Chest pain and ST-segment elevation 3 minutes after completion of adenosine pharmacologic stress testing (original) (raw)
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The American Heart Hospital Journal, 2009
Case history: a 76-year-old African-American female presented to a community hospital with complaints of chest pain. Her medical history was significant for hypertension, gastroesophageal reflux disease (GERD), hyperlipidemia, and bipolar disorder. On arrival at the emergency department, electrocardiogram showed acute inferior wall myocardial infarction (MI). The patient received thrombolytic therapy with tenecteplase (TNKase™) with successful reperfusion. On arrival at our hospital, the patient denied any chest pain and her electrocardiogram showed sinus bradycardia with small Q-waves in the inferior leads II, III, and AVF (see Figure 1). She was treated with aspirin, heparin, lisinopril, simvastatin, and clopidogrel. Beta-blocker was not started as the patient was having bradycardia. The patient was scheduled to undergo myocardial perfusion scan 48 hours following her uncomplicated inferior wall MI.
Medical & Clinical Research, 2017
Background: We sought to determine the prognostic importance of adenosine-induced ischemic ECG changes in patients with normal SPECT myocardial perfusion images. Methods: We performed a retrospective analysis of 765 patients undergoing adenosine MPI between January 2013 and January 2015. Patients with baseline electrocardiographic (ECG) abnormalities and/or abnormal scan were excluded. Results: Overall, 67 patients (8.7%) had ischemic ECG changes during adenosine infusion in the form of ST depression of ≥1mm. Of these, 29 (43% [3.8% of all patients]) had normal MPI (positive (+) ECG group). An ageand sex-matched group of 108 patients with normal MPI without ECG changes served as control subjects (negative (-) ECG group). During a mean follow-up of 33.3 ± 6.1 months, patients in the +ECG group had no significantly more adverse cardiac events than those in the-ECG group. One (0.9%) patient within the negative ECG group had a nonfatal MI (0.7% annual event rate after a negative MPI). A case only was admitted due to heart failure in the (-) ECG group) that proved to be secondary to pulmonary cause and not of CAD. A case in this (+) ECG group admitted as a CAD that ruled out by coronary angiography. Conclusion: Patients with normal myocardial perfusion scintigraphy in whom ST-segment depression develops during adenosine stress test appear to be with no increased risk for future cardiac events compared with similar patients without ECG evidence of ischemia.
Journal of Nuclear Cardiology, 2010
Patients with a normal myocardial perfusion scan have a low risk of adverse cardiac events, even when the adenosine stress electrocardiography test is positive. Background: Patients able to exercise adequately with normal myocardial perfusion imaging (MPI) have an annual hard cardiac event rate of approximately 1% per year. This rate increases to 1.3% to 2.3% per year in those assessed using adenosine who have normal MPI. In patients with both an abnormal adenosine stress electrocardiogram (ECG) test and an abnormal adenosine stress perfusion scan, the risk is greater than an abnormal scan alone. Objective: To determine if an abnormal adenosine stress ECG test in patients with normal MPI carries a worse prognosis. Design: Retrospective cohort study. Participants: Patients presenting for clinical reasons for MPI were retrospectively reviewed; 76 patients met inclusion criteria of a normal myocardial perfusion scan, abnormal adenosine stress ECG, no known coronary artery disease, and follow up >6 months. Methods: A 6-minute infusion adenosine stress ECG test was performed. Ischemic ECG was defined as either ≥1.5 mm upsloping ST-depression or ≥1.0 mm horizontal or downsloping ST-depression at 80 ms beyond the J-point in at least 3 consecutive beats in at least 2 contiguous leads. Post-stress imaging started at 45 to 60 minutes post-infusion. Cardiovascular events were defined as cardiac death, nonfatal myocardial infarction (MI), or coronary revascularization. Results: The mean age of participants was 66 years; 87% were women and 30% were diabetic. Follow-up was 24 ± 13 months. There were no cardiac deaths or nonfatal MIs in the cohort. Twenty two patients underwent angiography as a result of the adenosine stress myocardial perfusion scan. There were 11 patients who underwent revascularization; 10 occurred as a direct result of the initial perfusion scan, and 1 occurred 19 months later. Conclusions: The rate of cardiac death and MI was 0% at a mean follow-up interval of 24 months in this cohort of patients with adenosine stress-induced ST-depression but normal MPIs. The authors state that, "In the presence of normal MPI, the specificity of ischemic ECG changes during adenosine infusion for the detection of severe obstructive coronary artery disease is poor, although patients with multiple coronary risk factors, particularly diabetes mellitus, should undergo further investigation." Reviewer's Comments: The authors state that patients with an abnormal adenosine stress ECG but normal myocardial perfusion and who have multiple risk factors should undergo further investigation. Why? The rate of hard cardiac events (cardiac death or nonfatal MI) was 0% over 2 years in this cohort and in all subgroups of this cohort. They did not show that angiography was of benefit or that revascularization was of benefit in patients with a normal myocardial perfusion scan. On the contrary, the best conclusion from their data is that patients with a normal perfusion scan have a very low annual risk of a hard cardiac event, even if the stress adenosine test is positive. (Reviewer-Thomas F. Heston, MD).
