Case introduction
A 35-year-old male patient presented with recurrent precardiac pain without obvious cause 4 months ago. The pain lasted for tens of seconds and was relieved spontaneously. The frequency of pain increased 1 week ago. His blood pressure(BP) was 120/77 mmHg, heart rate 71 beats per minute. His physical examination did not hear heart murmur and friction sound, and no obvious abnormal signs were found. There was no obvious history of heart disease , hypertension and diabetes. However, there was a long-term smoking history of about 10 years, 15 cigarettes /one day, and drinking for 7 years, 100g/ one day. Laboratory examination showed that CK-MB, troponin and brain natriuretic peptide levels were not significantly abnormal. No obvious abnormality was found by echocardiography. ECG showed that the T wave of lead V4-V6 was inverted. Coronary angiography exhibited the wall of the middle segment of the left anterior descending artery and the distal segment of the circumflex artery was irregular, and no obvious stenosis was found. With the consent of the patient and the approval of the hospital ethics committee, ATP stress myocardial contrast electrocardiography (MCE) was used to detect the myocardial microvascular function of the patient.
ATP was injected into the fore arm cephalic vein at 140ug/min/Kg for 6 minutes. Ventricular wall motion, myocardial perfusion, blood flow spectrum of distal anterior descending branch, clinical symptoms, ECG and BP were observed before stress, 2-3 minutes after administration and during recovery period.
During MCE, the amount and speed of ultrasound microbubbles injected each time were the same. The results showed a slight delay in myocardial perfusion in the ventricular septal region at the apex of the heart before stress (at the end of the diastolic period of five cardiac cycles after ”flashing”) (Fig. 1A). At peak period, MCE showed perfusion delay areas decreased (diastolic end of two cardiac cycles after ”flashing”) ( Fig. 1B). Perfusion delay areas showed significantly larger than that before stress in the recovery phase (diastolic end of five cardiac cycles after ”flashing”) (Fig.1C). Coronary blood flow reserve CFR= mean diastolic coronary blood flow velocity before loading/mean diastolic coronary blood flow velocity during peak stress, which was 2.2. The diastolic blood flow spectrum resistance of coronary artery in recovery period was significantly higher than that before stress, showing a ”thumb” spectrum (Fig. 2A and B). The blood flow spectrum velocity integral changed from 17.16cm before stress to 11.93cm in recovery period. There was no obvious abnormality in left ventricular wall motion before stress, peak period and recovery period, and there was no significant change in ECG and BP. The patient had no obvious symptoms before stress and at the peak period, and had chest pain for about 30 seconds in the recovery period, which was similar to ordinary chest pain. No chest pain occurred after clinical treatment with Diltiazem hydrochloride tablets.