resulted in angina and/or ST segment changes accompanied by regional left ventricular contractile abnormalities, decreased ejection fraction, as well as decreased left ventricular end-diastolic and stroke volumes. After surgery with all grafts patent, atrial pacing at similar heart rates did not produce an ischemic response. Left ventricular contractile pattern remained normal, and there was no change in ejection fraction though end-diastolic and stroke volumes decreased. These studies demonstrate that aortocoronary bypass surgery can abolish both the ischemic response and left ventricular dysfunction that accompany atrial pacing.

Angina Pectoris↗
PubMed1992

Metabolic evidence of viable myocardium in regions with reduced wall thickness and absent wall thickening in patients with chronic ischemic left ventricular dysfunction.

Reduced end-diastolic wall thickness with absent systolic wall thickening has been reported to represent nonviable myocardium in patients with chronic coronary artery disease. To assess whether reduced regional end-diastolic wall thickness and absent wall thickening accurately identify nonviable myocardium, 25 patients with ischemic left ventricular dysfunction (ejection fraction at rest 27 +/- 10%) underwent positron emission tomography with oxygen-15-labeled water and 18fluorodeoxyglucose to assess metabolic activity and spin-echo gated nuclear magnetic resonance imaging to measure regional end-diastolic wall thickness and wall thickening. The presence of metabolic activity was defined as 18fluorodeoxyglucose uptake (corrected for partial volume) greater than 50% of that in normal regions. Of 355 myocardial regions evaluated, 266 were hypokinetic or normokinetic at rest and 89 were akinetic (that is, absent wall thickening). 18Fluorodeoxyglucose uptake was observed in 97% of the hypokinetic and normokinetic regions and in 74% of the akinetic regions. End-diastolic wall thickness was greater in akinetic regions with than in those without 18fluorodeoxyglucose uptake (11 +/- 4 vs. 7 +/- 3 mm, p less than 0.01). The highest values for sensitivity and specificity of end-diastolic wall thickness in predicting the absence of metabolic activity in akinetic regions were 74% and 79%, respectively, and corresponded to an end-diastolic threshold of 8 mm. However, the positive predictive accuracy was only 55% and did not improve for other end-diastolic wall thickness values. In all myocardial regions, there was only a weak correlation between 18fluorodeoxyglucose activity and either end-diastolic wall thickness (r = 0.17) or wall thickening (r = 0.32). Thus, metabolic activity is present in many regions with reduced end-diastolic wall thickness and absent wall thickening. These data indicate that assessment of regional anatomy and function may be inaccurate in distinguishing asynergic but viable myocardium from nonviable myocardium.

Adult↗
PubMed1989

Right ventricular dysfunction in septic shock: assessment by measurements of right ventricular ejection fraction using the thermodilution technique.

Right ventricular ejection fraction (RVEF) was measured by the thermodilution technique in a series of 127 consecutive critically ill patients monitored with a modified pulmonary artery (PA) catheter equipped with a fast response thermistor. Thermodilution RVEF was significantly lower in septic shock (23.8 +/- 8.2%, 93 measurements) than in sepsis without shock (30.3 +/- 10.1%, 118 measurements) or in the absence of sepsis or cardiopulmonary impairment (32.5 +/- 7.1%, 62 measurements). Both myocardial depression and pulmonary hypertension could account for this impairment of RV function. RVEF decreased from 35.1 +/- 9.8 to 24.2 +/- 10.4% (P less than 0.01) during development of septic shock and increased from 25.0 +/- 7.6 to 29.8 +/- 8.5% (P less than 0.05) during recovery (14 patients). Initial RVEF in septic shock was 27.8 +/- 8.6% in 11 patients who survived but only 20.9 +/- 6.7% (P less than 0.02) in the 23 patients who eventually died. Thus, RV dysfunction is common during septic shock, is directly related to its severity, and can easily be recognized in patients monitored with a PA catheter.

Adult↗
PubMed1986

Effects of substrate availability on myocardial C-11 palmitate kinetics by positron emission tomography in normal subjects and patients with ventricular dysfunction.

