Dobutamine
Cardiotonic Agents
Echocardiography, Stress
Echocardiography
Exercise Test
Myocardial Stunning
Ventricular Function, Left
Hemodynamics
Myocardial Ischemia
Ventricular Dysfunction, Left
Hydrazones
Coronary Disease
Thallium Radioisotopes
Tomography, Emission-Computed, Single-Photon
Technetium Tc 99m Sestamibi
Amrinone
Milrinone
Coronary Angiography
Sensitivity and Specificity
Dipyridamole
Predictive Value of Tests
Stroke Volume
Enoximone
Electrocardiography
Dogs
Myocardial Revascularization
Myocardium
Magnetic Resonance Imaging, Cine
Cardiac Output
Sympathomimetics
Atropine
Myocardial Infarction
Propanolamines
Feasibility Studies
Oxygen Consumption
Adrenergic beta-Antagonists
Observer Variation
Cardiomyopathy, Dilated
Receptors, Adrenergic, beta
Prospective Studies
Radionuclide Ventriculography
Tomography, Emission-Computed
Radiopharmaceuticals
Echocardiography, Doppler
Reversal of severe pulmonary hypertension with beta blockade in a patient with end stage left ventricular failure. (1/1123)
A 52 year old man with severe chronic left ventricular failure (New York Heart Association class IV) was considered unsuitable for cardiac transplantation because of high and irreversible pulmonary vascular resistance (PVR). In an attempt to produce symptomatic improvement, metoprolol was cautiously introduced, initially at 6.25 mg twice daily. This was slowly increased to 50 mg twice daily over a two month period and continued thereafter. After four months of treatment the patient's symptoms had improved dramatically. His exercise tolerance had increased and diuretic requirements reduced to frusemide 160 mg/day only. Assessment of right heart pressures was repeated and, other than a drop in resting heart rate, there was little change in his pulmonary artery pressure or PVR. His right heart pressures were reassessed showing a pronounced reduction in pulmonary artery pressure and a significant reduction in PVR, which fell further with inhaled oxygen and sublingual nitrates. He was then accepted onto the active waiting list for cardiac transplantation. A possible mechanism of action was investigated by assessing responses to beta agonists during treatment. Not only was there pronounced improvement in PVR but it was also demonstrated that beta receptor subtype cross-regulation may have contributed to the mechanism of benefit. (+info)Recovery of contractility of viable myocardium during inotropic stimulation is not dependent on an increase of myocardial blood flow in the absence of collateral filling. (2/1123)
OBJECTIVES: The purpose of this study was to determine whether contractile recovery induced by dobutamine in dysfunctioning viable myocardium supplied by nearly occluded vessels is related to an increase in blood flow in the absence of collaterals. BACKGROUND: Dobutamine is used to improve contractility in ventricular dysfunction during acute myocardial infarction. However, it is unclear whether a significant increase in regional blood flow may be involved in dobutamine effect. METHODS: Twenty patients with 5- to 10-day old anterior infarction and > or =90% left anterior descending coronary artery stenosis underwent 99mTc-Sestamibi tomography (to assess myocardial perfusion) at rest and during low dose (5 to 10 microg/kg/min) dobutamine echocardiography. Rest echocardiography and scintigraphy were repeated >1 month after revascularization. Nine patients had collaterals to the infarcted territory (group A), and 11 did not (group B). RESULTS: Baseline wall motion score was similar in both groups (score 15.9+/-1.3 vs. 17.4+/-2.0, p = NS), whereas significant changes at dobutamine and postrevascularization studies were detected (F[2,30] = 409.79, p < 0.0001). Wall motion score improved significantly (p < 0.001) in group A both at dobutamine (-5.3+/-2.2) and at postrevascularization study (-5.5+/-1.9), as well as in group B (-3.9+/-2.8 and -4.5+/-2.4, respectively). Baseline 99mTc-Sestamibi uptake was similar in both groups (62.9+/-9.7% vs. 60.3+/-10.4%, p = NS), whereas at dobutamine and postrevascularization studies a significant change (F[2,30] = 65.17, p < 0.0001) and interaction between the two groups (F[2,30] = 33.14, p < 0.0001) were present. Tracer uptake increased significantly in group A both at dobutamine (+ 10.9+/-7.9%, p < 0.001) and at postrevascularization study (12.1+/-8.7%, p < 0.001). Conversely, group B patients showed no change in tracer uptake after dobutamine test (-0.4+/-5.8, p = NS), but only after revascularization (+8.8+/-7.2%, p < 0.001). CONCLUSIONS: The increase in contractility induced by low dose dobutamine infusion in dysfunctional viable myocardium supplied by nearly occluded vessels occurs even in the absence of a significant increase in blood flow. (+info)Prognostic value of dobutamine stress echocardiography in predicting cardiac events in patients with known or suspected coronary artery disease. (3/1123)
