Ferenc Imre Suhai, Barbara Sipos, Milán Vecsey-Nagy, Bálint Szilveszter
Városmajor Heart and Vascular Centre, Cardiac CT Working Group, Budapest, Hungary
September 29, 2026
History
Why did the patient come for a CT exam?
A 29-year-old male patient, with a history of hypertension and bronchial asthma, was referred to the Városmajor Heart and Vascular Centre from the emergency department due to acute retrosternal chest pain and markedly elevated cardiac biomarkers.
His symptoms occurred in the setting of a recent upper respiratory tract infection with fever and follicular tonsillitis. He had been treated with azithromycin before admission.
At the emergency department, laboratory tests showed significant inflammatory activity and myocardial injury, with elevated C-reactive protein, leukocytosis with neutrophilia, and markedly elevated high-sensitivity troponin T, which increased from 1302 ng/L to 1689 ng/L. CK-MB was also elevated.
Electrocardiography showed ST-segment elevation in the inferior leads with reciprocal ST depression in aVL.
Transthoracic echocardiography revealed preserved left ventricular systolic function without regional wall motion abnormalities. Given the combination of acute chest pain, elevated troponin, inflammatory syndrome, and ECG changes, acute myocarditis was suspected; however, acute coronary syndrome had to be excluded.
Therefore, a coronary CT angiography was performed as the initial imaging modality to assess the coronary status. Cardiac magnetic resonance imaging was subsequently performed for detailed myocardial tissue characterization and confirmation of the diagnosis.
Diagnosis
What were the CT findings, and what happened to the patient after CT?
Coronary CT angiography was performed using a photon-counting detector CT on a Siemens NAEOTOM Alpha Peak scanner. Native calcium scoring, contrast-enhanced ECG-gated coronary CTA, and a 6-minute delayed-phase acquisition for myocardial tissue characterization and visual assessment of late iodine enhancement were performed.
The estimated radiation dose was 350 mGy·cm for the CCTA and 245 mGy·cm for the delayed scan.
Iomeron 400 was administered with a contrast volume of 80 mL. The patient received 75 mg oral metoprolol and 0.8 mg sublingual nitroglycerin prior to the examination. Heart rate during the scan was 85/min with sinus rhythm.
The coronary calcium score was 0.
The patient had a left-dominant coronary artery system and normal origin and course of the coronary arteries. No relevant coronary atherosclerosis or luminal stenosis were detected (Figure 1).
Figure 1. CT coronary angiography demonstrating normal coronary artery anatomy with no evidence of significant stenosis.
Cardiac magnetic resonance imaging was performed on a 1.5-T Siemens Aera scanner. Short-axis images demonstrate myocardial edema on T2-weighted fat-suppressed imaging and corresponding non-ischemic late gadolinium enhancement on LGE imaging in the mid-ventricular anterior-anterolateral and inferior-inferolateral left ventricular segments, predominantly in a subepicardial to midmyocardial distribution.
The concordant presence of edema and LGE supports acute myocarditis rather than ischemic infarction.
On the 6-minute delayed-phase PCCT images, visually detectable late iodine enhancement was observed, in a non-ischemic distribution. The enhancement involved the basal and midventricular anterolateral and inferolateral regions, the inferior segment in a subepicardial to midmyocardial pattern, and the apical inferior and lateral segments (Figure 2).
Figure 2. Electrocardiogram (ECG) During Prospective Sequential Cardiac CT Acquisition. Multimodality comparison of an acute myocardial injury from basal to apical short-axis images. The first column shows 6-minute delayed-phase PCCT images, the second column shows corresponding color-coded LUT maps, the third column shows iodine maps, and the fourth column shows matched cardiac MRI late gadolinium enhancement images. Blue arrows indicate areas of abnormal myocardial iodine enhancement on PCCT and corresponding non-ischemic myocardial injury on CMR. The abnormalities are predominantly located in the anterolateral, inferolateral, and inferior left ventricular segments, with a subepicardial to midmyocardial distribution, consistent with acute myocarditis.
The visual delayed iodine enhancement pattern indicated abnormal myocardial tissue characteristics and supported the diagnosis of an acute myocarditis.
Cardiac magnetic resonance (CMR) imaging was performed on a 1.5-T Siemens Aera scanner using Gadovist contrast agent. The CMR protocol included cine b-SSFP imaging, T2-weighted imaging, native T1 and T2 mapping, first-pass perfusion, late gadolinium enhancement imaging, and post-contrast T1 mapping for extracellular volume assessment.
