Measurement of cardiac troponin in serum is an essential part of diagnosing myocardial infarction in the emergency department. The guidelines suggest that high-sensitivity techniques should be used for measuring cardiac troponin I (cTnI) or cardiac troponin T (cTnT). The aim of our study was to correlate the values of both troponins, and to ascertain which type of troponin is more in agreement with the diagnosis. The patients were classified into four groups: 43 patients in non-ST-elevation myocardial infarction (NSTEMI), 7 in ST-elevation myocardial infarction (STEMI), 48 in Type 2 myocardial infarction, and 21 in the control group. A significant correlation between cTnI and cTnT was found in the NSTEMI (r = 0.70) and Type 2 (r = 0.75) groups while in the control group there was no association (r = −0.06). The ratios of cTnI and cTnT relative to their cut-off values were lower in Type 2 myocardial infarction compared to NSTEMI. This difference can be attributed to the pathophysiology of these two types of heart conditions. The ratio in the NSTEMI group was higher in female than in male patients (53.3 vs. 24.6 ng/L); the same difference was found for the ratio of cTnT (20.8 vs. 13.1 ng/L). In the same manner, the ratios in the Type 2 group were higher in female than in male patients for cTnI (25.6 vs. 12.7 ng/L) as well as for cTnT (19.0 vs. 6.73 ng/L). These differences could be due to biological differences, but they could also be influenced by other factors contributing to different damage responses.

Background: Intramyocardial dissecting hematoma (IDH) is a rare but potentially life-threatening complication, most commonly linked to myocardial infarction (MI) but also described in other settings such as cardiac interventions or severe chest trauma. Owing to the limited data on its diagnosis, management, and outcomes, treatment strategies for IDH remain controversial. Case presentation: We present a case of a 53-year-old female who was initially misdiagnosed with Takotsubo cardiomyopathy and later found to have an IDH complicated by anticoagulation dilemmas and infection. Despite initial conservative management, progressive dissection and elevation of inflammatory markers prompted surgical intervention. The patient underwent endoventricular patch repair (Dor procedure), with successful resolution and functional recovery through rehabilitation. Conclusions: This case highlights the importance of keeping IDH in the differential diagnosis, especially in patients with non obstructive coronary findings or unexplained myocardial wall abnormalities. Multimodal imaging, especially cardiac MRI, plays a key role in confirming the diagnosis and determining the extent of dissection. Treatment should be highly individualized, balancing the risks of hematoma expansion against the need for anticoagulation when intracavitary thrombi are present. Infection risk can further complicate the clinical course, necessitating early recognition and intervention. When conservative management is no longer viable, surgical repair—such as the Dor procedure—can stabilize the myocardium and lead to meaningful recovery.