Chest Pain

AI Used With Chest X-ray to Triage Chest Pain Patients

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A study published in Radiology reports that artificial intelligence (AI) may help improve care for patients who show up at the hospital with acute chest pain.

“To the best of our knowledge, our deep learning AI model is the first to utilize chest X-rays to identify individuals among acute chest pain patients who need immediate medical attention,” said the study’s lead author, Márton Kolossváry, MD, PhD, radiology research fellow at Massachusetts General Hospital (MGH) in Boston.

Acute chest pain syndrome may consist of tightness, burning or other discomfort in the chest or a severe pain that spreads to your back, neck, shoulders, arms, or jaw. It may be accompanied by shortness of breath.

Acute chest pain syndrome accounts for over 7 million emergency department visits annually in the United States, making it one of the most common complaints.

Fewer than 8% of these patients are diagnosed with the three major cardiovascular causes of acute chest pain syndrome, which are acute coronary syndrome, pulmonary embolism or aortic dissection. However, the life-threatening nature of these conditions and low specificity of clinical tests, such as electrocardiograms and blood tests, lead to substantial use of cardiovascular and pulmonary diagnostic imaging, often yielding negative results. As emergency departments struggle with high patient numbers and shortage of hospital beds, effectively triaging patients at very low risk of these serious conditions is important.

Deep learning is an advanced type of artificial intelligence (AI) that can be trained to search X-ray images to find patterns associated with disease.

For the study, Dr Kolossváry and colleagues developed an open-source deep learning model to identify patients with acute chest pain syndrome who were at risk for 30-day acute coronary syndrome, pulmonary embolism, aortic dissection or all-cause mortality, based on a chest X-ray.

The study used electronic health records of patients presenting with acute chest pain syndrome who had a chest X-ray and additional cardiovascular or pulmonary imaging and/or stress tests at MGH or Brigham and Women’s Hospital in Boston between January 2005 and December 2015. For the study, 5,750 patients (mean age 59, including 3,329 men) were evaluated.

The deep-learning model was trained on 23,005 patients from MGH to predict a 30-day composite endpoint of acute coronary syndrome, pulmonary embolism or aortic dissection and all-cause mortality based on chest X-ray images.

The deep-learning tool significantly improved prediction of these adverse outcomes beyond age, sex and conventional clinical markers, such as d-dimer blood tests. The model maintained its diagnostic accuracy across age, sex, ethnicity and race. Using a 99%sensitivity threshold, the model was able to defer additional testing in 14% of patients as compared to 2% when using a model only incorporating age, sex, and biomarker data.

“Analyzing the initial chest X-ray of these patients using our automated deep learning model, we were able to provide more accurate predictions regarding patient outcomes as compared to a model that uses age, sex, troponin or d-dimer information,” Dr Kolossváry said. “Our results show that chest X-rays could be used to help triage chest pain patients in the emergency department.”

According to Dr Kolossváry, in the future such an automated model could analyze chest X-rays in the background and help select those who would benefit most from immediate medical attention and may help identify patients who may be discharged safely from the emergency department.

Long-COVID Chest Pain: Main Causes, Ways to Relieve

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(Shutterstock)

Long COVID, or post-COVID conditions, are evolving terms, and as time passes, we’re learning more about the aftereffects of COVID-19 infection. One of the most common symptoms that have been observed is chest pain, which affects up to 22 percent of patients two months after acute infection.

“It’s very common with patients that experienced significant cough during their COVID infection, but can also be a sign of something more troubling,” Dr. Thomas Gut, medical director of the Post-COVID Recovery Center at Staten Island University Hospital, part of Northwell Health in New York, told The Epoch Times.

While this can be frightening for COVID survivors, it doesn’t always mean you’re experiencing a life-threatening condition.

Post-COVID Chest Pain Cause 1: Heart Disease and Blood Clotting

“COVID has been associated with heart disease and also abnormal blood clots,” observed Gut.

These can cause chest pain.

A large study found COVID-19 was linked to a severely increased risk of blood clot-related issues immediately after diagnosis compared to people never infected. This includes heart attack and stroke. Researchers also found that this risk remained higher for up to 49 weeks, although dropped sharply by the second week.