OBJECTIVES: The study sought to determine the utility of dobutamine stress echocardiography (DSE) in predicting cardiac events in the year after testing. BACKGROUND: Increasingly, DSE has been applied to risk stratification of patients. METHODS: Medical records of 1,183 consecutive patients who underwent DSE were reviewed. The cardiac events that occurred during the 12 months after DSE were tabulated: myocardial infarction (MI), cardiac death, percutaneous transluminal coronary angioplasty (PTCA), and coronary artery bypass surgery (CABG). Patient exclusions included organ transplant receipt or evaluation, recent PTCA, noncardiac death, and lack of follow-up. A positive stress echocardiogram (SE) was defined as new or worsened wall-motion abnormalities (WMAs) consistent with ischemia during DSE. Classification and regression tree (CART) analysis identified variables that best predicted future cardiac events. RESULTS: The average age was 68+/-12 years, with 338 women and 220 men. The overall cardiac event rate was 34% if SE was positive, and 10% if it was negative. The event rates for MI and death were 10% and 8%, respectively, if SE was positive, and 3% and 3%, respectively, if SE was negative. If an ischemic electrocardiogram (ECG) and a positive SE were present, the overall event rate was 42%, versus a 7% rate when ECG and SE were negative for ischemia. Rest WMA was the most useful variable in predicting future cardiac events using CART: 25% of patients with and 6% without a rest WMA had an event. Other important variables were a dobutamine EF <52.5%, a positive SE, an ischemic ECG response, history of hypertension and age. CONCLUSIONS: A positive SE provides useful prognostic information that is enhanced by also considering rest-wall motion, stress ECG response, and dobutamine EF. (+info)Integrated evaluation of relation between coronary lesion features and stress echocardiography results: the importance of coronary lesion morphology. (4/1123)
OBJECTIVES: The aim of this study was to analyze, in the same group of patients, the relationship between multiple variables of coronary lesion and results of exercise, dobutamine and dipyridamole stress echocardiography tests. BACKGROUND: Integrated evaluation of the relation between stress echocardiography results and angiographic variables should include not only the assessment of stenosis severity but also evaluation of other quantitative and qualitative features of coronary stenosis. METHODS: Study population consisted of 168 (138 male, 30 female, mean age 51+/-9 years) patients, on whom exercise (Bruce treadmill protocol), dobutamine (up to 40 mcg/kg/min) and dipyridamole (0.84 mg/kg over 10 min) stress echocardiography tests were performed. Stress echocardiography test was considered positive for myocardial ischemia when a new wall motion abnormality was observed. One-vessel coronary stenosis ranging from mild stenosis to complete obstruction of the vessel was present in 153 patients, and 15 patients had normal coronary arteries. The observed angiographic variables included particular coronary vessel, stenosis location, the presence of collaterals, plaque morphology according to Ambrose classification, percent diameter stenosis and obstruction diameter as assessed by quantitative coronary arteriography. RESULTS: Covariates significantly associated with the results of physical and pharmacological stress tests included for all three stress modalities presence of collateral circulation, percent diameter stenosis and obstruction diameter, as well as lesion morphology (p < 0.05 for all, except collaterals for dobutamine stress test, p = 0.06). By stepwise multiple logistic regression analysis, the strongest predictor of the outcome of exercise echocardiography test was only percent diameter stenosis (p = 0.0002). However, both dobutamine and particularly dipyridamole stress echocardiography results were associated not only with stenosis severity - percent diameter stenosis (dobutamine, p = 0.04; dipyridamole, p = 0.003) - but also, and even more strongly, with lesion morphology (dobutamine, p = 0.006; dipyridamole, p = 0.0009). As all of stress echocardiography results were significantly associated with percent diameter stenosis, the best angiographic cutoff in relation to the results of stress echocardiography test was: exercise, 54%; dobutamine, 58% and dipyridamole, 60% (p < 0.05 vs. exercise). CONCLUSIONS: Integrated evaluation of angiographic variables have shown that the results of dobutamine and dipyridamole stress echocardiography are not only influenced by stenosis severity but also, and even more importantly, by plaque morphology. The results of exercise stress echocardiography, although separately influenced by plaque morphology, are predominantly influenced by stenosis severity, due to a stronger exercise capacity in provoking myocardial ischemia in milder forms of coronary stenosis. (+info)Functional status and quality of life in patients with heart failure undergoing coronary bypass surgery after assessment of myocardial viability. (5/1123)