CMR demonstrated mildly reduced left ventricular systolic function, with an LVEF of 45.4%. Left ventricular volumes were within the normal range, stroke volume was preserved, and left ventricular myocardial mass was normal. Right ventricular size and systolic function were preserved, with an RVEF of 52.2%.
T2-weighted images demonstrated myocardial edema in the basal and midventricular anterolateral and inferolateral segments, the midventricular inferior and partly anterior segments, and the apical inferior segment, predominantly in a subepicardial to midmyocardial distribution (Figure 3).
Figure 3. Cardiac MRI confirmation of acute myocarditis: myocardial edema and non-ischemic injury
After gadolinium administration, pathological late gadolinium enhancement was observed in the same edematous myocardial segments.
Parametric mapping further supported the diagnosis. Native T1, T2, and ECV values were elevated in the affected lateral myocardial regions. ECV was increased in the basal lateral wall and midventricular lateral wall, while septal values remained within the normal range.
Overall, the CMR findings confirmed acute myocarditis with mildly reduced left ventricular ejection fraction and mild diffuse hypokinesis.
Comments
Is there any clinically interesting aspect of the case to discuss?
What difference did photon-counting CT make for the patient?
This case highlights the potential diagnostic value of photon-counting CT in patients presenting with acute chest pain, elevated cardiac biomarkers, and electrocardiographic changes suggestive of acute coronary syndrome.
The 6-minute delayed-phase acquisition allowed visual assessment of myocardial iodine retention. Delayed-phase spectral reconstruction using monoenergetic plus images and color-coded iodine maps improved visualization of myocardial iodine distribution and enabled myocardial tissue characterization.
Focal subepicardial to mid-myocardial iodine accumulation indicated abnormal myocardial tissue characteristics. The distribution of delayed iodine enhancement corresponded closely to the edema, late gadolinium enhancement, and elevated CMR-derived ECV values in the affected myocardial segments.
An important limitation is the additional radiation exposure associated with the delayed-phase of CT imaging. This is particularly relevant in young patients, in whom radiation dose should be carefully justified and minimized.
Therefore, delayed-phase PCCT acquisitions should not be considered for routine in all patients with suspected myocarditis, but rather reserved for selected cases in which the expected diagnostic benefit outweighs the additional dose, such as when CMR is contraindicated, unavailable, or unlikely to be feasible.
PCCT could serve as a comprehensive first-line imaging tool in selected patients with suspected myocarditis and possible acute coronary syndrome. Its inherent spectral capabilities, together with its high spatial resolution, allow rapid exclusion of obstructive coronary artery disease while also enabling visual myocardial tissue characterization through delayed-phase spectral imaging, monoenergetic reconstructions, and iodine mapping.
These capabilities support comprehensive coronary artery evaluation while simultaneously providing additional insights into myocardial tissue characteristics within a single examination.
Examination Protocol
Detail | Value |
|---|
Scanner | NAEOTOM Alpha.Peak |
Scan area | Heart |
Scan mode | QuantumPlus + HD (combined spectral and HighRes) |
Scan length | 141 mm |
Scan direction | Cranio-caudal |
Scan time | 0.507 s |
Tube voltage | 140 kV |
IQ level | 100 |
Dose modulation | CARE Dose4D |
CTDIvol | 17.5 mGy |
DLP | 245 mGy*cm |
Rotation time | 0.25 s |
Pitch | not applicable |
Slice collimation | 144 x 0.4 mm |
Slice width | 0.4 mm |
Reconstruction increment | 0.4 mm |
Reconstruction kernel | Qr44 Q4 |
keV level | 40 |
Spectral reconstruction | Monoenergetic Plus; iodine/water decomposition; iodine maps |
Heart rate | 57/min (delayed) |
Contrast | Iomeron 400, 400 mg/mL |
Volume | 80 mL + 10mL saline pacer + 30mL saline chaser (for CCTA) |
Flow rate | 5 mL/s |
Start delay | Bolus tracking triggered at 92 HU (CCTA), delayed acquisition performed 6 minutes after contrast administration. |
Disclaimer
The statements by customers of Siemens Healthineers described herein are based on results that were achieved in the customer’s unique setting. Because there is no “typical” hospital and many variables exist (e.g., hospital size, case mix, level of IT and/or automation adoption) there can be no guarantee that other customers will achieve the same results.
The products/features (mentioned herein) are not commercially available in all countries. Their future availability cannot be guaranteed.
