50-year-old woman with no PMH who presented with palpitations and regular narrow-complex tachycardia with HR in 200s on ECG in the emergency department.
hsTnT 18 –> 20 –> 25
She converted to normal sinus rhythm after adenosine administration. ECG post- adenosine showed normal sinus rhythm with no ST-T changes. She remained asymptomatic throughout. She was discharged home on oral metoprolol.
Teaching point: Benign tachyarrhythmias such as AV nodal re-entrant tachycardia may cause a mild hsTnT elevation even in the absence of myocardial ischemia.
60-year-old man with PMH of interior STEMI status post DES to RCA 8 months prior, HTN, HLD, chronic anemia of unclear etiology who presented with chest pressure worse on exertion relieved by nitroglycerin.
hsTnT 30 –> 41 –> 40
Hemoglobin was found to be reduced to 7.3 g/dL from baseline of 10 g/dL. TTE showed a normal LVEF with unchanged inferior regional wall motion abnormalities. After blood transfusion symptoms resolved. He was discharged with outpatient colonoscopy.
Teaching point: Because the oxygen delivery equation depends on hemoglobin, acute anemia may cause increased myocardial demand. Myocardial ischemia may resolve after addressing the anemia.
50-year-old woman with PMH of HTN, HLD, class III obesity presented to the emergency department after an episode of loss-of-consciousness for a few minutes while exercising followed by chest discomfort and diaphoresis.
hsTnT 179 –> 114 –> 99
ECG showed sinus tachycardia, RBBB, and no ST-T changes. TTE was unremarkable, but was technically limited given body habitus. Coronary CTA showed no evidence of coronary artery disease, but incidentally demonstrated a saddle pulmonary embolus. She was started on therapeutic anticoagulation.
Teaching point: It is important to consider other cardiopulmonary causes of troponin elevation. It is not sufficient to stop at ACS rule-out. A hsTnT elevation may occur from pulmonary embolism.
77-year-old man with PMH of Afib, COPD, CKD, who presented to the emergency department with epigastric pain, diarrhea and nausea. ECG showed nonspecific ST-T abnormalities.
hsTnT 71–>62–>63
A year prior he was admitted for COPD exacerbation and a TnT (4th generation assay) was 0.03–>0.04. TTE showed normal LV function and wall motion.
Teaching point: CKD may cause chronic elevation of troponin in the absence of significant myocardial ischemia. In this patient, hsTnT values obtained with the 5th generation assay correlated with values obtained a year prior with the 4th generation one. Therefore, chronicity of the troponin elevation was confirmed.
90-year-old woman with PMH of STEMI status post DES to LAD ten years prior, ischemic cardiomyopathy status post ICD, Afib, CKD, HTN, DM presented to the emergency department from her assisted living facility after symptoms of abdominal discomfort, nausea and vomiting which started shortly after she had soup with rice. She had no chest pain or shortness of breath. ECG showed anterior Q waves, no change from prior.
hsTnT 100–>132–>129
TTE showed severely reduced LVEF and wall motion abnormalities in the territory of the LAD, no change from a prior study a year ago. hsTnT was rechecked the following day and remained flat in the 150s.
Teaching point: A relatively mild uptrend in troponin may be seen in patient with CKD with baseline troponin elevation in the setting of a noncardiac acute illness. This is especially common in patient with underlying chronic ischemic heart disease.
87-year-old man with PMH of multivessel CAD status post multiple DES and known evidence of inferior wall ischemia on nuclear stress test, ischemic CM , CKD, COPD presented with constant nonexertional chest pressure over the past day or so. The chest pressure had been chronic, but slightly more prominent on this presentation. ECG showed LBBB and did not meet Sgarbossa criteria.
hsTnT 91–> 92–>107
Serum Cr was 2.06 mg/dL which was his baseline. TTE showed unchanged LVEF of 35% and regional wall motion abnormalities. LHC showed only 30% in-stent restenosis of his DES. His antianginals were uptitrated with good symptom relief.
Teaching point: CKD is a common cause of hsTnT elevation especially in patients with chronic ischemic heart disease.
89-year-old man with PMH of NSTEMI status post DES to the mid LCx a month prior with an unaddressed heavily calcified 80% mid LAD stenosis, CKD presented to the emergency department with dull L-sided chest pain started the same day as he was lifting boxes at home. Patient took two nitroglycerin tablets with some relief. ECG showed normal sinus rhythm with baseline LBBB and did not meet Sgarbossa criteria.
hsTnT 90 –> 174 –>571
During the recent hospitalization for NSTEMI his hsTnT peaked to 300. TTE showed borderline normal LV function with no regional wall motion abnormalities, no change from prior a month ago post-LHC. LHC was repeated and showed patent mid LCx stent and same mid LAD stenosis demonstrated a month prior. FFR of the LAD stenosis was 0.89 inconsistent with hemodynamic significance, so it was not stented. His antianginal therapy was maximized with some improvement in symptoms.
Teaching point: In this patient with CKD a chronic severe stenosis in the LAD caused a significant troponin elevation with anginal symptoms.
