This is a decision you and your doctor will make. For this medicine, the following should be considered:. Tell your doctor if you have ever had any unusual or allergic reaction to this medicine or any other medicines. Also tell your health care professional if you have any other types of allergies, such as to foods, dyes, preservatives, or animals.
For non-prescription products, read the label or package ingredients carefully. Appropriate studies have not been performed on the relationship of age to the effects of adenosine injection in the pediatric population.
Safety and efficacy have not been established. Appropriate studies performed to date have not demonstrated geriatric-specific problems that would limit the usefulness of adenosine injection in the elderly. There are no adequate studies in women for determining infant risk when using this medication during breastfeeding. Weigh the potential benefits against the potential risks before taking this medication while breastfeeding.
Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are receiving this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below.
The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive. Using this medicine with any of the following medicines is usually not recommended, but may be required in some cases. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines. Using this medicine with any of the following medicines may cause an increased risk of certain side effects, but using both drugs may be the best treatment for you.
Certain medicines should not be used at or around the time of eating food or eating certain types of food since interactions may occur. Using alcohol or tobacco with certain medicines may also cause interactions to occur.
Most users should sign in with their email address. If you originally registered with a username please use that to sign in. To purchase short term access, please sign in to your Oxford Academic account above. Don't already have an Oxford Academic account? Oxford University Press is a department of the University of Oxford.
It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume 9. Adenosine-induced chest pain in patients with silent and painful myocardiai ischaemia: another clue to the importance of generalized defective perception of painful stimuli as a cause of silent ischaemia.
Crea , F. Oxford Academic. Google Scholar. Cite Cite F. Select Format Select format. Permissions Icon Permissions. Abstract Adenosine is formed from adenosine triphosphate within the ischaemic cells from where it is released into the coronary circulation. Issue Section:. You do not currently have access to this article.
Download all slides. Three slices were oriented in the short-axis plane base, mid, apex , prescribed from the cine four-chamber view. A test scan was performed with 5 dynamic images to confirm absence of artifacts and proper visualization of the LV myocardium and blood pool. The sequence was copied and 60 dynamics were implemented for perfusion imaging. Four minutes into the infusion, the stress perfusion imaging was performed, with 0.
The perfusion pulse sequence was initiated 3 seconds prior to gadolinium infusion, followed by a breath-hold command, and lasted for approximately 1 min. Adenosine infusion was stopped after the acquisition. After a brief period, during which optional images, such as flow sequences, were obtained, rest perfusion was performed with a second dose of 0.
An additional 0. Multi-slice SSFP cine short-axis imaging was subsequently performed. Acquisition extended from the atrial side of the ventricular valve plane to just beyond the apex.
Approximately seven minutes after the final contrast dose, a multi-phase inversion-recovery SSFP scan was acquired in the mid short-axis plane, in order to determine the optimal inversion time TI to null normal myocardium for LGE imaging. The time that corresponded to the image with sufficiently nulled myocardium was entered as the TI into the subsequent inversion recovery segmented turbo flash sequence used for LGE imaging.
Acquisition was performed in the short-axis, and covered the same anatomic range as the SSFP cine short-axis stack. In addition, single slices were acquired in the vertical long-axis, four chamber and left ventricular outflow tract views to correspond to the cine acquisitions. The TI was increased as needed as time passed.
Left ventricular ejection fraction was calculated off-line from end-diastolic and end-systolic endocardial tracings of the multi-slice SSFP cine short-axis images using computer-assisted planimetry. A negative AS-CMR was defined as the absence of all of the following: resting wall motion abnormalities on cine images, perfusion defects during adenosine infusion, or LGE in a coronary disease-type pattern subendocardial enhancement.
A myocardial perfusion defect was reported if a segment was definitely darker than surrounding myocardium and persisted more than three images beyond initial peak enhancement of the segment which appeared most normal. LGE images were displayed with a gray scale to optimally show normal myocardium as dark and the regions of LGE or fat as bright. The follow-up was completed in October Cardiovascular events during follow-up were identified for these patients by reviewing their medical data from our comprehensive institutional electronic records for clinic visits, new emergency department visits or hospital admissions.
Cardiac death was defined as death associated with known or suspected acute myocardial infarction, life threatening arrhythmia, or cardiogenic pulmonary edema. Re-hospitalization for chest pain was defined as a recurrent episode of chest pain requiring hospital admission. Qualitative variables are presented as absolute and relative frequencies. During the 13 months of enrollment, patients, Patients' characteristics, demographic data and medications at baseline are listed in Table 1.
