Chest pain and ST-segment elevation 3 minutes after completion of adenosine pharmacologic stress testing (original) (raw)

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

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.

A 75-year-old woman with chest pain and transient severe left ventricular systolic dysfunction

Revista Portuguesa de Cardiologia, 2015

Introduction: Coronary spasm can cause myocardial ischemia and angina in both patients with and without obstructive coronary artery disease. However, provocation tests using intracoronary acetylcholine (ACh) have been rarely performed in the Western world. Case report: We report a case of a 75-year-old woman with a history of hypertension and a mechanical aortic prosthesis who presented in the emergency room with acute-onset chest pain, widespread ST-segment depression and severe left ventricular systolic dysfunction, with no signs of prosthesis dysfunction. Emergent coronary angiography excluded obstructive coronary artery disease. Pain relief and normalization of ST segment and systolic function occurred within six hours. The patient was treated for a possible thromboembolic myocardial infarction and was discharged home asymptomatic. Tw o weeks later, cardiac magnetic resonance was performed showing inferoseptal transmural infarct scar, inferior and inferolateral subendocardial infarct and mid-basal ischemia in the anterior and anterolateral walls. She was readmitted with recurrence of chest pain and it was decided to perform a provocation test with ACh. After injection of ACh into the left anterior descending artery, chest pain, ST-segment depression, blood flow impairment (TIMI 1) and transient grade 3 atrioventricular (AV) block occurred. Intracoronary administration of nitrates reversed the coronary spasm and AV conduction disturbances. Twenty minutes later, chest pain and ischemic ST changes recurred; there was no response to vasodilators and the patient developed cardiac arrest with pulseless electrical activity. Advanced life support was maintained for 32 minutes without return of spontaneous circulation. Conclusions: Provocation tests have a high sensitivity and specificity for the diagnosis of vasospastic angina. Although it is rare, these tests have the potential risk of irreversible spasm leading to arrhythmia and death.

ST Segment Elevation During Dipyridamole Stress Testing in a Patient Without Coronary Lesions

Revista Española de Cardiología (English Edition), 2004

We describe a patient who presented transient ST-segment elevation and typical chest pain during an ischemia test with dipyridamole and technetium-tetrofosmin. Chest pain and electrical alterations disappeared promptly with sublingual nitroglycerin. Coronary angiography showed no epicardial lesions, and coronary vasospasm was suspected. We discuss possible explanations for this complication.

Electrocardiographic quiz

Medical Journal Armed Forces India, 2007

A 55 years old lady, a known case of hypertrophic cardiomyopathy with severe left ventricular outflow tract obstruction, was admitted to hospital for worsening exertional dyspnea and fatiguability. On examination, the heart rate was varying from 30 -110 beats per minute, the rhythm was irregularly irregular, there were prominent 'a' waves on jugular venous pulse intermittently, S1 was varying in intensity and P2 was loud. She had been prescribed tab metoprolol 12.5 mg 12 hourly and tab digoxin 0.25 mg once a day for five

ST-Segment Elevation in Conditions of Non-cardiovascular Origin Mimicking an Acute Myocardial Infarction: A Narrative Review

Cureus

The most widespread presenting ailments among patients visiting the emergency department are chest pain and shortness of breath. These symptoms lead any doctor to a probable diagnosis of myocardial infarction (MI). Detailed patient history, testing of blood samples for cardiac biomarkers that are indicative of cardiovascular necrosis, ultrasound methods, electrocardiography, and coronary computed tomography (CT) could all be beneficial to support the diagnosis. Out of these, electrocardiography is the most important and commonly done investigation in the emergency departments for patients presenting with chest pain and shortness of breath. However, interpreting these patients' electrocardiograms (ECGs) may be a matter of concern and worry. T wave and ST-segment changes are often of interest in the early signs of myocardial ischemia. Despite its incredible sensitivity, ST-segment deviation (elevated or depressed) has a low specificity because it can be seen in a variety of other cardiac and non-cardiac diseases. When ST-segment anomalies are identified, clinicians must consider many additional characteristics (such as risk factors, symptoms, and anamnesis), as well as all other possible diagnoses. All of these scenarios of patients presenting in the emergency department with chest discomfort and shortness of breath showing ST-segment abnormalities can leave a healthcare professional wondering whether to start treatment for acute myocardial infarction, through either the administration of a fibrinolytic agent, exposing patients to both the benefits and risks of fibrinolysis, or invasive coronary angiography. An astute physician may be able to recognize fabricated differential diagnosis mimicking STsegment elevation myocardial infarction (STEMI) in some situations. Failure to recognize these imposters can result in inefficient resource utilization, which can expose patients to unjustified risk and increased rather than decreased death and morbidity. Since the danger of cerebral hemorrhage from blood thinners is significant, in patient-care scenarios, in order to rule out percutaneous coronary intervention (PCI), a thorough assessment of the ECG is essential to consider diseases other than acute myocardial infarction, especially the ones that are non-cardiac in origin. The goal of this narrative review is to give an overview of the significant disorders that are non-cardiac in origin that can mimic an ST-segment elevation myocardial infarction (STEMI).

Prevalence of ECG changes during adenosine stress and its association with perfusion defect on myocardial perfusion scintigraphy

Nuclear Medicine Communications, 2017

Objective Myocardial perfusion scintigraphy (MPS) is a valuable, noninvasive imaging modality in the evaluation of patients with coronary artery disease. Adenosine stress may occasionally be associated with ECG changes. This study evaluated the strength of association between adenosine stress-related ECG changes and perfusion defects on 99m Tc-MPS. Patients and methods 117 (mean age: 61.25 ± 9.27 years; sex: men 87, women 30) patients with known/suspected coronary artery disease underwent adenosine stress MPS. ECG was monitored continuously during adenosine stress for ST-depression. On the basis of the summed difference score, reversible perfusion defects were categorized as follows: normal: less than 4, mild: 4-8, moderate: 9-13, and severe: more than 13. Results ST-depression was observed in 27/117 (23.1%) and reversible perfusion defects were observed in 18/27 (66.66%) patients. 2/27, 6/27, and 10/27 patients had mild, moderate, and severe ischemia, respectively. 9/27 patients had normal perfusion. ECG changes and perfusion defects showed a moderate strength of association (correlation coefficient r = 0.35, P = 0.006). The sensitivity, specificity, positive predictive value, and negative predictive value of ECG findings for prediction of ischemia were 35.29, 86.36, 67.67, and 63.33%, respectively. Conclusion ECG changes during adenosine stress are not uncommon. It shows a moderate strength of association with reversible perfusion defects. ECG changes during adenosine merit critical evaluation of MPS findings. Nucl Med Commun 38:291