Ischemic electrocardiogram during pharmacologic stress with regadenoson
Journal of Nuclear Cardiology, 2011
Case Presentation. 90 year old male with a history of coronary artery disease, hyperlipidemia, peripheral vascular disease, and moderate aortic stenosis was referred for stress testing after being seen in clinic with recurrent left-sided exertional chest pain, relieved with rest and not associated with any other symptoms. His cardiac history was also significant for a remote non-ST elevation myocardial infarction in the setting of an acute gastrointestinal bleed. His work-up in the past included coronary angiography 20 years prior to his presentation which had demonstrated non-occlusive diffuse two-vessel coronary artery disease. Aortic valve area measured 1.1 cm 2 on an echocardiogram approximately 1 year prior. His medications included aspirin, metoprolol, omeprazole, pravastatin, tamsulosin, and acetaminophen as needed. Severe osteoarthritis of his back and knees precluded exercise stress testing and he therefore underwent vasodilator stress using regadenoson with planned SPECT myocardial perfusion imaging. His baseline ECG is normal (Figure 1A). He was administered regadenoson as a 400 mg intravenous bolus over 10 seconds as per standard protocol. He immediately developed severe chest discomfort and became tachycardiac and mildly hypotensive with a systolic blood pressure of 90-100 mmHg. An electrocardiogram performed at that time (Figure 1B) demonstrated sinus tachycardia with diffuse 4-5 mm flat
A rare complication of a common stress test
Journal of Cardiology Cases, 2014
In 2008, regadenoson, a selective adenosine2A (A 2A) receptor agonist, was approved by the US Federal and Drug Administration for use as a pharmacologic stress agent in myocardial perfusion studies. By stimulating A 2A receptors in coronary smooth muscle, it can increase coronary blood flow by 2.5fold or greater. Previous data showed non-inferiority of regadenoson in detecting reversible myocardial ischemia, compared to adenosine. Given less serious adverse effects, being better tolerated and easily administered, regadenoson has been widely used for myocardial perfusion imaging. As adenosine receptors have many sub-types and are located in multi-organ systems, regadenoson can cause various adverse effects, including bronchospasm, atrioventricular block, or hypotension. However, adverse effects on the central nervous system are rarely reported. As adenosine receptors (A 1 and A 2A receptors) play a major role in neuron-glial cells interaction, regadenoson can provoke seizure through A 2A receptor activation. We hereby report a case of regadenoson associated-seizure and review seizure mechanism. This may raise more concern for a rare serious adverse effect of regadenoson which should be taken into consideration when selecting cardiac stress modalities. <Learning objective: Regadenoson can provoke seizure through central A 2A receptor activation. This should be taken into consideration when selecting cardiac stress test modalities, particularly in patients with known seizure disorder or history of organic brain disease.>
Coronary spasm after completion of adenosine pharmacologic stress test
Annals of Nuclear Medicine, 2011
Adenosine is a frequently used pharmacologic stress agent in myocardial perfusion imaging. Its safety profile is well established, and most of its side effects are mild and transient. Coronary vasospasm occurs occasionally during or after adenosine stress test in rare cases, which may lead to seriously adverse outcomes. This study reported 3 such cases after completion of adenosine pharmacologic stress test.
High cardiac output measurements in a patient with congestive heart failure
Journal of Cardiothoracic Anesthesia, 1987
I N PATIENTS WITH cardiovascular instability, pharmacological interventions are often guided by cardiac output (CO) measurements using the thermodilution technique. This method of CO determination has gained wide acceptance because, under normal circumstances, it is simple, safe, and expedient. Although the accuracy of the thermodilution method is only on the order of plus or minus 10%, this error range has usually been found acceptable in the clinical setting. 13 Occasionally, however, unusual conditions can lead to marked false elevations or reductions in the obtained measurements. These conditions include (1) equipment malfunctions, (2) errors in methodology, and (3) disease entities such as low-flow states and intracardiac shunts. The following case demonstrates the unusual occurrence of an elevated CO measurement in a patient with evidence of congestive heart failure.