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.