OBJECTIVES: The aim of this study was to evaluate whether preoperative clinical and test data could be used to predict the effects of myocardial revascularization on functional status and quality of life in patients with heart failure and ischemic LV dysfunction. BACKGROUND: Revascularization of viable myocardial segments has been shown to improve regional and global LV function. The effects of revascularization on exercise capacity and quality of life (QOL) are not well defined. METHODS: Sixty three patients (51 men, age 66+/-9 years) with moderate or worse LV dysfunction (LVEF 0.28+/-0.07) and symptomatic heart failure were studied before and after coronary artery bypass surgery. All patients underwent preoperative positron emission tomography (PET) using FDG and Rb-82 before and after dipyridamole stress; the extent of viable myocardium by PET was defined by the number of segments with metabolism-perfusion mismatch or ischemia. Dobutamine echocardiography (DbE) was performed in 47 patients; viability was defined by augmentation at low dose or the development of new or worsening wall motion abnormalities. Functional class, exercise testing and a QOL score (Nottingham Health Profile) were obtained at baseline and follow-up. RESULTS: Patients had wall motion abnormalities in 83+/-18% of LV segments. A mismatch pattern was identified in 12+/-15% of LV segments, and PET evidence of viability was detected in 30+/-21% of the LV. Viability was reported in 43+/-18% of the LV by DbE. The difference between pre- and postoperative exercise capacity ranged from a reduction of 2.8 to an augmentation of 5.2 METS. The degree of improvement of exercise capacity correlated with the extent of viability by PET (r = 0.54, p = 0.0001) but not the extent of viable myocardium by DbE (r = 0.02, p = 0.92). The area under the ROC curve for PET (0.76) exceeded that for DbE (0.66). In a multiple linear regression, the extent of viability by PET and nitrate use were the only independent predictors of improvement of exercise capacity (model r = 0.63, p = 0.0001). Change in Functional Class correlated weakly with the change in exercise capacity (r = 0.25), extent of viable myocardium by PET (r = 0.23) and extent of viability by DbE (r = 0.31). Four components of the quality of life score (energy, pain, emotion and mobility status) significantly improved over follow-up, but no correlations could be identified between quality of life scores and the results of preoperative testing or changes in exercise capacity. CONCLUSIONS: In patients with LV dysfunction, improvement of exercise capacity correlates with the extent of viable myocardium. Quality of life improves in most patients undergoing revascularization. However, its measurement by this index does not correlate with changes in other parameters nor is it readily predictable. (+info)Effects of phosphodiesterase inhibitors after coronary artery bypass grafting. (6/1123)
The aim of this study was to estimate the postoperative effects of phosphodiesterase (PDE) inhibitors (milrinone and olprinone) after coronary artery bypass grafting (CABG). To prevent hypotension caused by the PDE inhibitors, low dose of catecholamines were used concomitantly. A total of 34 elective CABG cases were tested. In 12 cases, 0.25 microg kg(-1) min(-1) of milrinone, 3 microg kg(-1) min(-1) of dobutamine (DOB) and dopamine (DOA) were used concomitantly (Group-M). In another 10 patients, 0.1 microg kg(-1) min(-1) of olprinone and the same doses of the catecholamines were infused (Group-O). As a control, the same doses of DOA and DOB only were administered in 12 patients (Group-C). When the pump flow of the cardiopulmonary bypass (CPB) decreased to half, these drugs were given in all groups. Hemodynamics were recorded before CPB, just after the operation, and 3, 6, 12, 24, 48 and 72 h after the operation. Both milrinone and olprinone increased the cardiac index and decreased systemic vascular resistance to almost the same degree. Olprinone decreased mean aortic and pulmonary artery pressures, and also significantly reduced the preload of both right and left heart compared with milrinone. Significant hypotension was not detected due to the concomitant usage of low-dose catecholamines. This concomitant usage of PDE inhibitors and catecholamines allowed easy weaning from CPB, demonstrating excellent hemodynamics after CABG. Good oxygen demand and supply balance were maintained in peripheral tissue. These results suggest that these new PDE inhibitors may be effective not only for weaning from CPB but also for post-cardiotomy cardiogenic shock. (+info)The functional significance of chronotropic incompetence during dobutamine stress test. (7/1123)
