Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0008031 (chest pain)
17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenosine is a neuromodulator with both excitatory and inhibitory effects dependent in part upon preconditions; it can act as an algesic or an analgesic agent. Previously we found variations of pain intensity during constant infusion of adenosine. We therefore quantified pain intensity during constant infusion of adenosine at a rate of 140 microg/kg/min intravenously in healthy volunteers, placebo controlled, double blind, and the relation to hemodynamic, vasomotor and sudomotor responses of the sympathetic nervous system and to the role of peripheral beta-endorphin response. The perceived chest pain during adenosine infusion showed an oscillatory pattern. Painful periods of about 30s were interrupted by painfree periods, and pain was always preceded by an increase in vasomotor sympathetic activity and by increased sudomotor activity. Plasma beta-endorphin values were heterogenous but exhibited an increase during infusion.
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PMID:Oscillation of pain intensity during adenosine infusion. Relationship to beta-endorphin and sympathetic tone. 1140 18

We evaluated the use of adenosine, dobutamine and arbutamine with (99m)Tc-tetrofosmin myocardial perfusion imaging. Forty patients under investigation for suspected coronary artery disease were recruited. Each had a resting scan and two separate stress scans on different days, in a randomized cross-over study. Resultant images were blindly reported in 13 segments per scan as normal, reversible or fixed defects. A score was given (0-3) for segmental defect severity. Haemodynamic responses were as expected for each agent. Subjective side effect scores did not differ overall between agents. Adenosine caused a significantly higher incidence of abnormal taste (54%) than dobutamine and arbutamine (both 23%) and a lower incidence of palpitations (25% vs 69% and 54%, respectively), all P<0.05. Arbutamine caused significantly more chest pain than adenosine (77% vs 46%) though less flushing (35% vs 68%), both P<0.05. Comparison of the results obtained showed highly significant levels of segmental agreement for visual and semi-quantitative analysis between adenosine and arbutamine, kappa value and correlation coefficient of 0.78 and 0.86, respectively, dobutamine and adenosine 0.69 and 0.78, and arbutamine and dobutamine 0.75 and 0.78, all P<0.0001. Adenosine, arbutamine and dobutamine differ in their haemodynamic response and side effect profile but provide highly comparable results during (99m)Tc SPECT imaging.
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PMID:Assessment of adenosine, arbutamine and dobutamine as pharmacological stress agents during (99m)Tc-tetrofosmin SPECT imaging: a randomized study. 1171

Adenosine stress echocardiography was performed in nine patients (58 (+/-3) years, eight women) with documented microvascular angina. Global ventricular function was assessed by Tc(99m) blood pool imaging and Doppler, whereas longitudinal ventricular function was assessed by simultaneous tissue Doppler echocardiography of the lateral mitral annulus. Adenosine was infused incrementally to onset of chest pain in all patients. There was no significant change in global or longitudinal systolic function. Adenosine induced global diastolic dysfunction, demonstrated by blood pool imaging and by Doppler of the transmitral flow. All patients had long axis diastolic dysfunction at peak adenosine, revealed by a ratio of early to late diastolic velocity of lateral mitral annulus <1, which was absent at rest. Adenosine, as a stress agent, provokes regional and global diastolic dysfunction in microvascular angina, which may be a consequence of subendocardial ischaemia. Long axis diastolic dysfunction can be easily revealed by tissue Doppler of the lateral annular motion.
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PMID:Adenosine provokes diastolic dysfunction in microvascular angina. 1179 72

Intravenous dipyridamole increases the concentration of circulating adenosine and produces coronary vasodilation. However, it decreases global cerebral blood flow (CBF) due to hyperventilation side effect of adenosine. In the present study, changes in regional CBF during dipyridamole stress were identified in detail. In 11 healthy men (51-71 years of age), CBF was measured by positron emission tomography with oxygen-15-labeled water at rest (baseline) and during dipyridamole stress. All images were normalized to global CBF and transformed to standard brain anatomy. A t map between baseline and dipyridamole stress conditions was then created on a pixel-by-pixel basis. CBF was globally decreased during dipyridamole stress. However, a significant relative increase in CBF was observed bilaterally in the thalamus and prefrontal cortex, indicating neural activation in these regions. Adenosine plays an important role in the production of anginal pain by stimulation of A(1) adenosine receptors. Neural activation in the thalamus and prefrontal cortex during angina pectoris has been reported. Although no subject felt chest pain during dipyridamole stress, neural activation in the thalamus and prefrontal cortex indicates that stimulation of A(1) adenosine receptors during dipyridamole stress may produce input from the heart to the thalamus through the vagal fiber.
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PMID:Regional changes in human cerebral blood flow during dipyridamole stress: neural activation in the thalamus and prefrontal cortex. 1216 62