The study shows that if someone had COVID-19, “then they should be talking with their physicians about managing their cardiovascular risk, which is likely to be increased for some level of time,” study senior author Jonathan Sterne, a professor of medical statistics and epidemiology at England’s University of Bristol, said in a statement.

The U.S. Centers for Disease Control and Prevention report that COVID-19 survivors have twice the risk of developing pulmonary embolism (blood clot in the lungs) or respiratory conditions.

Chest pain after COVID-19 could also be related to pericarditis (inflammation of the lining of the heart), and coronary artery disease (low blood flow to the heart), according to Dr. Luis Ostrosky-Zeichner, division chief of Infectious Diseases and Epidemiology at UTHealth Houston and Memorial Hermann.

Pericarditis is often mild and goes away on its own. However, if not treated, some cases can become chronic and seriously affect your heart. While it can take weeks or months to recover, full recovery is most likely with rest and ongoing care, which can also reduce the risk of getting it again.

Post-COVID Chest Pain Cause 2: Inflammation of the Lung

COVID-19 can cause lung complications such as pneumonia and, in the most severe cases, acute respiratory distress syndrome (ARDS).

Newer coronavirus variants might also cause airway disease, like bronchitis, potentially severe enough for hospitalization.

These conditions can create inflammation in the chest severe enough to cause pain.

In those with COVID pneumonia, “the chest pain can come from direct inflammation of the lung lining, called the pleura,” said Dr. Jacob Teitelbaum, a board-certified internist and nationally known expert in the fields of chronic fatigue syndrome, fibromyalgia, sleep, and pain. “[The pain will] tend to get worse with deep breaths.”

This kind of chest pain can resolve with time (months) and anti-inflammatory treatments such as highly absorbable forms of curcumin or ibuprofen, he added.

It Can Be Benign Muscle Pain, One Way to Check

But the chest pain “usually will be benign,” said Teitelbaum.

Those younger than the typical age for increased heart attack risk can look for specific signs that the pain isn’t life-threatening.

For people under 50 years of age, where the pain: is worse upon taking a deep breath, changing position or pushing over the area; does not trigger sweats or left arm pain; isn’t worse with exertion; isn’t associated with coughing up blood or yellow mucus; and doesn’t go away with an antacid, it’s most often just going to be benign muscle pain in your chest-wall area, said Teitelbaum.

If chest pain goes away with an antacid, especially if the pain is worse while lying down or with burping, it’s most often going to be indigestion and acid reflux.

“Do not use PPI acid blockers, as these are toxic and can worsen COVID in general,” Teitelbaum advised. “Instead, use famotidine, which helps the body heal from COVID by improving immunity, or [use] chewable antacids.”

There is a simple way to check whether it’s just pain in your chest muscles.

Push over the area of pain with your fingertips using about five pounds of pressure, which is enough to make your fingernail bed turn white.

If you can “reproduce the pain” by pressing over a bony area, like the ribs, Teitelbaum said, it is most likely a benign muscle pain. The rib cage is like a suit of armor around our internal organs, and pushing on the outside will not make the heart or lung underneath it hurt.

But after having chest pain post-COVID, the first thing you should do is see your doctor immediately to make sure it’s not anything dangerous.

“With chest pain, better safe than sorry,” Teitelbaum said. Essentially, your doctor is ruling out that you are having an acute heart attack, angina, or serious lung issue. “Heart attacks can kill if treatment is delayed.”

As long as a doctor has determined your symptoms are not worrisome, then just using a heating pad and topical comfrey or other creams like Icy Hot (topical aspirin and menthol) can be helpful, advised Teitelbaum.

Evaluation and managment of chest pain

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https://www.gehealthcare.com/article/cardiovascular-resources-evaluation-of-chest-pain

Novel troponin test may rule out heart attack risk.

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A single measurement of the new high-sensitivity cardiac troponin T (hs-cTnT) and a normal electrocardiogram (ECG) might help doctors predict which patients with chest pain are at low risk of heart attack and can be sent home from the emergency department (ED), a study has shown.