OBJECTIVE: To investigate the functional significance of chronotropic incompetence during dobutamine stress echocardiography. PATIENTS AND METHODS: The functional significance of chronotropic incompetence was evaluated during dobutamine stress echocardiography in 512 patients without beta blocker treatment who underwent dobutamine stress echocardiography (up to 40 microg/kg/min) and completed the protocol or reached the target heart rate. Mean (SD) age was 60 (12) years (313 men, 199 women). Chronotropic incompetence was defined as failure to achieve 85% of the maximum exercise heart rate predicted for age and sex (220 - age in men; 200 - age in women) at maximum dobutamine dose. RESULTS: Chronotropic incompetence occurred in 196 patients (38%). Affected patients were significantly younger, more likely to be men (both p << 0.001) and smokers (p < 0.05), had a higher prevalence of previous myocardial infarction (p < 0.005) and resting wall motion abnormalities (p < 0. 05), and had a lower resting heart rate (p << 0.001) and systolic blood pressure (p << 0.001) than patients without chronotropic incompetence, but there was no difference in the overall prevalence of ischaemia and significant coronary artery disease. By multivariate analysis, independent predictors of chronotropic incompetence were a lower resting heart rate (p << 0.001), younger age (p << 0.001), and male sex (p << 0.001). CONCLUSIONS: The relations among sex, age, and chronotropic incompetence show the need to titrate the dobutamine dose using specific data based on age and sex related heart rate responses to dobutamine rather than to an exercise stress test. Obtaining specific heart rate criteria is necessary to determine whether chronotropic incompetence represents a real failure to achieve a normal response or is the result of applying an inappropriate gold standard. (+info)Functional and molecular biological evidence for a possible beta3-adrenoceptor in the human detrusor muscle. (8/1123)
The possible existence of a beta3-adrenergic receptor (beta3-AR) in the human detrusor muscle was investigated by in vitro functional studies and analysis of mRNA expression. Isoprenaline, noradrenaline and adrenaline each produced a concentration-dependent relaxation of the human detrusor. The rank order for their relaxing potencies was isoprenaline (pD2 6.37+/-0.07) > or = noradrenaline (pD2 6.07+/-0.12) > or = adrenaline (pD2 5.88< or =0.11). Neither dobutamine (beta1- and beta2-AR agonist) nor procaterol (beta2-AR agonist) produced any significant relaxation at concentrations up to 10(-5) M. BRL37344A, CL316243 and CGP-12177A (beta3-AR agonists), relaxed the preparations significantly at concentrations higher than 10(-6) M. The pD2 values for BRL37344A, CL316243 and CGP-12177A were 6.42+/-0.25, 5.53+/-0.09 and 5.74+/-0.14, respectively. CGP-20712A (10(-7) - 10(-5) M), a beta1-AR antagonist, did not affect the isoprenaline-induced relaxation. On the other hand, ICI-118,551, a beta2-AR antagonist, produced a rightward parallel shift of the concentration-relaxation curve for isoprenaline only at the highest concentration used (10(-5) > M) and its pKB value was 5.71+/-0.19. Moreover, SR58894A (10(-7) - 10(-5) M), a beta3-AR antagonist, caused a rightward shift of the concentration-relaxation curve for isoprenaline in a concentration-dependent manner. The pA2 value and slope obtained from Schild plots were 6.24+/-0.20 and 0.68+/-0.31. The beta1-, beta2- and beta3-AR mRNAs were all positively expressed in detrusor smooth muscle preparations in a reverse transcription polymerase chain reaction assay. In conclusion, the present results provide the first evidence for the existence of the beta3-AR subtype in the human detrusor. They also suggest that the relaxation induced by adrenergic stimulation of the human detrusor is mediated mainly through beta3-AR activation. (+info)During myocardial stunning, the heart muscle cells experience a temporary reduction in contractility and an increase in the amount of lactic acid produced. This can lead to symptoms such as chest pain, shortness of breath, and fatigue. In severe cases, myocardial stunning can progress to myocardial infarction (heart attack) or cardiac arrest.
