A 24-Year-Old Man (Patient K.) consulted his family doctor with symptoms of acute respiratory viral infection (sore throat, general weakness, increased body temperature to 38.5-39 ℃). Five days later (despite his temperature returning to normal), he began to experience severe crushing pain in the heart area, that worsens when breathing in, and a feeling of shortness of breath during minimal physical exertion. The preliminary electrocardiogram (ECG) examination revealed heart rate (HR) 96 beats/min and the presence of concave ST segment elevation in all leads, without evidence of reciprocity. Laboratory test results showed an increase of high-sensitivity cardiac troponin I up to 9818 ng/L (normal range up to 25 ng/L). Patient was taken to the emergency department. Upon initial examination his HR was 110 beats/min, blood pressure - 100/60 mm Hg, respiration rate - 18 breaths/min, and his temperature - 36.9 °C. Lung fields were clear: no wheezing, rales, or rhonchy are audible. During auscultation of the heart, no murmurs, rubs, or gallops are noted. Radial pulses are equal and palpable. ECG (Figure 1) demonstrates normal sinus rhythm at 92 beats/min, ST-segment elevation in the leads I, II, aVF and V2-V6, with a downward convexity in V3-V4 and rudimentary S wave. There were no reciprocal changes in the ST segment, and the PQ segment in lead II was shifted downward.
Transthoracic echocardiography (Echo) revealed normal heart chamber sizes (left ventricular (LV) end-diastolic volume (EDV) - 134 ml, left atrium (LA) diameter - 4.1 cm, LA volume - 49 ml), hypokinesis of the LV apical segments, normal global LV contractile function (LV ejection fraction (EF) - 65%) and a minimal pericardial effusion (3 mm) behind the right atrium. Repeated laboratory test results were within normal limits, with the exception of these elevated values:
- white blood cell (WBC) count: 25 x 109/L (reference range 3.5–10 x 109/L) (with a left shift: band cells 18%, segmented cells 63%);
- erythrocyte sedimentation rate (ESR): 36 mm/h (reference range < 10);
- C-reactive protein (CRP): 314 mg/L (reference range < 5);
- procalcitonin level: 0.13 ng/mL (reference range < 0.05)
- creatine kinase (CK): 964 IU/L (reference range up to 195 IU/L);
- CK -MB: 89.6 IU/L (reference < 25 IU/L);
- troponin I: 19.1 ng/mL (reference ≤ 0.3 ng/mL);
The patient underwent urgent coronary angiography (CAG) that revealed no hemodynamically significant lesions of the coronary arteries. Cardiac MRI, performed after the CAG, presented increased MR signal (T2-weighted image) from the intramural/subepicardial myocardium at the level of the apical segments of the LV with sreading to the lateral, posterior wall, and partially to the LV septum with a maximum thickness of 6-7 mm, with a length of 8-10 mm to 16 mm. There was a slight homogeneous effusion in the pericardium up to 3 mm behind the lateral wall of the heart with transition to the posterior wall, in the absence of any visible signs of thickening of the layers of the pericardium (Figure 2).
The patient’s preliminary diagnosis was: Infarct-like acute myocarditis. Heart failure (HF) stage B with preserved LVEF.
Initial in-patient department medication:
- carvedilol 3.125 mg twice daily,
- eplerenone 25 mg/day,
- perindopril 2 mg/day,
- extended-release trimetazidine 35 mg twice daily,
- torasemide 5 mg/day,
- non-narcotic analgesics.
After a few days of such therapy, the patient's condition improved: heart pain disappeared, feeling of shortness of breath decreased. A numerous of positive dynamics were observed, including a decrease in WBC count to 10.77 × 109/L, CK to 63 IU/L and CK-MB to 12.2 IU/L. The ECG showed no changes in the ST segment, but deep negative T waves formation were detected. (Figure 3).
However, despite a marked improvement in the patient's condition following a two-week treatment period, the temperature rose again to 38°C. The patient again began to complain of pain in the heart area without a clear connection to physical exertion, fatigue and breathlessness. Subsequently, the patient exhibited symptoms of a nonproductive cough, which was accompanied by inspiratory dyspnea and palpitations, particularly during minimal physical exertion and when in a recumbent position. Auscultation revealed weakened vesicular breathing over the lower lung fields. Subsequent laboratory tests demonstrated an increase in:
- the WBC count up to 13.49 × 109/L and to 17.74 × 109/L in 2 days;
- ESR up to 50 and then to 59 mm/h;
- CRP concentration up to 101.31 and then to 136.31 mg/L.