Researchers in Sweden sought to determine the negative predictive value of undetectable hs-cTnT (<5 ng/L) and an ECG without significant ST elevation or depression for the primary endpoint of myocardial infarction (MI) within 30 days among 14,636 patients (age >25 years) with chest pain who presented at the ED of a hospital in Sweden over a 2-year period. [Abstract 403-14-LB-13200; J Am Coll Cardiol 2014; doi:10.1016/j.jacc.2014.03.017]

Nearly 9,000 patients (61 percent) who had undetectable hs-cTnT (<5 ng/L) on initial testing (as measured with Elecsys® 2010, Roche Diagnostics) were included in the study. They were younger and less likely to have diabetes, chronic kidney disease, prior MI or stroke compared with patients who had increased hs-cTnT levels (5-14 and >14 ng/L).

Hospitalization rates were lower among patients with undetectable hs-cTnT (21 percent vs 44 and 82 percent for 5-14 and >14 ng/L, respectively). Diagnosis of MI increased with increasing levels of hs-cTnT (2 percent for <5 ng/L, 3.1 percent for 5-14 ng/L, 4.1 percent for >14 ng/L).

Within 30 days, 39 patients with undetectable hs-cTnT had MI (24 had significant ECG changes, 15 had normal ECG). The negative predictive value of the tests for MI was 99.8 percent (95% CI, 99.7-99.9) and 100 percent for death (95% CI, 99.9-100). After adjusting for age, sex, diabetes, prior MI and eGFR, there was no significant difference in the risk of death between patients discharged from the ED and those hospitalized within 365 days (hazard ratio [HR], 0.73; 955 CI, 0.48-1.12).

“Patients with chest pain who have an initial hs-cTnT of <5 ng/L and no signs of ischemia on ECG, independent of duration of chest pain and other risk factors, have a minimal risk of MI within 30 days, and no risk of death,” said lead investigator Dr. Nadia Bandstein from the Karolinska Institute in Stockholm, Sweden. “These patients can be safely discharged from the ED.”

The study has some clinical implications – it can reduce overcrowding of the ED, prevent unnecessary admissions, and save doctor-patient time. If MI can be ruled out more quickly, 20 to 25 percent of all hospital admissions for chest pain can be prevented, Bandstein said.

Panelist Dr. Allan Jaffe from Mayo Clinic, Rochester, Minnesotta, US, however, cautioned that the assay is likely to be effective only in low-risk groups. “We have to be careful in defining how we rule people in and out. In the long run, we will be able to validate the strategy… we need to do it a little bit more rigorously.”

Gastrobronchial fistula.

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A 67-year-old man presented with left anterior chest pain of sudden onset. On admission, chest radiography showed left lower lobe infiltrates.

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8 days later, chest radiography showed a cavitating lesion, consistent with a pulmonary abscess. CT of the chest revealed a pulmonary abscess in the left lower lobe. Suspecting an oesophagobronchial fistula, we did a barium contrast study, which showed a passage from the gastric fundus to the pulmonary abscess (figure). Oesophagogastroduodenoscopy confirmed the presence of a fistula in the gastric fundus; gastric contents were seen to enter the fistula. The fistula, and the left lower lobe to which it was adherent, were surgically resected, and the diaphragm was repaired. The patient’s recovery was uneventful.

Source: Lancet

Copeptin Helps “Copeptin Helps in the Early Detection Of Patients with Acute Myocardial Infarction”: the primary results of the CHOPIN Trial ONLINE FIRST.

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“Copeptin Helps in the Early Detection Of Patients with Acute Myocardial Infarction”: the primary results of the CHOPIN Trial ONLINE FIRST

Objectives  Demonstrate that copeptin level <14 pmol/L allows ruling out AMI when used in combination with cardiac troponin I (cTnI) <99th percentile and a non-diagnostic ECG at the time of presentation to the emergency department (ED).

Background  Copeptin is secreted from the pituitary early in the course of acute myocardial infarction (AMI).

Methods  This was a 16-site study in 1967 chest pain patients presenting to an ED within 6 hours of the onset of chest pain. Baseline demographics and clinical data were collected prospectively. Copeptin and a contemporary sensitive cTnI (99th percentile 40 ng/L; 10% coefficient of variation (CV) 0.03 μg/L) were measured in a core laboratory. Patients were followed for 180 days. The primary outcome was diagnosis of AMI. Final diagnoses were adjudicated by two independent cardiologists blinded to copeptin results.