The possibility of demonstrating noninvasively with C-11 palmitate and positron emission tomography (PET) changes in myocardial substrate metabolism in normal and diseased human myocardium in response to altered substrate availability in blood and disease-related abnormalities was examined in five normal volunteers and 16 patients with ventricular dysfunction. C-11 palmitate injection and serial PET imaging were performed after an overnight fast (control period) and again 2 hours later after oral glucose (50 gm). Myocardial C-11 time-activity curves from serial PET images revealed a biexponential clearance pattern. An early rapid phase, defined by relative size and clearance half-time, reflects C-11 palmitate oxidation and the late slow phase tracer deposition in the endogenous lipid pool. During the control period, the tracer fraction entering the early rapid phase averaged 47 +/- 13% (SD) in normal subjects and 45 +/- 12% in patients. Corresponding clearance half-times were 19 +/- 7 and 20 +/- 5 minutes, respectively. Heart rate and blood pressure remained unchanged after glucose, but plasma glucose levels rose by 72.5% in normal subjects and by 98.9% in patients, while free fatty acid levels fell by 72% and 42% (p less than 0.001), respectively. In normal subjects, the tracer fraction in the early rapid phase fell by 43% (p less than 0.005) and the clearance half-time increased by 46% (p less than 0.01). In patients, the response of C-11 palmitate tissue kinetics to glucose was variable. In nine patients, it was similar to that in normal subjects while in the other seven patients a "paradoxic" response occurred. The tracer fraction entering the rapid clearance phase increased after glucose by 30% (p less than 0.05) associated with a 36% (p less than 0.05) decline in clearance half-times. The paradoxic response was unrelated to disease etiology or plasma substrate levels but occurred mostly in left ventricles with more severely depressed function. Thus, PET and C-11 palmitate allow the noninvasive demonstration of the known response of substrate metabolism of the human heart to altered substrate availability. Glucose administration in fasted humans serves as a provocative test of substrate regulation which can be abnormal in myocardial disease and can be demonstrated noninvasively.

Adult↗
PubMed1984

Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction.

Cardiac dysfunction in animals has been associated with impairment of arterial and cardiopulmonary baroreflex control of the circulation. Chronic heart failure in human beings is associated with neurohumoral excitation, which could result in part from impairment in the inhibitory influence of baroreflexes. We postulated that (1) patients with left ventricular dysfunction (LVD) have impaired baroreflex modulation of vascular resistance and (2) administration of a digitalis glycoside would immediately restore baroreflex sensitivity. Eleven patients with LVD (NYHA class, 2.8 +/- 0.2, mean +/- SEM; baseline left ventricular ejection fraction, 18 +/- 2%; cardiac index, 2.4 +/- 0.21/min/m2; and pulmonary capillary wedge pressure, 26.0 +/- 3.2 mm Hg) were compared with 17 normal control subjects. We measured forearm vasoconstrictor responses to simulated orthostatic stress with use of lower body negative pressure (LBNP) at -10 and -40 mm Hg to unload cardiopulmonary and arterial baroreceptors. Baseline forearm vascular resistance (FVR) was higher in patients with LVD than in normal subjects: FVRLVD, 68.8 +/- 15.3 U; FVRN, 23.2 +/- 2.1 U (p less than .001). During unloading of baroreceptors with LBNP -10 mm Hg, normal subjects developed vasoconstriction (delta VRN at LBNP -10 mm Hg, +5.7 +/- 1.6 U) but patients with LVD failed to have vasoconstriction and tended to develop vasodilation (delta FVRLVD at LBNP -10 mm Hg, -8.6 +/- 8.5 U) (p = .05, normals vs patients with LVD at LBNP -10 mm Hg). A more marked disparity in response was seen during unloading of baroreceptors of LBNP -40 mm Hg: delta FVRN at LBNP -40 mm Hg, +16.6 +/- 1.5 U; delta FVRLVD at LBNP -40 mm Hg, -10.3 +/- 9.6 U (p less than .001, normals vs patients with LVD). Despite high baseline values for FVR, patients with LVD developed vasoconstriction during intra-arterial infusions of norepinephrine, thereby excluding a nonspecific depression of vascular reactivity as the mechanism for abnormal responses to LBNP in patients with LVD. We also studied the short-term effects of administration of a digitalis glycoside, ouabain 0.0075 mg/kg (seven patients) or lanatoside C (Cedilanid-D) 0.02 mg/kg (three patients), on baroreflex-mediated vasoconstrictor responses to LBNP in the patients with LVD. Digitalis glycoside reduced baseline FVR from 71.8 +/- 16.6 to 48.6 +/- 12.0 U (p less than .02). Responses to LBNP tended to be normalized after administration of digitalis glycoside: delta FVR during LBNP -40 mm Hg, -11.1 +/- 10.5 U before and +7.8 +/- 5.6 U after the drug (p less than .05).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1986