AS-CMR was performed in all cases without adverse events. The median duration of follow-up was days range to days. All cases were followed up. There was no myocardial infarction, cardiovascular death or death from other cause in the study population. A total of 14 patients Six of these 14 patients 5. Four patients refused further evaluation. From the remaining ten, five were advised to undergo coronary angiography, and all of these had obstructive CAD one received percutaneous coronary intervention.
Another four of the ten had known coronary anatomy from recent coronary angiography, and one with only a small area of ischemia was managed conservatively without undergoing coronary angiography. All patients received standard pharmacological treatment for secondary prevention of CAD.
During the follow-up period, the conservatively-managed patient with a small area of ischemia presented again with chest pain and was admitted; coronary angiography was performed revealing luminal irregularities with no need for interventional treatment. Another two patients with known CAD and scar in the original AS-CMR were readmitted because of chest pain and underwent coronary angiography, with no need for revascularization.
There were no readmissions for the patients who refused coronary angiography. Seven of them had a known history of CAD. During the period of follow-up a total of 9 patients presented again to the emergency department, all of them with atypical chest pain. Evaluation of chest pain with serial electrocardiograms, serial cardiac biomarkers of necrosis and non-invasive imaging studies did not reveal any case of acute coronary syndrome and all patients were discharged from the emergency department, without being admitted.
The present study has shown that a negative AS-CMR performed within 24 hours of patients presenting to the emergency department with low-risk chest pain, as indicated by negative serial electrocardiograms and cardiac biomarkers of necrosis, is associated with an excellent prognosis.
Therefore, non-invasive tests which reliably exclude significant CAD in the acute setting are of great value, as they have the potential to reduce inappropriate admissions without increasing the risk of missed diagnoses. The present study extends the findings of previous studies examining the predictive value of stress perfusion CMR [ 8 — 15 ]. Jahnke et al. However, their stress protocol was not solely employed in the acute setting and presenting symptoms included dyspnea as well as chest pain.
Also in the non-acute clinical setting, Pilz et al. In addition, only patients without perfusion defects or LGE were included, leaving outcomes to be compared to calculated event probabilities rather than observed outcomes of a group with positive AS-CMR. The high negative predictive value of AS-CMR found in the present study in patients presenting to the emergency department with low-risk chest pain concurs with findings from a prior study by Ingkanisorn et al [ 15 ], in which no patient with a normal AS-CMR had a subsequent diagnosis of CAD or an adverse outcome over a period of days.
While inclusion criteria were similar, all patients in the current study underwent AS-CMR from our Cardiac Decision Unit within 24 hours, whereas patients in Ingkanisorn et al.
Our study better validates the utilization of AS-CMR as an initial risk-stratifying diagnostic modality in the acute setting, selecting those patients who can be safely discharged. Also, only three short-axis slices were used for first-pass perfusion in the present study, compared with the "typically at least nine" slices obtained in Ingkanisorn et al.
Therefore, our protocol maintains the same diagnostic accuracy with a less labor intensive image acquisition protocol. Choosing the appropriate non-invasive evaluation for acute chest pain involves considering test characteristics, as well as the risks inherent to the test itself.
High sensitivity and negative predictive value, as demonstrated for AS-CMR in the present study, are essential. Adding nuclear myocardial perfusion imaging MPI to exercise protocols or pharmacologic stress improves sensitivity for detecting significant CAD, but results in significant exposure to ionizing radiation. Similarly, coronary computed tomography angiography CTA has a defined role in excluding CAD as the etiology of acute chest pain [ 17 — 20 ] but also involves radiation exposure and the administration of potentially nephrotoxic contrast agents.
While efforts to decrease the effective radiation dose of these studies are making headway, the attributable risk of fatal malignancy from a single nuclear MPI study or coronary CTA has been estimated at 1 in [ 21 ].
Stress echocardiography is an attractive alternative for the evaluation of acute chest pain as it avoids exposure to radiation or nephrotoxic contrast agents, and includes an evaluation of cardiac structure and function similar to AS-CMR.
However, the sensitivity of dobutamine stress echocardiography DSE with regional wall motion analaysis WMA for detection of significant CAD has been questioned, and its risks of induced arrhythmia and acute infarction are appreciable. Tsutsui et al. However, MPA is a technique not widely utilized. Contrary to these findings, Bedetti et al.
0コメント