Myocardial stunning is often seen in athletes who engage in intense exercise, such as marathon runners or professional football players. It can also occur in people with pre-existing heart conditions, such as coronary artery disease or hypertension.
Treatment of myocardial stunning typically involves addressing the underlying cause, such as reducing stress on the heart or improving blood flow to the myocardium. In severe cases, medications such as nitrates or beta blockers may be used to reduce the workload on the heart and improve contractility. In some cases, hospitalization may be necessary to monitor the condition and provide appropriate treatment.
Prevention of myocardial stunning involves taking steps to reduce the risk factors for heart disease, such as maintaining a healthy diet, exercising regularly, and managing stress. It is also important to seek medical attention if symptoms of myocardial stunning are present, as prompt treatment can help prevent more severe complications.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
There are several potential causes of LVD, including:
1. Coronary artery disease: The buildup of plaque in the coronary arteries can lead to a heart attack, which can damage the left ventricle and impair its ability to function properly.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can lead to LVD.
3. Cardiomyopathy: This is a condition where the heart muscle becomes weakened or enlarged, leading to impaired function of the left ventricle.
4. Heart valve disease: Problems with the heart valves can disrupt the normal flow of blood and cause LVD.
5. Hypertension: High blood pressure can cause damage to the heart muscle and lead to LVD.
6. Genetic factors: Some people may be born with genetic mutations that predispose them to developing LVD.
7. Viral infections: Certain viral infections, such as myocarditis, can inflame and damage the heart muscle, leading to LVD.
8. Alcohol or drug abuse: Substance abuse can damage the heart muscle and lead to LVD.
9. Nutritional deficiencies: A diet lacking essential nutrients can lead to damage to the heart muscle and increase the risk of LVD.
Diagnosis of LVD typically involves a physical exam, medical history, and results of diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and stress tests. Treatment options for LVD depend on the underlying cause, but may include medications to improve cardiac function, lifestyle changes, and in severe cases, surgery or other procedures.
Preventing LVD involves taking steps to maintain a healthy heart and reducing risk factors such as high blood pressure, smoking, and obesity. This can be achieved through a balanced diet, regular exercise, stress management, and avoiding substance abuse. Early detection and treatment of underlying conditions that increase the risk of LVD can also help prevent the condition from developing.
Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.
The symptoms of coronary disease can vary depending on the severity of the condition, but may include:
* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back
Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.
Preventative measures for coronary disease include:
* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.
There are different types of myocardial infarctions, including:
1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.
Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.
Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.
Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.
Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.
There are several possible causes of dilated cardiomyopathy, including:
1. Coronary artery disease: This is the most common cause of dilated cardiomyopathy, and it occurs when the coronary arteries become narrowed or blocked, leading to a decrease in blood flow to the heart muscle.
2. High blood pressure: Prolonged high blood pressure can cause the heart muscle to become weakened and enlarged.
3. Heart valve disease: Dysfunctional heart valves can lead to an increased workload on the heart, which can cause dilated cardiomyopathy.
4. Congenital heart defects: Some congenital heart defects can lead to an enlarged heart and dilated cardiomyopathy.
5. Alcohol abuse: Chronic alcohol abuse can damage the heart muscle and lead to dilated cardiomyopathy.
6. Viral infections: Some viral infections, such as myocarditis, can cause inflammation of the heart muscle and lead to dilated cardiomyopathy.
7. Genetic disorders: Certain genetic disorders, such as hypertrophic cardiomyopathy, can cause dilated cardiomyopathy.
8. Obesity: Obesity is a risk factor for developing dilated cardiomyopathy, particularly in younger people.
9. Diabetes: Diabetes can increase the risk of developing dilated cardiomyopathy, especially if left untreated or poorly controlled.