78-year-old woman with PMH of Afib who presented with sudden-onset chest pressure as a surprise birthday party was revealed to her. ECG showed ST elevations in the lateral leads with reciprocal changes in inferior leads.
hsTnT 129 –> 724 two hours later –> 500 the next day.
TTE showed LVEF of 40% with akinetic mid to apical segments (“apical ballooning”). Emergent LHC showed no significant CAD. Repeat TTE a week later showed a completely normal LV function.
Teaching point: Stress-induced cardiomyopathy can mimic an acute myocardial infarction including symptoms, ECG changes and troponin elevation.
75-year-old woman with PMH of HTN, anxiety, prior episode of stress-induced cardiomyopathy two years prior (LHC showed no evidence of CAD at that time) presented to the ED with nonradiating, nonexertional chest pressure which awoke her from sleep. ECG showed sinus tachycardia and nonspecific ST-T abnormalities.
hsTnT 276–>354–>409
TTE shows LVEF 35% with hypokinesis of apical and mid ventricular segments. After her prior episode of stress-induced cardiomyopathy which manifested with a similar wall motion pattern, her LV function had recovered completely. Patient did not have any signs or symptoms of decompensated heart failure. A repeat catheterization was not obtained. Her LVEF recovered completely after one month as seen on outpatient TTE.
Teaching point: Stress-induced cardiomyopathy can mimic an acute myocardial infarction including symptoms, ECG changes and troponin elevation.
67-year-old man with PMH of stable angina and 3-vessel CAD treated medically presented with sudden-onset crushing chest pain after using marijuana. Chest pain resolved with nitroglycerin.
hsTnT 50–>74–>89
ECG showed nonspecific ST-T changes. TTE showed new lateral wall hypokinesis. LHC the next day showed a severe LCx stenosis which was treated with a DES.
Teaching point: Although the troponin elevation may not be meteoric, the presence of either wall motion abnormalities on echo, EKG changes, or angina is sufficient to suggest that myocardial ischemia, not just myocardial injury, is present.
84-year-old man with PMH of HTN, HLD, CKD, NSTEMI status post DES to LAD five years prior and RCA two years prior presented after two episodes of L-sided chest pressure, the first a few days ago occurring on exertion and lasting 30 minutes, the second one today at rest lasting an hour. The second episode resolved spontaneously and was partially relieved by nitroglycerin. He had not had any chest discomfort since the last stent was placed until this presentation.
hsTnT 32–> 26 –> 43.
ECG showed nonspecific ST-T abnormalities. TTE showed normal LV function and no wall motion abnormalities. LHC shows critical in-stent restenosis of the prior LAD stent which was treated with a new stent.
Teaching point: It is possible for myocardial injury with myocardial ischemia to present with just anginal symptoms and troponin elevation without ECG and echo changes, so history taking is of utmost importance.
47-year-old man no PMH who presented to the emergency department with a three-week history of chest pain radiating to the left arm. The chest pain was initially only exertional, then started occurring at rest as well and became progressively more frequent and severe.
hsTnT 11–>11–>12
TTE was normal. He was medically treated for unstable angina. LHC the following day showed a severe stenosis of the mid LAD which was treated with a DES.
Teaching point: Unstable angina may present with low troponin and unremarkable echocardiographic findings. Thorough history taking is paramount for the diagnosis of unstable angina.
66-year-old man with PMH of NSTEMI status post DES to proximal LAD three years prior, HTN, HLD, CKD was admitted for an ischemic stroke. Patient had an allergic reaction to a medication and developed angioedema. while in the hospital He is given epinephrine intramuscularly with resolution of the angioedema. ECG shows sinus tachycardia. hsTnT is accidentally ordered and goes from his known baseline in the 40’s to the 135 and after several hours peaks at 342. He reported no chest pain or discomfort and no shortness of breath. TTE shows preserved LV function and no regional wall motion abnormalities.
Teaching point: Administration of epinephrine will increase myocardial oxygen demand and can cause troponin elevation especially with existing ischemic heart disease.
72-year-old woman with PMH of HTN and recent viral URI presented with palpitations and sharp, nonexertional, positional chest pain.
hsTnT 18–>235–>200
TTE showed a normal LVEF and a large pericardial effusion. She had a negative pulsus paradoxus and no echocardiographic signs of hemodynamic compromise. She underwent nonurgent pericardiocentesis and was treated for pericarditis with NSAID and colchicine. Serous pericardial fluid revealed reactive mesothelial cells and mixed inflammation, no malignant cells.
Teaching point: Myopericarditis may case significant hsTnT elevation which may mimic that of acute myocardial infarction.
55-year-old man with PMH of cocaine use disorder presented to the emergency department with chest pressure started one hour prior. Patient used cocaine most days of the week, last time the day of the presentation.
hsTnT 24–>35–>43
ECG shows nonspecific ST-T abnormalities. TTE shows borderline normal LV function with no regional wall motion abnormalities. Chest pain subsides after nitroglycerin. He was discharged. Subsequent outpatient coronary CTA showed no coronary artery disease and no coronary calcifications.
Teaching point: cocaine use may cause elevations in hsTnT in the absence of CAD.