Left ventricular dysfunction in patients with angina pectoris and normal coronary angiograms.

Left ventricular function was assessed in 201 patients who presented with angina pectoris and who were subsequently found to have completely normal coronary angiograms. Left ventricular angiograms from 187 patients were suitable for analysis of systolic regional wall motion; 121 were found to be normal and 66 had a total of 115 hypokinetic segments. Patients with hypokinesia had a significantly higher left ventricular end systolic volume and a significantly lower left ventricular ejection fraction and exercise capacity than those in whom regional wall motion was normal. Thirty one per cent of patients with normal wall motion and 30% of those with hypokinesia had a resting left ventricular end diastolic pressure greater than 15 mm Hg. There were significantly more smokers in the group with hypokinetic segments. Thus of patients with angina and normal coronary angiograms, 25% had evidence of left ventricular systolic dysfunction, 20% had evidence of diastolic dysfunction, and 11% had evidence of both systolic and diastolic dysfunction. The results suggest that smoking may be associated with left ventricular regional wall motion abnormalities.

Adult↗
PubMed1983

Coronary reperfusion for the treatment of acute myocardial infarction: postischemic ventricular dysfunction.

There has been recent interest in treating acute myocardial infarction with coronary reperfusion by fibrinolytic therapy. Experimental studies have shown that myocardial infarct size can be reduced by coronary reperfusion. However, return of cardiac function, high energy phosphate metabolism, and cardiac ultrastructure may be delayed within tissue which is salvaged by coronary reperfusion. This postischemic ventricular dysfunction is transient and has been termed the 'stunned myocardium' phenomenon. Although reperfused infarcts are hemorrhagic, the hemorrhage is confined well within tissue which is already necrotic and does not appear to exacerbate the extent of necrosis. Clinical trials designed to assess the benefits of reperfusion for the therapy of acute myocardial infarction should concentrate on long-term rather than short-term changes in cardiac function.

Animals↗
PubMed1991

Clinical heart failure trials and the design rationale of Studies of Left Ventricular Dysfunction (SOLVD).

Heart failure has become a major worldwide public health problem. Several million patients suffer with this malady and large epidemiologic studies have documented mortality that can be in excess of 50% at 5 years. Furthermore, morbidity is great with this disease and hospitalizations are increasing yearly. Attention must be placed on pharmacotherapeutic strategies that can attenuate the morbidity and high mortality seen in the heart failure milieu. Studies of Left Ventricular Dysfunction (SOLVD) is a large, multicenter, multinational, clinical research program with two, double-blind, randomized clinical trials designed to evaluate the effects of an angiotensin converting enzyme inhibitor, enalapril, on heart failure morbidity and mortality. The program also includes a registry and several substudies that are designed to better clarify heart failure pathophysiology. With over 13,000 subjects participating in this program, SOLVD is the largest clinical heart failure study ever mounted. It is important to consider the design rationale of this program.

Double-Blind Method↗
PubMed1990

Effects of a vasopressin antagonist with combined antipressor and antiantidiuretic activities in rats with left ventricular dysfunction.