10. Age: Dilated cardiomyopathy is more common in older adults, with the majority of cases occurring in people over the age of 65.
It's important to note that many people with these risk factors will not develop dilated cardiomyopathy, and some people without any known risk factors can still develop the condition. If you suspect you or someone you know may have dilated cardiomyopathy, it's important to consult a healthcare professional for proper diagnosis and treatment.
Dobutamine
Cardiac stress test
Adrenergic agonist
Pimobendan
Dopamine (medication)
Dopamine
Zygacine
Sympathomimetic drug
Single-photon emission computed tomography
Perfusion scanning
Eosinophilic myocarditis
Shock (circulatory)
Hypovolemic shock
Ractopamine
Dopexamine
Sepsis
Strain rate imaging
Intravenous sodium bicarbonate
Coronary ischemia
Amrinone
Vasodilatory shock
Levosimendan
Peripartum cardiomyopathy
Hibernating myocardium
Emergency medical services
Cardiac tamponade
Hypovolemia
Speckle tracking echocardiography
Roberto Ferrari (cardiologist)
Cardiac magnetic resonance imaging perfusion
DOBUTamine Injection USP
MedlinePlus - Search Results for: DOBUTAMINE
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Publication Detail
Cardiogenic Shock Symptoms
Forane (isoflurane) dosing, indications, interactions, adverse effects, and more
Dopamine3
- Dopamine was used in 8 patients, dobutamine in 5 patients, epinephrine in 2 patients, and norepinephrine in 2 patients. (cdc.gov)
- Drugs to advance the heart's pumping ability, such as dobutamine, dopamine and norepinephrine. (sahmy.com)
- Dopamine, dobutamine and adrenaline were the most common first-, second- and third-line anti-hypotensive drugs used. (who.int)
Echocardiography7
- The objective of this pilot study was to determine the safety and outcome of performing or deferring coronary interventions in patients with intermediate stenoses based on the results of dobutamine stress echocardiography (DSE). (bmj.com)
- 1. Cardioprotective effect of dexrazoxane during treatment with doxorubicin: a study using low-dose dobutamine stress echocardiography. (nih.gov)
- 3. Early diagnosis of anthracycline toxicity in asymptomatic long-term survivors: dobutamine stress echocardiography and tissue Doppler velocities in normal and abnormal myocardial wall motion. (nih.gov)
- 5. [The role of dobutamine stress echocardiography in early diagnosis of cardiac toxicity in long-term survivors of asymptomatic children treated with anthracycline]. (nih.gov)
- 6. Detection of early anthracycline-induced cardiotoxicity in childhood cancer with dobutamine stress echocardiography. (nih.gov)
- 8. Comparison of low-dose dobutamine stress echocardiography and echocardiography during glucose-insulin-potassium infusion for detection of myocardial viability after anterior myocardial infarction. (nih.gov)
- It is commonly used as a cardiotonic agent after CARDIAC SURGERY and during DOBUTAMINE STRESS ECHOCARDIOGRAPHY . (nih.gov)
Hydrochloride2
Negative dobutamine stress1
- Acute myocardial infarction after a negative Dobutamine stress echocardiogram in a patient with end-stage liver disease. (bvsalud.org)
Inotrope1
- Whether given orally, continuously intravenously, or intermittently intravenously, neither dobutamine nor any other cyclic-AMP-dependent inotrope has been shown in controlled trials to be safe or effective in the long-term treatment of congestive heart failure. (nih.gov)
Cardiac8
- In patients with depressed cardiac function, both dobutamine and isoproterenol increase the cardiac output to a similar degree. (nih.gov)
- In the case of dobutamine, this increase is usually not accompanied by marked increases in heart rate (although tachycardia is occasionally observed), and the cardiac stroke volume is usually increased. (nih.gov)
- At least in pediatric patients, dobutamine-induced increases in cardiac output and systemic pressure are generally seen, in any given patient, at lower infusion rates than those that cause substantial tachycardia (see PRECAUTIONS , Pediatric Use ). (nih.gov)
- Dobutamine is indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of adults with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures. (nih.gov)
- An autonomic link between inhaled diesel exhaust and impaired cardiac performance: insight from treadmill and dobutamine challenges in heart failure-prone rats. (nih.gov)
- 13. Lack of clinically significant cardiac dysfunction during intermediate dobutamine doses in long-term childhood cancer survivors exposed to anthracyclines. (nih.gov)