Forty-four patients with effort angina pectoris were evaluated with SUNY4001 (adenosine) thallium-201 (201Tl) myocardial scintigraphy to detect coronary artery disease. These patients had single-vessel disease (> or = AHA 90% stenosis) in either RCA or LAD. Adenosine was infused at the rate of 120 or 140 microg/kg/min for six minutes. 111 MBq of 201Tl was injected after three minutes of the start of the infusion. The early and delayed images were obtained by SPECT imaging. The sensitivity was 94.7% at 120 microg/kg/min and 84.2% at 140 microg/kg/min. Adenosine 201Tl myocardial scintigraphy showed high accuracy for detecting significant coronary artery disease. Adverse reactions occurred in 77.3% of the patients. Regarding the rates of the adverse reactions, there was no significant difference between 120 and 140 microg/kg/min. Major adverse reactions were Chest pain/discomfort (52.3%) and Flushing/Feeling of warmth (27.3%). No serious complication was observed at any infusion rate. Most of adverse reactions disappeared sortly. Only two patients required treatment for moderate chest pain, which, however, disappeared in several minutes. One of the treatments was merely the termination of adenosine infusion, and the other was sublingual spray of nitroglycerin. Adenosine infusion caused slight decrease in blood pressure and increase in heart rate. The hemodynamic changes resolved within several minutes after the adenosine infusion. Decrease in systolic blood pressure of more than 20 mmHg from the base level occurred in 26.1% and 52.4% at 120 and 140 microg/kg/min infusion rate respectively. Therefore, the adenosine infusion at 120 microg/kg/min should be considered safe and useful for the diagnosis of coronary artery disease by pharmacologic stress imaging.
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PMID:[Diagnosis of coronary artery disease by thallium-201 myocardial scintigraphy with intravenous infusion of SUNY4001 (adenosine) in effort angina pectoris--the clinical trial report at multi-center: phase II]. 1535 25

With two hundred and seven patients unable to exercise adequately, the diagnostic accuracy and adverse reaction of 201Tl myocardial scintigraphy with the pharmacologic stress by SUNY4001 (adenosine) infusion were studied. Adenosine was infused for six minutes at the rate of 120 microg/kg/min, and then 201Tl was injected after three minutes from the start of infusion. The early and delayed images were obtained by SPECT imaging. According to angiography, > or = AHA 90% stenosis was defined as significant. The sensitivity of detecting coronary artery disease was 87.1% and the specificity was 46.0%. Adverse reactions occurred in 66.7% of the patients, most of which disappeared shortly with no need for treatment. Major adverse reactions were chest pain/discomfort (30.4%), flushing/feeling of warmth (22.4%) and blood pressure decrease (17.4%). Adenosine infusion caused slight decrease in blood pressure and increase in heart rate. These hemodynamic changes were resolved within several minutes from the termination of adenosine infusion. We concluded that adenosine-201Tl imaging is safe and useful to detect coronary artery disease in patients unable to exercise adequately.
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PMID:[The diagnostic value for ischemic heart disease of thallium-201 myocardial scintigraphy by intravenous infusion of SUNY4001 (adenosine)--the report of clinical trial at multi-center: phase III]. 1535 26

Adenosine with its rapid onset and brief duration of action has a number of clinical applications including treatment of paroxysmal supraventricular tachycardia and maximal coronary vasodilatation during pharmacologic stress testing. The adverse effects of adenosine include dyspnea, nausea, headache, chest pain, flushing and bronchospasam. Although there were few reports which mentioned the occurrence of bronchospam after administration of adenosine, a number of studies indicated that the use of adenosine was not contraindicated in patients with chronic obstructive pulmonary disease (COPD) or asthma. We report here a male patient with pulmonary emphysema and lung bullous disease who developed severe constriction of the main bronchi after intravenous adenosine during general anesthesia. After treatment, the patient was discharged without complications. We have reviewed the related current literature and herein discuss the reason and management of the adenosine induced bronchospasm.
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PMID:Intraoperative bronchospasm after intravenous adenosine during general anesthesia. 1567 35