These experiments assessed the hemodynamic and aquaretic effects of an arginine vasopressin (AVP) antagonist with dual V1V2-receptor inhibiting properties in rats with congestive heart failure resulting from ischemic cardiomyopathy. The compound d(CH2)5-D-Tyr(Et)VAVP was used in these studies. Rats with limited or extensive myocardial infarcts (i.e., with less than 50% or greater than 66% necrosis of the left ventricular wall, respectively, induced by left coronary ligation) and sham-operated controls received the AVP antagonist (100 micrograms/kg i.v.) 4 weeks later. This agent produced an 18% increase in cardiac output (p less than 0.05) and 13% decrease in systemic vascular resistance in the severely damaged rats, both changes being significantly different from those seen in the normal controls or the rats with limited infarcts. All animals exhibited increases in urinary output of 4-10-fold over baseline. We conclude that the hemodynamic and renal effects of this agent are beneficial in animals with left ventricular dysfunction.

Animals↗
PubMed1984

The systolic arterial pressure/end-systolic volume relationship in patients with severe left ventricular dysfunction.

Performance of the intact left ventricle is well-defined by the end-systolic pressure/end-systolic volume relationship that appears independent of preload and afterload. To determine whether noninvasive measurements of this relationship could distinguish normal from abnormal subjects, we evaluated the relationship between arterial systolic pressure (determined by cuff sphygnomanometry) and radionuclide estimates of end-systolic volume in 12 normal subjects and 24 patients with severe left ventricular dysfunction. Data were acquired at rest, after atropine injection, and then during at least three increments of arterial pressure (average total increase approximately 45 mm Hg) using phenylephrine. The relationship between peak-systolic pressure (SP) and end-systolic volume (ESV) was found to be linear in all subjects (r greater than or equal to 0.91). The slope of this line was steeper in normal subjects than in myopathic patients (73 +/- 21.7 vs 20.8 +/- 8.7 mm Hg/volume unit/m2, P less than 0.001) and the zero pressure intercept also was greater (49.8 +/- 30 mm Hg vs 27.1 +/- 44.2 mm Hg, P less than 0.01). Similarly, resting ejection fraction (EF) was greater in the normals (0.71 +/- 0.88 vs 0.21 +/- 0.07% P less than 0.001) and end-diastolic volume (EDV) was smaller (4.14 +/- 0.88 vs 6.58 +/- 0.65 volume units, P less than 0.01). Systolic pressure/end-systolic volume relationship determined by these noninvasive methods was linear in both patients with severely reduced cardiac function and normal control subjects, clearly distinguishing normal from severely impaired left ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Reversibility of severe left ventricular dysfunction due to doxorubicin cardiotoxicity. Report of three cases.

Doxorubicin is a potent anticancer agent effective in a wide range of malignancies, but its use is limited by dose-dependent late cardiotoxicity. Severe doxorubicin cardiotoxicity has been associated with a poor prognosis and a high mortality rate, and until recently has been thought to be irreversible. We describe the cases of three patients with well-documented severe left ventricular dysfunction due to doxorubicin who had complete clinical recovery with return of cardiac function to normal. Because severe doxorubicin cardiotoxicity is reversible in some patients, aggressive supportive therapy is warranted.

Adult↗
PubMed1989

The effect of diabetes mellitus on prognosis and serial left ventricular function after acute myocardial infarction: contribution of both coronary disease and diastolic left ventricular dysfunction to the adverse prognosis. The MILIS Study Group.

Patients with diabetes mellitus experience a more adverse outcome after acute myocardial infarction compared with nondiabetic patients, although the mechanisms responsible for these findings are not clear. From the Multicenter Investigation of the Limitation of Infarct Size (MILIS) study, the course of acute infarction in 85 diabetic patients was compared with that in 415 nondiabetic patients, all of whom had serial assessments of left ventricular function. The diabetic patients experienced a more complicated in-hospital and postdischarge course than did the nondiabetic patients, including a higher incidence of postinfarction angina, infarct extension, heart failure and death, despite the development of a smaller infarct size and similar levels of left ventricular ejection fraction. Although diabetic patients had a worse profile of cardiovascular risk factors at the time of the index infarction, the increased incidence of adverse outcomes among them persisted despite adjustment for these baseline imbalances. Diabetic women had a poor baseline risk profile compared with the other groups categorized by gender and diabetic status, and experienced an almost twofold increase in cardiac mortality despite development of the smallest infarct size during the index event. The duration of diabetes and the use of insulin at the time of the index infarction were associated with a better in-hospital mortality rate, but the duration of diabetes did not exert a major influence on the outcome of the diabetic patients. The factors responsible for the increased incidence of adverse outcomes among diabetic patients may be related to an acceleration of the atherosclerotic process, diastolic left ventricular dysfunction associated with diabetic cardiomyopathy or other unidentified unfavorable processes.