- In vivo cardiac functional performance in response to dobutamine was determined by a computerized pressure-volume loop system. (cdc.gov)
- Additionally, inhalation of MWCNTs also reduced cardiac stroke work, stroke volume, and output in response to dobutamine in anesthetized rats. (cdc.gov)
Intravenous2
Infusion1
- The effective infusion rate of dobutamine varies widely from patient to patient, and titration is always necessary (see DOSAGE AND ADMINISTRATION ). (nih.gov)
Vein1
- Dobutamine is put in a vein and causes the heart to beat faster. (kembeo.com)
Rats1
- At 1 day postexposure, separate rats were catheterized for left ventricular pressure (LVP), contractility, and lusitropy and assessed for autonomic influence using the sympathoagonist dobutamine and surgical vagotomy. (nih.gov)
Exercise1
- A dobutamine stress echocardiogram ( DSE ) may be used if you are ineffective to exercise. (kembeo.com)
Stress3
- What is a dobutamine stress echocardiogram? (kembeo.com)
- Why might I need a dobutamine stress echocardiogram? (kembeo.com)
- Dobutamine stress echocardiogram (DSE) is generally a safe and reliable test for detection of myocardial ischaemia. (bvsalud.org)
Patients1
- Dobutamine is contraindicated in patients with idiopathic hypertrophic subaortic stenosis and in patients who have shown previous manifestations of hypersensitivity to dobutamine. (nih.gov)
Heart4
- Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the ß receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. (nih.gov)
- In animal studies, dobutamine produces less increase in heart rate and less decrease in peripheral vascular resistance for a given inotropic effect than does isoproterenol. (nih.gov)
- Dobutamine may cause a marked increase in heart rate or blood pressure, especially systolic pressure. (nih.gov)
- Medicines that increase blood pressure and blood flow out of the heart are called vasopressors and inotropes, including norepinephrine and dobutamine. (nih.gov)
Major1
- In human urine, the major excretion products are the conjugates of dobutamine and 3-O-methyl dobutamine. (nih.gov)
Echocardiography1
- Cite this: Dobutamine Stress Echocardiography in Preoperative and Long-Term Postoperative Risk Assessment of Elderly Patients - Medscape - Mar 01, 2003. (medscape.com)
Toxicity2
- desflurane increases toxicity of dobutamine by Mechanism: unknown. (medscape.com)
- ether increases toxicity of dobutamine by Mechanism: unknown. (medscape.com)
Cardiac7
- In patients with depressed cardiac function, both dobutamine and isoproterenol increase the cardiac output to a similar degree. (nih.gov)
- In the case of dobutamine, this increase is usually not accompanied by marked increases in heart rate (although tachycardia is occasionally observed), and the cardiac stroke volume is usually increased. (nih.gov)
- At least in pediatric patients, dobutamine-induced increases in cardiac output and systemic pressure are generally seen, in any given patient, at lower infusion rates than those that cause substantial tachycardia (see PRECAUTIONS , Pediatric Use ). (nih.gov)
- Dobutamine is indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of adults with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures. (nih.gov)
- An autonomic link between inhaled diesel exhaust and impaired cardiac performance: insight from treadmill and dobutamine challenges in heart failure-prone rats. (nih.gov)
- In vivo cardiac functional performance in response to dobutamine was determined by a computerized pressure-volume loop system. (cdc.gov)
- Additionally, inhalation of MWCNTs also reduced cardiac stroke work, stroke volume, and output in response to dobutamine in anesthetized rats. (cdc.gov)
Inotropic2
- Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the ß receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. (nih.gov)
- In animal studies, dobutamine produces less increase in heart rate and less decrease in peripheral vascular resistance for a given inotropic effect than does isoproterenol. (nih.gov)
Increases3
- isocarboxazid increases effects of dobutamine by pharmacodynamic synergism. (medscape.com)
- linezolid increases effects of dobutamine by pharmacodynamic synergism. (medscape.com)
- selegiline transdermal increases effects of dobutamine by pharmacodynamic synergism. (medscape.com)
Blood Pressure1
- Dobutamine may cause a marked increase in heart rate or blood pressure, especially systolic pressure. (nih.gov)