Today's definition of coronary artery disease (CAD) comprises two forms: obstructive and non-obstructive CAD. The 31-72% chance of a life-threatening event-like a myocardial infarction-with non-obstructive CAD is well documented in numerous studies. The objective in modern strategies of diagnosis and therapy should therefore be expedient identification of patients at high risk for coronary events, who will benefit from a customized therapy. Before initiating diagnostic procedures of CAD, a well defined strategy should be pursued. There are two possible primary objectives: ASSESSMENT OF THE INDIVIDUAL RISK FOR A CORONARY EVENT: Assessment of the individual "absolute" risk for a coronary event is not possible using single traditional risk factors. The individual risk can be estimated by integrating several of the traditional risk factors into a scoring system. These so-called risk scores (e.g. Framingham score and Procam score), however, have been associated with shortcomings: insufficient discrimination of high-risk from low-risk individuals. The calcium score has therefore become increasingly established; this Agatston score is independent of the traditional risk factors, so there is no correlation between Agatston and Procam scores. Today, the calcium score is considered the superior test for identifying individuals at high risk for a coronary event and its use is recommended by the European Society of Cardiology (ESC) guidelines for prevention of cardiovascular diseases. PROOF OR EXCLUSION OF A HEMODYNAMICALLY SIGNIFICANT CORONARY STENOSIS: Another concept is the definitive proof or exclusion of a hemodynamically "significant" coronary narrowing. The probability of an obstructive CAD is traditionally assessed by the type of chest pain, age, gender and stress-ECG. In patients with a low probability of an obstructive CAD, cardiac catheterization is not indicated, whereas in patients with a high probability of a hemodynamically significant coronary stenosis, an invasive strategy should be performed. Since non-invasive coronary angiography (CTA) with cardiac-CT has been shown to provide a high negative predictive value, CTA (with good imaging quality) is suitable for ruling out a significant obstructive CAD in the group at intermediate risk for an obstructive CAD. Another approach could be a functional test to initially prove a relevant, inducible myocardial ischemia: In a large cohort it was shown that patients will only prognostically benefit from revascularization procedures if the ischemic myocardial area is greater than 10%. Therefore, the assessment of the extent of myocardial ischemia is the domain of modern stress imaging tests. Stress-echocardiography and myocardial scintigraphy have almost the same sensitivity (74-80%, 84-90%, respectively) and specificity (84-89%, 77-86%, respectively), which are considerably higher than for stress-ECG. Cardiac MR is most suitable for the assessment of myocardial perfusion, because it traces the first pass dynamics of gadolinium at rest and during stress in reproducible slices at an acceptable spatial and a high temporal resolution without ionizing radiation. Whether the non-invasive coronary angiography with cardiac-CT and the Adenosin-perfusion imaging with cardiac-MR will completely replace diagnostic cardiac catheterization and stress-echocardiography as well as myocardial scintigraphy remains to be evaluated in further studies.
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PMID:[Impact of both cardiac-CT and cardiac-MR on the assessment of coronary risk]. 1641 70

This study investigated plasma brain natriuretic peptide (BNP) levels in normotensive and hypertensive patients with suspected coronary artery disease during radionuclide pharmacological stress testing. Twenty-seven normotensive patients (15 males, aged 63.0+/-4.5 years and 12 females, aged 63.0+/-4.1 years) and 38 essential hypertensive patients (25 males, aged 63.3+/-3.3 years and 13 females, aged 64.6+/-2.6 years) with chest pain and exercise stress testing inconclusive for coronary artery disease underwent myocardial perfusion single-photon emission computed tomography (SPECT) using adenosine infusion. SPECT identified patients without (16 normotensive and 22 hypertensive) and patients with (11 normotensive and 16 hypertensive) transient perfusion defects. Basal BNP levels in normotensive patients without transient myocardial ischemia (3.1+/-1.2 fmol/ml) were significantly (P<0.01) lower than those observed in normotensive patients with transient ischemia (8.2+/-1.2 fmol/ml), whereas BNP levels in hypertensive patients without transient ischemia (8.2+/-1.0 fmol/ml) did not significantly differ from those in hypertensive patients with transient ischemia (8.1+/-2.0 fmol/ml). No significant difference was found in BNP levels between males or females either in normotensive or hypertensive patients without or with ischemia. Adenosine infusion did not significantly change BNP levels in any subject group without or with myocardial perfusion defects. Our findings show that increases in BNP allow early detection of myocardial ischemia in normotensive patients, but not in hypertensive patients with suspected coronary artery disease. Adenosine-induced myocardial ischemia does not affect BNP production already activated by coronary artery disease in normotensive patients and by hemodynamic changes in hypertensive patients.
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PMID:Plasma brain natriuretic peptide at rest and after adenosine-induced myocardial ischemia in normotensive and essential hypertensive patients with suspected coronary artery disease. 1895 35

Adenosine is widely used as a pharmacologic agent for stress myocardial perfusion imaging. Vasospasm as a side effect of adenosine has been reported a few times in other countries, but it has not been reported in Japan. A 65-year-old woman was admitted to our hospital because of chest pain at rest and during exercise. She underwent myocardial scintigraphy, to rule out myocardial ischemia. After adenosine infusion, she felt chest pain and the electrocardiogram (ECG) showed ST elevation in inferior leads. Adenosine infusion was stopped immediately. Her chest pain resolved, and the ECG reverted to baseline. Perfusion image presented reverse redistribution in inferior segments, and coronary angiography revealed insignificant lesions. Transient ST elevation during adenosine infusion is thought to be due to coronary vasospasm, judging from scintigraphic and angiographic findings.
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PMID:Coronary arterial spasm during adenosine myocardial perfusion imaging. 1930 35


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