65-year-old woman with with PMH of 3-vessel CAD status post CABG 10 years prior, recent upper respiratory infection with poor-oral intake presented to the ED after one episode of near-syncope as she was standing up followed by chest pressure which resolved by arrival of paramedics.
hsTnT 10–>14–>18.
TTE showed low-normal EF, no regional wall motion abnormalities, no changes from prior study a few years ago. She had positive orthostatic vital signs and symptoms which resolved after IVF.
Teaching point: Transient hypotension may cause hsTnT elevation.
88-year-old man with PMH of HTN, DM, ESRD on HD was referred for an outpatient pharmacological nuclear stress test given complaints of chest pressure and shortness of breath on exertion for the past month. After regadenoson administration patient felt “not himself”, almost lost consciousness and felt a sharp R-sided chest pain all of which were reversed with aminophylline. Blood pressure dropped significantly after regadenoson administration and recovered after aminophylline. ECG was unremarkable.
hsTnT 94–>88–>71
TTE showed low-normal LVEF and no wall motion abnormalities. LHC showed a 50% stenosis in the proximal LAD which was not hemodynamically significant by FFR.
Teaching point: transient hypotension may cause a significant troponin elevation. This patient’s baseline troponin was already elevated due to his ESRD.
90-year-old woman with PMH of advanced dementia presented to the emergency department after a mechanical fall at assisted living facility. She is unable to provide any meaningful history. ECG was unremarkable.
hsTnT 24 –> 64–>31
which correlated with total creatine kinase 233–>424–>356 IU/L. TTE showed normal LV function and wall motion. She was given IV fluids.
Teaching point: Troponin T is present in skeletal muscle as well as in the myocardium. Therefore, a physical trauma may result in troponin T elevation. Correlating troponin T trend with creatine kinase may help inform the cause of the troponinemia.
80-year-old man with PMH of CAD (status post PCI to LAD and OM1), obstructive sleep apnea, DM, HTN was admitted with bilateral lower extremity weakness and was found to have elevated creatinine kinase (9000 IU/L) and Cr (2.4 mg/dL, baseline 1.0 mg/dL).
hsTnT 97–>98–>99
ECG showed normal sinus rhythm without ST-T changes. TTE showed normal LV function. Patient had LHC in three years prior that showed patent OM1 and LAD stents. He was diagnosed with rhabdomyolysis and given IV fluids.
Teaching point: Troponin T is released from injured skeletal muscle. Rhabdomyolysis will increase troponin T along with creatine kinase.
32-year-old man with no PMH presented with shortness of breath, mild chest discomfort (anterior chest, reproducible with palpations) of two days duration. Patient has had a maculopapular rash on the extensor surfaces of his limbs and on his back and suspicion for dermatomyositis. He has elevated creatine kinase, aldolase, C-reactive protein and erythrocyte sedimentation rate.
hsTnT 124–>117–>105
ECG showed sinus rhythm with no significant ST-T segment changes. TTE was unremarkable. Biopsy of right quadriceps showed chronic inflammatory myopathy.
Teaching point: Troponin T is released from injured skeletal muscle. Dermatomyositis may increase troponin levels in the absence of myocardial ischemia.
67-year-old man with PMH DM, HTN, HLD, TIA who presents to the emergency department as a catheterization lab activation in the setting of R-sided chest crushing pain that woke him up from sleep. ECG showed ST elevation in the anterolateral leads with reciprocal changes in the inferior leads. Emergent LHC showed an occluded mid LAD which was stented and a 70% stenosis of the proximal LCx.
hsTnT 230 at presentation peaked at 5630 12 hours later.
TTE showed LVEF 29% with akinesis of the apex, mid and apical septal, anteroseptal and anterolateral segments. A few days later he underwent staged PCI of the LCx stenosis.
Teaching point: hsTnT usually has an impressive upward trend in STEMI.
32-year-old woman with no PMH presented to the emergency department five days after delivering her second child with progressively worsening shortness of breath without any chest discomfort or pain. The patient was hypertensive.
hsTnT 10—>12—>14
BNP was 548. CXR showed signs of pulmonary edema. CTA chest ruled out a pulmonary embolism. Her symptoms improved after diuresis. TTE was normal. This patient was diagnosed with post-partum preeclampsia.
Teaching point: Mild or minimal hsTnT elevation may be seen in young otherwise healthy patients with disorders related to pregnancy such as pre-eclampsia.
55-year-old woman with PMH of non-small-cell lung carcinoma on carboplatin, pemetrexed and pembrolizumab presented to the emergency department with chest pain.
HsTnT 80–>313–>534
Patient was known to have no coronary calcium on prior imaging. Coronary CTA showed nonobstructive CAD. TTE showed a normal LVEF with mid septal akinesis. Cardiac MRI showed evidence of focal myocardial edema in the septum. She was treated with high-dose corticosteroids and her troponin downtrended to normal.
Teaching point: In patients receiving immune checkpoint inhibitors, such as pembrolizumab, be vigilant of the possibility that troponin elevation is occurring from ICI myocarditis.
Case vignettes were written by Kene Mezue, MD, and Giorgio Mottola, MD. These case vignettes are for educational purposes only.