Repeated Echo revealed the separation of the pericardial layers behind the LV posterior wall (up to 3 mm) and along the contour of the right chambers (up to 13 mm). This finding was accompanied by substantial thickening of the pericardial layers and indications of initial constriction (Inferior vena cava (IVC) 2.3 cm with collapse on inspiration < 50%). Minimal quantity of fluid was also identified in the right pleural sinus (Figure 4).
Multislice computed tomography of the chest organs excluded pulmonary embolism, but revealed CT signs of bilateral lower lobe pneumonia and pleurisy (fluid accumulation up to 14 mm deep on the right and 12.5 mm deep on the left), as well as pericarditis (uneven thickening of the pericardium up to 12.3 mm, mainly in the right sections due to fluid content), and pleural effusion (fluid accumulation up to 12.5 mm deep on both sides). The patient was prescribed antibacterial therapy (moxifloxacin 400 mg/day) and intravenous dexamethasone (8 mg/day) in addition to the ongoing therapy. After five days, dexamethasone was replaced with methylprednisolone at a daily dose of 12 mg per os. After five days of glucocorticoids (GCs) and antibiotic treatment, clinical improvement was noted (normalisation of temperature, cessation of pain, reduction in coughing and increased performance), as well as positive dynamics in laboratory and instrumental parameters. A repeat laboratory test showed a decrease in WBC count to 12.33 × 10⁹/L, ESR - to 12 mm/hour and CRP - to 4.34 mg/L.
The results of a repeated Echo, taken just 7 days after treatment began, showed that there was no fluid in either the pericardium or the pleural cavities. Follow-up MSCT of the chest organs revealed CT signs of post-inflammatory changes in the pulmonary tissue of both lungs, with no signs of fluid in the pericardium or pleural cavities. Thus, the final diagnosis was Infarction-like acute myocarditis. Dressler's syndrome (pericarditis, pleurisy and pneumonitis). HF Stage B with preserved LVEF. Given the positive dynamics of clinical, laboratory and instrumental parameters, the patient was discharged from the clinic under the supervision of a cardiologist at their place of residence with the following recommendations:
- restriction of physical activity;
- adherence to a water-salt regimen;
- blood pressure, heart rate, and laboratory tests monitoring;
- echocardiography once a month.
- To continue taking prescribed medication:
- carvedilol 25 mg twice daily;
- eplerenone 25 mg/day;
- esomeprazole 40 mg/day;
- perindopril 10 mg/day;
- torasemide 5 mg once every 7 days;
- methylprednisolone at a dose of 12 mg per day for three months.
Three months later, while continuing treatment, the patient underwent a repeat examination. ECG: normal sinus rhythm at 65 beats/min. Slightly negative T waves in leads II, III, aVF, V5–V6 and biphasic (+/-) T waves in V3–V4 were detected (Figure 5).
The Echo showed that the cavities (LV EDV 117 ml) and walls (0.9 cm) were within normal limits. Valve function and structure were normal. No segmental LV abnormalities were detected. LV contractile function was good (LVEF 61%). LV diastolic function was normal. The pericardial layers no changes without effusion. Laboratory test results: WBC count – 8.32 x 10⁹/L; ESR – 4 mm/h; monocytes – 7.5%; CRP – <4 mg/L; troponin I – 0.15 ng/mL; CK – 80 IU/L; CK-MB – 12.7 IU/L; NT-proBNP – 22.42 pg/mL (reference range < 125). The repeated contrast-enhanced cardiac MRI showed MR signs of post-inflammatory LV myocardial fibrosis (substitutive, mild, more posterior-lateral LV wall). There was no enlargement of the heart chambers, and overall LV contractility was preserved. There were also no signs of inflammatory activity (oedema/inflammatory infiltration of the myocardium) or pathological effusion in the pericardial cavity (Figure 6).
The patient was advised to gradually reduce the daily dose of methylprednisolone until it is withdrawn completely. This was followed by the withdrawal of esomeprazole, torasemide, eplerenone, and perindopril, and a gradual reduction in the dose of carvedilol.