Results  AMI was the final diagnosis in 156 patients (7.9%). A negative copeptin and cTnI at baseline ruled out AMI for 58% of patients, with a NPV of 99.2% (95% CI 98.5-99.6). AMIs not detected by the initial cTnI alone were picked up with copeptin >14 pmol/L in 23/32 patients (72%). NSTEMIs undetected by cTnI at 0h were detected with Copeptin >14 pmol/L in 10/19 patients (53%). Projected average time-to-decision could be reduced by 43% (from 3.0 hours to 1.8 hours) by the early rule out of 58% of patients. Both abnormal copeptin and cTnI were predictors of death at 180 days (p<0.0001 for both, c index 0.784 and 0.800, respectively). Both were independent of age and each other and provided additional predictive value (all p<0.0001).

Conclusion  Adding copeptin to cTnI allowed safe rule out of AMI with a NPV >99% in patients presenting with suspected ACS. It has the potential to rule out AMI in 58% of patients without serial blood draws.

Source: JACC

Chest Pain: What Happens After the Emergency Department?

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Patients who follow up with cardiologists do best.

 

Researchers examined patterns of follow-up care and outcomes in high-risk patients with chest pain who presented to Ontario emergency departments (EDs) from 2004 to 2010. High risk was defined as having a prior diagnosis of cardiovascular disease, diabetes, or both. The primary outcome was a composite of all-cause death and hospitalization for myocardial infarction within 1 year after the index visit.

Of nearly 57,000 patients, 17% followed up with a cardiologist (with or without a visit to primary care) within 30 days after ED discharge, 57% followed up with a primary care practitioner only, and 25% did not have a visit to a physician recorded. After adjustment for clinical, demographic, and hospital characteristics, the cardiologist group had a significantly lower hazard ratio for the composite outcome (HR, 0.79; P<0.001) than the no–follow-up group and the PCP-only group (HR, 0.85; P<0.001). PCP-only follow-up was significantly beneficial compared to no follow-up (HR, 0.93; P<0.023). Patients seen by cardiologists underwent more testing and received more evidence-based therapies within 100 days after discharge.

Comment: These robust results demonstrate that what happens after the emergency department visit is as important as what happens during the ED visit, and that postdischarge care for patients with high-risk chest pain should include timely assessment by a cardiologist.

 

Source: Journal Watch Emergency Medicine

Rapid Rule-Out Protocol for Patients with Suspected Cardiac Chest Pain.

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The combination of TIMI score of zero at presentation, no new ischemic changes on initial electrocardiogram, and negative troponin results at zero and 2 hours had a sensitivity of 99.7%.

In a prospective observational study of 1975 patients who presented to two hospitals in Australia and New Zealand with chest pain suggestive of acute coronary syndrome, researchers assessed whether or not an accelerated diagnostic protocol could identify patients at low risk for major adverse cardiac events within 30 days. Patients with ST segment elevation on initial electrocardiogram (ECG) were excluded. Patients received usual care, including serial troponin testing, in accordance with international guidelines; each hospital used its standard troponin test.

The protocol consisted of a Thrombolysis in Myocardial Infarction (TIMI) score at presentation, initial ECG results, and troponin I concentrations at zero and 2 hours; patients with a TIMI score of zero, no new ischemic changes on initial ECG, and negative troponin results at zero and 2 hours were deemed low risk.

Major adverse cardiac events (acute myocardial infarction, death, cardiac arrest, cardiogenic shock, emergency revascularization, and ventricular dysrhythmia requiring intervention) occurred in 302 patients (15%), usually within 10 days. The protocol identified 392 patients (20%) as being low risk; one of these patients (0.25%) had a major cardiac event (myocardial infarction diagnosed on the basis of an elevated troponin result at 12 hours). The sensitivity and negative predictive value of the protocol for identifying patients with major adverse cardiac events were both 99.7%, and the specificity was 23.4%.

Comment: This study begs for a randomized trial in which low-risk patients are actually sent home, but such a study is unlikely to ever be conducted. The study’s strength is its use of current (i.e., not highly sensitive) troponin assays from two different manufacturers. These findings support institutions developing internal protocols to efficiently evaluate patients with low-risk chest pain. Developers of such protocols should recognize that most patients will require further testing, such as exercise tolerance testing, to exclude ischemia.

Source: Journal Watch Emergency Medicine