Cardiovascular Diseases↗
PubMed1985

Acute myocardial infarction complicated by left ventricular dysfunction and respiratory failure. The effects of continuous positive airway pressure.

The cardiopulmonary effects of continuous positive airway pressure (CPAP) were studied in 14 patients with acute myocardial infarction complicated by circulatory and respiratory failure. Cardiac performance, lung mechanics, and gas exchange were assessed during 50 percent mechanical ventilatory support at end-expiratory airway pressure levels of 0, 5, 10, and 15 mm Hg. The increase in airway pressure resulted in significantly improved arterial blood oxygenation (p less than 0.001) and in a substantial reduction in the spontaneous respiratory effort (p less than 0.001). We observed a slight decrease in stroke volume index (p less than 0.05) with increasing airway pressure in patients who had moderate left ventricular dysfunction, and a trend of improvement (NS) in those who had severe pump failure. Relatively high levels of CPAP can be used to improve pulmonary function in patients with acute myocardial infarction and left ventricular failure. In fact, circulatory depression is less likely to occur when cardiac performance is poor.

Aged↗
PubMed1987

Left atrial abnormalities indicating diastolic ventricular dysfunction in cardiopathy of obesity.

Electrocardiograms and M-mode echocardiograms were evaluated in lean and obese patients, either normotensive or hypertensive, who were paired for mean arterial pressure, age, and sex. Electrocardiographic evidence of left atrial abnormalities (LAA) occurred more frequently (p less than 0.01) and left atrial size was greater in the obese than in the lean patients (p less than 0.01). The left atrial emptying index, an indicator of early diastolic ventricular function, was reduced in obese patients (p less than 0.01), most markedly in those with obesity-hypertension. The left atrial emptying index was reduced in obese patients with electrocardiographic LAA compared to obese patients without this electrocardiographic sign (p less than 0.02). A close correlation (r = 0.61, p less than 0.001) was obtained between the left atrial emptying index and atrial ECG abnormalities. These left atrial abnormalities in obesity and particularly in obesity-hypertension indicate diastolic ventricular dysfunction.

Adult↗
PubMed1987

Hemodynamic effects of the beta 1-adrenoceptor partial agonist xamoterol in relation to plasma norepinephrine levels during exercise in patients with left ventricular dysfunction.

A new cardioselective beta 1-adrenoceptor partial agonist, xamoterol, has been developed for the treatment of heart failure, especially that associated with ischemic heart disease. To investigate the hemodynamic effect of xamoterol in relation to sympathetic nervous activity, hemodynamic variables and plasma norepinephrine (NE) levels were measured at rest and during three graded bicycle exercise tests before and after a single intravenous dose of 0.15 mg/kg xamoterol in 10 patients with mild-to-moderate left ventricular dysfunction. Plasma NE increased with increasing grade of exercise and a linear correlation between plasma NE and heart rate was observed at four time points (at rest and three exercise levels) before and after xamoterol. After administration of xamoterol, the slope of the regression line of plasma NE-heart rate relation was significantly less steep than that before drug. Predose and postdose regression lines crossed at 440 pg/ml of plasma NE. Similar effects were observed on the plasma NE-cardiac index and plasma NE-systolic blood pressure relations (regression lines crossed at 380 and 530 pg/ml of plasma NE, respectively). Thus, xamoterol had a dual agonist-antagonist effect in relation to plasma NE, and the crossover point lay approximately between 400 pg/ml and 500 pg/ml. This level of plasma NE was achieved at a low exercise level and at a heart rate of about 100 beats/min. These results indicate that xamoterol has intrinsic sympathomimetic activity comparable to relatively low sympathetic activity (400 to 500 pg/ml of plasma NE) and therefore acts as a beta 1-agonist when sympathetic nervous activity is below this level and as an antagonist when sympathetic activity is above this level.

Adrenergic beta-Antagonists↗